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Effect of 6 months of exercise training on cardiovascular and hormonal responses to head up tilt in elderly men and women

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Title:
Effect of 6 months of exercise training on cardiovascular and hormonal responses to head up tilt in elderly men and women
Creator:
Carroll, Joan F
Publication Date:
Language:
English
Physical Description:
xvii, 228 leaves : ill. ; 29 cm.

Subjects

Subjects / Keywords:
Blood pressure ( jstor )
Cough ( jstor )
Endurance ( jstor )
Exercise ( jstor )
False positive errors ( jstor )
Head up tilt ( jstor )
Heart rate ( jstor )
Older adults ( jstor )
Plasmas ( jstor )
Treadmills ( jstor )
Cardiovascular system -- Effect of exercise on ( lcsh )
Dissertations, Academic -- Exercise and Sport Sciences -- UF
Exercise and Sport Sciences thesis Ph.D
Exercise for the aged ( lcsh )
Hypotension, Orthostatic -- Effect of exercise on ( lcsh )
Treadmill exercise tests ( lcsh )

Notes

Thesis:
Thesis (Ph.D.)--University of Florida, 1992.
Bibliography:
Includes bibliographical references (leaves 208-227).
General Note:
Typescript.
General Note:
Vita.
Statement of Responsibility:
by Joan F. Carroll.

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Source Institution:
University of Florida
Holding Location:
University of Florida
Rights Management:
Copyright [name of dissertation author]. Permission granted to the University of Florida to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
Resource Identifier:
001751602 ( ALEPH )
26529405 ( OCLC )
AJG4538 ( NOTIS )

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EFFECT OF 6 MONTHS OF EXERCISE TRAINING ON CARDIOVASCULAR
AND HORMONAL RESPONSES TO HEAD UP TILT IN ELDERLY MEN
AND WOMEN











BY


JOAN F. CARROLL


DISSERTATION PRESENTED TO THE GRADUATE SCHOOL
THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY

























This work is dedicated to my parents who always believed in me, and to my
husband, who helped me accomplish my goals.













ACKNOWLEDGEMENTS


A project of the magnitude and scope of this could not have been

accomplished without the cheerful and endless assistance from a great


number of individuals.


First and foremost, I would like to thank all those


who helped conduct the tilt tests and associated laboratory analyses: Lindsey


Reider, Keith Engelke, Mike Welsch,


Jennifer Gulick,


Lynn Panton, Linda


Garzarella, Brian Elliott, Judson Bruno, Evan Korn, Kevin Kenney, Dr. Jay


Graves, Dr. Marie Knafelc, and Dr. Greg Guillen.
the project could not have succeeded. Special tha


Without their dedication,


inks go to Brian Elliott and


Judson Bruno, who spent many long hours on data verification and


computer data entry.


Many thanks also go to all the undergraduate and


graduate students who assisted with the training of our subjects over the

course of this project.

I would also like to thank all those who helped me learn the

techniques of plasma volume and hormone analysis: Dr. Charles Wood,


Maureen Keller-Wood, Christine


Taranovich


, Curt Kane, Anne Bowers, and


"Mike"


Merz.


Their help and friendship over many months enabled me to


complete a sometimes frustrating task.


Thanks also go to Michelle Wiltshire-


Clement and Anne Bowers for their work in completing hormone analyses.


A most sincere thanks you goes to Carolyn Hansen,


who despite the








Finally, I would like to thank the members of my committee--Drs.


Michael L. Pollock


, James E. Graves,


Victor A. Convertino, Charles E.


Wood


and David T


Lowenthal--for their help in launching the project and in


bringing this manuscript to fruition.


I am indebted to all of them for the time


and dedication they put forth on this project; I also owe a special thank you to


Drs.


Wood and Convertino for their helpful evaluations of this manuscript


in its final weeks.


Finally, I offer special thanks to my committee chair, Dr.


Michael L. Pollock, for all his help and assistance during the last four years,

and for his work on this manuscript.















TABLE OF CONTENTS


ACKNOWLEDGEMENTS ...................................................... ... .......... .. ............................111

LIST OF TABLES........... ........ .............................................................................v

LIST OF FIURES .................................................. .................. ... .. ... x

ABSTRACT..............................................................................................................xv

CHAPTERS


Statement of the Problem
Research Hypothesis.........
Justification ........................
Assumptions.......................
Delimitations ............. .........
Limitations.......................
Definition of Terms.............


REVIEW OF LITERATURE ..... .. .. ....... ..a ... ...... ..... ........ ...... ...... ... ......12


Introduction.


Responses to Endurance Training..............................
Resting Heart Rate (HR), Stroke Volume (SV) a
O utput (Q )...........................................................
Blood Pressure (BP) .............................................
Mamimal Aerobic Power.......................................
Increase in Strength and Muscle Mass...................
Responses to Strength Training ..................................
Hormonal, and Blood/Plasma Volume Responses


Resting Values..... ........................-.........................
Blood / Plasma Volume. ..............................................................


nd Cardiac


. Traini..ng..:0 .. .. .... ...
. .. 0 .. .. 000 .. .' .. a. a..
to Training:


....... ..22
......... .22


INTRODUCTION ...........~...~.....~......~.......~... 1


.....,.......'12









Cardiovascular, Hormonal, and Plasma


Volume Responses to


Tilt: Pre- and Post-training .....................................................t..,............35
Heart Rate, Stroke Volume, Cardiac Output, and Blood


Pressure................................................................... ................
Blood/Plasm a Volum e ................................................ ........................


Vasoactive


......36
......40


Hormones...................................


Hormones Associated with Fluid Volume Control:
Aldosterone (ALDO)..................................................
Adrenocorticotropic Hormone (ACTH).....................


Protein (PROT),


Sodium (Na+) and Potassium (K+)..


Mechanisms Potentially Responsible for Changes in Orthostatic
R esponses................ .......................................... ..... ............ ...........................
Plasma Volume Change........ ........ .................................................
Muscle Mass Changes ................................................................
Changes in Baroreceptor Sensitivity ...........................................
Altered Hormonal Response .....................................................
Summar y ....................... ...............................................................


Subjects.... ....................... .................................. ............... ...
Type of Data Needed ..... ...........................................
Methods of Data Collection ....................................
Maximal Oxygen Uptake (VO2max) Test............


Tilt Table


Strength


Test...................


Testing.............


Body Composition........... ..................... ...............................
Blood Sample Analyses..............................................
Training ...... .... ......... ..................................................... ........
Data Analysis ....................................................................
Dependent measures............................... ...................
Statistical analyses........... ...................................................


RESUL


Subject Characteristics ......................................................................
Training Responses................................... ...... ................ ............
Maximal Oxygen Uptake.......................................................
Strength................. ........................... ...................................
Body Composition...................................................................


Cnrrinvacnilar RPCnnncpC 1n


Tilt


-C.-


TS ~...~ .................. ..~...~....... ...~.......... ..~~....~~..~... ~~~.~.~~.. ................ ................77


IMIETHOLXILOGY .............~.................~...~~...


...


........................................








Responses of Subject Experiencing Presyncopal Symptoms................
Responses to the Cough Test.......................................................................
Analyses to Average Data .....................................................................
Analyses of Cough Responses.............................. ...........................
Analyses of Beat by Beat Data................................................................


..114
..134
..134


Introduction..


Exercise Training and Cardiovascular Responses to Head-up Tilt.......
Heart Rate, Stroke Volume, and Cardiac Output................................
Possible M mechanism s............ ............... ...................................... .................


Exercise


Exercise


Training, Resting Plasma


Volume and Resting


Training and the Hormonal and Plasma


Volume


Response to Head-up Tilt.............................................................
Responses of Fainters..........................................................................
Stroke Volume and Cardiac Output.... .... .................. ............
Blood Pressure.................................................................. ........
Hormonal Responses........... ............. ............ ..................... ..........


Responses to Cough T
Conclusions..................


Directions for Future Research


DEMOGRAPHIC, MEDICAL AND ACTIVITY


QUESTIONNAIRES......


INSTITUTIONAL REVIEW BOARD


**t******* 55......... ...,,........... 1 62


APPROVAL LETTER..................181


D DATA COLLECTION FORMS FOR TILT TEST................... ....... .............. 183

E INDIVIDUAL FAIN TERS' DATA................................................................ 188

LIST OF REFERENCES ...............................................................................................208

BIOGRAPHICAL SKETCH.........................................................................................228


'est. ..................~ ,,,,,,..,,,, .................~ ......~~....~.~..~


DISCUSSION AND CONCLUSIONS ................... ................... ...............~.~. ,146


)-Iormonal Responses...............~.............~.


APPENL)ICES ,,..,,..,,,,, ,,..,,..,,,,,, ,..,,.,.,,,,,, ..,,.,,..,,,, ,,..,,


INFORMED CONSENT L~CUMENT .,..,,,,.,,,, ,,,..,,,,,,,, ..................1 '73














LIST OF TABLES


Table


Page


Characteristics of Control,


Treadmill


and Treadmill/Resistance


Training Groups at the Start of 6 Months of Exercise Training.


VO2max


(ml*kg-1 min-1) Responses of Control,


Treadmill,


and Treadmill/Resistance Groups Before (Ti) and After(T3) 6


Months of Exercise


Training.................


Strength


Testing Scores of Control,


Treadmill, and


Treadmill/Resistance Groups Before (T1) and After (T3) 6
M months of Exercise Training ...............................................

Body Composition Measurements for Control, Treadmill,
Treadmill/Resistance Groups Before (T1) and After (T3) 6


and


Months of Exercise


Overall Heart Rate


Stroke Volume


, Cardiac Output, Blood


Pressure and Peripheral Resistance Response to
Over Groups and Tests ......................... .............


Tilt, Averaged
". ..... .. ...'... **...'4 ....'.''8 5


Analyses to Average Data: Type I Error Rates for Detecting a


Time Effect Within Each Time Period for Heart Rate,
Volume, Cardiac Output, Blood Pressure, and Total


Peripheral Resistance ...................................


Averaged Heart Rate and Stroke Volume Responses to 700


Head-up Tilt for Control,


Stroke


....................o..........o.............87


Treadmill, and


Treadmill/Resistance Groups Before (T1) and After (T3) 6


Months of Exercise


Training...............


Averaged Cardiac Output Responses to 70


Head-up


Tilt for


Control,


Treadmill


, and Treadmill/Resistance Groups Before


(TI) and After (T3) 6 Months of Exercise Training................


............... 2


........77


.........78


Training .....~............. ~~.~...~...... ....~~.....


...................88


.............~~89








4-10


Averaged Mean Arterial Blood Pressures and Total
Peripheral Resistance Responses to 700 Head-up Tilt for


Control,


Treadmill, and Treadmill/Resistance Groups Before


(T1) and After (T3) 6 Months of Exercise Training.............


4-11


Effect of Training on Supine Resting Heart Rate,


Stroke


Volume, Cardiac Output, Blood Pressure, and Total


Peripheral Resistance Measurements for Control,


Treadmill


and Treadmill/Resistance Groups Before (T1) and After (T3) 6


months of Exercise


Training...................


4-12


Wilks'


Lambda Values for 2 X 3 X 11 (Test X Group X Time)


Repeated Measures Analysis for Heart Rate, Stroke Volume,
Cardiac Output, Blood Pressure, and Peripheral Resistance


Responses to 70


Head-up


Tilt ....


4-13


Analysis of the Effect of 6 Months of Exercise Training on the
Relative and Absolute Change in Stroke Volume and Cardiac


Output from Rest to 700 Head-up


Tilt for Control


, Treadmill,


..........98


and Treadmill/ Resistance Groups. ....... ................... ...... ..............


4-14


Post Hoc Analysis for


Time Effect to Detect Changes in Heart


Rate, Stroke Volume, and Cardiac Output as a Result of 700


Head-up


4-15


4-16


Tilt .........


Post Hoc Analysis for Time Effect to Detect Changes in
Systolic, Diastolic, and Mean Arterial Pressure as a Result of
70 H ead-up Tilt .............................. .... .... ............... ........................ ...102


Post Hoc Analysis for Time Effect to Detect Changes in Total


Peripheral Resistance as a Result of 70 Head-up Tilt


........................103


Responses of Plasma
Volume to 700 Head-i
Months of Exercise Tr


Volume, Blood Volume, and Red Cell
ip Tilt Before (T1) and After (T3) 6
raining in the Control and Exercise


Training Groups .... ........ ...


4-18


.................105


Probabilities for Type I Error in Detecting a Change in Plasma
Volume, Blood Volume and Red Cell Volume as a Result of


Head-up


Tilt or Exercise


3'rainirtg..... ...


......106


4-19


Hemoglobin and Hematocrit Measurements at Rest and


rtlL~, flnta.. In~ PTri ... Al,. It C~ n


........92


.......6. .... .......4................... ..... .... 94


4-17


..................91


......~...100


n,.~,, u,, 1








4-20


Probabilities for


Type I Error in Detecting a Change in


Hemoglobin and Hematocrit as a Result of 700 Head-up


Before (TI) or After (T3) 6 Months of Exercise


4-21


Percent Change in Plasma


Volume


, Blood Volume, and Red


Cell Volume During 700 Head-up Tilt Before (T1) and After
(T3) 6 Months of Exercise Training in the Control and


Exercise Training Groups ........................................

Hormonal/Electrolyte Response to 700 Head-up


and After 6 Months of Exercise
Exercise Training Groups ..........


...... .......... ...............109

Tilt Before


Training in the Control and


.........111


Probabilities for Type I Error in Detecting a Change in
Hormone Concentration as a Result of 70 Head-up Tilt
Before (Tl) or After (T3) 6 Months of Exercise Training ........................112


4-24


Heart Rate Responses of Fainters (F


n=4)


(NF; n=24) to 700 Head-up Tilt Before (T1),


mnd Nonfainters
After 3 Months


(T2), and After 6 Months (T3) of Exercise Training.


Stroke Volume Responses of Fainters (F; n=4) and
Nonfainters (NF; n=24) to 700 Head-up Tilt Before (T1), After


3 Months (T2),


and After 6 Months (T3) of Exercise Training.........116


4-26


Cardiac Output Responses of Painters (F,


n=4) and


Nonfainters (NF; n=24) to 700 Head-up Tilt Before (T1), After


3 Months (T2), and After 6 Months (T3) of Exercise


Training


Systolic and Diastolic Blood Pressure Responses of Painters
(F; n=4) and Nonfainters (NF; n=24) to 700 Head-up Tilt


Before (TI), After 3 Months (T2),


and After 6 Months (T3) of


Exercise Training...........................................................................

Mean Arterial Blood Pressure and Total Peripheral
Resistance Responses of Fainters (F; n=4) and Nonfainters


n=24) to 700 Head-up


(T2),


and After 6 Months (T3) of Exercise


Comparison of Subject Characteristics,


Training................


Aerobic Capacity,


Strength, and Body Composition of Nonfainters (n=24) vs.
Painters (n=4) Prior to Exercise Training............................................1....30


4-23


4-25


4-27


4-28


4-29


Tilt Before (T1), After 3 Months


'Iiaining ................... 1 09


~~..~~..~...115








4-31


Overall Responses to


Three Supine and Three


Tilt Cough


Trials


, Values Averaged Over Tests and Groups...............................1...35


4-32


Analyses to Average Cough Data:
Detecting a Difference Among the


Type I Error Rates for
Three Cough Trials for


4-33


Mean Supine and Tilt Cough


Variable


Treadmill, and Treadmill/Resistance


Averaged Over


Values for Control,
Training Groups


Three Supine and Three 700 Head-up


Cough Trials Before (T1) and After (T3) 6 Months of Training


4-34.


Summary of the Effect of Tilt and Training on the Responses


to the Cough Test...............


4-35


Heart Rate Values Averaged Every Five Beats for 40 Beats


Post-Cough for Control,


Treadmill, and Treadmill/Resistance


Groups for Supine and 700 Head-up Tilt Cough Tests Before
(T1) and After (T3) 6 Months of Training ............................................


4-36


Probabilities for Type I Error for Detecting a Difference in
Heart Rate Values at Each Time Point Post-Cough During


Supine and 700 Head-up


Tilt Cough Tests Before (Ti) and


After (T3) 6 months of Exercise Training


4-37


Heart Rate Response to Supine and 700 Head-up


Tilt Cough


Tests Before (T1) and After (T3) 6 Months of Exercise


Training,


Values Averaged Over Groups for Every Five Beats


for 40 Beats Post-Cough


Supine and Tilt Cough Tests ...........~.........~..................


....~...........~..~..~.~.~~140













LIST OF FIGURES


Table


Page


Mean test responses of control (CONT),


treadmill (TREAD),


and treadmill/resistance (TREAD/RESIST) groups to 700
head-up tilt before (Tl) and after (T3) 6 months of exercise


training: a) stroke volume (SV)


b) cardiac output (Q)..


Percent change (A) in mean test response from prior to
exercise training (T1) to after (T3) 6 months of exercise


training in control (CONT),


treadmill (TREAD),


treadmill/resistance (TREAD/RESIST) exercise groups: a)
mean test stroke volume (SV) and b) mean test cardiac


output (Q).......................


Responses of fainters vs. nonfainters to 700 head-up tilt prior
to exercise training: a) heart rate (HR); b) stroke volume (SV);


c) cardiac output (


......................................................97


.....120


Responses of fainters vs.


nonfainters to 700 head-up tilt after


3 months of exercise training: a) heart rate (HR); b) stroke
volume (SV); c) cardiac output (Q)...........................................................1

Responses of fainters vs. nonfainters to 700 head-up tilt after
6 months of exercise training: a) heart rate (HR); b) stroke


volume (SV)


Responses of fainters vs.


nonfainters to 700 head-up tilt


before exercise training: a) systolic blood pressure (SBP); b)
diastolic blood pressure (DBP); c) mean arterial pressure
(M A P )..............................................................................................


Responses of fainters


vs. nonfainters to 700


head-up tilt after


3 months of exercise training: a) systolic blood pressure (SBP);


b) diastolic blood pressure (DBP)


c) mean arterial pressure


-l a a -


Q)


.~.........~~..~~.. ~.96


c) cardiac output(Q).. ...~~........~~.....~...................








b) diastolic blood pressure (DBP); c) mean arterial pressure
(MAP)..........................................................................................................126


4-10


4-11


Total peripheral resistance response of fainters vs.
nonfainters to 700 head-up tilt: a) before exercise training; b)
after 3 months of exercise training; c) after 6 months of
exercise training. ........................................................................................127

Hormonal responses of fainters and nonfainters to supine
rest (pretilt) and 700 head-up tilt before (T1) and after (T3) 6
months of exercise training: a) vasopressin (AVP); b)
adrenocorticotropic hormone (ACTH). .............................................134

Heart rate (HR) response to cough test in supine and 700
head-up tilt positions by control group before (T1) and after


(T3) 6 month training protocol......


4-12


4-13


Heart rate (HR) response to cough test in supine and 700
head-up tilt positions by treadmill exercise group before (Tl)
and after (T3) 6 month training protocol.....................................


Heart rate (HR) response to cough test in supine and 700
head-up tilt positions by treadmill/resistance exercise group
before (Ti) and after (T3) 6 month training protocol................


Relationship between the relative change in resting plasma
volume and the relative change in the HR response to tilt ..


Responses of female fainter A to 700 head-up tilt before (T1),
after 3 months (T2), and after 6 months (T3) of exercise
training: a) heart rate (HR); b) stroke volume (SV); c) cardiac


output (


Percent change (A) from supine rest in response to 700 head-
up tilt in female fainter A before (T1), after 3 months (T2), and
after 6 months (T3) of exercise training: a) heart rate (HR); b)


stroke volume (SV); c) cardiac output (Q)......


Blood pressure responses of female fainter A to 700


head-up


tilt before (T1), after 3 months (T2), and after 6 months (T3) of


exercise training: A) systolic (SBP)


b) diastolic (DBP); c) mean


arterial (MAP) uressure..............................................


......190


........................................


Q)


.........143








training: a) systolic (SBP); b) diastolic (DBP); c) mean arterial
(M A P) pressure ...... .... ................................ ................................


Total peripheral resistance (TPR) response of female fainter A
to 70 head-up tilt before (T1), after 3 months (T2), and after 6
months (T3) of exercise training: a) absolute response; b)
percent change (A) from supine rest... ................... ...........................


Responses of female fainter B to 70 head-up tilt before (TI),


after 3 months (T2), and af
training: a) heart rate (HR)


ter 6 months (T3) of exercise
; b) stroke volume (SV); c) cardiac


output (


Percent change (A) from supine rest in response to 700 head-
up tilt in female fainter B before (T1), after 3 months (T2), and
after 6 months (T3) of exercise training: a) heart rate (HR); b)
stroke volume (SV); c) cardiac output (Q).....................................


Blood pressure responses of female fainter B to 70 head-up
tilt before (Tl), after 3 months (T2), and after 6 months (T3) of


exercise training: A) systolic (SBP)
arterial (MAP) pressure................


b) diastolic (DBP)


c) mean


Percent change (A) from supine rest in blood pressure
response to 700 head-up tilt in female fainter B before (T1),
after 3 months (T2), and after 6 months (T3) of exercise


training: a) systolic (SBP)


E-10


E-11


b) diastolic (DBP); c) mean arterial


(M A P) pressure .................................... ............................. ..........

Total peripheral resistance (TPR) response of female fainter B
to 70 head-up tilt before (T1), after 3 months (T2), and after 6
months (T3) of exercise training: a) absolute response; b)
percent change (A) from supine rest. ................................................

Responses of male fainter A to 700 head-up tilt before (T1),
after 3 months (T2), and after 6 months (T3) of exercise
training: a) heart rate (HR); b) stroke volume (SV); c) cardiac


output (


E-12


Percent change (A) from supine rest in response to 70 head-
up tilt in male fainter A before (T1), after 3 months (T2), and


ra jvrn -is -. a ~e /TTI


I -'


..........191


Q)


Q)








exercise training: A) systolic (SBP)
arterial (MAP) pressure..................


E-14


b) diastolic (DBP); c) mean


.........200


Percent change (A) from supine rest in blood pressure


response to 700 head-up tilt in male fainter A


before (TI),


after 3 months (T2), and after 6 months (T3) of exercise


training: a) systolic (SBP)


b) diastolic (DBP)


c) mean arterial
.......................................201


(MAP) pressure................................ .................


E-15


E-16


Total peripheral resistance (TPR) response of male fainter A
to 700 head-up tilt before (T1), after 3 months (T2), and after 6
months (T3) of exercise training: a) absolute response; b)
percent change (A) from supine rest.............. .................................202


Responses of male fainter B to 700 head-up tilt before (T1),
after 3 months (T2), and after 6 months (T3) of exercise
training: a) heart rate (HR); b) stroke volume (SV); c) cardiac


output (


E-17


Q )" ................ ..................0.... 0. ......0..... ............


...... ..~....... ... .. ...... 203


Percent change (A) from supine rest in response to 700 head-
up tilt in male fainter B before (Ti), after 3 months (T2), and
after 6 months (T3) of exercise training: a) heart rate (HR); b)


stroke volume (SV); c) cardiac output (Q)


E-18


........204


Blood pressure responses of male fainter B to 700 head-up tilt
before (Ti), after 3 months (T2), and after 6 months (T3) of


exercise training: A) systolic (SBP)
arterial (MAP) pressure..................


E-19


b) diastolic (DBP); c) mean


Percent change (A) from supine rest in blood pressure


response to 700 head-up tilt in male fainter B


before (T1),


after 3 months (T2), and after 6 months (T3) of exercise


training: a) systolic (SBP)


E-20


b) diastolic (DBP); c) mean arterial


Total peripheral resistance (TPR) response of male fainter B
to 700 head-up tilt before (T1), after 3 months (T2), and after 6
months (T3) of exercise training: a) absolute response; b)
percent change (A) from supine rest...................................................207


(MAP) pressure. ...........,....... ..... ..................~ ................... .......













Abstract of Dissertation Presented to the Graduate School
of the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Doctor of Philosophy


EFFECT OF 6 MONTHS OF EXERCISE TRAINING ON CARDIOVASCULAR
AND HORMONAL RESPONSES TO HEAD UP TILT IN ELDERLY MEN


AND


Joan F


May


WOMEN


Carroll


1992


Chairman:


Michael L. Pollock


Ph.D.


Major Department:


Exercise and Sport Sciences


To evaluate the effect of 6 months of exercise training on heart rate,


stroke volume (SV),


cardiac output (Q),


blood pressure, and hormonal


responses to head-up tilt (HUT), 22
assigned to treadmill exercise (TREA


women and 11 men (60 to 82 years) were

AD; n = 14), treadmill plus resistance


exercise (TREAD/RESIST; n


= 10), or non-exercising control (n


= 9) groups.


Tilt testing before (T1) and after (T3) training consisted of 30 minutes of


supine rest, 15 minutes of 700


HUT, and 15 minutes of supine recovery.


Plasma volume (PV), aldosterone (ALDO),


vasopressin (AVP),


,A -YA ,~ .AL -AlH n t A s~ a a A "TLT .1 an. -I: a aL~ -: ( f A \








protein (PROT) were measured after 30 minutes of supine rest.
were also measured after 15 minutes of HUT.
Training increased maximal aerobic power in TREAD and


Hormones


TREAD/RESIST by 16.4% and 13.


, respectively (p


< 0.05).


TREAD decreased


body weight and skinfold measurements while


elbow flexion and extension strength (p


TREAD/RESIST increased


< 0.05).


Resting SV


Q increased 20.6% and 13.4%,


0.01); resting Q decreased 9.1


respectively,


in TREAD/RESIST (p


0.05).


in TREAD


Average tilt


test SV


and Q increased 15.0


and 9.3


, respectively, in TREAD; average test


Q decreased 9.8% in TREAD/RESIST (p


0.05).


The combined training group


increased PV by 9.5%,


while resting plasma levels of ACTH,


AVP


ALDO


Na+


PROT


, and EPI were not changed with training.


Four subjects


experienced presyncopal symptoms at T1 associated with large increases in


ACTH and AVP


Improved responses at T3 may be related to increased SV


and Q.
The results suggest a) endurance training increases resting and


orthostatic SV


resting and orthostatic Q.
related to changes in PV


while endurance plus resistance training decreases


The difference between training groups may be
and venous return; b) PV increases with training in


the elderly but resting hormonal levels are unchanged, suggesting a change in
the stimulus-response relationship between blood volume and hormone
secretion via volume sensitive cardiopulmonary receptors; c) training


improves responses of older,


intolerant subjects to tilt, mediated by increased












CHAPTER 1
INTRODUCTION


Changing demographics in the United States in the latter half of the 20th


and into the early


21st century indicates that persons over the age of 65 comprise


the fastest growing segment of the population.


In 1980


of the population


was over the age of 65 but this proportion is expected to increase to 18% by the


year 2030 (Abrams & Berkow, 1990).


When the elderly population is further


delineated, it can be seen that the oldest group in our society (85+ years) has


increased by 24.8


since 1980.


During this period,


the 75-84 year old group grew


while the 65-74 year old group increased by 11


In absolute numbers,


there are expected to be 34.9 million elderly by the year 2000, an increase of


over 1987 (Beck, 1989).


Thus, an understanding of the physiological


changes associated with aging and how these changes impact on homeostatic
responses in older persons takes on a great deal of importance.

Changes in the cardiovascular system that are associated with aging may
predispose older individuals toward disorders of blood pressure (BP) control


mechanisms.


Acute BP changes are buffered by the high-pressure carotid and


aortic baroreflex system.


In the elderly, an attenuation of baroreflex sensitivity


has been attributed to a decrease in arterial compliance, which results in a
decreased deformation of the baroreceptors during a given pressure change


(Lipsitz, 1990) and thus an attenuated afferent signal.


There may also be a





2

aging change that limits the ability of the senescent heart to increase end-diastolic
volume (EDV) and/or decrease end-systolic volume (ESV); this results in a
decreased ability to compensate for declines in cardioacceleration capacity by
way of an increase in stroke volume (SV) (Shannon, Maher, Santinga, Royal, &


Wei, 1991).


Finally, either a decrease in f3-receptor sensitivity in the peripheral


vasculature or a decrease in vascular compliance may lead to diastolic BP or
peripheral resistance responses to orthostasis that are not easily modified


(Sowers,


1987).


The neuroendocrine system is also altered with age.


There is a decrease in


the secretary rate and plasma concentration of aldosterone when sodium intake


is unrestricted


there is also a decline in aldosterone secretion in response to


sodium restriction (Gregerman & Bierman,


1981


McGinty, Stem, & Akshoomoff,


1988).


This decline parallels the decline in basal levels of renin activity.


Although vasopressin levels may not be affected by aging, the ability of the
kidney to concentrate urine is decreased due to a decrease in glomerular


filtration rate rather than to a decrease in sensitivity to vasopressin.


These


changes might be expected to decrease the body's ability to augment plasma


volume (PV) with endurance training.


Vasoconstrictive responses may also be


affected: although there is an increase in plasma norepinephrine concentration
with age, there is a diminished vascular contractile response (Gregerman &


Bierman, 1981


McGinty et al.,


1988).


This, together with the decrease in renin


activity, may affect the ability of the senescent vasculature to adequately respond
to hypotensive stimuli.
One manifestation of aging changes is the presence of orthostatic








estimates a 20 to 30% rate of postural hypotension in the noninstitutionalized


elderly.


These rates, however, may reflect the presence of risk factors associated


with postural hypotension (hypertension, varicose veins, central nervous system
disorders, certain medications); the presence of postural hypotension in the
healthy elderly may be lower than this (Dambrink & Wieling, 1987; Mader,


Josephson, & Rubenstein,


1987).


In younger populations, there have been both cross-sectional and
longitudinal studies that have sought to determine the factors associated with
orthostatic intolerance and the best training regimen to improve the responses to


orthostasis.


A training-induced hypervolemia has been hypothesized as a


mechanism for improving cardiovascular responses to an orthostatic stress.
Convertino, Montgomery, and Greenleaf (1984) found that a decrease in the HR
and rate-pressure product responses to a 600 head-up tilt after 8 days of cycle


ergometer training correlated significantly (r


increase in blood volume.


= -0.68) with a training-induced


Similarly, Shvartz, Convertino, Keil, and Haines


(1981) found that improvement in tilt tolerance and a decreased HR response to
head-up tilt after training was related to an increased PV.
An increase in muscle mass is another mechanism hypothesized to help


improve responses to orthostasis.


According to this theory, an increase in muscle


mass or tone limits venous pooling during orthostasis and thus better maintains


venous return, cardiac output (Q), and arterial pressure.


Support for this theory


was provided by several studies showing that postural hypotension in response
to simulated microgravity was associated with decreased musculature,
particularly in the lower extremities, and increased compliance in the leg





4

found that 3 months of gymnastic training on "heavy apparatus" was superior to
volleyball and general conditioning for improving the systolic BP and pulse
pressure response to a 10-minute standing test. It was hypothesized that an
increase in abdominal muscle strength in the gymnastics group could explain the

results; however, abdominal strength was not measured. In the later study
(1969), Shvartz found that a 7-week program of upper body resistance-type
exercises was superior to a program of bench-stepping for improving the systolic


BP and pulse pressure response during head-up tilt.


This appeared to indicate


that some mechanism involved in the adaptation to resistance training was
responsible for the improvement, but no explanatory mechanisms were offered
by the author.
A third mechanism proposed to improve responses to orthostasis is an


increase in baroreceptor responsiveness.


This refers to the HR increment


resulting from a given arterial pressure decrement.


Several recent cross-sectional


studies have compared the baroreceptor response of weightlifters and
endurance-trained subjects to lower body negative pressure and/or a


phenylephrine infusion (Smith, Graitzer, Hudson, & Raven,


Raven, 1986).


1988; Smith &


Both investigations have found that the peripheral resistance


response of the two groups was similar and concluded that the more effective
maintenance of BP in the weight-trained individuals was due to an enhanced


baroreceptor sensitivity.


Weight training may therefore play a role in improving


responses to orthostasis either by increasing baroreceptor responsiveness and/or
by increasing muscle mass.
Finally, altered neuroendocrine secretion or altered vascular sensitivity to








1988; Convertino, Brock, Keil,


Bernauer, & Greenleaf, 1980; Convertino, Keil, &


Greenleaf, 1983; Convertino, Mack, & Nadel, 1991


Wade, Dressendorfer,


O'Brien, & Claybaugh, 1981), norepinephrine often decreases (Hagberg, Montain,


Martin, & Ehsani,


1991).


1989b; Kiyonaga, Arakawa, Tanaka, & Shindo, 1985; Tipton,


This is thought to reduce BP responses through decreases in HR and Q.


Altered vascular sensitivity to pressor hormones, in particular an increased (3-
adrenergic receptor sensitivity, may also play a role in altering responses to


orthostasis after training (Wiegman, Harris,


Joshua, & Miller,


1981


Wiegman,


1981).
Whether physical training can improve the responses to an orthostatic
stress in the elderly is not known. Some of the components involved in the reflex
responses to orthostasis may be irreversibly altered in the elderly (e.g., aortic


distensibility, 13-adrenergic sensitivity, cardiac and vascular compliance).


In the


young, an improved response to tilt after training consists of a decrease in HR
and rate-pressure product associated with an increase in PV (Convertino et al.,


1984; Shvartz et al.,


1981).


However, in the elderly, the HR and systolic BP


responses to tilt are already attenuated (Dambrink & Wieling, 1987; Jansen,


Lenders, Thien, & Hoefnagels,


1989; Kenny, Lyon, Bayliss, Lightman, & Sutton,


1987), due possibly to a decrease in the sensitivity of the baroreflex response


(Gribbin et al.


,1971).


An improved response to tilt in the elderly after training


may therefore involve increases, rather than decreases, in HR or systolic BP. It is
possible that an increase in muscle mass after training would increase the systolic


BP response to tilt through an improved venous return and SV


However, there


may be a limit to the effect of this mechanism due to a decrease in left ventricular








1988).


Finally, there may be a limit to the role that increased PV can play in the


improvement in venous pressure because of impaired renal sodium conservation
in the elderly (Gregerman & Bierman, 1981; Mader, 1989).


Based on the data from investigations with younger subjects,


it appears


that promising modes of training for the improvement in orthostatic responses


are either weight training (Shvartz,


1968a


1968b


, 1969; Smith et al.,


1988; Smith &


Raven


, 1986), or endurance training with a resistive component, such as cycling


(Convertino et al., 1984; Greenleaf, Brock, Sciaraffa, Polese, & Elizondo, 1985;


Shvartz et al.


,1981) or uphill treadmill walking.


Endurance exercise training


with a resistive component for the elderly would combine some of the
advantages of endurance and resistive training alone while eliminating some of


the disadvantages.


Endurance exercise training can improve aerobic capacity


(VO2max) in the elderly an average of 15-30% (Adams & deVries,


1973; Hagberg


et al.


, 1989b; Meredith et al.,


1989; Seals, Hagberg, Hurley, Ehsani,


& Holloszy,


1984).


It can also cause a beneficial change in body composition (Graves, Panton,


Pollock, Hagberg, & Leggett, unpublished), and a decrease in resting BP


(Cononie et al.


1991


Hagberg, 1990; Hagberg & Seals,


1987), particularly in those


who are hypertensive (Hagberg, Montain, & Martin, 1987; Hagberg et al.,


1989b).


Finally, endurance training is associated with increases in PV (Convertino et al.,


1984; Oscai, Williams, & Hertig, 1968; Shvartz et al.,


1981) although this effect has


not been verified in older subjects.

One disadvantage of endurance training in the elderly is that elderly
women appear to be more susceptible than elderly men to orthopedic injury
related to high impact endurance activities such a jogging and fast walking





7

reduce injury occurrence in the elderly while providing an adequate stimulus for


an increase in aerobic capacity (Hagberg et al.,


1989a) and an increase in leg


strength (Pollock et al.,


1991).


It is possible that muscle atrophy in the sedentary


elderly is marked and that uphill treadmill walking would provide enough
stimulus to improve muscular strength and thus improve the cardiovascular

responses to orthostasis through enhanced venous return.

Resistance training induces increases in muscular strength in the elderly


(Fiatarone et al


., 1990; Frontera, Meredith, O'Reilly, Knuttgen, & Evans,


1988;


Kauffman, 1985; Perkins & Kaiser, 1961) and may be beneficial in ameliorating


the effects of decreased muscle mass on postural hypotension.


Resistance


training may also improve responses to orthostasis by an increase in


baroreceptor sensitivity (Smith et al.,


1988; Smith & Raven,


1986).


A training


program combining resistance training and uphill walking may therefore
provide optimal fitness and health benefits while minimizing injuries.


Statement of the Problem


Most researchers investigating the effect of training on orthostatic
responses have used young to middle-aged populations (Beetham & Buskirk,


1958; Convertino et al.,


1984; Greenleaf et al.,


1985; Greenleaf et al.,


1988; Shvartz


et al.


,1981).


No research has been conducted to date to determine whether any


form of physical training can help improve the responses to an orthostatic


challenge in the elderly.


Consequently, different types of training programs


using elderly subjects need to be conducted.
The specific aims of this research are a) to describe the cardiovascular and





8

uphill walking or a combination of uphill walking plus selected resistance
training exercises can improve the cardiovascular responses of elderly
individuals to a 700 head-up tilt; and c) if orthostatic responses improve, to
evaluate the mechanisms involved in the improvement.


Research Hypothesis

It is hypothesized that uphill treadmill walking of an intensity sufficient to
induce significant changes in aerobic capacity and/or resistance training of an
intensity to increase muscular strength of the arms and legs will result in positive


adaptations in the cardiovascular responses to an orthostatic stress (700


tilt).


head-up


It is also hypothesized that one or more of the following training


adaptations will correlate with the adaptations in orthostatic responses:


increased lower body muscle mass and/or strength, an increased PV


increased


baroreceptor responsiveness, and/or changes in pressor hormone secretion.


justification


The increase in the elderly population in the United States and the
increased cost of medical and pharmacological intervention to ameliorate the
effects of aging underlines the importance of less costly interventions in the


treatment of aging manifestations.


In younger populations, there have been


some promising results indicating that exercise training can improve the


cardiovascular responses to orthostatic stresses (Convertino et al.,


1984;


Greenleaf et al


., 1985; Shvartz 1968a


, 1969; Shvartz et al.,


1981).


Yet the effect of


exercise training


on orthostatic responses has not been investigated in older





9

investigated in other populations of elderly, e.g., those with documented

orthostatic hypotension. Ultimately, exercise training may prove to be an
alternative treatment for physiologic (aging-related) occurrences of orthostatic

hypotension.


Assumptions

1. All laboratory equipment will yield accurate, reliable results over the
course of repeated testing.

2. Subjects will follow instructions given to them regarding food, drink,
and drug intake prior to testing.

3. Subjects will follow instructions given to them regarding the
maintenance of current lifestyle (e.g., diet and exercise) outside of the
prescribed program.


Delimitations

The following delimitations were imposed:

1. Subjects were over the age of 60 years.

2. Subjects recruited were sedentary and free from cardiovascular,
pulmonary, peripheral vascular, or orthopedic diseases, or conditions
that would limit their full participation in an exercise program.

3. Subjects were not diabetic.

4. Subjects had resting systolic and diastolic BP less than 160/100.

5. Subjects were not taking anti-anginal or digitalis medication.

6. Subjects did not previously have a myocardial infarction, coronary
artery bypass surgery, or percutaneous transluminal coronary
angioplasty.
n te 4 -








Subjects had a normal HR and BP response to maximal treadmill
testing.


Strenuous exercise was not allowed within 12


hours prior to most


testing procedures; strenuous exercise was not allowed within 24
hours prior to tilt testing.


Subjects were at least 3 hours but not more than 12


hours post-


prandial during testing sessions; no caffeine was consumed within 3
hours prior to any test.

No alcohol was consumed within 24 hours prior to testing.

Subjects took usual prescribed medications prior to testing.


Limitations


Major limiting factors included the following:


Forty-four elderly subjects (14 males, 30 females) volunteered to serve
as subjects.

Diet and day-to-day activity could not be regulated.


Definition of Terms


Aerobic exercise consists of activities that can be maintained continuously


and involve rhythmic movement of large muscle groups.


Aerobic activities, such


as walking, jogging, running, swimming, cycling, and rope-skipping, are used to
improve cardiorespiratory function.

Baroreflex responsiveness refers to the magnitude of the HR change in


response to a given arterial pressure change.


A decreased responsiveness refers


to an attenuated HR response to a given pressure change.
T4xmnrrn nrroara 24c 2ali rrna m on in hi an nan im








Orthostasis is an environmental perturbation that produces qualitative
effects similar to those induced by upright stationary posture (ConvertinoHR
1987).


Orthostatic (postural) hypotension is a reduction of 20 mmHg or more in


systolic BP upon


standing upright (Lipsitz,


1990).


Orthostatic intolerance is the inability of the cardiovascular reflexes to
maintain arterial pressure for adequate cerebral blood perfusion, eventually
leading to syncope (Convertino, 1987).
Resistance exercises consist of activities designed to increase muscular


strength and/or endurance.


These activities generally involve concentric and/or


eccentric contractions of a muscle group against a constant or variable resistance
and use free weights, and/or constant or variable resistance machines.
Syncope is synonymous with fainting.












CHAPTER 2
REVIEW OF LITERATURE


Introduction


The response to orthostasis involves an activation of reflex systems
designed to maintain blood pressure (BP) homeostasis and cerebral perfusion
despite the translocation of approximately 800 ml of blood from the central


circulation to the periphery (Blomqvist & Stone, 1983).


These reflexes include


enhancement of myocardial function, increases in arterial and venous tone,
increases in neuroendocrine secretion, and reflexes mediated by high- and
low-pressure baroreceptors.
Endurance training in young individuals appears to be associated with


alterations in some of the reflex responses to orthostasis.


There may be a


reduction in chronotropic responsiveness, and in the sensitivity of the high-


and low- pressure baroreceptor systems.


In addition, there may be an


alteration in the sensitivity of vascular receptors, an increase in venous
compliance, and an attenuation of vasoactive hormone release (Convertino,


1987).


These changes would appear to compromise the body's ability to


withstand an orthostatic challenge.


On the other hand


, training-induced


adaptations that would appear to enhance the body's ability to withstand
orthostasis include an increase in blood volume (BV) and an increase in
muscle mass, particularly in the lower extremities.








response to orthostasis when compared with younger persons.


There is


generally a smaller reflex increase in heart rate (HR) (Dambrink & Wieling,


1987


Ebert, Hughes,


Tristani, Barney, & Smith,


1982


Frey & Hoffler, 1988)


most likely due to a decreased HR responsiveness in the high-pressure


baroreflex system (Gribbin et al.,


1971).


Mean arterial pressure (MAP) may


therefore be maintained with less of a reliance on HR (Jansen et al.,


1989) and


more of a reliance on increases in peripheral vascular resistance and diastolic


blood pressure (DBP) (Ebert et al.,


1982


Frey & Hoffler,


1988).


In addition,


while younger persons usually demonstrate an increase or no change in
systolic blood pressure (SBP) when moving from sitting to standing


(Convertino et al.


, 1984; Dambrink & Wieling, 1987),


older persons often see a


decrease (Dambrink & Wieling, 1987).


This may be due to arterial rigidity,


which decreases the ability of the vasculature to adjust to changes in pressure


(Jansen et al.,


1989; Smith and Fasler, 1983),


or to baroreflex impairment


(Lipsitz,


1989).


Whether the responses to an orthostatic stress can be improved after


endurance training in the elderly is not known.


Some of the components


involved in the reflex responses to orthostasis may be irreversibly altered in
the elderly (e.g., aortic distensibility, j3-adrenergic sensitivity, cardiac and


vascular compliance).


Another problematic issue is that some of the changes


produced by the aging process are in the same direction as those produced in


younger persons who "improve"


their responses to orthostasis after training.


For example, an improved response to head-up tilt after training in young
persons generally involves a decrease in HR and rate-pressure product








training may therefore involve increases, rather than decreases,


in HR or


SBP.

An understanding of the responses of elderly persons to an orthostatic

stress after training first involves an investigation of how resting parameters

may be altered with training and how training interacts with aging to produce


changes.


The response to an orthostatic stress before and after a period of


training must also be described, taking into account both training and possible

aging effects.


Responses to Endurance


Training


Resting Heart Rate (HR),


Stroke Volume (SV), and Cardiac Output (O)


The decline in resting HR after endurance training is well documented


in young and middle-aged persons.


The magnitude of the decrease ranges


from 4 to 8 beats*min-1 (Convertino et al.,


1980a; Convertino et al.,


1983;


Convertino et al.


, 1984; Convertino et al.,


1991; Greenleaf,


Sciaraffa


, Shvartz,


Keil, & Brock, 1981; Hartley et al.,


1969; Oscai et al.,


1968; Pollock et al.,


1976


Pollock et al.


,1971; Seals & Chase, 1989) and may be related to training-


induced hypervolemia (Fortney, Wenger, Bove, & Nadel,


1983).


Other factors


related to this decrease include decreased sympathetic nervous system (SNS)


activity (Bjorntorp, 1987


Katona, McLean,


Dighton,


& Guz, 1982) and/or


increased in parasympathetic tonus (Barney,
Kenney, 1985; Seals & Chase, 1989). Declines


Ebert, Groban, & Smith, 1985;


in resting HR may be


independent of the body position in which the HR is measured.


Greenleaf et








Some authors claim that a resting bradycardia does not occur with


training in the elderly (Lampman & Savage, 1988).


However, this conclusion


is based partially on the results from studies on institutionalized subjects


(Clark, Wade,


Massey


& Van Dyke, 1975


Stamford


,1972) or on programs


using "light"


exercise (Emes, 1979).


Nevertheless, even some studies using a


moderate exercise intensity (Barry, Daly, Pruett, Steinmetz, Page,


Birkhead


Rodahl


, 1966; Meredith et al.,


1989; Schocken,


Blumenthal


, Port, Hindle,


Coleman, 1983) have failed to documented significant decreases in resting
HR. This is in contrast to other studies showing declines in resting HR in the

elderly after training to be of approximately the same magnitude as


documented in younger subjects.


Braith et al. (1990) found a small (3


beats *min-1) but significant decrease in HR after 3 months of endurance


training at 50-70% HRRmax in healthy 60 to 79 year olds.


A similar small


decrease was noted by Adams and deVries (1973) in elderly women after 3


months of training at a minimum of 60


VO2max.


Cononie et al. (1991)


found a slightly greater decline (5 beats *min1) in healthy 70-79 year olds after


six months of endurance training at 75-85


VO2max


. Older hypertensives


may have even larger reductions in HR as a result of training (e.g.,


Hagberg et al.,


8-13 beats;


1989b).


Stroke volume at rest has been shown to be unchanged (Ekblom,
Astrand, Saltin, Stenberg, & Wallstrom, 1968) or increased (Convertino et al.,


1991


Hartley et al.,


1969) after strenuous physical training in young and


middle-aged persons.


Increases may be related to training-induced


hypervolemia and elevated central venous pressure (CVP) (Convertino et al.,








, due to the reduction in resting HR (Convertino et al.,


1991


Hartley et al.,


1969).


The data on changes in resting SV or Q with training in the elderly are


scarce.


In one of the few reported studies,


Hagberg et al. (1989b) found that


elderly hypertensives did not increase their resting SV or their blood or
plasma volumes after 9 months of low- or moderate-intensity exercise
training. However, the low-intensity exercise group had a reduction in
resting Q, while the moderate-intensity group had a reduction in total


peripheral resistance.


No potential mechanisms were proposed to explain the


different responses.


Similarly


Schocken et al. (1983) reported that neither


resting Q nor resting SV changed after training in the elderly.


They also


found that contractile function, as measured by an increase in left ventricular


(LV) ejection fraction and LV ESV


did not change with training.


Blood Pressure (BP)


Since the level of mean BP is the product of flow (Q


= HR X SV) and


peripheral resistance, changes in one or both of these factors as a result of


exercise training could effect BP changes.


reductions in HR and


If SV remains unchanged,


Q will provide a blood pressure-lowering effect.


Reductions in peripheral resistance may also act to lower BP.
Mechanisms associated with these changes include a decrease in SNS
activity, resetting and/or increased sensitivity of baroreceptors, altered


distribution of BV


, altered pressure-natriuresis function, alterations in the


renin-angiotensin axis, altered sensitivity of vascular a- and P-receptors, and








central nervous system that stimulate central endorphin production and
cause a decrease in resting HR and Q through central inhibition of SNS


activity (Bjorntorp, 1987).


In addition, since insulin is stimulated by 3-


adrenergic activity, lowered SNS activity may also result in a decrease in


plasma insulin concentration.


This may help to decrease BP by decreasing


sodium (Na+) reabsorption in the kidney (Bjorntorp, 1987


Zambraski, 1984).


Kenney &


Greenleaf et al. (1981) hypothesize that the drop in diastolic


BP after training is a result of the continued stimulation of both vasopressin
and the renin-angiotensin system during exercise, resulting in a diminished


vasoconstrictive response for some time after exercise; i.e.,


"fatigue"


of the


vasoconstrictor response.


Confounding factors include a concomitant weight


loss with training, which independently decreases catecholamine release and
BP (Tipton, 1991).
According to several recent reviews, endurance training in young and
middle-aged persons with mild essential hypertension can lower both SBP
and DBP 8-10 mmHg (Bjorntorp, 1987; Hagberg, 1990; Hagberg & Seals, 1987).


Training in older (>


60 years) hypertensives (Hagberg et al.,


normotensives (Braith et al.,


1990; deVries,


1989b) and


1970; Emes, 1979; Stamford, 1972)


can have the same effect.


Despite the reductions seen in some


normotensives, it is commonly thought that the BP-lowering benefits to be
derived from endurance training are dependent on the initial BP level:
persons with normal initial BP often do not see reductions with training


(Adams & deVries, 1973; Kilbom et al.,


1969; Pollock et al.,


1976; Schocken et


, 1983) while those with mild to moderate elevations in BP (>


140/90








75-85%


VO2max,


there were decreases in SBP


DBP


and mean arterial blood


pressure (MAP) of 4, 5, and 4 mmHg, respectively.


However, when subjects


with initial blood pressures of >140/90 mmHg were analyzed separately, the


decreases were 8, 9,


and 8 mmHg for SBP


DBP


and MAP


, respectively.


Maximal Aerobic Power


Endurance training programs of

American College of Sports Medicine's

maintaining cardiorespiratory fitness (A


12 months duration that meet the


(ACSM) criteria for developing and

LCSM, 1990) generally result in


improvements in


VO2max ranging from 15-30%.


The magnitude of


improvement is dependent on the frequency,


intensity and duration of


training (Atomi,


, Iwasaski, & Miyashita,


1978; Gettman et al.,


1976; Milesis


et al.


, 1976).


Although there is a decrease in maximal aerobic power with age


(Buskirk & Hodgson, 1987),


the relative training-induced improvement in


VO2max that can be made by healthy elderly individuals is similar to that


seen in younger individuals (Cress et al.,


1991


Hagberg et al.,


1989a


Meredith


et al.


, 1989; Seals et al.,


1984; Sidney & Shephard,


1978) when training


programs are designed according to the ACSM (1990) recommendations.


example,


training for more than two days per week at either 60 or 80%


maximal HR reserve (HRRmax), resulted in improvements in


VO2max of 14


and 29%,
Similarly,
in a 20%


respectively


in elderly persons (Sidney & Shephard, 1978).


training 3 days per week for six months at 75-85


improvement in


HRRmax resulted


VO2max in elderly men and women (Hagberg et








central (i.e., increased maximal SV


maximal


Q, and maximal myocardial


oxygen [02] consumption) and peripheral (increased maximal arteriovenous
02 difference) adaptations have resulted from endurance training in young


and middle-aged men (Ekblom et al.,


1968; Hartley et al.,


1969) and in cardiac


patients (Ehsani,


Heath, Martin,


Hagberg, & Holloszy, 1984; Ehsani,


Martin,


Heath


, & Coyle,


1982),


the evidence for improved central parameters after


training in elderly individuals is sparse and inconclusive (Ehsani,


1987).


Indirect evidence for central adaptations is provided by Heath, Hagberg,
Ehsani, and Holloszy (1981) who found that values for maximal 02 pulse


were similar for young and master athletes,
group of sedentary middle-aged individuals.


and both were higher than for a
This suggested that the higher


VO2max in the master athletes compared with the sedentary subjects could


have been mediated through a higher maximal SV


similar between the two groups.
02 difference cannot be ruled out.


since maximal HR was


However, a higher maximal arteriovenous
Schocken and coworkers (1983) also


provide evidence for an increase in maximal SV in the elderly.


They found


that although moderate- to high-intensity training (70-85% HRmax) did not


change resting SV


ESV, or EDV in elderly subjects,


the calculated maximal


exercise SV increased approximately 13 ml as a result of an increase in


maximal LV EDV


. Maximal


Q increased from 9.94 to 11.40 L*min-1


but this


was not statistically significant.
Meredith and coworkers (1989) provided evidence for the peripheral


adaptation hypothesis. After 12


weeks of cycle ergometer training at 70%


HRRmax, they found that elderly subjects demonstrated significant increases









young and old subjects made nearly identical absolute increases in


VO2max


(5.5 and 5.3 ml*kg-l min-1


, respectively).


In relative terms, the elderly


subjects increased


VO2max 19.9


, compared with 1


for the young


subjects.


Seals et al. (1984) also found evidence for peripheral,


training adaptations in the elderly.


but not central,


They found that after 6 months of low-


intensity training followed by 6 months of high-intensity training, 61-67 year-


old men and women increased


VO2max approximately 30%.


Since maximal


Q was not significantly increased, the increase in


VO2max appeared to be


mediated primarily through a 14% increase in the maximal arteriovenous 02

difference.


Increase in Strength and Muscle Mass

Changes in body composition as a result of endurance training are

commonly assessed using hydrostatic weighing or skinfolds. Using these

methods, lean body mass changes either not at all (Hagberg et al., 1989a;


Kilbom et al.


, 1969) or increases a small amount (Boileau,


Buskirk, Horstman,


Mendez, & Nicholas,


1971


Wilmore et al.


,1980) as a result of endurance


training.


Using urinary creatinine as a measure of muscle mass, Meredith et


al. (1989) also found no increase in muscle mass after 1


training at 70%


weeks of endurance


VO2max in the elderly.


Due to the specific nature of training adaptations,


it would not be


expected that strength would substantially increase as a result of endurance








elderly.


In a more recent study, however (Graves et al., unpublished),


there


was a strong trend toward an increase in leg strength in endurance trained 70-
79 year olds, many of whom used uphill treadmill walking as a mode of
training.


Responses to Strength Training

Although the response to strength training varies widely among


individuals and studies


, the average improvement in strength for young and


middle-aged men and women for most muscle groups appears to be
approximately 25-30% (Fleck & Kraemer, 1987) and is often associated with an


increase in fat free weight (FFW) (Hurley et al.,


1984).


Older individuals are


capable of making comparable changes with appropriately designed programs


(Aniansson & Gustafsson


,1981; Aniansson, Ljungberg, Rundgren, &


Wetterqvist, 1984; Chapman, deVries,


& Swezey


1972; Liemohn,


1975;


Moritani & deVries


however


, 1980).


, moderate- to higl


In some studies using elderly individuals,
h- intensity resistance training has resulted in


greater increases in strength (e.g., 50-230%) (Fiatarone et al.,


1990


Frontera et


., 1988; Kauffman, 1985; Perkins & Kaiser, 1961).


This may be due to the


lower initial level of strength and thus the greater relative potential for


strength


development.


Changes in muscle morphology that occur with aging include a
decrease in the total number of both Type I and Type II fibers, with a greater


proportional loss of the Type II fibers (Evans,


1986; Larsson,


Sjodin,


Karlsson, 1978; Larsson,


Grimby, & Karlsson,


1979).


This age-related atrophy





22


Although aging-related changes in muscle morphology can be partially

reversed as a result of resistance training, the reported changes vary among


studies.


This may be due to differences in training intensity, muscle groups


trained or tested, or even possibly to gender-specific adaptations.


(1991) found an increase in the


Cress et al.


Type IIb fiber cross-sectional area, with


maintenance of the Type I and Ha fiber cross-sectional area,


after 50 weeks of


low to moderate aerobic/resistance training in septuagenarian women.


Both


Aniansson and Gustafsson (1981) and Aniansson et al. (1984) noted an

increase in the percentage, but not in the cross-sectional area, of Type IIa fibers


after resistance training in elderly men and women.


On the other hand


Larsson (1982) found that the cross-sectional area of both Type I and Type II


fibers increased 31.8 and 51


, respectively, with 15 weeks of knee extensor


training in 56-65 year old men.


Frontera et al.


(1988) also found significant


increases of 33.5 and


.6% in Type I and II fiber cross-sectional area after 12


weeks of strength training in 60-72 year old men.


Hormonal,


and Blood/Plasma


Volume Responses to


Training: Resting


Values


Blood/Plasma


Volume


While some early studies reported no change in BV


as a result of


training (Bass,


Buskirk, lampietro, & Mager, 1958; Dill,


Hall


Hall, Dawson, &


Newton


,1966),


most recent studies show that endurance training increases


BV (Convertino et al.


, 1980a; Convertino, Greenleaf, & Bernauer, 1980;


w 'a a a 1- 1 100'2,,,~,, fllhla taa a al lflA. fl. -- A nr -


r,,,,,,c:,, ,r. ,1


----


A A


1 nnl








the hemoglobin (Hb) concentration but a constancy in the Hb content


(Convertino et al.


, 1980a; Oscai et al.,


1968).


The training parameters of intensity, frequency and duration have all


been hypothesized to affect BV increases.


Two studies by Convertino and


colleagues illustrate the possible effect of training intensity on BV expansion


(Convertino et al.


,1980a; Convertino et al.,


1977).


Both studies utilized an 8-


day training protocol involving 2 hoi
intensity for the former study was 65


VO2max for the latter study.


an 18.


irs of cycle ergometer exercise per day;


of VO2max while it was 50


The regimen with the higher intensity produced


(72 ml) higher increase in BV.


Intensity,


however, cannot be the only factor influencing the


magnitude of PV expansion.


In two studies by Convertino and colleagues


(Convertino et al.


, 1980a; Convertino et al.,


1983),


identical 8-day cycle


ergometer training protocols at an intensity of 65


of VO2max for


2 hours


per day induced 1


1 and 12.3% increases, respectively,


in PV


However, a


different investigative group (Greenleaf et al.,


1981) found a similar (1


increase in PV after a comparable training protocol at an exercise intensity of


only 44% of VO2max


It might be hypothesized that the potential for PV


expansion is greater when the initial volume is lower since the relative
volume expansions in these studies were similar, but the absolute increases

were smaller in the Greenleaf et al. (1981) (385 ml vs. 427 ml in both
Convertino et al. studies), indicating a smaller initial PV. On the other hand,
Convertino et al. (1980a) compared the fitness level and relative
hypervolemia of the subjects in their study with those of Oscai et al. (1968).








initial PV (3500 ml


vs. 3196 ml), yet they were able to achieve a greater


relative PV expansion (1


vs 6.4%


427 ml vs.


204 ml).


Frequency and duration of training are thought to affect training-


induced hypervolemia.


It has been speculated that regimens with


consecutive days of training and/or exercise durations of two hours or more


per day produce a greater hypervolemia than those which allow 1


days


recovery between training sessions and/or use shorter exercise sessions


(Convertino et al., 1980a).


If program duration is held constant, particularly


with shorter (e.g.,


8 days) programs, this may hold true.


An equally important


factor in BV expansion, however, may be the total amount of work


performed during the entire program.


For example, Convertino et al. (1991)


produced a 13% increase in PV with a 10-week training regimen where
subjects exercised for 4 days per week, 30 minutes per day at 75-80% of


VO2max


In the Convertino et al. (1980a) study


a 12.1


increase in PV was


achieved with an 8-day protocol, where subjects exercised for


at 65% of VO2max


2 hours per day


It is possible that the lower training frequency and shorter


duration in the former study was offset by the higher intensity and longer


program duration to produce an equivalent PV


In contrast, Oscai et al.


expansion.


(1968) produced only a 6.4% increase in PV with


training for 30 minutes per day, 3 days per week for 16 weeks.


Although the


training intensity relative to


VO2max was not specified,


the training HR data


suggest an intensity similar to that used in the Convertino et al. (1991) study.


Clearly


there are other factors or combinations of factors influencing the


degree to which PV can be expanded due to a training regimen.








facilitate retention of Na+ and water; and an increase in plasma albumin
content, which provides an increased water-binding capacity for the blood


(Convertino et al.


, 1980a; Convertino, Keil,


Bernauer, & Greenleaf, 1981).


This


conclusion is supported by data from Greenleaf et al. (1981) who found that
subjects exercising in the heat had greater increases in AVP and PRA during


exercise and a larger PV
moderate temperature.


after training than subjects exercising in a more
Resting values of AVP and PRA, however, were


unchanged with training (Convertino et al.,


1980a; Convertino et al.,


1983;


Greenleaf et al.


1981


Convertino et al


., 1991).


Few studies have documented the PV responses to training in older
individuals. Resting PV does not appear to change with age up to age 40
(Chien, Usami, Simmons, McAllister, & Gregersen, 1966) but cross-sectional


and longitudinal data with older individuals are lacking.


Convertino et al.


(1980a) hypothesized that training-induced hypervolemia might be less in


older individuals due to a decreased physical working capacity.


However,


since training intensity expressed as a percentage of VO2max appears to be a


potent stimulus for PV


expansion, the relative hypervolemia induced by


training in older individuals may be equal to that of younger individuals


training at the same relative intensity.


Indirect evidence for the Convertino


et al. hypothesis is offered by the data of Kilbom et al.


(1969).


In this study, 38-


year old men increased


VO2max by 14% after 2 months of endurance


training; however, there were no changes in resting Hb and Hct.


Although


PV was not measured, the data suggest that it did not change since an increase
in PV is usually accompanied by decreases in Hb and Hct (Convertino et al.,








would more likely contribute to a lack of change in PV in older persons


(Gregerman & Bierman, 1981


McGinty et al.,


1988).


Vasoactive


Hormones


Vasopressin


(AVP).


The most potent stimulus for AVP secretion is an


increase in blood osmolality sensed by osmoreceptors in or near the


hypothalamus.


Increases as small as 1


above 280 mOsmeL


-1 are sufficient


to elicit AVP secretion.


A secondary influence on AVP secretion is a BV


change sensed by both high- and low-pressure mechanoreceptors.


The high-


pressure baroreceptors in the carotid sinus and aortic arch are sensitive to
changes in arterial pressure while low-pressure (cardiopulmonary)


baroreceptors, located in the atria,


the pulmonary veins, and within the walls


of the heart, respond to changes in intracardiac pressures.


arterial

up tilt,


Reductions in


, central venous, or atrial pressure, such as would be induced by head-
decrease afferent nerve activity and release inhibitory activity in the


cardiovascular centers of the central nervous system.


A series of reflexes


ensue which act to maintain arterial pressure by increasing Q and/or


peripheral resistance.


The end result is an increase in HR and contractility,


increased veno- and vasoconstriction, and reduced blood flow to the skin,


skeletal muscles


, kidney and splanchnic area (Convertino, 1987;


Guyton, 1991


Goodman & Frey, 1988).


An increase in vasoactive hormone (AVP,


norepinephrine, and renin-induced angiotensin II [An]) release is an integral


part of this response.


Conversely, increases in central venous or atrial


pressure induced by supine posture or water immersion would produce








Training-induced increases in BV


cause parallel increases in CVP


(Convertino et al.


, 1991) and are of the magnitude (10-15%


Convertino et al.,


1980a


Convertino et al.


,1983; Convertino et al.,


1991


Greenleaf et al.


, 1981)


where AVP would be expected to decrease.


Cross-sectional studies have


found that acute volume expansion or water immersion stimulate the

suppression of AVP and secretion of atrial natriuretic factor both in animals


(Johnson,


Zehr, & Moore,


1970) and humans (Gauer & Henry, 1963; Norsk,


Bonde-Petersen, & Warberg, 1985;


Thompson,


Tatro, Ludwig, & Convertino,


1990; Volpe et al.,


1989).


Conversely, Harrison et al.


(1986) found that acute


changes in central BV induced by dehydration and orthostasis induced


increases in AVP


In contrast, Norsk,


Bonde-Petersen, & Warberg (1986) did


not find a relation between acute CVP changes,


induced by lower body


negative pressure (LBNP) or lower body positive pressure, and AVP secretion,
and concluded that the cardiopulmonary mechanoreceptors did not strongly
influence AVP secretion.

Although studies using acute volume changes to stimulate or suppress
AVP provide evidence that cardiopulmonary receptors play a role in AVP
secretion, they do not adequately address the issue of the effect of chronic


changes in volume and CVP on hormonal secretion.


It has been


hypothesized that endurance training causes a resetting and/or a decrease in


the sensitivity of the cardiopulmonary receptors (Convertino, 1987).


This


results in unchanged basal levels associated with increased BV, together with
either a reduced suppression of AVP when CVP is increased (e.g., during
water immersion or lower body positive pressure), or a reduced secretion of








individuals have resting levels of AVP similar to those of sedentary


individuals.


A decrease in sensitivity of the cardiopulmonary receptors is


suggested by studies which have found that endurance-trained individuals


exhibited a lesser diuretic response (i.e.,


a reduced suppression of AVP) in


response to water immersion (Boning & Skipka,


1979; Claybaugh et al.,


1986;


Skipka, Boning, Deck,

(Claybaugh et al., 1986


Kulpmann, & Meurer,


i; Freund et al.,


1979) or water intake


1988) as evidenced by a lower urine flow.


Longitudinal studies provide the best insight into the response of
resting AVP levels to physical training and into possible alterations in


cardiopulmonary baroreceptor sensitivity.


Convertino et al. (1980a) and


Convertino et al. (1983; 1991) found that resting AVP did not change after


training programs that increased


VO2max by 8-20%.


In their most recent


investigation,


Convertino et al.


(1991) measured BV


CVP, and resting


hormonal le'
BV and CVP


vels.


They found that training resulted in parallel increases in


, but without any increase in MAP or vascular compliance.


addition, there were no changes in resting levels of AVP


, ALDO, or atrial


natriuretic factor suggesting that the chronic increase in CVP caused a
resetting of the cardiopulmonary stimulus-response mechanism.


Renin.


Renin is synthesized and secreted into the blood by the


juxtaglomerular (JG) cells in the afferent arterioles of the glomeruli.
Juxtaglomerular cells secrete renin in response to decreased pressure in the
afferent arterioles as well as in response to sympathetic stimulation, decreased


Na+ load in the tubular fluid
1988; Kiowski & Julius, 1978)


/ or a drop in atrial pressure (Goodman & Frey,
. All of these stimuli are related to a decrease in








I mi-1 h-1 (Labhart,


1986)


, but may be lower in the elderly (Cleroux et al.,


1989; Gregerman & Bierman, 1981).
Although it might be expected that training-induced increases in BV


(Convertino et al.


, 1980a; Convertino et al.,


1980b; Convertino et al.,


1983;


Convertino et al.


1991


Oscai et al.


, 1968) or decreases in SNS activity


(Bjorntorp, 1987


Katona et al., 1982) would reduce renin secretion as it does in


acute volume changes (Thompson et al.,


1990),


the increase in volume is not


associated with increases in mean arterial pressure (Convertino et al.,


with changes in plasma Na+ concentrations (Convertino et al.,


1991) or


1980a; Freund


et al.


, 1988).


Accordingly, most studies find that renin activity in younger


individuals does not change with training.


Both Convertino et al. (1980a) and


Convertino et al. (1983) found unchanged resting levels after an exercise


protocol (8 days of cycle ergometry for 2 hours per day at 65%


VO2max) that


induced 1


1-12.3% increases in PV


. Wade et al. (1981) also found resting


levels to be unchanged in endurance runners during and after 20 days of
running an average of 28 km per day.

The data from cross-sectional studies largely support this conclusion.


Both Freund et al.


(1988) and Skipka et al. (1979) found no difference in


resting PRA levels between trained and untrained individuals.


study (Fagard et al


However


., 1985) found lower resting PRA values in endurance-


trained athletes.

The data regarding changes in resting levels of renin after training in


the elderly are sparse and contradictory.


Braith et al.


(1990) found decreases in


resting PRA associated with decreases in resting BP in healthy 60 to 79 year








both exercising and control groups.


This did not appear to be associated with


the BP changes,


however: subjects exercising at low (50%


VO2max) intensity


experienced significantly greater reductions in BP than the control or


moderate-intensity (70-85


VO2max) exercise groups, but with equivalent


reductions in PRA.


Catecholamines.


Norepinephrine (NE) levels are generally considered


representative of sympathetic tone (Mazzeo, 1991),


although this conclusion


has been challenged (Floras et al.,
concentrations may not represent


1986).


The possibility that plasma NE


sympathetic activity after training because


of down regulation of adrenergic receptors has not been investigated (Tipton,


1991).


Resting plasma levels of NE average 66-390 pg*ml-1 while resting EPI


levels average 10-70 pg*ml-1 (Cryer, 1980).


Resting levels of NE are increased


with age, while EPI concentrations remain unchanged (Gregerman &


Bierman, 1981


Lipsitz, 1989).


Training is associated with a decrease in SNS activity as evidenced by a
decrease in plasma NE concentration, particularly in hypertensives (Hagberg


et al.


, 1989b; Kiyonaga et al.,


1985


Tipton, 1991).


However, Convertino et al.


(1991) found no change in resting levels of NE after 10 weeks of training in


young normotensive men.


Changes in body weight associated with training


may independently result in decreases in catecholamine release, rendering
conclusions about the effect of training alone difficult (Tipton, 1991). The
reduction in resting NE is thought to result in a decrease in BP through


decreases in resting HR and Q.


However, the data regarding the response of


peripheral resistance are inconsistent: some investigators have found that the








Data on post-training resting catecholamine concentrations in the


elderly are scarce.


Hagberg et al.


(1989b) found that 9 months of exercise


training in elderly hypertensives did not reduce supine or standing NE levels


compared with initial within-group levels.


However, because of an increase


in NE in the control group, the changes from pre- to post-training in the


exercise groups were significant.


Epinephrine (EPI) levels (both supine and


standing) did not change with training in either exercise group.


Summary.


Based on results from studies inducing acute central BV


changes, increases in BV should produce increased stimulation of the
cardiopulmonary baroreceptors and induce a suppression of AVP and renin.
The bulk of the data, both cross-sectionally and longitudinally, suggest that
this does not occur when central BV is increased chronically. This supports


the hypothesis (Convertino et al.,


1991) that the continual stimulation of the


cardiopulmonary receptors produces an attenuation of the stimulus-response
mechanism or a resetting of the receptors to operate at a higher CVP.


Norepinephrine levels,


with training.


however, are more commonly seen to decrease


These reduced levels are associated with decreases in BP or


peripheral resistance.


Training-induced losses in body weight may


independently reduce catecholamine levels.


Hormones Associated with Fluid Volume Control:


Aldosterone (ALDO)


The plasma concentration of AII is the most potent stimulus for ALDO
secretion; increased adrenocorticotropic hormone (ACTH) and potassium


(K+) concentrations are also potent stimuli.


Since the rate-limiting step in the








increase ALDO secretion.


Increased ALDO causes an increase in the


reabsorption of Na+ in the renal collecting ducts along with an obligatory


retention of water, and an increase in the excretion of K+


. Normal resting


values for supine subjects range from 20-100 pg*ml-1 (Labhart, 1986).


Resting


levels in the elderly are approximately 40% lower (Gregerman & Bierman,

1981).


Most studies show that training does not affect resting ALDO levels.


This is not surprising in

previously cited. Conve


light of the constancy of resting renin activity levels

rtino and coworkers (1991) found no changes in


resting ALDO levels after a 10 week (4 days per week at 75-80% of VO2max)


training regimen.


Cross-sectional studies (Freund et al.,


1988; Wade et al.,


1981) also have found no differences in resting ALDO levels between trained


and untrained individuals.


One study


however, did find that trained


subjects had lower resting levels of ALDO compared with untrained subjects,

but that this difference did not correspond to the resting renin activity levels


(Skipka et al.,


1979).


Data on training changes in resting ALDO concentrations in the elderly


are scarce.


Braith et al. (1990) found that 3 months of exercise training in 60 to


79 year-olds did not alter resting ALDO levels, despite evidence for a decrease

in both resting potassium (K+) and resting renin activity.


Adrenocorticotropic Hormone (ACTH)


Adrenocorticotropic hormone causes the adrenal cortex to secrete


cortisol and ALDO.


However, ACTH is not as important a regulator of ALDO








rhythm,


with highest levels in the early morning.


Morning values for the


healthy adult range from 10-100 pg*mll-


20 pg*ml-1 (Labhart, 1986).


, while evening values range from


Aging does not appear to change resting ACTH


levels (Everitt, 1980


Gregerman & Bierman,


1981).


The response of resting ACTH levels to training is not known.
However, since acute distension of the right atrium inhibits ACTH release
(Cryer & Gann, 1974), it might be hypothesized that the increase in BV that


accompanies training would reduce basal ACTH secretion.


On the other


hand, if there is a resetting and/or a reduction in sensitivity of the atrial
receptors mediating ACTH release as there appears to be for AVP and renin
release, basal levels would not be affected.


Protein (PROT).


Sodium (Na+) and Potassium (K+)


The normal resting value for PROT in the plasma is 1


7.3 gm*dl-1


.2 mOsm L


, while the normal resting values for Na+ and K+ are 143 and 4.2


mOsm L


, respectively (Guyton,


1991).


Protein and K+ together provide only


about


of the total plasma osmolar activity while Na+ is responsible for


approximately 51


of the total osmolar activity.


Changes in plasma Na+


concentrations affect osmoreceptors in or near the anterior hypothalamus,
which in turn control AVP secretion by the posterior pituitary gland.
Plasma proteins are responsible for producing capillary osmotic
pressure since they do not readily diffuse through the capillary membrane.
Although, from a homeostatic point of view, it would not be expected that


the concentrations of PROT


Na+, or K+ would change with training, the





34

system is sensitive to small changes in osmolality, and because resting levels

of AVP appear to be unchanged with training (Convertino et al., 1980a;


Convertino et al.


, 1983; Convertino et al.,


1991),


it would be expected that


resting plasma levels of Na+ would be unaltered with exercise training.


Indeed


Convertino et al.


(1980a) found that an 8.1


(457 ml) increase in BV


was accompanied by an increase in total osmolar and PROT


content, but not


concentration.
This conclusion is supported by the cross-sectional data of Freund et al.


(1988) who noted similar plasma Na+


and PROT


concentrations in trained


and untrained subjects.


One study


however, noted a lower resting PROT


concentration in trained subjects (6.35 g*dl-1) compared with their untrained

counterparts (6.9 g*dl-1) (Boning & Skipka, 1979).
There has also been a report of decrease in plasma K+ from 4.2 to 3.7


mEq*L


-1 as a result of 4 months of intensive training (Rose, 1975).


This may


be due to the post-exercise increase in ALDO that occurs in response to

transient episodes of hyperkalemia during exercise, and which results in a


"rebound"


hypokalemia.


Cross-sectional data (Claybaugh et al.,


1986; Wade et


al., 1981) showing an increased ALDO response in trained individuals to

water immersion and daily long-distance running lend indirect support to


this theory.


However, the finding of greater ALDO responsiveness in trained


individuals is not universal (Freund et al.,


1988; Skipka et al.,


1979).


An alternative explanation for the resting hypokalemia seen after
training involves an increase in resting muscle membrane potential,


favoring a movement of K+ into the muscle cells.


Six weeks of treadmill








Data on the response of resting K+


in elderly individuals are sparse. B

resting K+ from 4.24 to 3.94 mEq*L


Na+, and PROT levels after training


;raith et al. (1990) found a decrease in


, but an unchanged resting ALDO, in


elderly subjects after 3 months of endurance training; no mechanisms were

proposed to explain the result.


Cardiovascular, Hormonal,


and Plasma


Volume Responses to


Tilt: Pre- and


Post-training

Head-up tilt is a method used to study the reflex mechanisms


associated with the response to orthostasis.


Because muscular activity in the


legs can be minimized, as compared with passive standing, the contribution

of cardiovascular reflexes to the maintenance of arterial pressure can be better


distinguished.


As a response to the venous pooling induced by upright tilt,


CVP


EDV


Q are sequentially reduced.


There is also a gradual


decrease in blood flow in the kidney, and in the resting arm and leg muscles


(Convertino,


1987).


If Q is decreased without an increase in peripheral resistance,

pressure and cerebral perfusion will fall, and syncope will ensue. Th


arterial


te ability


of the body to resist the fall in arterial pressure is dependent on the

responsiveness and interaction high- and low-pressure baroreceptor systems,

myocardial function, arterial and venous tone, and neuroendocrine

secretions.

The cardiovascular and hormonal responses to tilt cannot be directly

compared among different investigations due to the widely differing


fl1 41%,,,,, fl I1. nn~l tt- -t,,LI ~


r*nlrrn~ln


I[l.. -








(Fitzpatrick,


Theodorakis,


Vardas


, & Sutton, 1991): for example, a 450 tilt


represents approximately 70% of the stresses imposed by upright posture


(Jansen et al.,


1989) while a 700


head-up tilt is nearly equivalent to the stress of


upright posture (Lye,


Vargas, Faragher, Davies, & Goddard,


1990


Wieling et


, 1983).


The magnitude of cardiovascular and hormonal responses would


be expected to vary accordingly, as documented for the HR and thoracic BV


responses by Smith et al. (1984).


Nevertheless


, it may be possible to deduce


qualitative conclusions from earlier studies.


Heart Rate,


Stroke Volume, Cardiac Output, and Blood Pressure


The increase in HR from supine to upright posture in young subjects is

well documented and appears to vary based on the angle and duration of tilt.

Increases of approximately 10 to 30 beats*min-1 are generally reported


(Beetham & Buskirk


, 1958; Convertino et al.


1984; Davies, Slater,


Forsling, &


Payne,


1976; Greenleaf et al.,


1981


Huber et al., 1988; Lee, Lindeman, Yiengst,


& Shock


, 1966; Matalon & Farhi,


Secher, 1990; Sannerstedt, Julius,


1979; Matzen, Knigge, Schutten,

& Conway, 1970; Shannon et al.,


Warberg, &


1991


Solomon, Atherton, Bobinski, & Green, 1986; Vargas et al.,


1986; Wieling et


1983


Williams


Walsh


, Lightman, & Sutton,


1988)


, although smaller


increments have been seen (Dambrink & Wieling,


1987).


Stroke volume


decrements during tilt range from 30 to 50% (Banner et al.,

Stone, 1983; Mangseth & Bernauer, 1980; Matalon & Farhi,


1990; Blomqvist &


1979


Sannerstedt


et al.


,1970; Vargas et al.,


1986).


Despite compensatory increases in HR, Q


generally decreases approximately 20-30% (Banner et al.,


1990; Blomqvist &








The changes with posture in older individuals are generally of a


smaller magnitude.


On an absolute basis, HR increments during tilt are less


than in young persons, although at least one study found no difference in the


response (Lipsitz, Mietus, Moody,


& Goldberger, 1990).


Increases of only 10-15


beats *min-1


are common (Kenny et al.,


1987; Lee et al.,


1966


Lye et al.,


1990;


Shannon et al.


1991


Vargas et al.,


1986).


However, one investigation (Ecoffey,


Edouard


, Pruszczynski,


Taly and Samii,


1985) found that HR did not increase


in elderly men during 30


tilt used


Although this may be due to the low angle of


, another investigation (Dambrink and Wieling, 1987) also found


small HR increments (0-5 beats*min-1) in 60 to 90 year-olds during a 700 tilt.


Even on a relative basis


, HR increments during tilt are smaller in older


individuals.


Jansen et al.


(1989) reported that elderly normotensives had a 10-


increases in HR compared with


20-25% increments in young


normotensives.


Several investigators (Dambrink & Wieling, 1987;


Norris,


Shock, &


Yiengst, 1953; Smith,


Barney, Groban, Stadnicka,


& Ebert, 1985) have


also found that the peak steady state HR response to orthostatic changes or to

neck suction took longer to achieve in older individuals.

Stroke volume during tilt decreases approximately 25-40% in older


individuals (Lee et al. 1966; Lye et al.,


1990; Shannon et al.,


1991


Vargas et al.,


1986).


Shannon et al. (1991) found that the greater reduction in SV in older,


as compared with younger, individuals was related to their inability to


decrease ESV despite similar reductions in EDV


It was hypothesized that the


inability to decrease ESV was due to aging changes in the vascular system.


The data comparing postural changes in


Q in young and old subjects





38


young subjects, but found that young subjects increased Q by 19% during a 600


tilt while old subjects experienced an 18


decrease.


Finally,


Lee et al. (1966)


found that older subjects had a 12


saw only a 3


fall in cardiac index while young subjects


drop.


A comparison of the BP responses of old and young subjects during tilt


reveals a variety of response patterns.


Most investigations have found that


SBP remains unchanged,


both in young (Beetham & Buskirk,


1958;


Convertino et al.


, 1984; Davies et al.


1976; Huber et al.,


1988; Matzen et al.,


1990; Williams et al., 1988) and elderly (Kenny et al.,


1987; Lee et al.,


1966; Lye


et al.


,1990) subjects.


Two cross-sectional studies comparing the BP response


to head-up tilt in young, middle-aged,


age-related differences.


and elderly subjects also did not find


Kaijser and Sachs (1985) evaluated the SBP and DBP


response to 8 minutes of 600 tilt and found no difference in response among


the groups.


Similarly, Smith et al. (1984) found that the MAP response did


not differ among different age groups in response to tilt.


However,


Vargas et


al. (1986) found that SBP decreased and DBP increased during 700 head-up tilt
in both old and young subjects, with young subjects showing greater increases


in DBP


Peripheral resistance increased equally for young and old subjects.


contrast, Dambrink and Wieling (1987) found that SBP decreased in older
subjects but remained stable in young subjects during an upright tilt.


However, the age-related DBP response was in agreement with


Vargas et al.


(1986).


Similarly, Lipsitz,


Maddens, Pluchino, Schmitt, and Wei (1986) found


that the peripheral resistance response to standing was greater in young, as


compared with old subjects,


after one minute of standing.


Equivalent





39

peripheral resistance increases more in older subjects have attributed the
enhanced response to a compensatory mechanism for the decreased HR and
Q response.
Few longitudinal studies document the cardiovascular responses to tilt
after a period of physical training but several have addressed the issue of
training-induced responses to tilt by comparing trained and untrained


subjects in a cross-sectional design.


Diaz and Rivera (1986) showed that


trained subjects had a significantly lower HR both during supine rest and
during a 30-minute tilt. During the tilt, trained subjects increased HR by 17


beats *min-1


while untrained subjects increased HR by 24 beats *min-1


may be related to training-induced hypervolemia.


Klein


. This


, Wegmann, Bruner


and Vogt (1969) and Klein,


Bruner


, Jovy,


Vogt, and Wegmann (1969) also


found that trained subjects had lower HRs under both rest and tilt conditions.
While the magnitude of the change from rest to tilt reported by Klein,


Wegmann,


Bruner and Vogt (1969) was 6.2 beats*min-1


lower in the trained


subjects, the relative increases were nearly identical (33.


vs. 32.3%


beats min-1 for trained and untrained subjects,


respectively).


Similarly


Harma and Lansimies (1985) did not find a difference between fit and
untrained men in the relative magnitude of the HR response to tilt.
In an early longitudinal study, Beetham and Buskirk (1958) found that
physical conditioning did not change the HR or BP response to 700 tilt in


young subjects.


On the other hand


Shvartz et al.


(1981) found a lower HR


and better maintenance of BP during tilt table testing in 5 of 10 subjects after


training and/or heat acclimation.


However, the lack of a true control (non-








training at 65


of VO2max


.Mean tilt duration to syncope increased by 6


minutes


associated with an increase in PV and a decrease of 9 beats*min-1


the HR response to tilt.


However, the heart rate acceleration from supine to


tilt positions only declined 4 beats *min-1 due to a 5 beats-min-1


resting HR.


reduction in


The BP response to tilt was unchanged by training.


The HR response to tilt after training in elderly individuals has not


been characterized.


However, there are some animal data to suggest that


exercise training increases NE content in the heart (Gwathmey et al.,


this may indicate an increased adrenergic responsiveness.


1990)


Whether this


would result in an increased HR response during tilt is not known;


confounding factors might include increases in SV


and/or BV


which would


tend to offset any increase in HR.


Blood/Plasma


Volume


Hagan, Diaz, and Horvath (1978) studied the effect of 35 minutes of
supine posture, followed by 35 minutes of standing, on Hct, Hb concentration,


plasma PROT


and PV in young subjects.


After 35 minutes in the supine


posture, PV increased by 440 ml, representing an increase of 11.7%.
Assumption of the standing position resulted in an increase of 10.3% and


10.8% for Hct and Hb, respectively, and an increase of 20.8


proteins.


in plasma


Hydrostatic pressure produced a fluid efflux of 593 ml and reduced


BV and PV by 9.5 and 16.2


, respectively. Red cell mass was unchanged by


posture.


Davies et al.


After 45 minutes


(1976) found similar results in a 45-minute, 850 tilt.


, PV had decreased 16.8%


, with a corresponding increase in








(Williams et al.,


1988).


Tarazi, Melsher, Dustan, and Frohlich (1970),


however, found somewhat smaller PV


decreases during a 20-minute, 500 tilt.


Their subjects experienced a PV decrease of 113 ml, corresponding to a 3.9%


decrement.


Data from studies with the elderly demonstrate results similar to


the majority of studies with young subjects.


Lye et al. (1990) found that a 10-


minute, 70 head-up tilt elicited a 10.8% decrease in PV in healthy elderly
subjects.
Physical training does not appear to affect the magnitude of the PV


decrement during tilt.


Convertino et al. (1984) found that although the


absolute PV decrease during a 600 tilt was greater after 8 days of training (544


ml vs.


479 ml),


the relative decrement remained the same (13.9% vs. 13.6%).


Similar results were found by Greenleaf et al.


(1988) who studied the response


to a 600 head-up tilt before and after a 6-hour water immersion protocol both
prior to and after 6 months of exercise training in young to middle-aged men.


Plasma volume decreases ranged from 9.0


procedures.


to 12.6% during the four tilt


In addition, neither pre- nor post-tilt Hb and Hct values were


changed with training.


Hemoglobin increased from 14.5 to 15.8 while Hct


increased from approximately 37.0 to 39.9 during tilt both pre- and post
training.


Vasoactive


Hormones


Vasopressin (AVP).


Upright posture translocates approximately 500 ml


of blood to the lower extremities while another 200-300 ml may be transferred


to the veins in the buttocks and pelvis (Blomqvist & Stone,


1983); prolonged





42

That AVP secretion during tilt is stimulated by volume receptors is

supported by research showing that dehydration results in greater resting and


tilt AVP concentrations.


Harrison et al.


(1986) found that resting levels of


AVP were five times higher, while tilt values were approximately 6.5


higher in dehydrated subjects.


times


Similarly, Greenleaf et al. (1988) found that


AVP levels were increased in response to tilt after,


but not before


a 6 hour


water immersion which reduced body weight by 1.12


Vasopressin secretion during head-up tilt may also be affected by
increases in the renin-AII axis resulting from generalized sympathetic


stimulation


decreased renal blood flow and/or pressure, or decreased


osmolar load at the juxtaglomerular cells (Mouw, Bonjour, Malvin,


Vander


1971


Ramsay,


Keil, Sharpe, & Shinsako, 1978).


Hypotension is also a


potent stimulator of AVP secretion (Share, 1976).
Vasopressin promotes homeostasis during orthostasis by increasing the
permeability of cells in the collecting ducts to water, thus increasing the


reabsorption of fluid in the kidney.


Vasopressin also limits filtration of


plasma into the interstitial space by the selective vasoconstriction of skeletal


muscle and skin arterioles.


The result is both a redistribution of vascular


volume to critical tissues (e.g., the brain), and a lowering of capillary pressure
which favors net reabsorption of fluid from the interstitial space. The


increased peripheral resistance induced by


AVP does not usually increase BP


because of baroreceptor-induced compensatory changes in HR and Q. In
addition, AVP may cause a reduction in cardiac contractility as a result of
coronary arteriolar constriction (Goodman & Frey, 1988).








Sander-Jensen et al.,


1986; Williams et al., 1988).


Davies et al. (1976) found


that tilt values were approximately

to a tilt duration of 30 minutes, after
3-4.5 times basal values. This occur


when PV had reached its nadir (-17%).


1.6-1.9 times higher than basal values up
er which time AVP increased strikingly to

red when HR and BP were stable but


These data support the role of volume


receptors in regulating AVP during postural stress.


Davies, Forsling and


Slater (1977) also documented large increases (approximately 700


) in AVP


release only after 30 minutes of tilt and hypothesized that the delayed increase
was due to the increase in renin and AII.

Basal values of AVP may be higher in the elderly but the magnitude of


increase during tilt may not differ between young and old (Vargas et al.,


1986).


The increase in AVP secretion is most likely due to volume receptors since


osmolality generally remains constant (Greenleaf et al.,


1988; Harrison et al.,


1986


Sander-Jensen et al.,


1986)


however, hyperosmolality cannot be


disregarded since it has been shown to increase (Vargas et al.,


1986).


Differences among studies attempting to document the AVP response
of elderly and young subjects may be due to the existence of responderss" an<


"nonresponders"


Rowe


, Minaker, Sparrow, and Robertson (1982) found that


some subjects did not increase AVP during 8 minutes of quiet standing, and


that the prevalence of "nonresponders" increased with age from 8.3


in young subjects to 46.


(1 of 12)


(7 of 15) in elderly subjects.


Despite the presence of appropriate stimuli and the apparent beneficial
effects of AVP in maintaining BP homeostasis, not all studies have


documented AVP increases during tilt.


Mohanty et al.


(1985) found that AVP








hypothesis is offered by Ecoffey et al. (1985) who found that AVP did not


change in elderly men during tilt when MAP remained constant.


However,


the low angle of tilt (300) may be responsible for the nonresponsivenss of the


neurohumoral system.


, Secher, Astrup, and Warberg (1986) found


unchanged AVP during 200


and 400


tilts associated with unchanged or


increased MAP


Although MAPs were not reported, both Banner et al. (1990)


and Greenleaf et al. (1988) also found no change in AVP during tilt protocols


utilizing 45 and 600


angles, respectively.


The data regarding the AVP response to tilt after physical training are


not entirely consistent.


Greenleaf et al.


(1985) found that AVP increased


during tilt before, but not after, a 12-day heat acclimation/exercise program.
Convertino et al. (1984) also found a decrease in the AVP response to a 600 tilt
after 8 days of training. Compared with the response prior to training, the


peak AVP response declined 37.7%;


statistically significant.


however, this was not found to be


A decline in the AVP response to tilt after training is


consistent with the hypothesis that a training-induced increase in PV better


maintains central BV


and pressure (Convertino et al.,


1984).


In contrast, Greenleaf et al. (1988) found that AVP levels did not


increase during a 600 tilt either before or after 6 months of training.


However,


both pre- and post-training values of AVP were significantly increased by an
identical tilt protocol after 6 hours of water immersion, lending support to
the hypothesis that AVP secretion is not stimulated by reductions in central
BV until PV losses reach approximately 20%.


Renin (PRA).


Renin release from the JG cells in the kidney is








reinforcing its own vasoconstrictor action.


In addition, All increases cardiac


contractility by increasing calcium influx in cardiac myocytes. The
combination of these effects markedly increases BP and makes AII a potent


pressor agent.


AII also contributes to maintenance of salt and water balance


through the stimulation of both ALDO and AVP secretion (Davies et al.,


Goodman & Frey,


1977


1988).


Because of its indirect role in BP and fluid volume homeostasis


renin


is increased during tilt, stimulated by high- and low-pressure baroreceptors


and through n-receptor-mediated mechanisms (Grassi et al.,


1988; Kiowski &


Julius, 1978).


Upright PRA values average 1.9 ng AIeml-1 hr1


, compared


with 1.1 ng AI*ml-1*hr-1 for resting values (Thomas, 1985).

however, the increments during tilt appear to vary widely.


Like AVP


In general,


appears that longer tilt durations elicit greater PRA concentrations, even


when the tilt angle is low.


after a 60-minute


A 74% increase was shown by Banner et al. (1990)


, 450 tilt, while Davies et al. (1976, 1977) found increases of


60-80% during 30 minutes of 85 tilt.

2 hour, 450 protocol (Williams et al.,


Increases of 110-120% were found with a


1988) and with a


minute upright


protocol (Solomon et al.,


1986).


In contrast, Mohanty et al. (1985) found only a


44% increase in young to middle-aged subjects during a 5-minute, 800 tilt


while Lye et al. (1990) saw a 50


increase in PRA in elderly subjects during a


10-minute


, 70 head-up tilt.


One exception to this generalization was the 110-


increase shown by Huber et al. (1988) with a 10 minute upright tilt.


Most authors have found that supine and orthostatic PRA


values


decline with age (Cleroux et al.,


1989; Crane & Harris, 1976; Hayduk et al.,


1973;








decrease in cardiopulmonary baroreceptor sensitivity.


Cleroux et al. (1989)


found that elderly subjects did not increase renin activity during LBNP


despite significant decreases in CVP,
demonstrated significant increases ix
Ecoffey et al. (1985) and Kenny et al.
increase in elderly individuals during


while young and middle-aged subjects
n PRA with equivalent changes in CVP.

(1987) also found that PRA did not
g tilt. However, the low tilt angles used


in these studies may have affected the results:


Ecoffey et al.


(1985) used a 15-


minute, 30 head-up tilt in elderly men, while Kenny et al.


hour, 400 tilt in asymptomatic elderly men and women.


(1987) utilized a


Gender differences


may also have affected the renin response to orthostasis in the Kenny et al.


(1987) study.


Gregerman and Bierman (1981) state that in one-third of females


over the age of 70, renin activity levels are not only low but fail to rise with


postural change.


The use of a combined sample of males and females may


have masked a possible tilt-induced increase in the elderly males.
The PRA response to tilt after training is potentially important since it
may be a primary mechanism for the increase of peripheral resistance


through AII formation.


A decrease in the peripheral resistance response to


orthostasis as a result of endurance training has been proposed as a
mechanism of reduced orthostatic tolerance in trained subjects (Goldwater,


DeLada


, Polese, Keil,


& Luetscher, 1980; Mangseth & Bernauer, 1980).


However, the data are scant and contradictory.


On the one hand


Greenleaf et


al. (1988) found that PRA increased in response to a 600


tilt prior to, but not


after 6 months of exercise training in young and middle-aged men. In
contrast, Convertino et al. (1984) found that 8 days of training did not change








Mohanty et al.,


1985; Vargas et al.,


1986; Williams et al.,


1988; Zerbe, Henry


Robertson, 1983).


Increases can range from a low of 60-80% (Banner et al.,


1990; Jensen et al.,


1989; Sander-Jensen et al.,


1986;


Williams et al.


, 1988) to 150-


170% (Cleroux et al.,


1989; Huber et al.,


1988).


Although some researchers


have found that NE levels are greater at rest (Gregerman & Bierman, 1981


Jensen et al.,


1989


Vargas et al.,


1986) and during tilt (Vargas et al.,


1986) in


elderly subjects when compared to young subjects, Cleroux et al. (1989) found


similar resting NE levels in young (16-30 years),


middle-aged (37-49 years) and


elderly (61-73 years) subjects.


However, Cleroux et al.


(1989) found that the


NE response to an equivalent drop in CVP induced by LBNP was significantly


less in elderly subjects,


and attributed this decline to a reduction in the


sensitivity of the cardiopulmonary baroreceptors.


A reduction in NE


secretion in response to tilt in the elderly is also suggested by comparing the


results of Sander-Jensen et al. (1986) and Ecoffey et al. (1985).


In the former


study, a significant increase in NE was found in response to a 300 tilt in young


subjects,


while in the latter study, no increase in NE was found in 58 to 82


year old men during a 15-minute tilt at the same angle.

The basal function of the adrenal medulla does not appear to change

with age; thus resting levels of EPI remain constant (Gregerman & Bierman,


1981).


Low angles of tilt (e.g., 300) do not appear to stimulate EPI secretion


either in young (Sander-Jensen et al.,


1986) or old (Ecoffey et al.,


1985) subjects.


In contrast, greater angles of tilt (e.g., 450 and 60) stimulated EPI secretion in


young subjects (Banner et al.,


1990


Sander-Jensen et al.,


1986).


The effect of


tilt duration is less clear.


Although some researchers using protocols of


5 and








There are scant data characterizing the catecholamine response to tilt


after training.


The only data appear to be from a heat acclimation/exercise


study by Greenleaf and coworkers (1985); it was found that EPI and NE did not


increase in response to a 700 head-up tilt test prior to 1


days of heat


acclimation and exercise. However, increases were noted during the tilt test
at the end of the 12-day study. The response of elderly individuals after


training has not been studied.


Summary.


Vasopressin, renin, and NE all act to maintain BP


homeostasis during orthostasis via a variety of mechanisms.


Although


increases in these hormones during head-up tilt have not been universally
documented, differences in protocols may account for some of the
discrepancies.

Hormones Associated with Fluid Volume Control: Aldosterone (ALDO)


Increased ALDO causes an increase in the reabsorption of Na+ and water


and an increase in the excretion of K+ in the renal collecting ducts.


its role in defending BV


ALDO.


Because of


head-up tilt increases, while supine posture inhibits,


Upright ALDO levels average 30-280 pg*ml-1 (Loriaux & Cutler, 1986),


compared with 20-100 pg*ml-1 for supine values (Labhart, 1986).

While some investigators have indeed found an increase in ALDO


during head-up tilt (Bie et al.,


1986; Mohanty et al.,


1985; Sander-Jensen et al.,


1986; Vargas et al.,


1986),


other investigators have found increases in ALDO


during tilt only under pathological conditions.


For example,


Harrison and


coworkers (1986) found that tilt-induced ALDO secretion occurred only








Although some authors have found that aging decreases resting
plasma levels of ALDO due to a concomitant decrease in PRA (Crane &


Harris, 1976; Saruta et al.,


1980),


Vargas et al. (1986) found that there was no


age difference between young and elderly subjects in resting ALDO values. In
addition, both age groups increased ALDO secretion to the same extent during


a 10-minute, 700 head-up tilt.


Both resting and tilt findings are consistent


with their data on the renin response.


In contrast, Lye et al.


(1990) did not


find a significant increase in plasma ALDO concentration in elderly subjects
as a result of an identical tilt protocol.


Data on the tilt response of ALDO after training are scarce.


However


data from a cross-sectional study (Skipka et al., 1979) indicate that the response
of ALDO to water immersion may be higher (i.e., less suppressed) in trained
subjects, suggesting a decreased sensitivity of cardiopulmonary receptors.
There may also be an uncoupling of the renin and ALDO responses with


training: Skipka et al.


(1979) found that the responsiveness of ALDO secretion


did not correspond to renin activity levels, which were not significantly
different between trained and untrained subjects at rest and which declined at
a similar rate during immersion.

Adrenocorticotropic Hormone (ACTH)


Because almost any type of physical or mental stress can lead to greatly


enhanced ACTH secretion


, ACTH levels would be expected to increase during


head-up tilt.


In addition


, ACTH secretion is sensitive to atrial stretch (Cryer &


Gann


,1974) so that a decrease in right atrial volume would result in an








maintenance of central BV


during orthostasis (Convertino et al.,


1984).


addition


, a training-induced increase in muscle mass may facilitate venous


return and enhance CVP during orthostasis and thus contribute to CVP

maintenance.

Only two studies have noted the response of ACTH to orthostasis: one

found that there were no changes (Galen, Louisy, Habrioux, Lartigue, &

Guezennec, 1988) while the other found an approximate 100% increase


(Huber et al.,


1988).


Both studies utilized an upright tilt position;


interestingly, it was the shorter of the two protocols (Huber et al.,


1988; 10


minutes vs. 25 minutes) which produced the significant increase in ACTH.

No studies have recorded the ACTH response to tilt after a program of

physical training in either young or elderly subjects.


Protein (PROT),


Sodium (Na+) and Potassium (K+)


Researchers who have measured Na+


, and/or osmolality during a


variety of head-up tilt protocols have generally reported no change (Davies et


,1977; Harrison et al., 1986; Huber et al.,


1988; Mohanty et al.,


1985; Sander-


Jensen et al.,


1986).


Mohanty et al.


(1985) attribute the constancy of K+ to the


secretion of NE which, via a P2-adrenoreceptor-mediated activation of


adenylate cyclase, stimulates the Na+/K+


muscle.


-ATP-ase that pumps K+ into skeletal


When NE secretion during tilt was prevented by bromocriptine


administration, there was a significant increase in plasma K+ concentration.


Sander-Jensen et al. (1986) found small increases in PROT


during both


300 (from 8.27 to 8.63 g*dl


, 4.3%) and a 60


(8.15 to 8.30 g*/dl


, 1.8%) head-








Training does not appear to affect the PROT


tilt in young person

changed during 700

acclimation program


S .


or electrolyte response to


Greenleaf et al. (1985) did not find that Na+ or K+


head-up tilt, either before or after a 12-day heat

i. Greenleaf et al. (1988) also found similar electrolyte


responses during a 600 tilt to tolerance before and after a 6-month training
program; the only exception appeared to be a significant increase in K+ during


tilt prior to training.


Although Greenleaf and coworkers (1985; 1988) found


that PROT increased during tilt both before and after training and/or heat
acclimation, no direct comparisons were made on whether the magnitude of


increase was similar at the two time points.


Data on the PROT or electrolyte


response to tilt after training in older persons are lacking.



Mechanisms Potentially Responsible for Changes
in Orthostatic Responses


Plasma


Volume Changes


One hypothesis regarding improvements in orthostatic responses after
training postulates that an increased BV helps in maintaining orthostatic

integrity by providing a larger fluid volume reserve against which fixed


gravitational forces act (Blomqvist and Stone,


1983


, Bungo, Charles, &


Johnson, 1985; Convertino et al.


,1984; Hyatt and West,


1977


Shvartz et al.,


1981).


Convertino et al.


(1984) and Shvartz et al.


(1981) both document that


decreases in orthostatic HR were related to increases in BV


. Conversely,


Harrison, Kravik,


Geelen, Keil,


& Greenleaf (1985) documented a relationship


Ilflr I. -1 Irr a








physical and physiological variables on peak LBNP tolerance.


Blood volume


contributed to LBNP tolerance in a multiple regression model but the slope
was negative, indicating that a high BV was associated with a lower LBNP


tolerance.


Levine et al. (1991) also found that the subjects with the lowest


LBNP tolerance had the greatest resting PV


. They speculated that the


mechanism responsible for this apparent anomaly might involve a training-


induced increase in left ventricular compliance


this would result in greater


decreases in EDV and SV for a given reduction in EDP during orthostasis and
negate the advantage of an increase in BV.
Paradoxically, the increase in BV together with the parallel increase in


CVP (Convertino et al.


, 1991) may serve to produce a resetting of the low-


pressure cardiopulmonary baroreceptors
volume at equivalent hormonal levels.


This allows an increased fluid


There may also be an attenuation of


the cardiopulmonary receptor stimulus-response mechanism leading to a
reduction in AVP or renin secretion for an equivalent CVP decrement during


orthostasis (Convertino et al.


,1984; Greenleaf et al.,


1988).


An attenuated


hormonal response may result in a reduction in the cardiac output or


peripheral resistance response to orthostasis.


Since higher levels of PRA and


AVP during orthostasis appear to play a major role in maintaining tolerance


(Harrison et al.


, 1985; Sather et al.,


1985; Sather, Goldwater


Montgomery, &


Convertino, 1986; Shvartz et al.,


1981), a reduced response would be


counterproductive.

Muscle Mass Changes








Q and arterial pressure during orthostasis.


Postural hypotension in response


to simulated microgravity has been associated with decreased musculature,


particularly in the lower extremities,


and increased compliance in the leg


vasculature (Convertino et al.


,1989; Duvoisin et al.,


1989).


Early training


studies (Shvartz, 1968a; Shvartz, 1969) suggested that resistance training
improved chronotropic responsiveness to standing or head-up tilt. However,
it could not be determined whether the improved responses were due to
increases in muscle mass or changes in baroreceptor sensitivity.


Changes in Baroreceptor Sensitivity

High-pressure baroreceptors in the carotid sinus and aortic arch are


mechanoreceptors sensitive to changes in arterial pressure.


pressure, such as is induced during orthostasis,


A fall in arterial


decreases afferent nerve


activity and releases inhibitory activity in the cardiovascular centers of the


central nervous system.


A series of reflexes ensue which act to maintain


arterial pressure by increasing Q and/or peripheral resistance.


is an increase in HR and contractility


The end result


increased veno- and vasoconstriction,


and reduced blood flow to the skin, skeletal muscles,


area (Convertino


kidney and splanchnic


, 1987).


The effect of physical conditioning on baroreflex sensitivity is a
controversial issue, partially due to the use of different experimental designs


(cross-sectional vs. longitudinal).


An early cross-sectional study by


Stegemann, Busert, and Brock (1974) found that the HR and BP responses to
both neck suction and neck pressure were less in trained runners than in








(Raven, Graitzer, Smith, & Hudson,


1985; Raven, Rohm-Young, &


Blomqvist, 1984).


In contrast, Barney et al.


(1985) found that young endurance


trained men had increased baroreceptor responses to neck suction when


compared to untrained men.


Finally


some cross-sectional studies provide


evidence that training does not affect the baroreflex.


Falsetti


, Burke, and


Tracy (1982) found that the HR responses of trained swimmers and untrained


controls to neck suction and neck pressure were similar.


In addition, MAP


responses of the two groups to LBNP were not significantly different.
Hudson, Smith and Raven (1987) also found that baroreflex sensitivity at


mmHg of LBNP was similar for trained and untrained women.


(1991) found similar baroreflex responses in high-


Levine et al.


mid-, and low-fit young


men in response to neck suction and neck pressure.


Finally,


Fiocchi


, Fagard,


Vanhees, Grauwels,


and Amery (1985) found that baroreflex sensitivity did


not correlate with


VO2max in trained cyclists.


However, the low correlation


= 0.05) may be partly due to the homogeneity in the


VO2max values (54.1 _+


1.4 ml-kg-1*min-1).


Longitudinal animal data provide equally equivocal results.


Tipton,


Matthes, and Bedford (1982) and Bedford and Tipton (1987) provide animal
data in support of the hypothesis that endurance training attenuates


baroreflex control of BP


, particularly during hypotensive episodes.


In their


experiments, trained rats experienced greater and faster falls in arterial
pressure during LBNP than untrained controls; the group differences were


abolished with baroreceptor denervation.
Mass, & Jones (1990), using a dog model,


The data from Gwirtz, Brandt,

support this conclusion. However,








Longitudinal training data in humans is scarce.


Somers, Conway,


Johnson, & Sleight (1991) reported that 6 months of endurance training in
middle-aged hypertensives resulted in an increase in baroreceptor sensitivity


as measured during phenylephrine infusions.


decreases of 9.7


This was accompanied by


and 6.8 mmHg in systolic and diastolic pressures, respectively,


a prolongation of the R-R interval, and an increase in the R-R variability.
They noted, however, that hypertension is associated with a decrease in


baroreceptor sensitivity and a decrease in the R-R variability,


appeared to normalize with training.


and that these


Whether normotensive individuals


would see the same changes was not investigated.
In contrast, Seals and Chase (1989) suggest that training has no effect on


baroreceptor responsiveness.


They found that 11 weeks of endurance training


in middle-aged and older men did not alter the baroreflex control of HR in


response to neck suction, neck pressure, or LBNP. Similarly,


Vroman, Healy,


& Kertzer (1988) report that 12 weeks of endurance training in young men
produced no change in the baroreflex sensitivity (as measured by AHR/ASBP)


during LBNP at -40 mmHg.


While baroreflex sensitivity


decreases with age


(Gribbin et al.


1971


Lipsitz, 1989), the effect of training on this parameter has


not been investigated.

Altered Hormonal Response


The response of vasoactive hormones to orthostasis may be affected by
training if low- and/or high-pressure baroreflex sensitivity is altered.
Although basal AVP secretion does not appear to change with training









1986; Skipka et al., 1979).


Kiyonaga et al.,


A reduction in resting (Hagberg et al.,


1989b;


1985) and orthostatically-induced (Goldwater et al.,


1980) NE


secretion after training may be a mechanisms for reducing renin secretion


after training (Davies et al.,


1977).


Changes in vascular sensitivity to pressor hormones may also play a


role in altering responses to orthostasis.


Wiegman et al.


(1981) found


decreases in vasoconstrictor, and possibly venoconstrictor,


response to NE


after 6 weeks of endurance training in rats, and hypothesized (Wiegman,


1981) that P3-adrenergic sensitivity was increased.


This could play a role in


altered BP and peripheral resistance responses during orthostasis.

Summary


Physiological responses hypothesized to contribute to the maintenance
of arterial pressure during orthostasis are altered by physical training. The
direction of change, however, is not always consistent with an improvement
in the orthostatic responses, when each mechanism is considered separately.
Blood volume increases may provide a larger fluid volume reserve to offset
fluid translocation during orthostasis; however, the effect of this larger
volume may be to reduce cardiopulmonary baroreceptor sensitivity and


vasoactive hormone release.


The chronotropic responsiveness of the high-


pressure baroreceptors may also be attenuated


this may be offset somewhat by


a larger BV


and an improved SV


. Finally


training may improve muscle


mass and tone and thus improve responses to orthostasis via an improved













CHAPTER 3
METHODOLOGY


Subiects


Eighty-three subjects, ranging in age from 60 to 82 years, volunteered to


participate in this study.


An initial screening by telephone was used to


identify subjects who were within the desired age range, had been sedentary
for at least one year, and who had no overt history of cardiovascular or
pulmonary disease, or any orthopedic limitations to exercise testing and


training.


Subjects meeting these criteria reported to the laboratory where the


entire study protocol,


the inherent risks and hazards of the study, and the


necessary time commitment were explained.


Subjects were also asked to


complete demographic, medical history, and activity questionnaires


(Appendix A).


These forms were reviewed by the investigator; subjects not


meeting the physical and health requirements for the investigation were


notified and excluded from the study.

were scheduled for a further screening


Subjects meeting the requirements
visit. Written informed consent was


obtained from each subject who wished to continue (Appendix B).


Based on


this orientation, eight subjects were disqualified due to prior cardiac disease (n


= 5) or other medical or orthopedic problems (n


= 3).


Ten subjects elected not


to continue.


All procedures were approved by the University of Florida


'nllhlrnro h Srf NKnA Tnoe-eIiTan flnrtr.. f. IT A / C'\








cardiovascular physical examination, including a resting 12-lead


electrocardiogram (ECG).


If any clinically significant findings such as


hypertension (blood pressure [BP] exceeding 160/100 mmHg at rest),


angina


pectoris, or an abnormal resting ECG (ST segment depression or elevation
that is horizontal or downsloping greater than 1 mm, 0.08 seconds from the J-
point, or the presence of abnormal Q waves) were found, the subject was
referred to his/her personal physician and excluded from participation in the
study.

Subjects that were deemed suitable were then administered a graded
treadmill exercise test (GXT) according to the Naughton protocol (Naughton


& Haider, 1973).


The protocol used a constant speed of


2 miles *hour-1


grade was 0


initially and increased 3.5


every


2 minutes.


The test continued


until the subject reached voluntary maximal exertion or became symptomatic


with positive hemodynamic or medical indices.


Heart Rate (HR) and ECG


were monitored continuously throughout the exercise and recovery periods.
A 12-lead ECG was recorded at the end of each stage of exertion, at peak


exercise, and at each minute for


7 minutes of recovery; a 3-lead ECG rhythm


strip was recorded at the intermediate minute of each exercise stage.


Blood


pressure was measured by auscultation at rest prior to exercise, at the end of


each stage of exercise, immediately post-exercise, and at minutes 1,


3, 5, and


of recovery. Rating of perceived exertion (RPE) using the Borg scale (Borg,
1982) was determined during each minute of exercise.
For subjects to continue in the study, the test must have been
terminated by the subject because of fatigue with no significant evidence of





59

horizontal or downsloping ST segment depression that was greater than 3
mm at 0.08 seconds after the J-point, second or third degree heart block, onset


of bundle branch block,


ventricular couplets (> 2/min), ventricular


tachycardia (2 3 consecutive PVC's),


RonT


premature ventricular


contractions (PVCs),


frequent unifocal PCVI


10/min),


frequent multifocal


PVCs (>4/min),


a BP in


excess


of 250/110, or a drop in systolic BP (American


College of Sports Medicine, 1991).


All GXTs were supervised by a physician


trained in cardiovascular exercise testing. A crash cart with all necessary
emergency medications and a defibrillator was immediately adjacent to the
treadmill during every GXT.

Based on the physical examination and GXT, 21 subjects were


disqualified from further participation in the study.
disqualification included elevated resting BP (a = 5)


Reasons for


, other resting ECG


abnormalities (n


= 2), abnormal HR or BP response to exercise (a


segment depression during exercise (n


= 10).


= 4), and ST


Thus, 44 subjects (14 males, 30


females) were accepted into the study.


Type of Data Needed


The criterion measures indicative of the cardiovascular response to an


orthostatic stress were the HR


, stroke volume (SV), cardiac output (Q) and BP


responses during a 30-minute supine rest; a 15-minute,


700 head-up tilt; and a


15-minute supine recovery. These responses were recorded during initial (T1)
testing and also at the midpoint (13 weeks; T2) and end (26 weeks; T3) of a
physical training program (Appendix D).








baroreflex function, c) increased muscle mass, and d) improved hormonal


response.


An appropriate analysis of each mechanism was needed to


determine which factor, if any, contributed to improved orthostatic responses.
Blood volume was measured at T1 and T3 using the Evan's Blue dye


technique (Greenleaf et al.,


1979) while baroreflex responsiveness was assessed


by analyzing the HR response to coughing in the supine and 70 tilt positions


(Cardone et al.


1987


Maddens, Lipsitz, Wei,


Pluchino, & Mark, 1987;


Wei &


Harris


,1982).


Lower body muscle mass was assessed using dual x-ray


absorptiometry (Haarbo, Gotfredsen, Hassager, & Christiansen, 1991).
Increases in vasoactive hormones in response to upright tilt act to


maintain blood pressure.


Therefore, the levels of vasopressin (AVP),


plasma


renin activity (PRA), norepinephrine (NE) and epinephrine (EPI) were


assessed at rest and during upright tilt.


Other hormones and electrolytes


instrumental in fluid volume control and the stress response


adrenocorticotropicc hormone [ACTH],


aldosterone [ALDO],


sodium [Na+],


potassium [K+],


and protein [PROT]) were also measured at rest and during


Finally, data from a maximal oxygen uptake test and strength tests were


used to


assess


the presence and magnitude of the training response.


Methods of Data Collection


Maximal Oxygen Uptake (VO2max) Test


Prior to testing, a 20 or


gauge, 1 1/2


inch venous catheter was placed


under aseptic conditions in an antecubital vein for blood sampling to





61

Subjects rested in the supine position for 20 minutes after catheter placement
before a 24-26 ml blood sample was drawn for determination of resting


hormones, PROT


and electrolyte values.


The blood sample was divided


among pre-chilled vacuum-type collection tubes (Vacutainer, Becton-


Dickinson, Rutherford,


(for ACTH, AVP
electrolytes, EPI,


minutes at


NJ) containing ethylenediaminetetracetic acid (EDTA)


, PRA, ALDO), or heparin/EGTA/glutathione (for PROT,
NE). The samples were centrifuged at 3500 rpm for 15


2-4 C. The plasma was placed into separate polypropylene tubes


and kept frozen at -200


C (ACTH, AVP,


PRA


, ALDO, PROT


electrolytes) or


-800 C (NE, EPI) until analysis.


The subject then performed a symptom limited maximal treadmill test


to determine peak oxygen consumption.


protocol; however


The test consisted of the Naughton


if the subject walked for longer than 12 minutes during


the initial screening GXT


miles hr-1


the initial speed during the


, rather than 2 miles hr-1


VO2max test was 3


During the V0O2max test, the subject


breathed through a mouthpiece attached to a low-resistance breathing valve
and had a nose clip in place; expired air was collected in meteorological


balloons.


The expired air was analyzed for fractional oxygen and carbon


dioxide concentrations using gas analyzers (Ametek-Thermox, Pittsburgh,


PA) calibrated with precision gases.


Expired gas volumes were measured with


a 120 liter


Tissot spirometer (Collins,


During the


Braintree, MA).


VO2max test, the subject's HR, ECG,


and RPE were


monitored in the same manner as during the screening GXT


signs and symptoms used for stopping the GXT


and the same


prior to the subject's








initial


VO2max protocol except that blood samples were not taken at T2.


Ambient temperature during the test was kept at 23-240C.


Tilt Table


Test


Preparation for testing included the placement of ECG electrodes (for


monitoring standard and augmented limb leads),


and mylar-coated


aluminum electrode tapes around the neck and thorax (for monitoring HR,


A 20 or


gauge, 11/2


inch venous catheter was placed under


aseptic conditions in an antecubital vein for a) PV measurement, and b) blood


sampling to determine plasma hormones,


PROT, electrolytes, Hb and Hct


before and after the tilt procedure. The catheter was kept patent during the
entire test period with sterile heparinized saline. A small (approximately 1
ml) venous blood sample was taken at the time of the catheter insertion for
the determination of Hct, which was necessary for the calculation of SV with
the impedance cardiograph.

The subject assumed a supine position on the motorized tilt table


(Model 720, Tri W-G,


, Valley City


ND) and was connected to ECG


(Quinton, Seattle,


WA) and cardiac impedance (Minnesota Impedance


Cardiograph, Model 304B,


Surcom, Inc.,


Minneapolis, MN) monitoring


devices.


A BP cuff was fitted around the upper arm for manual BP


measurement.


Heart rate, SV


and BP were measured during a 30-minute


supine control period after 15,


and 30 minutes.


Stroke volume was


measured with the impedance cardiograph using three representative
waveforms during the first 15-20 seconds of each measurement period. Heart





63

output was calculated by the impedance cardiograph as the product of HR and
SV. Systolic and diastolic BP were measured manually with a mercury


sphygmomanometer (PyMoh,


Somerville


, NJ) and stethoscope after the


impedance measurements were made.


A digital readout of the HR was


continually available on the ECG monitor and a 6-second rhythm strip was


recorded along with the cardiac impedance measurements.


A 24-26 ml


venous blood sample was drawn after approximately 28 minutes of supine
rest for the duplicate determinations of plasma hormones, PROT, and


electrolytes; blood samples were treated as described for the


VO2max test.


blood sample for triplicate measurements of Hct and Hb was placed in a pre-
chilled EDTA-treated vacuum-type collection tube and placed on ice or
refrigerated until analysis.

At the end of 30 minutes of supine rest, baroreflex responsiveness was


assessed by the response to coughing (Cardone et al.,


1987


Wei & Harris,


1982).


A 1-minute baseline period commenced and the BP was measured


during the final 30 seconds of this period. The subject was then instructed to
cough by inhaling deeply and coughing forcefully 3 times in rapid succession.
Blood pressure was measured immediately on cessation of the cough. An
ECG strip was recorded continually beginning 10 seconds prior to the cough to
provide the baseline R-R interval, and ending 1 minute after cough cessation.
The sequence was repeated two more times.
Plasma volume (PV) measurement was then made. For this
measurement, a 23 gauge butterfly infusion set was inserted into an
antecubital, wrist or hand vein on the arm opposite the one in which the








minutes after the injection (Greenleaf et al., 1979).


The blood was placed in a


heparin-treated vacuum-type collection tube and centrifuged at 3500 rpm for


15 minutes at 2-40 C.


frozen at


The plasma was placed in a polypropylene tube and kept


-20 C until analysis.


After PV determination


, the fixed-speed motorized tilt table was


brought from supine to the 700 head-up position, taking approximately 15-20


seconds.


The 15-minute tilt period began once the subject was in the 700


head-up position (To).


A HR rhythm strip was recorded every minute during


the first 6 seconds of each minute. Impedance measurements were made
during the first 15-20 seconds of each minute. Blood pressures were recorded


30 seconds after TO and after impedance measurements at minutes 1,


and 15.


2, 3, 4, 5,


A 24-26 ml venous blood sample was drawn between minutes 13-


15 of the tilt procedure and analyzed for Hct, Hb, plasma hormones,


PROT


and electrolytes. At the end of the 15-minute tilt, the subject again repeated
the cough sequence while in the 700 head-up position.


The tilt test was discontinued if any of the following occurred:


a) the


subject reached the predetermined time limit for the tilt portion of the test; b)
presyncopal symptoms such as a fall in systolic BP greater than 15 mmHg
between adjacent 1 minute measurements and/or a sudden bradycardia

greater than 15 beats *min-1 occurred; c) the systolic BP fell below 80 mmHg;
or d) the subject requested to stop due to dizziness, nausea, or discomfort


(Sather et al.


,1986).


Following completion or discontinuance of the tilt portion of the test,
the subject was returned to the supine position in approximately 15-20








refrain from conversation, aside from answering any questions from the

investigators regarding their status, and from unnecessary movement.


Temperature during the test was kept at 23-240C.


The tilt test was repeated at


T2 and T3 and was identical to the initial test except that PV was not
measured and blood samples were not taken at T2.


Strength


Testing


One repetition maximum (1-RM) leg


NautilusTM (Dallas,


TX) Leg Press machine.


strength was assessed using the

Arm strength was assessed with


the NautilusTM Biceps Curl machine and the NautilusTM Triceps Extension


machine.


Subjects with range-of-motion limitations in the hip, knee, or


shoulder were tested by either adjusting the seat position on the machine or


by "double pinning" the weight stack.
pain-free part of their range-of-motion.


Thus subjects were tested through the
These variations were recorded so


that subjects were tested in the same manner at T2 and T3.


warming up with 4-5 submaximal repetitions.


subsequent single lift was increased by


Subjects began by


The resistance on any


10 pounds according to the difficulty


with which the subject executed the previous lift; a one minute rest was


allowed between trials.


The 1-RM was considered to be the maximum


amount of weight that could be lifted through the subject'


pre-determined


full range-of-motion.

Lumbar extension strength was assessed with a MedXTM (Ocala, FL)


Lumbar Extension machine.


Subjects underwent a multiple joint angle test


consisting of maximum voluntary isometric contractions at seven angles (0









Testing always proceeded consecutively from


to 0


of flexion.


criterion measure consisted of the maximum strength averaged over the
number of angles tested.

Body Composition


Muscle mass was assessed noninvasively using a Dual-Energy X-ray


Absorptiometer (Lunar Radiation,


Madison,


WI).


The subject lay in a supine


position while the X-ray scanner performed a series of transverse scans


moving from head to toe at 1 cm intervals.


Measurements of total and


regional bone mineral content, fat mass and fat free mass were obtained.

Measurements of skinfold thickness were made with Lange calipers


(Cambridge, MA) at the triceps, chest, axilla, subscapula,


abdomen,


suprailium, and thigh, following the procedures outlined by Pollock and


Wilmore (1990).


Measurements from the seven sites were summed (17).


Body circumferences were measured with a steel tape at the shoulder,


abdomen, waist, gluteus, right thigh,


and right upper arm following the


procedures outlined by Pollock and Wilmore (1990).


Blood Sample Analyses


Plasma volume analysis.


T-1824 (Evan's blue) dye analysis was based


on the methods of Greenleaf et al.


(1979).


The dye from the plasma sample


was extracted onto a wood-cellulose powder (Solka Floc


SW-40A)


chromatoeraDhic column after it had been spnaratfrp from thp al nhrmirn hr ho








water mixture.


The addition of KH2PO4 buffered the pH of the eluate to 7.0;


the absorbance of the eluate was read at 61


nm.


Plasma volume was


calculated from the formula:


(VXD)(STXv)


1.03(T)


where


= volume (ml) of T-1824 dye injected (22.6 mg/5 ml)
= dilution of standard (1:250)
= absorbance of standard
= volume of sample extracted (1.0 ml)
= absorbance of plasma sample
= correction factor for dye uptake by tissues


BV was calculated as PV/(1


- 0.91Hct).


Hemoglobin (Hb) concentration was


determined with triplicate measurements using the cyanmethemoglobin


method (Sigma Diagnostics, St. Louis,


MO) and a Spectronic 20D


spectrophotometer (Milton Roy Company, Rochester


NY).


Hematocrit (Hct)


was measured in triplicate with a microhematocrit centrifuge (IEC,


Model


, Needham Heights,


MA) and a Fisher Micro-capillary


Tube Reader.


Hematocrit measurements were not corrected for trapped plasma or for


whole body hematocrit.


Percent changes in PV


BV and red cell volume


(RCV) during the tilt procedure were calculated from Hb and Hct

measurements according to the formulas of Dill and Costill (1974):


BVA
RCVA
PVA
ABV,%
ARCV,
APV,%


= BVB (HbB/HbA)
= BVA (HctA)/100


=BVA


-CVA


= 100 (BVA
= 100 (CVA
= 100 (PVA


- BVB)/BVB
-CVB)/CVB
-PVB)/PVB


Hemoglobin; hematocrit.








Hormone analyses.


Vasopressin was extracted from 0.5 ml plasma


samples by adsorption to bentonite and was eluted from the bentonite with a


(volume to volume) mixture of acetone and 1.0 N HC1.


Average recovery


was 80


results were not corrected for recovery.


Dried extracts were


reconstituted to 0.25 ml with assay buffer (0.05 M phosphate buffer containing


0.01 M EDTA and 0


bovine serum albumin; pH


= 7.4).


Vasopressin was


measured by radioimmunoassay (RIA) using a highly specific anti-AVP


polyclonal antibody (raised in the laboratory of Dr. Charles Wood,


of Florida).


University


125I-labeled AVP (DuPont, Welmington, DE) was used as tracer,


and AVP (Sigma) was used as standard.


The range of the standard curve was


from 0.05 to 10 pg per tube.


The detection limit of the assay (90


of maximal


binding) was 0.078 pg per tube, which translated to 0.39 pg*ml-1 after


extraction of 0.5 ml of plasma.


Values below 0.39 pg*ml-1 were assigned a


value of 0.39 pg*ml-1 for statistical purposes. T
variation for a low pool (0.40 pg per tube) was 4


he intra-assay coefficient of

% (n = 10) and for a high pool


(4.0 pg per tube) was 14%


(0.35 pg per tube; n


= 10).


= 13) (Raff, Kane


Interassay coefficient of variation was

, & Wood, 1991).


For ACTH analysis, plasma samples and standard (0


ml) were


extracted on powdered Coming glass (0.35mg per 0.5 ml of plasma, 100-200


mesh in double-distilled water, Coming Glass Works,


Coming, NY) and


eluted from the glass with a 1:1 (volume to volume) mixture of 0.25 N HC1


and acetone.


Dried extracts were reconstituted to 0.5 ml in assay buffer (0


phosphate buffer, pH


7.4).


Adrenocortocotropic hormone was measured by


RIA using an antibody specific to 1-39 hACTH raised in rabbits in the








Medicine)


125I-labeled ACTH was used as tracer.


Values for extracted plasma


samples were corrected for recovery using extracted standard.


The lowest


standard used in the assay was 20 pg*ml-1; values below this were assigned
the value of 20 pg*ml-1 for statistical purposes. Interassay coefficients of


variation were 19


and 9.8% from samples of mean concentrations of 33


pg*ml-1 (n


= 24) and 76 pg*m1-1 (n


= 24),


respectively (Bell, Wood, & Keller-


Wood, 1991).
Aldosterone was measured using a RIA kit from Diagnostic Products


Corporation (Los Angeles, CA).


Unextracted plasma samples were placed in


ALDO antibody-coated tubes to which 125I-ALDO was added; samples were


then incubated for 3 hours at 370 C.


to 1200 pg*ml-1


. Values below


pg*ml-1 for statistical purposes. Intr
by Diagnostic Products) ranged from


The range of the standard curve was from

pg*ml-1 were assigned the value of 25
aassay coefficients of variation (provided


for samples with a mean


concentration of 803 pg*ml-1 to 8.3% for samples with a mean concentration


of 52 pg*ml-1


Interassay coefficients of variation (provided by Diagnostic


Products) ranged from 3.9


for samples with a mean concentration of 468


pg*ml-1 to 10.4% for samples with a mean concentration of 51 pgml-1.
Due to inadequate storage the plasma samples for PRA were damaged
and the data is not presented.
Epinephrine (EPI) and norepinephrine (NE) were analyzed using high
performance liquid chromotography (HPLC) using a Waters (Millipore


Corporation, Milford,


MA) HPLC system consisting of an injector unit (WISP


TM Model 712B), pump (Model 510),


and electrochemical detector (Model








extracted from this solution by adsorption onto alumina and were eluted


from the alumina with a


1:1 (volume) mixture of glacial acetic acid,


10%


sodium disulfide


, and 5% EDTA. A 20 ml sample of extract was injected onto


a reverse-phase C18 column and EPI and NE were measured by


electrochemical detection of the column effluent.
recovery using the internal standard. The intraa


Values were corrected for


ssay coefficient of variation


for NE was 1.4% while the interassay coefficient of variation was 3.8%


(Convertino et al


., 1991).


Total plasma PROT


was determined using refractometry.


This method


is based on refraction and change in velocity of light waves as they cross an


air/fluid interfac

(Raphael, 1976).


e.


The higher the solute content, the greater the refraction


Using this method, a 20 jl drop of plasma was placed on the


refractometer glass; light was admitted through a prism and PROT


determination made to the nearest 0.:
determined to the nearest 0.1 mEq L


. Both Na+ and K+ were


-1 from plasma samples using a Nova I


ion-specific electrode system (Nova Biomedical,


Waltham, MA).


Training

The 44 subjects who completed the initial testing were randomly


assigned to one of two experimental (exercising) groups,


exercising control group.


or to a non-


The experimental groups undertook endurance


training on a treadmill (Trackmaster, Model TM 200E, JAS Mfg., Carrollton,


TX) (TREAD; n


= 16), or endurance-plus-resistance (NautilusTM plus MedXTM)


training (TREAD/RESIST; n


= 17).


The remaining 11 subjects were assigned








Training for


TREAD and TREAD/RESIST


consisted of three sessions


per week for 26 weeks.


All training sessions began with 5 to 10 minutes of


warm-up exercises and ended with a


5 minute cool-down walk.


Initially all


subjects exercised for 20 minutes at 40 to 50%

reserve (HRRmax) (Pollock & Wilmore, 1990).


of their maximal heart rate

Exercise duration was increased


by 5 minutes every


2 weeks until exercise time was 40 minutes.


week, exercise intensity was gradually increased to 60-70


After the fifth


HRRmax.


Intensity


was increased first by increasing the walking speed until the subject reached a


, brisk pace; further increases in intensity were accomplished by


raising the treadmill grade. O

duration and 60-70% HRRmax

through the 14th week. Ratin;


sessions averaged approximately 1


nce subjects reached 40 minutes of exercise

, the intensity and duration were maintained

g of perceived exertion (RPE) during these


13 initially (light/somewhat hard) and


progressed to 13-14 (somewhat hard/hard,


intensity for weeks 1-13 was 62.6 + 4.2


heavy).


HRRmax.


The average training


A VO2max test was


administered at T2 and training heart rates were adjusted for the latter half of


the study based on the results of this test.


Beginning in the 15th week,


subjects gradually increased their intensity to 75-85


HRRmax


while duration


was increased to 45 minutes.


The average training intensity and RPE for


weeks 15-26 was 78.


7 +4.6


HRRmax and 14-15 (hard),


respectively.


The subjects in


TREAD/RESIST


additionally performed selected


resistance training exercises during the 26 weeks of the study.


One set each of


8-15 repetitions of biceps curl, triceps extension and leg press was performed 3


times per week, while one set of 8-12


repetitions of lumbar extensions was


comfortable








that produced volitional muscle fatigue in 12-20 repetitions.


could consistently complete 12-15
repetitions for the leg exercise, or


When subjects


repetitions for the arm exercises, 15-20
10-15 repetitions for the lumbar extension


exercise, resistance was increased by approximately 5%.


Based on a comparison to the


1-RM values, training intensity for


the first 13 weeks averaged 67.9, 85.4, and 99.6


1-RM for the leg press,


biceps


curl and triceps extension exercises, respectively.


weeks averaged 73.


Intensity for the final 13


, and 97.5% of the T2 1-RM for the leg press, biceps


curl, and triceps extension, respectively.


Training intensity for the lumbar


extension averaged 61.5% of the Ti peak torque during weeks 1-13, and 66.4%
of the T2 peak torque during weeks 14-26.


Data Analysis


Dependent Measures


The dependent measures consisted of the HR, SV


and BP


measurements taken at successive time intervals during the tilt test.


Calculated variables, such as mean arterial pressure (MAP


= DBP + 0.33 [SBP


DBP]), TPR (MAP/ Q) and Q were also dependent measures during the test.
Due to the assessment of several potential contributing mechanisms to
any possible improvements in orthostatic response, other variables assumed


dependent status in the various analyses.


These variables included PV


total


body and regional muscle mass,


VO2max,


maximal strength, hormonal response to tilt,


and the response to cough.









Statistical Analyses

Forty-one of the original 44 subjects completed training and/or their


obligations as control subjects.


Of these 41


8 were eliminated from statistical


analyses due to p-blockade medication (n


- 3),


the presence of advanced


cancer (n_


= 1), or pre-syncopal symptoms during T1 tilt testing (n_


=4).


Data


from the subjects experiencing pre-syncopal symptoms during T1 tilt testing


were analyzed separately.
unless otherwise indicated


Therefore, the sample size used for all analyses,


is 33.


Group characteristics,


VO2max


, strength, and body composition.


order to determine whether initial group characteristics were similar, the


age,


height, weight,


and relative


VO2max (ml kg'- min-1) were each


analyzed using


a one-way anlaysis of variance (ANOVA) with Duncan's


multiple range test.


The change in


and relative


VO2max values over 26


weeks was analyzed in a


2 X 3 (time X group) repeated measures ANOVA


design.


A one-way


ANOVA and a Duncan's


multiple range post-hoc test


performed on lower body lean mass measurement, and on the


Tl maximum


strength values for leg press (LP),


biceps curl (BI),


and triceps extension (TRI)


values, and lumbar extension (LE) indicated that there were initial group
differences that could be accounted for by including gender in the T1


ANOVA.

done in a


Therefore, the analyses of the strength and lean mass changes were

2 X 3 (time X group) analysis of covariance (ANCOVA) design using


the T1 score as the covariate.





74

suggested that the multiple time measurements for each variable could be
collapsed in order to provide a smaller number of representative values.
Therefore a one-way repeated measures ANOVA using the four resting
supine measurements was performed for each of the dependent measures.
High type I error rates indicated that differences among the four values were

due to random variation; the four values for each variable were therefore
averaged to provide a single resting measurement.


Similarly, a series of repeated measures analyses for HR, SV


DBP


Q, SBP


MAP, and TPR were performed on the measurements made during tilt


(TILT) and supine recovery (REC).


Separate analyses for HR, SV


, and Q were


done on the measurements from minutes


and REC.


, 6-10 and 11-15 for both TILT


Analyses of the BP variables and TPR were done on measurements


from minutes


during both


TILT and REC.


An a priori decision was made


not to include the raw data from TILTO, TILT1


RECo, and RECi in these


analyses since these time points represented transitional periods where
values were rapidly changing.


T1 resting values of HR, SV


SBP


DBP


MAP


and TPR were


compared among the three groups using a one-way


ANOVA.


The effect of


training on the resting variables was investigated in a


2 X 3 (test X group)


repeated measures ANOVA.


Using the collapsed resting, tilt and recovery values,


a 2 X 3 X 11 (test X


group X time) repeated measures ANOVA was used to compare rest, tilt and


recovery values for each dependent variable.


A significant test effect for a


particular variable was further evaluated by creating a mean value (collapsed








and test.


A significant time effect for a particular variable was evaluated by


comparing the TILT and REC values, collapsed over group and test, to the


resting value in a one-way


ANOVA with 11 levels of time.


Plasma volume and hormone/electrolyte responses.


Plasma volume


measurements were obtained successfully at both T1 and T3 in only 18 of 33


subjects.


Because of the small number of subjects with duplicate PV


measurements in each of the training groups,


TREAD/RESIST


analyses.


subjects in TREAD and


were combined into a single group (TRAIN) for PV statistical


In order to determine whether initial group values were similar,


the T1 pretilt PV


RCV


, Hb, and Hct were each analyzed using a one-way


ANOVA with Duncan's multiple range post-hoc test.


To determine whether


tilt and/or training affected these variables, PV


RCV


, Hb, and Hct were


each analyzed in a 2 X 4 (group X time) repeated measures ANOVA design.


The time levels represented pretilt and tilt at both T1 and T3.


The percent


change in PV


, and RCV during tilt at T1 and T3 were analyzed in a


2X2


(group X time) repeated measures ANOVA.


combining


Because of the necessity of


TREAD and TREAD/RESIST into a single group for the various


BV analyses, the hormonal responses were similarly analyzed in


X time) repeated measures ANOVA designs.


2X4 (group


The time levels represented


pretilt and tilt at both T1 and T3.


Cough test.


The parameters measured during the cough test


represented the reflex responses in the presumed baroreceptor-mediated
event; no direct measure of the reflex stimulus (e.g., intra-arterial pressure


measurements) was available.


The resting R-R interval for each cough test





76

after cough cessation at which the minimum R-R interval occurred, and the
number of R-R intervals occurring between the cessation of coughing and the


minimum R-R.


From these parameters, the difference between the resting


and minimum R-R was calculated (A R-R).


Means and standard deviations of


the first 40 intervals after the cough were calculated and transformed to HR


values with the formula: HR


= 60/R-R.


To determine whether values from the three supine and three tilt


cough trials were comparable, the resting R-R,


minimum R-R


, A R-R, time of


minimum R-R, and interval of minimum R-R were each analyzed in a one-


way repeated measures ANOVA.


Based on the results of these tests, the three


supine and three tilt values were each averaged. Using the averaged values,
group differences at T1 were assessed using a one-way ANOVA and Duncan's


multiple range test.


The effect of training was analyzed with an ANCOVA


design with the TI values as the covariate.

Analysis of the 40 beats after the cessation of coughing was done on HR


values averaged every five beats.


A one-way


ANOVA with nine levels of


time was used to compare the resting HR with the eight averaged post-cough


HRs for each test and group.


assess


the effect of tilt and training, a 4 X 3


(test X group) repeated measures ANOVA was performed for each of the


nine time points.


The four tests were


T1 supine,


T1 tilt,


T3 supine and T3 tilt.


In all cases, statistical probabilities are presented as the chances of
concluding wrongly that the mean values obtained during the tilt test were
due to true differences and did not arise from random variability given the


sample size of this experiment. A p


< 0.05 was required for statistical













CHAPTER 4
RESULTS


Subject Characteristics


Descriptive data on age, height, weight, and sum of seven skinfolds


(7) at the start of training are presented for the control (CONT),


treadmill


(TREAD), and treadmill plus resistance (TREAD/RESIST) groups in Table 4-1.


The results of the ANOVA performed to


assess


differences in initial subject


characteristics indicated a large type I error rate for weight (gp


= 0.15),


height (p


= 0.14) and


= 0.49).


Thus


, any differences in these three variables at the


start of the training program were due to random variation.


However, the


probability of a type I error for the age analysis was small (p


= 0.01).


Post hoc


analysis using Duncan'


multiple range test indicated that TREAD was older


than CONT at the start of the program.


Table 4-1


Characteristics of Control


, Treadmill, and Treadmill/Resistance


Training Groups at the Start of 6 Months of Exercise Training.


Group


CONT (n =
TREAD (n


Age
(yrs)


65.8 + 6.7
72.4 + 4.5*


= 14)


TREAD/RESIST (n


= 10)


7 3.8


Height
(cm)


164.9 +
161.4


168.8 + 11.4


Weight
(kg)


71.0 + 1


61.8 +


73.4 + 17.8


7
(mm)


18654


173
150 +


Values are mean S.D.










Training Responses


Maximal Oxygen Uptake


Tl and T3


VO2max (ml* kg-1 min-1) values for CONT


TREAD,


and TREAD/RESIST are listed in Table 4-2.


The results of the ANOVA to


assess


differences in T1


values indicated that any differences among groups in


initial


VO2max were due to random variation (p


= 0.32).


The 2 X 3 (test X


group) repeated measures analysis used to


assess


the effects of training


resulted in a type I error rate of


< 0.01 for detecting a test X group interaction.


Follow up analyses showed that after 26 weeks of training,


TREAD and


TREAD/RESIST increased


VO2max by 16.4% and 13.


, respectively (p


0.01).


The 5.3% decline in the


VO2max of CONT during the 26 week study


period could be ascribed to random variation (p


= 0.11).


Table 4-2.


VO2max (ml*kg-1*min-1) Responses of Control,


Treadmill, and


Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise
Training.


Group n Ti T3


CONT 9 22.8 3.7 21.6 + 4.1
TREAD 14 22.0 + 4.4 25.6 + 5.6*
TREAD/RESIST 10 24.8 5.0 28.2 + 5.4*

Values are mean S.D.


CONT


= Control; TREAD


< 0.01


= Treadmill; TREAD/RESIST


, greater than corresponding TI value


= Treadmill/Resistance





79



Strength

In strength testing, there were 10 subjects who did not complete T3 leg


press (LP) testing.


Seven subjects had sustained back or knee injuries over the


6 month interval which precluded LP testing and/or training; three subjects


did not complete their


strength testing obligations at T3.


Four subjects did not


complete T3 biceps curl (BI) and triceps extension (TRI) testing; two of these

subjects had sustained injuries which precluded testing and/or training,


while the other two subjects did not complete their


T3 testing obligations.


Therefore, the sample size for LP 1-RM strength testing was 23,


and TRI testing it was 29.


while for BI


The sample size for lumbar extension (LE) testing


was 19.


The T1 and T3 values for LP, BI, TRI,


and LE strength are listed in Table


The results of the ANOVA used to


assess


differences in T1 values


indicated a low probability of a type I error in the detection of group


differences for LP (p


< 0.01),


BI (


< 0.01),


TRI(a


= 0.05) and LE (p


= 0.03).


results of Duncan'


post hoc test indicated that TREAD/RESIST had higher


strength scores than TREAD in LP


both TREAD and CONT in LE.


BI, and TRI and had higher scores than


However, when gender was used as a


covariate in the TI analysis,


the resulting high p-values (p


= 0.71


, 0.74, 0.58,


0.67 for LP


, TRI, and LE respectively) indicated that once gender was


accounted for, any differences among groups were due to random variation.
The effect of training on all strength measures was therefore analyzed


with an analysis of covariance (ANCOVA) design using the


T1 strength scores








accounted for by random variation (


= 0.55).


Thus, strength training by


TREAD/RESIST did not improve leg/buttocks strength to a greater extent

than the changes seen in TREAD and CONT. Using absolute strength scores,

TREAD/RESIST increased strength in LP by 16.5% after 26 weeks of training.


However, TREAD and CONT also increased LP strength by 18.9


and 8.2%,


respectively.


Table 4-3.


Strength Testing Scores of Control, Treadmill,


Treadmill/Resistance Groups Before (T1) and After (T3) 6 Months of
Training.


Exercise


Variable


Group


Adjusted


LP Obs)


CONT
TREAD


114.0
108.1


TREAD/RESIST


49.9
63.2


216.3 127.5**


123.3 +
128.5 +


37.6


251.9 149.8


154.6 10.8
166.7 6.9
170.0 + 9.5


BI (Ibs)


47.1


CONT
TREAD


TREAD/RESIST


TRI (Ibs)


22.7


35.9 14.1


57.2


CONT
TREAD


22.8**


36.7 16.9


28.2


TREAD/RESIST


43.1 17.3**


46.3 21.5
36.6 + 16.1
71.9 + 32.5


35.8 16.6
29.3 10.1
55.8 24.1


43.8 +


46.5 1.6
58.2 + 2.0t


33.4 +


36.7 +1.6
46.0 1.9t


LE (Nm)a


CONT
TREAD


TREAD/RESIST


145.1 39.8
142.4 + 52.8
269.9 +156.3*


149.4 +
147.8


33.9
71.9


274.8 170.8


190.6 12.8
191.9 11.9
182.1 14.2


T1 and T3 values are mean + S.D.; Adjusted T3 values are mean S.E.


CONT


= Control; TREAD


= Treadmill;


TREAD/RESIST


= Treadmill/Resistance;


LP = Leg press; BI
extension


= Biceps curl; TRI


= Triceps extension; LE


= Lumbar


Adjusted for TI strength scores








Analysis of covariance results indicated that the adjusted T3 BI scores


of TREAD/RESIST were greater than those of either TREAD (p


< 0.01) or


CONT (Ep


< 0.01).


The adjusted TRI scores for TREAD/RESIST were also


greater than those for both TREAD (p


< 0.01) and CONT (p


< 0.01).


Using


absolute strength scores, TREAD/RESIST increased strength in BI and TRI by

25.7% and 29.5%, respectively, while both TREAD and CONT showed changes

of less than 5% in these exercises.

Analysis of covariance results for LE strength indicated that differences

among groups in adjusted T3 LE scores could be accounted for by random


variation (


= 0.88).


Thus, lumbar extension training by


TREAD/RESIST


not improve lower back strength to a greater extent than the changes seen in


TREAD and CONT


. Using absolute strength scores, TREAD/RESIST


increased strength in LE by 1.8% after 26 weeks of training.


However


TREAD


and CONT also increased LE strength by 3.8% and 3.0%,


respectively.


Body Composition


Two control subjects did not complete testing obligations at T3;
therefore, calculation of muscle mass data was based on a sample size of 32,
while sum of seven skinfold (17) and girth data were based on a sample size


of 31.


Means and standard deviations for CONT


TREAD/RESIST for body weight,

measures are listed in Table 4-4.


TREAD


, arm and leg girths,


and lean mass


The results of the ANOVA used to


assess


group differences in Ti values indicated a low probability of a type I error for


lower body lean mass (p


= 0.04) and for arm lean mass (p


= 0.04).


The results








Table 4-4.


Body Composition Measurements for Control,


Treadmill, and


Treadmill/Resistance Groups Before (T1) and After (T3) 6 Months of Exercise
Training.


Adjusted


CONT


7 (mm) (n = 7)
Body weight (kg) (n
Arm girth (cm) (n =
Leg girth (cm) (n =


186+54
71.0 12


= 11)


Arm lean mass (kg) (n=8)
Trunk lean mass (kg) (n=8)
Total body lean mass (kg) (n = 8)
Lower body lean mass (kg) ( = 8)


31.0
54.8
3.8
18.9


40.7 f 10.7


14.0


191 62


72.4 14.2


31.9 +
54.9
3.9
19.2


41.3 10.6


14.6


4.0 1.2
20.4 0.5


7 0.3
7 0.2


TREAD (in
7 (mm)


= 14)


173 57


Body weight (kg)
Arm girth (cm)
Leg girth (cm)
Arm lean mass (kg)
Trunk lean mass (kg)
Total body lean mass (kg)
Lower body lean mass (kg)


61.8 14.2


28.8
49.7
3.2
18.9
37.0
12.5


159 58
60.8 14.6
28.5 3.7
48.3 3.9


3.4


18.7


37.1
12.7


4.1 0.9
20.0 0.3
41.0 0.3
14.3 0.2


TREAD/RESIST (n
7 (mm)
Body weight (kg)
Arm girth (cm)
Leg girth (cm)


= 10)


150 73
73.4 17.8


31.5


52.7


Arm lean mass (kg)
Trunk lean mass (kg)
Total body lean mass (kg)
Lower body lean mass (kg)


4.9
23.0


47.1 13.8


16.4


4.5t


146 67
73.7 17.9


32.2
51.5
5.1


22.5


46.8 13.1


16.7


4.5


4.1 1.1
19.8 0.4
41.0 0.3
14.4 0.2


T1 and T3 values are mean


CONT


= Control;


TREAD


r..~..A..1 Jn an nt.l ,


adjusted T3 values are mean S.E.


= Treadmill;


TREAD/RESIST


- r"7


C,.. I *IP A. I *


__ I








weight, total body lean mass, and trunk lean mass were 0.07,


0.27, 0.49, 0.15,


0.10, 0.49 respectively.


When gender was used as a covariate in the T1 analyses for arm and
lower body lean mass, the resulting high p-values (p = 0.35 and 0.52,
respectively) indicated that, once gender was accounted for, any initial


differences among groups were due to random variation.


The effect of


training on all lean mass measures was therefore analyzed with an ANCOVA


design using the Ti measure as the covariate.


The results indicated that the


changes with training for total body lean mass, lower body lean mass, arm

lean mass, and trunk lean mass could be ascribed to random variation (p =


and 0.64, respectively).


Analyses of the effect of training on


girth were each done in a


body weight, arm girth and leg


2 X 3 (time X group) repeated measures ANOVA.


The type I error rates for detecting a time X group interaction for


body


weight, arm girth,


and leg girth were 0.03, 0.05, 0.01,


and 0.37 respectively.


Follow up analyses indicated that there was a decrease in the


= 0.01) and


body weight (p


= 0.02) for TREAD.


Differences in


and body weight between


T1 and T3 for CONT (p


0.32 0.62


= 0.41 and 0.23


, respectively) and TREAD/RESIST (p


, respectively) were due to random variation.


The follow up analysis


for arm girth indicated that TREAD/RESIST had an increase in arm girth (p


0.03),


while changes in arm girth for


TREAD and CONT from T1 to T3 were


due to random variation (p2


=.16 and 0.10, respectively).




Full Text

PAGE 1

EFFECT OF 6 MONTHS OF EXERCISE TRAINING ON CARDIOVASCULAR AND HORMONAL RESPONSES TO HEAD UP TILT IN ELDERLY MEN AND WOMEN BY JOAN F CARROLL A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 1992 u !V ITY OF FLORI A u:~ ~.:s

PAGE 2

This work is dedicated to my parents who always believed in me, and to my husband, who helped me accomplish my goals

PAGE 3

ACKNOWLEDGEMENTS A project of the magnitude and scope of this could not have been accomplished without the cheerful and endless assistance from a great number of individuals. First and foremost, I would like to thank all those who helped conduct the tilt tests and associated laboratory analyses: Lindsey Reider, Keith Engelke, Mike Welsch, Jennifer Gulick, Lynn Panton, Linda Garzarella, Brian Elliott, Judson Bruno, Evan Korn, Kevin Kenney, Dr. Jay Graves, Dr Marie Knafelc, and Dr. Greg Guillen. Without their dedication, the project could not have succeeded. Special thanks go to Brian Elliott and Judson Bruno, who spent many long hours on data verification and computer data entry. Many thanks also go to all the undergraduate and graduate students who assisted with the training of our subjects over the course of this project. I would also like to thank all those who helped me learn the techniques of plasma volume and hormone analysis: Dr Charles Wood, Dr Maureen Keller-Wood, Christine Taranovich, Curt Kane, Anne Bowers, and "Mike" Merz. Their help and friendship over many months enabled me to complete a sometimes frustrating task. Thanks also go to Michelle Wiltshire Clement and Anne Bowers for their work in completing hormone analyses A most sincere thanks you goes to Carolyn Hansen, who despite the many demands of her career and family life, gave generously of her time to help with statistical analyses. iii

PAGE 4

Finally, I would like to thank the members of my committee--Drs Michael L. Pollock, James E Graves, Victor A Convertino, Charles E. Wood and David T Lowenthal--for their help in launching the project and in bringing this manuscript to fruition I am indebted to all of them for the time and dedication they put forth on this project; I also owe a special thank you to Drs. Wood and Convertino for their helpful evaluations of this manuscript in its final weeks Finally, I offer special thanks to my committee chair, Dr Michael L. Pollock, for all his help and assistance during the last four years, and for his work on this manuscript. iv

PAGE 5

TABLE OF CONTENTS ACKNOWLEDGEMENTS ................................ .. ... ......... ..... ..... ........ ...... .. ..... ..... ...... .iii LIST OF TABLES ....... .. .... .. .... ......... ... .. ........... ................................. ... ................ ...... .. viii LIST OF FIGURES .. ........ .... ...... ........................ ......... ... ....... .. ........ .............................. xii ABSTRACT ... .. .............................................................................................................. xvi CHAPTERS 1 INTRODUCTION ................................................................................................ 1 Statement of the Problem ........ ...... ... ..... .... ... ........ ............ ........ .... ................ .... 7 Research Hypothesis .................. .. ... .. .................................. .. ........... ...... .. ....... ... 8 Justification ............. .......... ................................. .. .................. ... ............. .... ..... ...... 8 Assumptions ... .... ... .............................................................................................. 9 Delimitations .................. .... ................................... .......................... .... ....... ......... 9 Limitations .......................................................................................................... 10 Definition of Terms ................................ ...... .. .................... .......................... .. .. 10 2 REVIEW OF LITERATURE ................. ............. ....... ......... .... ..... ......... ............ 12 Introduction ........................................................................................................ 12 Responses to Endurance Training ................................................................. 14 Resting Heart Rate (HR), Stroke Volume (SV) and Cardiac Output ( Q) ............................................................................................... 14 Blood Pressure (BP) ..................................................................................... 16 Mamimal Aerobic Power ...................................... ............. ...................... 18 Increase in Strength and Muscle Mass .................................................... 20 Responses to Strength Training ..................................................................... 21 Hormonal, and Blood/Plasma Volume Responses to Training: Resting Values ... ........ . . ....... ............................... ... .... .......... ...................... 22 Blood/Plasma Volume .............................. ... .............................................. 22 Vasoactive Hormones ................................................................................ 26 Hormones Associated with Fluid Volume Control: Aldosterone (ALDO) ........ ........................... ..... .... ... ............... ..... ...... ... 31 Adrenocorticotropic Hormone (ACTH) ................................................. 32 Protein (PROT), Sodium (Na+) and Potassium (K+) ........ ... ................. 33 V

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Cardiovascular, Hormonal, and Plasma Volume Responses to Tilt: Preand Post-training ... . .. . ............ .... . .. ...... . .. ...... . . .. .. . ....... . .... 35 Heart Rate, Stroke Volume, Cardiac Output, and Blood Pressure .. . ......... ........... .. .. .. .. .. .. ..... .. ..... ..... ....... .. .. . ... . . ....... .. . .. .. .... 36 Blood/Plasma Volume . ..... .. ... ...... ... .. ... ........ ... .. . ... .. .... ............ .. .. .. ... . 40 Vasoacti ve Hormones .. ... . . ... .. .. .. ...... .. ..... ...... .. . . .. .. .... .. ...... .... .. ... .... 41 Hormones Associated with Fluid Volume Control: Aldosterone (ALDO) ..... .... . .. .... .. . .. ...... ..... ..... . .. . .... .... ....... ........ ..... ... 48 Adrenocorticotropic Hormone (ACTH) .... ... ........ ... ... ... .... ...... .. .. ... ..... 49 Protein (PROT), Sodium (Na+) and Potassium (K+) . ...... . . . ....... ... ... 50 Mechanisms Potentially Responsible for Changes in Orthostatic Responses .. ... ....... ..... ........ ... .... ... .. ... . .. .. ... ... .. .... ... ...... ....... .... ....... ... .. . 51 Plasma Volume Change .... . .. .. ... .. .. ... . .. .. . ... ... ...... .. ........ .. .. . .. . . .... . . .. 51 Muscle Mass Changes . .. . . .. .. .. .. .. .... .... .. . ...... . .. ... .... .. .. .. .. ........ ... .. .. . 52 Changes in Baroreceptor Sensitivity .... ... .. .. .... .. .. . .. ... .. ... .. . .. .. .. .. . . .53 Altered Hormonal Response .... .. ..... . ... .. .. ... .. .. ... . .. ... .. ..... .. .. .... . ...... .55 Summary .. ... .. ... ............. .. .......... . .. ........... ... ..... ........ .. .. .. ........ ... .... ..... . 56 3 METHOOOLcx;Y .... . .. .. . ............ .. . .. . ..... ... .. .. ..... .. ........ ... .. ........ .. ...... .... .. .. .. .. 57 Subjects ... .. .... . .. ... . ........ . .. .. . . .. .. ...... .. .. . . .... ..... .... ... .... ... ..... ..... .. ......... ... ... 57 Type of Data Needed .............. .......... .. .... ......... ...... .. ....... . .. ... .... ... ..... . .. . . 59 Methods of Data Collection ...... ....... .. .. . ....... .. ....... ..... ..... .. ..... .. . .. . . ... . .. .... 60 Maximal Oxygen Uptake (V02max) Test ...... . ....... .. .... .. . .. .... . .. ... ... .. .. 60 Tilt Table Test .. .... .. . .. ............ .. ............... .. ...... .. ...... .. ... ........ .. . ... .. .. .. ........ 62 Strength Testing .. . .. ... .. ...... .. ..... ........ ........ .... .. .... ....... ... .......... ..... . .. .... 65 Body Composition .... . ....... ...... .. .... . ....... .. ...... ........ . ....... . .. ......... .. . .. .. .. 66 Blood Sample Analyses ... . .. ....... . .. ... .... .. .... ... ........ .... .. ............. ... ... ..... 66 Training .... .... .. .............. .. .... .. . .. ....... . ...... . ......... ....... .. ...... .... . .... .. .. ... . ....... . 70 Data Analysis ........ ...... ..... .. .. .. ... ........ .. .... ... .. .... . .. .... .. ... .. .. . .. ... ... .. .... .. . ... ... 72 Dependent measures .... . . . .... . ....... ... .. .. . ..... ... .. . ... .. ..... .. ... .. .. . ... .. ... .... 72 Statistical analyses . ..... .. ......... ...... . ... ..... .. ... ... ... ..... ... .... . . . .. .. . ... .. ...... 73 4 RESULTS ... .. .... .... ..... ... ... ........ .... .. ............. .. ..... ... .. ....... ..... . .. . ... ... ...... .... . ... 77 Subject Characteristics .. ... . . ..... .... .. .. . .. .. .. ...... .... .. .. .. ... .. ...... .... .... .. . .. ..... ..... 77 Training Responses .... ........ .. ... .. ........ ... ... . .... ... .. . .... .... .... .. ... ... .. . ... . .. ... .. .. 78 Maximal Oxygen Uptake .... ...... .. ......... ..... .. ..... .... .. ... ... .. .. .. ...... .... ..... .. 78 Strength .. ... .. ..... .. ... .. ... ... ..... . ... .. ... .. ... ... .. .. .... .. .. ... .. .. ... ... .. ..... .. .. . ...... .. ... 79 Body Composition ..... .... .... ... .. .... .. .. .. . .... . . .. .. . ... ... ..... . .... .. ... .. . . ...... 81 Cardiovascular Responses to Tilt ...... ..... . .. .... . ... ........ ... ... .. .. ... ... ... ... ... .. .. ..... 84 Analyses to Average Data .. . ...... .. .... . ... . .. . .. .. .. .. ......... .. .. .. ... ..... ...... .. ... 84 Effect of Training on Resting Variables .... .... ..... .... ..... ...... .... .... .. .. . .. .. .. 87 Effect of Training on the Cardiovascular Responses to Tilt ..... ..... .... 94 Hormonal and Plasma Volume Response to Training and Tilt.. . . .... 104 vi

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Responses of Subject Experiencing Presyncopal Symptoms .. .. ........... . 114 Responses to the Cough Test. ..... .. .. ........... ........... . . .... .. ..... .. ... ........... . 134 Analyses to Average Data . .. .... .. . .. ... .. .. ... . .. . ..... . . .... .. .. . ... .. .. . .. . ... 134 Analyses of Cough Responses ............ . ... .......... ... .... ........... ... .. .. ...... .. 137 Analyses of Beat by Beat Data ......... .......... ................... . .. ...... .. .......... 140 5 DISCUSSION AND CONCLUSIONS ........ .... ......... .. .. ...... .. ........ ... .......... ... 146 Introduction . .... . . .. ....... . ... . ........ .. . . ....... ....... .. .. ....... .. .... ... ... ... .. .. ... ... .. .. 146 Exercise Training and Cardiovascular Responses to Head-up Tilt ....... 147 Heart Rate, Stroke Volume, and Cardiac Output .. ... .. . ..... .. .. .. ... ...... 147 Possible Mechanisms ....... . .. ..... ... .. ........ .. ........ .. ......... . ... . ... . ..... .... .. ... 150 Exercise Training, Resting Plasma Volume and Resting Hormonal Responses .. .. .... .... .... .. ......... ... .... . ... .. ... ....... .. .......... ........ .. 151 Exercise Training and the Hormonal and Plasma Volume Response to Head-up Tilt. ..... .. .. .. .......... .. ................. .. ...... ... ..... .. . .. ...... 153 Responses of Fainters ....... .... . ........ .. .... .. . .. .. .. ...... ........................... ........ . 154 Stroke Volume and Cardiac Output .... ......... ... ..... . .. ... .... .. . ... .. ... ... .. .. 154 Blood Pressure .... ........... .. ..... .. ........ .... .. ........ ......... ...... ... .. . . .. ............. 155 Hormonal Responses ..... . . .. .. .......... .. .. ... . .. .. .. .... .. ... ... .. . ... ... . ....... ... .. 156 Responses to Cough Test. . .. ... ... .. .. ... .... ... .. ..... .. ..... ........... ... ...... .. . .......... 157 Conclusions ... .... ... ... .. ... ... ....... .. ... .. ........... ....... . .......... ...... . ....... .. .. ....... . 158 Directions for Future Research . .... .. .... .. .. .. ... .. . .... .. ... ........ .. ........ .. .... .. .... .. 159 APPENDICES ............................. ........... .. .... ........ ....... .. ......... . .. ....... .. . . . .. ..... ..... 162 A DEMOGRAPHIC, MEDICAL AND ACTIVITY QUESTIONNAIRES ... .... ............... .. . ........ .. .... .... .... .. .. .. ........ .. ... .... .. .. ....... 162 B INFORMED CONSENT DOCUMENT .. ....... .......... .... ... ... .. .... .. .. ... ... ... 173 C INSTITUTIONAL REVIEW BOARD APPROVAL LETTER. ...... . .. .... .. 181 D DATA COLLECTION FORMS FOR TILT TEST ... .... . .... .. . .. .. .. .. ... ... . . 183 E INDIVIDUAL FAINTERS' DATA .. ........ . ... .... . .. ... ... ....... .. ......... ... ........ 188 LIST OF REFERENCES . . ... .. . ...... .. ..... ...... ........ ... ....... .... .. ......... ............. ....... ...... 208 BIOGRAPHICAL SKETCH . . ... ..... . ........ .. .. .... .... ... ... .. . .. . ... . .. .. .... ... .. . ... . .. .... .... 228 vii

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LIST OF TABLES Table Page 4-1 Characteristics of Control, Treadmill, and Treadmill/Resistance Training Groups at the Start of 6 Months of Exercise Training .... ... 77 4-2 V0 2 max (mlkg lmin-1) Responses of Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After(T3) 6 Months of Exercise Training ................. ... .... ... ........ .. ... ... ... ..... .. ... ...... 78 4-3 Strength Testing Scores of Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training .............. ....... .... ..... ....... ... ............ .. ...... .. ..... 80 4-4 Body Composition Measurements for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training .. ...... .. ......... .. .... ...... ... .... ...... .. .... .. .... .......... .. 82 4-5 Overall Heart Rate, Stroke Volume, Cardiac Output, Blood Pressure and Peripheral Resistance Response to Tilt, Averaged Over Groups and Tests ..................... .. .. .. ........ .. ...... .... .... .... ...... .......... .. .... 85 4-6 Analyses to Average Data: Type I Error Rates for Detecting a Time Effect Within Each Time Period for Heart Rate, Stroke Volume, Cardiac Output, Blood Pressure, and Total Peripheral Resistance .... .. ........ .... ....... .... ... ..... .... .... .. .. .. ... ........ .. ...... ....... . 87 4-7 Averaged Heart Rate and Stroke Volume Responses to 70 Head-up Tilt for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training ........ ...... .... .... ............. .. .. .. ........ .. .................. 88 4-8 Averaged Cardiac Output Responses to 70 Head-up Tilt for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training .. .. ...... ..... ..... .. .. .... .. 89 4-9 Averaged Systolic and Diastolic Blood Pressure Responses to 70 Head-up Tilt for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training .... .... .. ... .... .. .. .... .... ........ .. ... ............... ........... 90 viii

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4-10 Averaged Mean Arterial Blood Pressures and Total Peripheral Resistance Responses to 70 Head-up Tilt for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training .... ...... . .. .... . ... .. .... 91 4-11 Effect of Training on Supine Resting Heart Rate, Stroke Volume, Cardiac Output, Blood Pressure, and Total Peripheral Resistance Measurements for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 months of Exercise Training .... .. .... .. .. ........ .. .................. .. ........ .... .. .. .. .. .... 92 4-12 Wilks Lambda Values for 2 X 3 X 11 (Test X Group X Time) Repeated Measures Analysis for Heart Rate, Stroke Volume Cardiac Output, Blood Pressure, and Peripheral Resistance Responses to 70 Head-up Tilt .. .. ...... .. ...... .. .......... .... ... .. .. .. .......... .. .... .. .. .. 94 4-13 Analysis of the Effect of 6 Months of Exercise Training on the Relative and Absolute Change in Stroke Volume and Cardiac Output from Rest to 70 Head-up Tilt for Control, Treadmill, and Treadmill/Resistance Groups ..... .... .. .. .. .. ........ .... ...... .... .. .. .. .... .. .. ...... 98 4-14 Post Hoc Analysis for Time Effect to Detect Changes in Heart Rate, Stroke Volume, and Cardiac Output as a Result of 70 Head-up Tilt .. .. ..... .. .... ........ .. .. .......... .. .... .......................................... .. .. .. .... 100 4-15 Post Hoc Analysis for Time Effect to Detect Changes in Systolic, Diastolic, and Mean Arterial Pressure as a Result of 70 Head-up Tilt .. ...... .... .... .. ........ .. ............ .... .... ...... ...... ..... .. .. .. .. .......... ... 102 4-16 Post Hoc Analysis for Time Effect to Detect Changes in Total Peripheral Resistance as a Result of 70 Head-up Tilt .. .. .... ...... .... .... 103 4-17 Responses of Plasma Volume, Blood Volume, and Red Cell Volume to 70 Head-up Tilt Before (Tl) and After (T3) 6 Months of Exercise Training in the Control and Exercise Training Groups ........ ... ........ .... .... ... ... .. .... ...... .. .. .. .. .. ..................... ...... 105 4-18 Probabilities for Type I Error in Detecting a Change in Plasma Volume, Blood Volume and Red Cell Volume as a Result of 70 Head-up Tilt or Exercise Training .. .. .... .... .. ......... .. .... ........ .. .... ..... ... 106 4-19 Hemoglobin and Hernatocrit Measurements at Rest and During 70 Head-up Tilt Before (Tl) and After (T3) 6 Months of Exercise Training in Control and Exercise Training Groups .. .... ... .... ... .. ....... .... . .. ... . ......... ..... . .... .... ...... .. . .... ... .. ... .. .. .. .. .. ..... .. ...... 108 ix

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4-20 Probabilities for Type I Error in Detecting a Change in Hemoglobin and Hematocrit as a Result of 70 Head-up Tilt Before (Tl) or After (T3) 6 Months of Exercise Training .. ........ .. .... .. 109 4-21 Percent Change in Plasma Volume, Blood Volume, and Red Cell Volume During 70 Head-up Tilt Before (Tl) and After (T3) 6 Months of Exercise Training in the Control and Exercise Training Groups .. .. .... . .. .... ........ .... ...... ...... .. .. .. .. .. ... . .. .... ... . 109 4-22 Hormonal/Electrolyte Response to 70 Head-up Tilt Before and After 6 Months of Exercise Training in the Control and Exercise Training Groups ... .... .. .... ........ ...... ... . .. . .... .. ........ ................. 111 4-23 Probabilities for Type I Error in Detecting a Change in Hormone Concentration as a Result of 70 Head-up Tilt Before (Tl) or After (T3) 6 Months of Exercise Training .... . . .. ......... 112 4-24 Heart Rate Responses of Fainters (F; n=4) and Nonfainters (NF; n=24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training .... .. ..... . .... ......... .. 115 4-25 Stroke Volume Responses of Fainters (F; n=4) and Nonfainters (NF; n=24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training ......... 116 4-26 Cardiac Output Responses of Fainters (F; n=4) and Nonfainters (NF; n=24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training .. .. .. 117 4-27 Systolic and Diastolic Blood Pressure Responses of Fainters (F; n=4) and Nonfainters (NF; n=24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training ... .. . .. ...... ... .. .. ... ....... ............. . .. . . . . ... .. .. ... .. .. . ... ... . 118 4-28 Mean Arterial Blood Pressure and Total Peripheral Resistance Responses of Fainters (F; n=4) and Nonfainters (NF; n=24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training .... ........ .. .. .. .. . .. .. 119 4-29 Comparison of Subject Characteristics, Aerobic Capacity, Strength, and Body Composition of Nonfainters (n=24) vs Fainters (n=4) Prior to Exercise Training .... ... ... .. ... ...... .. . ... . ... . .. .... .. 130 4-30 Comparison of Blood Volume and Hormone Responses of Nonfainters (n=24) vs. Fainters (n=4) to 70 Head-up Tilt Before and After 6 Months of Exercise Training .. ... .... ...... . ... ..... ... .. 132 X

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4-31 Overall Responses to Three Supine and Three Tilt Cough Trials, Values Averaged Over Tests and Groups .. .. ..... ...... . .. .. ... ... . .. 135 4-32 Analyses to Average Cough Data: Type I Error Rates for Detecting a Difference Among the Three Cough Trials for Supine and Tilt Cough Tests ... . ... ..... .... ....... . .. .. ... .. .. ...... . .. ... .. .......... 136 4-33 Mean Supine and Tilt Cough Variable Values for Control, Treadmill, and Treadmill/Resistance Training Groups Averaged Over Three Supine and Three 70 Head-up Tilt Cough Trials Before (Tl) and After (T3) 6 Months of Training 4-34. Summary of the Effect of Tilt and Training on the Responses to the Cough Test ... ............. ..... ....... .... .. ..... .. .. ... ...... . ....... . .. ....... .... . .. 140 4-35 Heart Rate Values Averaged Every Five Beats for 40 Beats Post-Cough for Control, Treadmill, and Treadmill/Resistance Groups for Supine and 70 Head-up Tilt Cough Tests Before (Tl) and After (T3) 6 Months of Training ....... . ..... ..... .. .... ...... .... .... . 141 4-36 Probabilities for Type I Error for Detecting a Difference in Heart Rate Values at Each Time Point Post-Cough During Supine and 70 Head-up Tilt Cough Tests Before (Tl) and After (T3) 6 months of Exercise Training .. ... .. .... .... . .. . .. .. ... ... .... . .... 144 4-37 Heart Rate Response to Supine and 70 Head-up Tilt Cough Tests Before (Tl) and After (T3) 6 Months of Exercise Training, Values Averaged Over Groups for Every Five Beats for 40 Beats Post-Cough .. .. .. ........ ... ... .... ..... .... ...... .. .. ... . .... ... .... . ........... 144 xi

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LIST OF FIGURES Table Page 4-1 Mean test responses of control (CONT), treadmill (TREAD), and treadmill/resistance (TREAD/RESIST) groups to 70 head-up tilt before (Tl) and after (T3) 6 months of exercise training: a) stroke volume (SV); b) cardiac output ( Q) .......... .. .... .. .. .. 96 4-2 Percent change(~) in mean test response from prior to exercise training (Tl) to after (T3) 6 months of exercise training in control (CONT), treadmill (TREAD), and treadmill/resistance (TREAD/RESIST) exercise groups: a) mean test stroke volume (SV) and b) mean test cardiac output ( Q) ... .... .. .... .. .. ................ .... .................... .. .......... .... .......... .. ...... .. .. ...... 97 4-3 Responses of fainters vs nonfainters to 70 head-up tilt prior to exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output ( Q) .. .... .... .... .... ........ .. .... .... .... .. .... .. .......... .. .. .. ........ .. ...... .. 120 4-4 Responses of fainters vs nonfainters to 70 head-up tilt after 3 months of exercise training : a) heart rate (HR); b) stroke volume (SV); c) cardiac output (Q) ........ .. .. .. .... .... ...... .... .... .... ............ .. 122 4-5 Responses of fainters vs nonfainters to 70 head-up tilt after 6 months of exercise training : a) heart rate (HR); b) stroke volume (SV); c) cardiac output ( Q) ................ .. ...... .. .. ........ .. ...... ...... .. ... 123 4-6 Responses of fainters vs nonfainters to 70 head-up tilt before exercise training: a) systolic blood pressure (SBP); b) diastolic blood pressure (DBP); c) mean arterial pressure (MAP) .. .... .. .. .. .......... .. .. ...... .. .... ........ .. .. .. .... .. .. .... .................. .... .. .. ................ 124 4-7 Responses of fainters vs. nonfainters to 70 head-up tilt after 3 months of exercise training: a) systolic blood pressure (SBP) ; b) diastolic blood pressure (DBP); c) mean arterial pressure (MAP) .. .. .... .. .... ........ .. .... .......... ...... ...................... ............ .. .. .. ...... .. ........ .. .... 125 4-8 Responses of fainters vs. nonfainters to 70 head-up tilt after 6 months of exercise training : a) systolic blood pressure (SBP); xii

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b) diastolic blood pressure (DBP); c) mean arterial pressure (MAP) .. . ... .. .. ..... .. ......... .. . .... ...... .. ........ .. . ..... .. .... .... . .. ........ .. . . .. .......... 126 4-9 Total peripheral resistance response of fainters vs. nonfainters to 70 head-up tilt: a) before exercise training; b) after 3 months of exercise training; c) after 6 months of exercise training .............. .. .. ...... .. .... .. ......... ....... ... ... . .... ....... .. ..... . ... .. .. 127 4-10 Hormonal responses of fainters and nonfainters to supine rest (pretilt) and 70 head-up tilt before (Tl) and after (T3) 6 months of exercise training: a) vasopressin (A VP); b) adrenocorticotropic hormone (ACTH) . ... ..... .. .. .... .. ...... ... .. .... .... .. 134 4-11 Heart rate (HR) response to cough test in supine and 70 head-up tilt positions by control group before (Tl) and after (T3) 6 month training protocol.. . ... .... .... .... .. ........ .. ...... . ...... .. .... . ...... 142 4-12 Heart rate (HR) response to cough test in supine and 70 head-up tilt positions by treadmill exercise group before (Tl) and after (T3) 6 month training protocol.. .... .. . .. .. ... ... .. ...... .. ......... .. . 143 4-13 Heart rate (HR) response to cough test in supine and 70 head-up tilt positions by treadmill/resistance exercise group before (Tl) and after (T3) 6 month training protocol.. ... .. .... . ...... .. .. 145 5-1 Relationship between the relative change in resting plasma volume and the relative change in the HR response to tilt . .. .. ..... 148 E-1 Responses of female fainter A to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output (Q) . .. ..... ............ ..... ........ .. .. ...... .... .. .... . .. .. .... ....... ....... ... ..... .. .... 188 E-2 Percent change (~) from supine rest in response to 70 head up tilt in female fainter A before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output ( Q) ................. ..... .. .. ... ... ... .. .... 189 E-3 Blood pressure responses of female fainter A to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: A) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure .......... ... .. . .. ... .. ..... ..... . .. .... .... ... ...... .. .. .... .. .. 190 E-4 Percent change (~) from supine rest in blood pressure response to 70 head-up tilt in female fainter A before (Tl), after 3 months (T2), and after 6 months (T3) of exercise xiii

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training: a) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure .......................................................................................... 191 E-5 Total peripheral resistance (TPR) response of female fainter A to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) absolute response; b) percent change (.1) from supine rest. ..................................................... 191 E-6 Responses of female fainter B to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output ( Q) ............... ................... .. ............ ........................ .............. ............ 193 E-7 Percent change (.1) from supine rest in response to 70 head up tilt in female fainter B before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output (Q) ........................................... 194 E-8 Blood pressure responses of female fainter B to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: A) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure ........ ... ................. ............ ........ ............. ............... 195 E-9 Percent change (.1) from supine rest in blood pressure response to 70 head-up tilt in female fainter B before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure .... ..................... ......................................... .. .. .. ........ ....... .. 196 E-10 Total peripheral resistance (TPR) response of female fainter B to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) absolute response; b) percent change (.1) from supine rest. ...................................... .............. 197 E-11 Responses of male fainter A to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output (Q) ................................................................................................... 198 E-12 Percent change (.1) from supine rest in response to 70 head up tilt in male fainter A before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output ( Q) ........................................... 199 E-12 Blood pressure responses of male fainter A to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of xiv

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exercise training: A) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure .......................... .. .. .. ........ .... ...... .. .. .. ...... .. ............ 200 E-14 Percent change(~) from supine rest in blood pressure response to 70 head-up tilt in male fainter A before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure .. .. .. ... .. .. ... .. ... .. ... .......... .. .................. .. .................... ...... .. . .. 201 E-15 Total peripheral resistance (TPR) response of male fainter A to 70 head-up tilt before (Tl), after 3 months (12), and after 6 months (T3) of exercise training: a) absolute response; b) percent change (~) from supine rest .. .......... .. .. ... . ........ ......... ............ 202 E-16 Responses of male fainter B to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output ( Q) .. .. ...... ... .. ... ... ..... .......... .. .. .... ......... ...... .... ... .. ... .... .. .... ...... .. .... 203 E-17 Percent change(~) from supine rest in response to 70 head up tilt in male fainter B before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output ( Q) ...... .... .... ........ .. ......... .... .. .... 204 E-18 Blood pressure responses of male fainter B to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training : A) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure . .... .... ... ....... .. ...... .. .. .. ...... .. ...... ... .. .. ................... 205 E-19 Percent change(~) from supine rest in blood pressure response to 70 head-up tilt in male fainter B before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure ... .. ...... ... ...... .. ....... .. . ......... ..... .. .... ...... ... .. .. .... . .. ... ...... 206 E-20 Total peripheral resistance (TPR) response of male fainter B to 70 head-up tilt before (Tl), after 3 months (12) and after 6 months (T3) of exercise training: a) absolute response; b) percent change (~) from supine rest.. .. ...... ........... .. .......... .. .... .. .. .... .. .. .. 207 xv

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Abstract of Dissertation Presented to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy EFFECT OF 6 MONTHS OF EXERCISE TRAINING ON CARDIOVASCULAR AND HORMONAL RESPONSES TO HEAD UP TILT IN ELDERLY MEN AND WOMEN By Joan F. Carroll May, 1992 Chairman: Michael L. Pollock, Ph D. Major Department: Exercise and Sport Sciences To evaluate the effect of 6 months of exercise training on heart rate, stroke volume (SV), cardiac output (Q), blood pressure, and hormonal responses to head-up tilt (HUT), 22 women and 11 men (60 to 82 years) were assigned to treadmill exercise (TREAD; n = 14), treadmill plus resistance exercise (TREAD/RESIST; n = 10), or non-exercising control (n = 9) groups Tilt testing before (T1) and after (T3) training consisted of 30 minutes of supine rest, 15 minutes of 70 HUT, and 15 minutes of supine recovery Plasma volume (PV), aldosterone (ALDO), vasopressin (AVP), adrenocorticotropic hormone (ACTH), plasma renin activity (PRA), norepinephrine (NE), epinephrine (EPI), sodium (Na+), potassium (K+), and xvi

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protein (PROT) were measured after 30 minutes of supine rest. Hormones were also measured after 15 minutes of HUT. Training increased maximal aerobic power in TREAD and TREAD /RESIST by 16.4% and 13.7%, respectively (p $ 0.05). TREAD decreased body weight and skinfold measurements while TREAD/RESIST increased elbow flexion and extension strength (p $ 0.05). Resting SV and Q increased 20.6% and 13.4%, respectively, in TREAD (p $ 0.01); resting Q decreased 9.1% in TREAD/RESIST (p 0.05). Average tilt test SV and Q increased 15.0% and 9.3%, respectively, in TREAD; average test Q decreased 9.8% in TREAD/RESIST (p $ 0.05). The combined training group increased PV by 9.5%, while resting plasma levels of ACTH, A VP, ALDO, K+, Na+, PROT, NE, and EPI were not changed with training. Four subjects experienced presyncopal symptoms at Tl associated with large increases in ACTH and AVP. Improved responses at T3 may be related to increased SV and Q. The results suggest a) endurance training increases resting and orthostatic SV and Q, while endurance plus resistance training decreases resting and orthostatic Q. The difference between training groups may be related to changes in PV and venous return; b) PV increases with training in the elderly but resting hormonal levels are unchanged, suggesting a change in the stimulus-response relationship between blood volume and hormone secretion via volume sensitive cardiopulmonary receptors; c) training improves responses of older, intolerant subjects to tilt, mediated by increased SV and Q. xvii

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CHAPTER 1 INTRODUCTION Changing demographics in the United States in the latter half of the 20th and into the early 21st century indicates that persons over the age of 65 comprise the fastest growing segment of the population In 1980, 11 % of the population was over the age of 65 but this proportion is expected to increase to 18% by the year 2030 (Abrams & Berkow, 1990). When the elderly population is further delineated, it can be seen that the oldest group in our society (85+ years) has increased by 24.8% since 1980. During this period, the 75-84 year old group grew 17.1 % while the 65-74 year old group increased by 11 %. In absolute numbers, there are expected to be 34.9 million elderly by the year 2000, an increase of 17.1 % over 1987 (Beck, 1989). Thus, an understanding of the physiological changes associated with aging and how these changes impact on homeostatic responses in older persons takes on a great deal of importance. Changes in the cardiovascular system that are associated with aging may predispose older individuals toward disorders of blood pressure (BP) control mechanisms. Acute BP changes are buffered by the high-pressure carotid and aortic baroreflex system. In the elderly, an attenuation of baroreflex sensitivity has been attributed to a decrease in arterial compliance, which results in a decreased deformation of the baroreceptors during a given pressure change (Lipsitz, 1990) and thus an attenuated afferent signal There may also be a decrease in the efferent baroreceptor-mediated responsiveness of heart rate (HR) acceleration during hypotensive stimuli (Gribbin, Pickering, Sleight, & Peto, 1971; Lipsitz, 1990). A decrease in cardiac compliance in the elderly is another 1

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2 aging change that limits the ability of the senescent heart to increase end-diastolic volume (EDV) and/ or decrease end-systolic volume (ESV); this results in a decreased ability to compensate for declines in cardioacceleration capacity by way of an increase in stroke volume (SV) (Shannon, Maher, Santinga, Royal, & Wei, 1991). Finally, either a decrease in J3-receptor sensitivity in the peripheral vasculature or a decrease in vascular compliance may lead to diastolic BP or peripheral resistance responses to orthostasis that are not easily modified (Sowers, 1987). The neuroendocrine system is also altered with age. There is a decrease in the secretory rate and plasma concentration of aldosterone when sodium intake is unrestricted; there is also a decline in aldosterone secretion in response to sodium restriction (Gregerman & Bierman, 1981; McGinty, Stern, & Akshoomoff, 1988) This decline parallels the decline in basal levels of renin activity. Although vasopressin levels may not be affected by aging, the ability of the kidney to concentrate urine is decreased due to a decrease in glomerular filtration rate rather than to a decrease in sensitivity to vasopressin. These changes might be expected to decrease the body's ability to augment plasma volume (PV) with endurance training. Vasoconstrictive responses may also be affected: although there is an increase in plasma norepinephrine concentration with age, there is a diminished vascular contractile response (Gregerman & Bierman, 1981; McGinty et al., 1988). This, together with the decrease in renin activity, may affect the ability of the senescent vasculature to adequately respond to hypotensive stimuli. One manifestation of aging changes is the presence of orthostatic (postural) hypotension. In their review, Robbins and Rubenstein (1984) estimate that approximately 20% of those over age 65 have postural hypotension and that the prevalence in persons over age 75 may exceed 30%. Lipsitz (1990) also

PAGE 20

3 estimates a 20 to 30% rate of postural hypotension in the noninstitutionalized elderly. These rates, however, may reflect the presence of risk factors associated with postural hypotension (hypertension, varicose veins, central nervous system disorders, certain medications); the presence of postural hypotension in the healthy elderly may be lower than this (Dambrink & Wieting, 1987; Mader, Josephson, & Rubenstein, 1987). In younger populations, there have been both cross-sectional and longitudinal studies that have sought to determine the factors associated with orthostatic intolerance and the best training regimen to improve the responses to orthostasis A training-induced hypervolemia has been hypothesized as a mechanism for improving cardiovascular responses to an orthostatic stress. Convertino, Montgomery, and Greenleaf (1984) found that a decrease in the HR and rate-pressure product responses to a 60 head-up tilt after 8 days of cycle ergometer training correlated significantly (r = -0.68) with a training-induced increase in blood volume. Similarly, Shvartz, Convertino, Keil, and Haines (1981) found that improvement in tilt tolerance and a decreased HR response to head-up tilt after training was related to an increased PV An increase in muscle mass is another mechanism hypothesized to help improve responses to orthostasis According to this theory, an increase in muscle mass or tone limits venous pooling during orthostasis and thus better maintains venous return, cardiac output (Q), and arterial pressure. Support for this theory was provided by several studies showing that postural hypotension in response to simulated microgravity was associated with decreased musculature, particularly in the lower extremities, and increased compliance in the leg vasculature (Convertino, Doerr, Mathes, Stein, & Buchanan, 1989; Duvoisin, Convertino, Buchanan, Gollnick, & Dudley, 1989). Two early training studies by Shvartz (1968a, 1969) also tend to lend support to this theory. In 1968, Shvartz

PAGE 21

4 found that 3 months of gymnastic training on "heavy apparatus" was superior to volleyball and general conditioning for improving the systolic BP and pulse pressure response to a 10-minute standing test. It was hypothesized that an increase in abdominal muscle strength in the gymnastics group could explain the results; however, abdominal strength was not measured. In the later study (1969), Shvartz found that a 7-week program of upper body resistance-type exercises was superior to a program of bench-stepping for improving the systolic BP and pulse pressure response during head-up tilt. This appeared to indicate that some mechanism involved in the adaptation to resistance training was responsible for the improvement, but no explanatory mechanisms were offered by the author. A third mechanism proposed to improve responses to orthostasis is an increase in baroreceptor responsiveness. This refers to the HR increment resulting from a given arterial pressure decrement. Several recent cross-sectional studies have compared the baroreceptor response of weightlifters and endurance-trained subjects to lower body negative pressure and/ or a phenylephrine infusion (Smith, Graitzer, Hudson, & Raven, 1988; Smith & Raven, 1986). Both investigations have found that the peripheral resistance response of the two groups was similar and concluded that the more effective maintenance of BP in the weight-trained individuals was due to an enhanced baroreceptor sensitivity. Weight training may therefore play a role in improving responses to orthostasis either by increasing baroreceptor responsiveness and/ or by increasing muscle mass Finally, altered neuroendocrine secretion or altered vascular sensitivity to pressor hormones may affect responses to orthostasis. Although most cross sectional and longitudinal studies do not find that training changes the resting plasma levels of vasopressin and renin (Freund, Claybaugh, Hashiro, & Dice,

PAGE 22

5 1988; Convertino, Brock, Keil, Bernauer, & Greenleaf, 1980; Convertino, Keil, & Greenleaf, 1983; Convertino, Mack, & Nadel, 1991; Wade, Dressendorfer O Brien, & Claybaugh, 1981), norepinephrine often decreases (Hagberg, Montain, Martin, & Ehsani, 1989b; Kiyonaga, Arakawa, Tanaka, & Shindo, 1985; Tipton, 1991). This is thought to reduce BP responses through decreases in HR and Q Altered vascular sensitivity to pressor hormones, in particular an increased~ adrenergic receptor sensitivity, may also play a role in altering responses to orthostasis after training (Wiegman, Harris, Joshua, & Miller, 1981; Wiegman, 1981) Whether physical training can improve the responses to an orthostatic stress in the elderly is not known Some of the components involved in the reflex responses to orthostasis may be irreversibly altered in the elderly (e g aortic distensibility, f3-adrenergic sensitivity, cardiac and vascular compliance). In the young, an improved response to tilt after training consists of a decrease in HR and rate-pressure product associated with an increase in PV (Convertino et al 1984; Shvartz et al 1981) However, in the elderly, the HR and systolic BP responses to tilt are already attenuated (Dambrink & Wieling, 1987; Jansen, Lenders, Thien, & Hoefnagels, 1989; Kenny, Lyon, Bayliss, Lightman, & Sutton, 1987), due possibly to a decrease in the sensitivity of the baroreflex response (Gribbin et al 1971) An improved response to tilt in the elderly after training may therefore involve increases, rather than decreases, in HR or systolic BP. It is possible that an increase in muscle mass after training would increase the systolic BP response to tilt through an improved venous return and SV However, there may be a limit to the effect of this mechanism due to a decrease in left ventricular compliance in the elderly (Shannon et al., 1991). Blood pressure responses may also be limited by the decreased responsiveness of the vasculature to vasoactive hormones such as norepinephrine (Gregerman & Bierman, 1981; McGinty et al

PAGE 23

6 1988). Finally, there may be a limit to the role that increased PV can play in the improvement in venous pressure because of impaired renal sodium conservation in the elderly (Gregerman & Bierman, 1981; Mader, 1989). Based on the data from investigations with younger subjects, it appears that promising modes of training for the improvement in orthostatic responses are either weight training (Shvartz, 1968a, 1968b, 1969; Smith et al., 1988; Smith & Raven, 1986), or endurance training with a resistive component, such as cycling (Convertino et al., 1984; Greenleaf, Brock, Sciaraffa, Polese, & Elizondo, 1985; Shvartz et al 1981) or uphill treadmill walking Endurance exercise training with a resistive component for the elderly would combine some of the advantages of endurance and resistive training alone while eliminating some of the disadvantages. Endurance exercise training can improve aerobic capacity ( V0 2 max) in the elderly an average of 15-30% (Adams & de Vries, 1973; Hagberg et al 1989b; Meredith et al 1989; Seals, Hagberg, Hurley, Ehsani, & Holloszy, 1984). It can also cause a beneficial change in body composition (Graves, Panton, Pollock, Hagberg, & Leggett, unpublished), and a decrease in resting BP (Cononie et al. 1991; Hagberg, 1990; Hagberg & Seals, 1987), particularly in those who are hypertensive (Hagberg, Montain, & Martin, 1987; Hagberg et al., 1989b). Finally, endurance training is associated with increases in PV (Convertino et al. 1984; Oscai, Williams, & Hertig, 1968; Shvartz et al., 1981) although this effect has not been verified in older subjects. One disadvantage of endurance training in the elderly is that elderly women appear to be more susceptible than elderly men to orthopedic injury related to high impact endurance activities such a jogging and fast walking (Pollock et al. 1991; Carroll et al., in press). Uphill treadmill walking, which provides a resistive component to the gluteal and hamstring muscles, but which allows a slower walking cadence and thus a reduction in impact forces, seems to

PAGE 24

7 reduce injury occurrence in the elderly while providing an adequate stimulus for an increase in aerobic capacity (Hagberg et al., 1989a) and an increase in leg strength (Pollock et al., 1991). It is possible that muscle atrophy in the sedentary elderly is marked and that uphill treadmill walking would provide enough stimulus to improve muscular strength and thus improve the cardiovascular responses to orthostasis through enhanced venous return. Resistance training induces increases in muscular strength in the elderly (Fiatarone et al., 1990; Frontera, Meredith, O'Reilly, Knuttgen, & Evans, 1988; Kauffman, 1985 ; Perkins & Kaiser, 1961) and may be beneficial in ameliorating the effects of decreased muscle mass on postural hypotension Resistance training may also improve responses to orthostasis by an increase in baroreceptor sensitivity (Smith et al., 1988; Smith & Raven, 1986). A training program combining resistance training and uphill walking may therefore provide optimal fitness and health benefits while minimizing injuries Statement of the Problem Most researchers investigating the effect of training on orthostatic responses have used young to middle-aged populations (Beetham & Buskirk, 1958; Convertino et al., 1984; Greenleaf et al., 1985 ; Greenleaf et al 1988; Shvartz et al 1981) N o research has been conducted to date to determine whether any form of physical training can help improve the responses to an orthostatic challenge in the elderly. Consequently, different types of training programs using elderly subjects need to be conducted. The specific aims of this research are a) to describe the cardiovascular and endocrine responses of elderly individuals to a 70 head-up tilt before and after 6 months of either uphill treadmill walking or a combination of uphill treadmill walking plus selected resistance training exercises; b) to determine whether

PAGE 25

uphill walking or a combination of uphill walking plus selected resistance training exercises can improve the cardiovascular responses of elderly individuals to a 70 head-up tilt; and c) if orthostatic responses improve, to evaluate the mechanisms involved in the improvement. Research Hypothesis 8 It is hypothesized that uphill treadmill walking of an intensity sufficient to induce significant changes in aerobic capacity and/ or resistance training of an intensity to increase muscular strength of the arms and legs will result in positive adaptations in the cardiovascular responses to an orthostatic stress (70 head-up tilt). It is also hypothesized that one or more of the following training adaptations will correlate with the adaptations in orthostatic responses: increased lower body muscle mass and/or strength, an increased PV, increased baroreceptor responsiveness, and/ or changes in pressor hormone secretion Justification The increase in the elderly population in the United States and the increased cost of medical and pharmacological intervention to ameliorate the effects of aging underlines the importance of less costly interventions in the treatment of aging manifestations In younger populations, there have been some promising results indicating that exercise training can improve the cardiovascular responses to orthostatic stresses (Convertino et al., 1984; Greenleaf et al 1985 ; Shvartz 1968a, 1969; Shvartz et al., 1981). Yet the effect of exercise training on orthostatic responses has not been investigated in older individuals Exercise training in healthy elderly individuals may provide information about potential mechanisms by which orthostatic responses may be improved in this population. In future studies, these mechanisms can be

PAGE 26

investigated in other populations of elderly, e.g., those with documented orthostatic hypotension. Ultimately, exercise training may prove to be an alternative treatment for physiologic (aging-related) occurrences of orthostatic hypotension Assumptions 1. All laboratory equipment will yield accurate, reliable results over the course of repeated testing 2 Subjects will follow instructions given to them regarding food, drink, and drug intake prior to testing. 9 3 Subjects will follow instructions given to them regarding the maintenance of current lifestyle (e g diet and exercise) outside of the prescribed program Delimitations The following delimitations were imposed: 1 Subjects were over the age of 60 years 2. Subjects recruited were sedentary and free from cardiovascular pulmonary, peripheral vascular, or orthopedic diseases, or conditions that would limit their full participation in an exercise program. 3 Subjects were not diabetic 4. Subjects had resting systolic and diastolic BP less than 160/100. 5. Subjects were not taking anti-angina! or digitalis medication 6 Subjects did not previously have a myocardial infarction, coronary artery bypass surgery, or percutaneous transluminal coronary angioplasty. 7. Subjects did not have any resting or exercise electrocardiogram abnormalities indicative of significant ischemia or high grade dysrhythrnia

PAGE 27

8. Subjects had a normal HR and BP response to maximal treadmill testing 9. Strenuous exercise was not allowed within 12 hours prior to most testing procedures; strenuous exercise was not allowed within 24 hours prior to tilt testing. 10 10 Subjects were at least 3 hours but not more than 12 hours post prandial during testing sessions; no caffeine was consumed within 3 hours prior to any test. 11 No alcohol was consumed within 24 hours prior to testing 12. Subjects took usual prescribed medications prior to testing Limitations Major limiting factors included the following : 1. Forty-four elderly subjects (14 males, 30 females) volunteered to serve as subjects. 2 Diet and day-to-day activity could not be regulated. Definition of Terms Aerobic exercise consists of activities that can be maintained continuously and involve rhythmic movement of large muscle groups. Aerobic activities, such as walking, jogging, running, swimming, cycling, and rope-skipping, are used to improve cardiorespiratory function Baroreflex responsiveness refers to the magnitude of the HR change in response to a gi v en arterial pressure change. A decreased responsiveness refers to an attenuated HR response to a given pressure change. Hypervolemia is an increase in blood volume

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Orthostasis is an environmental perturbation that produces qualitative effects similar to those induced by upright stationary posture (ConvertinoHR 1987). 11 Orthostatic (postural) hypotension is a reduction of 20 mmHg or more in systolic BP upon standing upright (Lipsitz, 1990). Orthostatic intolerance is the inability of the cardiovascular reflexes to maintain arterial pressure for adequate cerebral blood perfusion, eventually leading to syncope (Convertino, 1987). Resistance exercises consist of activities designed to increase muscular strength and/ or endurance These activities generally involve concentric and/ or eccentric contractions of a muscle group against a constant or variable resistance and use free weights, and/ or constant or variable resistance machines. Syncope is synonymous with fainting.

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CHAPTER2 REVIEW OF LITERATURE Introduction The response to orthostasis involves an activation of reflex systems designed to maintain blood pressure (BP) homeostasis and cerebral perfusion despite the translocation of approximately 800 ml of blood from the central circulation to the periphery (Blomqvist & Stone, 1983). These reflexes include enhancement of myocardial function, increases in arterial and venous tone, increases in neuroendocrine secretion, and reflexes mediated by highand low-pressure baroreceptors. Endurance training in young individuals appears to be associated with alterations in some of the reflex responses to orthostasis There may be a reduction in chronotropic responsiveness, and in the sensitivity of the high and lowpressure baroreceptor systems In addition, there may be an alteration in the sensitivity of vascular receptors, an increase in venous compliance, and an attenuation of vasoactive hormone release (Convertino, 1987) These changes would appear to compromise the body's ability to withstand an orthostatic challenge On the other hand, training-induced adaptations that would appear to enhance the body's ability to withstand orthostasis include an increase in blood volume (BV) and an increase in muscle mass particularly in the lower extremities. The responses to orthostasis after endurance training in elderly persons have not been characterized However, normal, healthy elderly persons demonstrate a quantitative and sometimes qualitative, difference in their 12

PAGE 30

13 response to orthostasis when compared with younger persons. There is generally a smaller reflex increase in heart rate (HR) (Dambrink & Wieling, 1987; Ebert, Hughes, Tristani, Barney, & Smith, 1982; Frey & Hoffler, 1988) most likely due to a decreased HR responsiveness in the high-pressure baroreflex system (Gribbin et al., 1971). Mean arterial pressure (MAP) may therefore be maintained with less of a reliance on HR (Jansen et al., 1989) and more of a reliance on increases in peripheral vascular resistance and diastolic blood pressure (DBP) (Ebert et al., 1982; Frey & Hoffler, 1988). In addition, while younger persons usually demonstrate an increase or no change in systolic blood pressure (SBP) when moving from sitting to standing (Convertino et al., 1984; Dambrink & Wieling, 1987), older persons often see a decrease (Dambrink & Wieling, 1987) This may be due to arterial rigidity, which decreases the ability of the vasculature to adjust to changes in pressure (Jansen et al., 1989; Smith and Fasler, 1983), or to baroreflex impairment (Lipsitz, 1989). Whether the responses to an orthostatic stress can be improved after endurance training in the elderly is not known Some of the components involved in the reflex responses to orthostasis may be irreversibly altered in the elderly (e g., aortic distensibility, !3-adrenergic sensitivity, cardiac and vascular compliance) Another problematic issue is that some of the changes produced by the aging process are in the same direction as those produced in younger persons who "improve" their responses to orthostasis after training For example, an improved response to head-up tilt after training in young persons generally involves a decrease in HR and rate-pressure product associated with an increase in plasma volume (PV) (Convertino et al., 1984; Shvartz et al., 1981). In the elderly, the HR and SBP responses to tilt are already attenuated (Gribbin et al., 1971) and an improved response to tilt after

PAGE 31

training may therefore involve increases, rather than decreases, in HR or SBP. 14 An understanding of the responses of elderly persons to an orthostatic stress after training first involves an investigation of how resting parameters may be altered with training and how training interacts with aging to produce changes. The response to an orthostatic stress before and after a period of training must also be described, taking into account both training and possible aging effects. Responses to Endurance Training Resting Heart Rate (HR), Stroke Volume (SV), and Cardiac Output (O) The decline in resting HR after endurance training is well documented in young and middle-aged persons. The magnitude of the decrease ranges from 4 to 8 beatsmin1 (Convertino et al., 1980a; Convertino et al., 1983; Convertino et al., 1984; Convertino et al., 1991; Greenleaf, Sciaraffa, Shvartz, Keil, & Brock, 1981; Hartley et al., 1969; Oscai et al., 1968; Pollock et al., 1976; Pollock et al., 1971; Seals & Chase, 1989) and may be related to training induced hypervolemia (Fortney, Wenger, Bove, & Nadel, 1983). Other factors related to this decrease include decreased sympathetic nervous system (SNS) activity (Bjorntorp, 1987; Katona, McLean, Dighton, & Guz, 1982) and/or increased in parasympathetic tonus (Barney, Ebert, Groban, & Smith, 1985; Kenney, 1985; Seals & Chase, 1989). Declines in resting HR may be independent of the body position in which the HR is measured Greenleaf et al. (1981) found nearly equal decreases in resting HR in the supine and sitting positions after 8 days of cycle ergometry training (8 and 7 beatsmin-1, respectively).

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15 Some authors claim that a resting bradycardia does not occur with training in the elderly (Lampman & Savage, 1988). However, this conclusion is based partially on the results from studies on institutionalized subjects (Clark, Wade, Massey, & Van Dyke, 1975; Stamford, 1972) or on programs using ''light'' exercise (Emes, 1979). Nevertheless, even some studies using a moderate exercise intensity (Barry, Daly, Pruett, Steinmetz, Page, Birkhead, & Rodahl, 1966; Meredith et al., 1989; Schocken, Blumenthal, Port, Hindle, & Coleman, 1983) have failed to documented significant decreases in resting HR. This is in contrast to other studies showing declines in resting HR in the elderly after training to be of approximately the same magnitude as documented in younger subjects. Braith et al. (1990) found a small (3 beatsmin1 ) but significant decrease in HR after 3 months of endurance training at 50-70% HRRmax in healthy 60 to 79 year olds. A similar small decrease was noted by Adams and deVries (1973) in elderly women after 3 months of training at a minimum of 60% V0 2 max. Cononie et al. (1991) found a slightly greater decline (5 beatsmin1 ) in healthy 70-79 year olds after six months of endurance training at 75-85% V0 2 max. Older hypertensives may have even larger reductions in HR as a result of training (e.g 8-13 beats; Hagberg et al., 1989b). Stroke volume at rest has been shown to be unchanged (Ekblom, Astrand, Saltin, Stenberg, & Wallstrom, 1968) or increased (Convertino et al., 1991; Hartley et al., 1969) after strenuous physical training in young and middle-aged persons. Increases may be related to training-induced hypervolemia and elevated central venous pressure (CVP) (Convertino et al 1991), or to changes in such cardiac loading conditions as decreased peripheral resistance and increased left ventricular EDV (Ehsani, 1987). In instances where SV was increased, resting Q remained the same despite an increased

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16 BV, due to the reduction in resting HR (Convertino et al., 1991; Hartley et al., 1969). The data on changes in resting SV or Q with training in the elderly are scarce. In one of the few reported studies, Hagberg et al. (1989b) found that elderly hypertensives did not increase their resting SV or their blood or plasma volumes after 9 months of lowor moderate-intensity exercise training. However, the low-intensity exercise group had a reduction in resting Q, while the moderate-intensity group had a reduction in total peripheral resistance. No potential mechanisms were proposed to explain the different responses. Similarly, Schocken et al. (1983) reported that neither resting Q nor resting SV changed after training in the elderly. They also found that contractile function, as measured by an increase in left ventricular (L V) ejection fraction and L V ESV, did not change with training. Blood Pressure (BP) Since the level of mean BP is the product of flow ( Q = HR X SV) and peripheral resistance, changes in one or both of these factors as a result of exercise training could effect BP changes. If SV remains unchanged, reductions in HR and Q will provide a blood pressure-lowering effect. Reductions in peripheral resistance may also act to lower BP. Mechanisms associated with these changes include a decrease in SNS activity, resetting and/ or increased sensitivity of baroreceptors, altered distribution of BV, altered pressure-natriuresis function, alterations in the renin-angiotensin axis, altered sensitivity of vascular aand ~-receptors, and alterations in the release or actions of endothelium-derived vasorelaxants and vasoconstrictors (Kenney & Zambraski, 1984; Tipton, 1991). It has also been hypothesized that physical activity sends specific afferent signals to the

PAGE 34

17 central nervous system that stimulate central endorphin production and cause a decrease in resting HR and Q through central inhibition of SNS activity (Bjorntorp, 1987) In addition, since insulin is stimulated by~ adrenergic activity, lowered SNS activity may also result in a decrease in plasma insulin concentration This may help to decrease BP by decreasing sodium (Na+) reabsorption in the kidney (Bjorntorp, 1987; Kenney & Zambraski, 1984) Greenleaf et al. (1981) hypothesize that the drop in diastolic BP after training is a result of the continued stimulation of both vasopressin and the renin-angiotensin system during exercise, resulting in a diminished vasoconstrictive response for some time after exercise; i.e., "fatigue" of the vasoconstrictor response Confounding factors include a concomitant weight loss with training, which independently decreases catecholamine release and BP (Tipton, 1991) According to several recent reviews, endurance training in young and middle-aged persons with mild essential hypertension can lower both SBP and DBP 8-10 mmHg (Bjorntorp, 1987; Hagberg, 1990; Hagberg & Seals, 1987). Training in older(> 60 years) hypertensives (Hagberg et al., 1989b) and normotensives (Braith et al., 1990; deVries, 1970; Emes, 1979; Stamford, 1972) can have the same effect. Despite the reductions seen in some normotensives, it is commonly thought that the BP-lowering benefits to be derived from endurance training are dependent on the initial BP level: persons with normal initial BP often do not see reductions with training (Adams & deVries, 1973; Kilborn et al., 1969; Pollock et al., 1976; Schocken et al., 1983) while those with mild to moderate elevations in BP (> 140/90 mmHg) are likely to see improvements with training (Kiyonaga et al., 1985). This phenomenon has been documented by Cononie and coworkers (1991) in a study on healthy 70-79 year olds. After six months of endurance training at

PAGE 35

75-85% V0 2 max, there were decreases in SBP, DBP, and mean arterial blood pressure (MAP) of 4, 5, and 4 mmHg, respectively. However, when subjects with initial blood pressures of >140/90 mmHg were analyzed separately, the decreases were 8, 9, and 8 mmHg for SBP, DBP, and MAP, respectively. Maximal Aerobic Power 18 Endurance training programs of 6 to 12 months duration that meet the American College of Sports Medicine's (ACSM) criteria for developing and maintaining cardiorespiratory fitness (ACSM, 1990) generally result in improvements in V0 2 max ranging from 15-30%. The magnitude of improvement is dependent on the frequency, intensity and duration of training (Atomi, Ito, lwasaski, & Miyashita, 1978; Gettman et al., 1976; Milesis et al., 1976). Although there is a decrease in maximal aerobic power with age (Buskirk & Hodgson, 1987), the relative training-induced improvement in V0 2 max that can be made by healthy elderly individuals is similar to that seen in younger individuals (Cress et al., 1991; Hagberg et al., 1989a; Mered i th et al., 1989; Seals et al., 1984; Sidney & Shephard, 1978) when training programs are designed according to the ACSM (1990) recommendations. For example, training for more than two days per week at either 60 or 80% maximal HR reserve (HRRmax), resulted in improvements in V0 2 max of 14 and 29%, respectively, in elderly persons (Sidney & Shephard, 1978). Similarly, training 3 days per week for six months at 75-85% HRRmax resulted in a 20% improvement in V0 2 max in elderly men and women (Hagberg e t al., 1989a). It appears that improvements in V0 2 max in the elderly are due primarily to peripheral, as opposed to central, adaptations. While both

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19 central (i.e., increased maximal SV, maximal Q, and maximal myocardial oxygen [02] consumption) and peripheral (increased maximal arteriovenous 02 difference) adaptations have resulted from endurance training in young and middle-aged men (Ekblom et al., 1968; Hartley et al., 1969) and in cardiac patients (Ehsani, Heath, Martin, Hagberg, & Holloszy, 1984; Ehsani, Martin, Heath, & Coyle, 1982), the evidence for improved central parameters after training in elderly individuals is sparse and inconclusive (Ehsani, 1987). Indirect evidence for central adaptations is provided by Heath, Hagberg, Ehsani, and Holloszy (1981) who found that values for maximal 02 pulse were similar for young and master athletes, and both were higher than for a group of sedentary middle-aged individuals. This suggested that the higher V0 2 max in the master athletes compared with the sedentary subjects could have been mediated through a higher maximal SV, since maximal HR was similar between the two groups. However, a higher maximal arteriovenous 02 difference cannot be ruled out. Schocken and coworkers (1983) also provide evidence for an increase in maximal SV in the elderly. They found that although moderateto high-intensity training (70-85% HRmax) did not change resting SV, ESV, or EDV in elderly subjects, the calculated maximal exercise SV increased approximately 13 ml as a result of an increase in maximal LV EDV. Maximal Q increased from 9 94 to 11.40 Lmin-1, but this was not statistically significant. Meredith and coworkers (1989) provided evidence for the peripheral adaptation hypothesis. After 12 weeks of cycle ergometer training at 70% HRRmax, they found that elderly subjects demonstrated significant increases of 27 and 118% in muscle glycogen content and muscle oxidative capacity a t rest, while younger subjects showed nonsignificant increases of 14 and 28%, respectively. However, part of the disparity in the results may be because both

PAGE 37

young and old subjects made nearly identical absolute increases in VO2max (5.5 and 5.3 mlkg-lemin-1, respectively). In relative terms, the elderly subjects increased VO 2 max 19.9%, compared with 12 1 % for the young subjects. 20 Seals et al. (1984) also found evidence for peripheral, but not central, training adaptations in the elderly. They found that after 6 months of low intensity training followed by 6 months of high-intensity training, 61-67 year old men and women increased VO 2 max approximately 30%. Since maximal Q was not significantly increased, the increase in VO 2 max appeared to be mediated primarily through a 14% increase in the maximal arteriovenous 02 difference. Increase in Strength and Muscle Mass Changes in body composition as a result of endurance training are commonly assessed using hydrostatic weighing or skinfolds. Using these methods, lean body mass changes either not at all (Hagberg et al., 1989a; Kilborn et al., 1969) or increases a small amount (Boileau, Buskirk, Horstman, Mendez, & Nicholas, 1971; Wilmore et al., 1980) as a result of endurance training. Using urinary creatinine as a measure of muscle mass, Meredith et al. (1989) also found no increase in muscle mass after 12 weeks of endurance training at 70% VO2max in the elderly Due to the specific nature of training adaptations, it would not be expected that strength would substantially increase as a result of endurance training. Consequently, very few endurance training studies have incorporated or reported strength testing measures. An early study (Barry, Steinmetz, Page, & Rodahl, 1966) found no increase in knee extension or elbow flexion strength after 3 months of cycle ergometer training in the

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21 elderly. In a more recent study, however (Graves et al., unpublished), there was a strong trend toward an increase in leg strength in endurance trained 7079 year olds, many of whom used uphill treadmill walking as a mode of training Responses to Strength Training Although the response to strength training varies widely among individuals and studies, the average improvement in strength for young and middle-aged men and women for most muscle groups appears to be approximately 25-30% (Fleck & Kraemer, 1987) and is often associated with an increase in fat free weight (FFW) (Hurley et al., 1984). Older individuals are capable of making comparable changes with appropriately designed programs (Aniansson & Gustafsson, 1981; Aniansson, Ljungberg, Rundgren, & Wetterqvist, 1984; Chapman, deVries, & Swezey, 1972; Liemohn, 1975; Moritani & deVries, 1980). In some studies using elderly individuals, however, moderateto highintensity resistance training has resulted in greater increases in strength (e.g., 50-230%) (Fiatarone et al., 1990; Frontera et al., 1988; Kauffman, 1985; Perkins & Kaiser, 1961) This may be due to the lower initial level of strength and thus the greater relative potential for strength development Changes in muscle morphology that occur with aging include a decrease in the total number of both Type I and Type II fibers, with a greater proportional loss of the Type II fibers (Evans, 1986; Larsson, Sjodin, & Karlsson, 1978; Larsson, Grimby, & Karlsson, 1979). This age-related atrophy is thought to be caused by either a reduction in physical activity (Aniansson & Gustafson, 1981; Larsson et al., 1978) or a reduced capacity to repair or replace damaged muscle cells (Evans, 1986).

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22 Although aging-related changes in muscle morphology can be partially reversed as a result of resistance training, the reported changes vary among studies This may be due to differences in training intensity, muscle groups trained or tested, or even possibly to gender-specific adaptations. Cress et al. (1991) found an increase in the Type IIb fiber cross-sectional area, with maintenance of the Type I and Ila fiber cross-sectional area, after 50 weeks of low to moderate aerobic/resistance training in septuagenarian women. Both Aniansson and Gustafsson (1981) and Aniansson et al (1984) noted an increase in the percentage, but not in the cross-sectional area, of Type Ila fibers after resistance training in elderly men and women On the other hand, Larsson (1982) found that the cross-sectional area of both Type I and Type II fibers increased 31.8 and 51.5%, respectively, with 15 weeks of knee extensor training in 56-65 year old men. Frontera et al. (1988) also found significant increases of 33.5 and 27 6% in Type I and II fiber cross-sectional area after 12 weeks of strength training in 60-72 year old men Hormonal, and Blood/Plasma Volume Responses to Training : Resting Values Blood/Plasma Volume While some early studies reported no change in BV as a result of training (Bass, Buskirk, Iampietro, & Mager, 1958; Dill, Hall, Hall, Dawson, & Newton, 1966), most recent studies show that endurance training increases BV (Convertino et al., 1980a; Convertino, Greenleaf, & Bernauer, 1980; Convertino et al ., 1983; Convertino et al., 1984; Convertino et al., 1991; Oscai et al., 1968). Associated with the increase in the plasma fraction of the blood and the constant red cell volume, there is a decrease in the hematocrit (Hct) and

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the hemoglobin (Hb) concentration but a constancy in the Hb content (Convertino et al., 1980a; Oscai et al., 1968) 23 The training parameters of intensity, frequency and duration have all been hypothesized to affect BV increases. Two studies by Convertino and colleagues illustrate the possible effect of training intensity on BV expansion (Convertino et al., 1980a; Convertino et al., 1977). Both studies utilized an 8day training protocol involving 2 hours of cycle ergometer exercise per day; intensity for the former study was 65% of VO2max while it was 50% of VO 2 max for the latter study. The regimen with the higher intensity produced an 18.7% (72 ml) higher increase in BV. Intensity, however, cannot be the only factor influencing the magnitude of PV expansion. In two studies by Convertino and colleagues (Convertino et al., 1980a; Convertino et al., 1983), identical 8-day cycle ergometer training protocols at an intensity of 65% of VO 2 max for 2 hours per day induced 12.1 and 12.3% increases, respectively, in PV. However, a different investigative group (Greenleaf et al., 1981) found a similar (12 2%) increase in PV after a comparable training protocol at an exercise intensity of only 44% of VO 2 max. It might be hypothesized that the potential for PV expansion is greater when the initial volume is lower since the relative volume expansions in these studies were similar, but the absolute increases were smaller in the Greenleaf et al. (1981) (385 ml vs. 427 ml in both Convertino et al. studies), indicating a smaller initial PV. On the other hand, Convertino et al. (1980a) compared the fitness level and relative hypervolemia of the subjects in their study with those of Oscai et al. (1968). The subjects in the Convertino et al. investigation had a higher initial fitness level (57 mlkg1 min1 vs approximately 38.5 mlkg-lmin 1) and a higher

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initial PV (3500 ml vs. 3196 ml), yet they were able to achieve a greater relative PV expansion (12.1 % vs 6.4%; 427 ml vs. 204 ml) Frequency and duration of training are thought to affect training induced hypervolemia. It has been speculated that regimens with 24 consecutive days of training and/or exercise durations of two hours or more per day produce a greater hypervolemia than those which allow 1-2 days recovery between training sessions and/ or use shorter exercise sessions (Convertino et al., 1980a). If program duration is held constant, particularly with shorter (e g 8 days) programs, this may hold true. An equally impor t ant factor in BV expansion, however, may be the total amount of work performed during the entire program For example, Convertino et al. (1991) produced a 13% increase in PV with a 10-week training regimen where subjects exercised for 4 days per week, 30 minutes per day at 75-80% of V0 2 max. In the Convertino et al. (1980a) study, a 12 1% increase in PV was achieved with an 8-day protocol, where subjects exercised for 2 hours per day at 65% of V0 2 max. It is possible that the lower training frequency and shorter duration in the former study was offset by the higher intensity and longer program duration to produce an equivalent PV expansion. In contrast, Oscai et al. (1968) produced only a 6.4% increase in PV w i th training for 30 minutes per day, 3 days per week for 16 weeks Although the training intensity relative to V0 2 max was not specified, the training HR data suggest an intensity similar to that used in the Convertino et al. (1991) study Clearly, there are other factors or combinations of factors influencing the degree to which PV can be expanded due to a training regimen. Hormonal factors associated with training-induced hypervolemia appear to be the stimulation of vasopressin (AVP) and renin (PRA) production during exercise (approximately fiveto ninefold increases), which

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25 facilitate retention of Na+ and water; and an increase in plasma albumin content, which provides an increased water-binding capacity for the blood (Convertino et al., 1980a; Convertino, Keil, Bernauer, & Greenleaf, 1981). This conclusion is supported by data from Greenleaf et al. (1981) who found that subjects exercising in the heat had greater increases in A VP and PRA during exercise and a larger PV after training than subjects exercising in a more moderate temperature Resting values of A VP and PRA, however, were unchanged with training (Convertino et al., 1980a; Convertino et al., 1983; Greenleaf et al., 1981: Convertino et al., 1991) Few studies have documented the PV responses to training in older individuals Resting PV does not appear to change with age up to age 40 (Chien, Usami, Simmons, McAllister, & Gregersen, 1966) but cross-sectional and longitudinal data with older individuals are lacking Convertino et a l. (1980a) hypothesized that training-induced hypervolemia might be less in older individuals due to a decreased physical working capacity. However, since training intensity expressed as a percentage of V0 2 max appears to be a potent stimulus for PV expansion, the relative hypervolemia induced by training in older individuals may be equal to that of younger individuals training at the same relative intensity. Indirect evidence for the Convertino et al. hypothesis is offered by the data of Kilborn et al (1969) In this study, 3855 year old men increased V0 2 max by 14% after 2 months of endurance training ; however, there were no changes in resting Hb and Hct. Although PV was not measured, the data suggest that it did not change since an increase in PV is usually accompanied by decreases in Hb and Hct (Convertino et al., 1980a; Oscai et al., 1968) An aging effect (a decrease in aldosterone secretion, and a decrease in plasma concentration and renal sensitivity to vasopressin [anti-diuretic hormone]), and not the decline in physical working capacity,

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would more likely contribute to a lack of change in PV in older persons (Gregerman & Bierman, 1981; McGinty et al., 1988). Vasoactive Hormones 26 Vasopressin (AVP). The most potent stimulus for A VP secretion is an increase in blood osmolality sensed by osmoreceptors in or near the hypothalamus. Increases as small as 1-2% above 280 mOsmL-1 are sufficient to elicit AVP secretion. A secondary influence on AVP secretion is a BV change sensed by both highand low-pressure mechanoreceptors. The high pressure baroreceptors in the carotid sinus and aortic arch are sensitive to changes in arterial pressure while low-pressure (cardiopulmonary) baroreceptors, located in the atria, the pulmonary veins, and within the walls of the heart, respond to changes in intracardiac pressures. Reductions in arterial, central venous, or atrial pressure, such as would be induced by head up tilt, decrease afferent nerve activity and release inhibitory activity in the cardiovascular centers of the central nervous system. A series of reflexes ensue which act to maintain arterial pressure by increasing Q and/ or peripheral resistance. The end result is an increase in HR and contractility, increased venoand vasoconstriction, and reduced blood flow to the skin, skeletal muscles, kidney and splanchnic area (Convertino, 1987; Guyton, 1991; Goodman & Frey, 1988). An increase in vasoactive hormone (AVP, norepinephrine, and renin-induced angiotensin II [All]) release is an integral part of this response Conversely, increases in central venous or atrial pressure induced by supine posture or water immersion would produce opposite changes. Supine resting values of AVP average 2.7 1.4 pgml-1 (Labhart, 1986).

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27 Training-induced increases in BV cause parallel increases in CVP (Convertino et al., 1991) and are of the magnitude (10-15%; Convertino et al., 1980a; Convertino et al., 1983; Convertino et al., 1991; Greenleaf et al., 1981 ) where A VP would be expected to decrease. Cross-sectional studies have found that acute volume expansion or water immersion stimulate the suppression of AVP and secretion of atrial natriuretic factor both in animals (Johnson, Zehr, & Moore, 1970) and humans (Gauer & Henry, 1963; Norsk Bonde-Petersen, & Warberg, 1985; Thompson, Tatro, Ludwig, & Convertino, 1990; Volpe et al., 1989). Conversely, Harrison et al. (1986) found that acute changes in central BV induced by dehydration and orthostasis induced increases in AVP. In contrast, Norsk, Bonde-Petersen, & Warberg (1986) did not find a relation between acute CVP changes, induced by lower body negative pressure (LBNP) or lower body positive pressure, and A VP secret i on, and concluded that the cardiopulmonary mechanoreceptors did not strongly influence AVP secretion. Although studies using acute volume changes to stimulate or suppress A VP provide evidence that cardiopulmonary receptors play a role in A VP secretion, they do not adequately address the issue of the effect of chronic changes in volume and CVP on hormonal secretion. It has been hypothesized that endurance training causes a resetting and/ or a decrease in the sensitivity of the cardiopulmonary receptors (Convertino, 1987). This results in unchanged basal levels associated with increased BV, together with either a reduced suppression of A VP when CVP is increased (e g., during water immersion or lower body positive pressure), or a reduced secretion o f A VP when CVP is reduced (e.g., during tilt or LBNP). A resetting of the stimulus-response relation between BV, CVP, and AVP secretion is suggested by the data of Freund et al. (1988) who found that endurance-trained

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28 individuals have resting levels of AVP similar to those of sedentary individuals. A decrease in sensitivity of the cardiopulmonary receptors is suggested by studies which have found that endurance-trained individuals exhibited a lesser diuretic response (i.e a reduced suppression of A VP) in response to water immersion (Boning & Skipka, 1979; Claybaugh et al 1986; Skipka, Boning, Deck, Kulpmann, & Meurer, 1979) or water intake (Claybaugh et al., 1986; Freund et al., 1988) as evidenced by a lower urine flow Longitudinal studies provide the best insight into the response of resting AVP levels to physical training and into possible alterations in cardiopulmonary baroreceptor sensitivity. Convertino et al. (1980a) and Convertino et al. (1983; 1991) found that resting AVP did not change after training programs that increased V0 2 max by 8-20%. In their most recent investigation, Convertino et al. (1991) measured BV, CVP, and resting hormonal levels They found that training resulted in parallel increases in BV and CVP, but without any increase in MAP or vascular compliance. In addition there were no changes in resting levels of A VP, ALDO or atrial natriuretic factor suggesting that the chronic increase in CVP caused a resetting of the cardiopulmonary stimulus-response mechanism Renin. Renin is synthesized and secreted into the blood by the juxtaglomerular (JG) cells in the afferent arterioles of the glomeruli. Juxtaglomerular cells secrete renin in response to decreased pressure in the afferent arterioles as well as in response to sympathetic stimulation, decreased Na+ load in the tubular fluid, or a drop in atrial pressure (Goodman & Frey, 1988 ; Kiowski & Julius, 1978) All of these stimuli are related to a decrease in BV and/ or a drop in arterial pressure Normal supine resting values for renin activity in normotensive individuals range from 1-2 ng Angiotensin

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Iml-lh-1 (Labhart, 1986), but may be lower in the elderly (Cleroux et al., 1989; Gregerman & Bierman, 1981). 29 Although it might be expected that training-induced increases in BV (Convertino et al 1980a; Convertino et al., 1980b; Convertino et al 1983; Convertino et al. 1991; Oscai et al., 1968) or decreases in SNS activity (Bjorntorp, 1987; Katona et al., 1982) would reduce renin secretion as it does in acute volume changes (Thompson et al., 1990), the increase in volume is not associated with increases in mean arterial pressure (Convertino et al., 1991) or with changes in plasma Na+ concentrations (Convertino et al., 1980a; Freund et al., 1988) Accordingly, most studies find that renin activity in younger individuals does not change with training. Both Convertino et al. (1980a) and Convertino et al. (1983) found unchanged resting levels after an exercise protocol (8 days of cycle ergometry for 2 hours per day at 65% VO2max) that induced 12.1-12 3% increases in PV. Wade et al. (1981) also found resting levels to be unchanged in endurance runners during and after 20 days of running an average of 28 km per day. The data from cross-sectional studies largely support this conclusion Both Freund et al. (1988) and Skipka et al. (1979) found no difference in resting PRA levels between trained and untrained individuals. However, one study (Fagard et al., 1985) found lower resting PRA values in endurance trained athletes. The data regarding changes in resting levels of renin after training in the elderly are sparse and contradictory. Braith et al. (1990) found decreases in resting PRA associated with decreases in resting BP in healthy 60 to 79 year olds after 3 months of exercise training at 50-70% HRRmax On the other hand, Hagberg et al. (1989b) found that after 9 months of exercise training in elderly hypertensives, there were equivalent reductions in resting PRA for

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30 both exercising and control groups. This did not appear to be associated with the BP changes, however: subjects exercising at low (50% V02max) intensity experienced significantly greater reductions in BP than the control or moderate-intensity (70-85% VO 2 max) exercise groups, but with equivalent reductions in PRA. Catecholamines. Norepinephrine (NE) levels are generally considered representative of sympathetic tone (Mazzeo, 1991), although this conclusion has been challenged (Floras et al., 1986). The possibility that plasma NE concentrations may not represent sympathetic activity after training because of down regulation of adrenergic receptors has not been investigated (Tipton, 1991). Resting plasma levels of NE average 66-390 pgml1 while resting EPI levels average 10-70 pgml1 (Cryer, 1980). Resting levels of NE are increased with age, while EPI concentrations remain unchanged (Gregerman & Bierman, 1981; Lipsitz, 1989). Training is associated with a decrease in SNS activity as evidenced by a decrease in plasma NE concentration, particularly in hypertensives (Hagberg et al., 1989b; Kiyonaga et al., 1985; Tipton, 1991). However, Convertino et al. (1991) found no change in resting levels of NE after 10 weeks of training in young normotensive men. Changes in body weight associated with training may independently result in decreases in catecholamine release, rendering conclusions about the effect of training alone difficult (Tipton, 1991). The reduction in resting NE is thought to result in a decrease in BP through decreases in resting HR and Q. However, the data regarding the response of peripheral resistance are inconsistent: some investigators have found that the decrease in NE is associated with a decrease in peripheral resistance while others have found either an increase or no change (Tipton, 1991).

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31 Data on post-training resting catecholamine concentrations in the elderly are scarce. Hagberg et al. (1989b) found that 9 months of exercise training in elderly hypertensives did not reduce supine or standing NE levels compared with initial within-group levels. However, because of an increase in NE in the control group, the changes from preto post-training in the exercise groups were significant. Epinephrine (EPI) levels (both supine and standing) did not change with training in either exercise group. Summary Based on results from studies inducing acute central BV changes, increases in BV should produce increased stimulation of the cardiopulmonary baroreceptors and induce a suppression of A VP and renin. The bulk of the data, both cross-sectionally and longitudinally, suggest that this does not occur when central BV is increased chronically. This supports the hypothesis (Convertino et al., 1991) that the continual stimulation of the cardiopulmonary receptors produces an attenuation of the stimulus-response mechanism or a resetting of the receptors to operate at a higher CVP. Norepinephrine levels, however, are more commonly seen to decrease with training. These reduced levels are associated with decreases in BP or peripheral resistance Training-induced losses in body weight may independently reduce catecholamine levels Hormones Associated with Fluid Volume Control: Aldosterone (ALDO) The plasma concentration of All is the most potent stimulus for ALDO secretion; increased adrenocorticotropic hormone (ACTH) and potassium (K+) concentrations are also potent stimuli. Since the rate-limiting step in the production of All is the cleavage by renin of angiotensinogen to angiotensin I (AI), the secretion of renin by the kidney is a major regulator of ALDO secretion. Therefore, the forces that stimulate renin secretion will ultimately

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32 increase ALDO secretion. Increased ALDO causes an increase in the reabsorption of Na+ in the renal collecting ducts along with an obligatory retention of water, and an increase in the excretion of K+. Normal resting values for supine subjects range from 20-100 pgml1 (Labhart, 1986). Resting levels in the elderly are approximately 40% lower (Gregerman & Bierman, 1981) Most studies show that training does not affect resting ALDO levels. This is not surprising in light of the constancy of resting renin activity levels previously cited. Convertino and coworkers (1991) found no changes in resting ALDO levels after a 10 week (4 days per week at 75-80 % of V0 2 max) training regimen. Cross-sectional studies (Freund et al., 1988; Wade et al., 1981) also have found no differences in resting ALDO levels between trained and untrained individuals One study, however, did find that trained subjects had lower resting levels of ALDO compared with untrained subjects, but that this difference did not correspond to the resting renin activity levels (Skipka et al., 1979) Data on training changes in resting ALDO concentrations in the elderly are scarce Braith et al. (1990) found that 3 months of exercise training in 60 to 79 year-olds did not alter resting ALDO levels, despite evidence for a decrease in both resting potassium (K+) and resting renin activity Adrenocorticotropic Hormone (ACTH) Adrenocorticotropic hormone causes the adrenal cortex to secrete cortisol and ALDO However, ACTH is not as important a regulator of ALDO secretion as is All, but it is required for optimal secretion (Goodman, 1988; Guyton, 1991). An important factor in the measurement of resting ACTH levels is the time of day of measurement: ACTH demonstrates a circadian

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33 rhythm, with highest levels in the early morning. Morning values for the healthy adult range from 10-100 pgml1 while evening values range from 520 pgml1 (Labhart, 1986). Aging does not appear to change resting ACTH levels (Everitt, 1980; Gregerman & Bierman, 1981). The response of resting ACTH levels to training is not known However, since acute distension of the right atrium inhibits ACTH release (Cryer & Gann, 1974), it might be hypothesized that the increase in BV that accompanies training would reduce basal ACTH secretion. On the other hand, if there is a resetting and/ or a reduction in sensitivity of the atrial receptors mediating ACTH release as there appears to be for A VP and renin release, basal levels would not be affected. Protein (PROT), Sodium (Na+) and Potassium (K"!:) The normal resting value for PROT in the plasma is 1.2 mOsmL1 or 7.3 gmdl1 while the normal resting values for Na+ and K+ are 143 and 4.2 mOsmL 1 respectively (Guyton, 1991). Protein and K+ together provide only about 2% of the total plasma osmolar activity while Na+ is responsible for approximately 51 % of the total osmolar activity. Changes in plasma Na+ concentrations affect osmoreceptors in or near the anterior hypothalamus, which in turn control A VP secretion by the posterior pituitary gland Plasma proteins are responsible for producing capillary osmotic pressure since they do not readily diffuse through the capillary membrane Although, from a homeostatic point of view, it would not be expected that the concentrations of PROT, Na+, or K+ would change with training, the training-induced increase in BV would require that the total PROT and osmolar content increase in parallel in order to retain the added fluid and maintain homeostasis In addition, because the osmolality-AVP feedback

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34 system is sensitive to small changes in osmolality, and because resting levels of AVP appear to be unchanged with training (Convertino et al., 1980a; Convertino et al., 1983; Convertino et al., 1991), it would be expected that resting plasma levels of Na+ would be unaltered with exercise training Indeed, Con vertino et al. (1980a) found that an 8.1 % ( 457 ml) increase in BV was accompanied by an increase in total osmolar and PROT content, but not concentration This conclusion is supported by the cross-sectional data of Freund et al (1988) who noted similar plasma Na+, K+, and PROT concentrations in trained and untrained subjects. One study, however, noted a lower resting PROT concentration in trained subjects (6.35 gdl1 ) compared with their untrained counterparts (6 9 gdl 1 ) (Boning & Skipka, 1979). There has also been a report of decrease in plasma K+ from 4 2 to 3.7 mEqL1 as a result of 4 months of intensive training (Rose, 1975) This may be due to the post-exercise increase in ALDO that occurs in response to transient episodes of hyperkalemia during exercise, and which results in a "rebound" hypokalemia Cross-sectional data (Claybaugh et al 1986; Wade et al., 1981) showing an increased ALDO response in trained individuals to water immersion and daily long-distance running lend indirect support to this theory. However, the finding of greater ALDO responsiveness in trained individuals is not universal (Freund et al., 1988; Skipka et al., 1979) An alternative explanation for the resting hypokalemia seen after training involves an increase in resting muscle membrane potential, favoring a movement of K+ into the muscle cells Six weeks of treadmill training in dogs increased the muscle membrane potential from -91 to -103 mV Hyperpolarization has also been seen in humans trained for long distance running and correlates linearly with the V0 2 max (Knochel, 1985).

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35 Data on the response of resting K+, Na+, and PROT levels after training in elderly individuals are sparse. Braith et al. (1990) found a decrease in resting K+ from 4.24 to 3 94 mEqL-1, but an unchanged resting ALDO, in elderly subjects after 3 months of endurance training; no mechanisms were proposed to explain the result Cardiovascular, Hormonal, and Plasma Volume Responses to Tilt: Preand Post-training Head-up tilt is a method used to study the reflex mechanisms associated with the response to orthostasis. Because muscular activity in the legs can be minimized as compared with passive standing, the contribution of cardiovascular reflexes to the maintenance of arterial pressure can be better distinguished. As a response to the venous pooling induced by upright tilt, CVP, EDV, SV, and Qare sequentially reduced There is also a gradual decrease in blood flow in the kidney, and in the resting arm and leg muscles (Convertino, 1987) If Q is decreased without an increase in peripheral resistance, arterial pressure and cerebral perfusion will fall, and syncope will ensue. The ability of the body to resist the fall in arterial pressure is dependent on the responsiveness and interaction highand low-pressure baroreceptor systems, myocardial function, arterial and venous tone, and neuroendocrine secretions The cardiovascular and hormonal responses to tilt cannot be directly compared among different investigations due to the widely differing protocols. Differences exist in the length of the pre-tilt control period, the angle and duration of tilt, use of a saddle or footplate, and the timing of measurements. The angle of tilt may be a particularly important parameter

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36 (Fitzpatrick Theodorakis, Vardas, & Sutton, 1991): for example, a 45 tilt represents approximately 70% of the stresses imposed by upright posture (Jansen et al 1989) while a 70 head-up tilt is nearly equivalent to the stress of upright posture (Lye, Vargas, Faragher, Davies, & Goddard, 1990; Wieling et al 1983) The magnitude of cardiovascular and hormonal responses would be expected to vary accordingly, as documented for the HR and thoracic BV responses by Smith et al. (1984) Nevertheless, it may be possible to deduce qualitative conclusions from earlier studies Heart Rate, Stroke Volume, Cardiac Output, and Blood Pressure The increase in HR from supine to upright posture in young subjects is well documented and appears to vary based on the angle and duration of tilt. Increases of approximately 10 to 30 beatsmin1 are generally reported (Beetham & Buskirk 1958; Convertino et al., 1984; Davies, Slater, Forsling, & Payne, 1976; Greenleaf et al., 1981; Huber et al 1988; Lee, Lindeman, Yiengst, & Shock, 1966; Matalon & Farhi, 1979; Matzen, Knigge, Schutten, Warberg, & Secher, 1990; Sannerstedt, Julius, & Conway, 1970; Shannon et al., 1991 ; Solomon, Atherton, Bobinski, & Green, 1986; Vargas et al., 1986; Wieling et al., 1983; Williams, Walsh, Lightman, & Sutton, 1988), although smaller increments have been seen (Dambrink & Wieling, 1987) Stroke volume decrements during tilt range from 30 to 50% (Banner et al., 1990; Blomqvist & Stone, 1983; Mangseth & Bernauer, 1980; Matalon & Farhi 1979; Sannerstedt et al., 1970; Vargas et al., 1986) Despite compensatory increases in HR, Q generally decreases approximately 20-30% (Banner et al., 1990; Blomqvist & Stone, 1983 ; Mangseth & Bernauer, 1980; Matalon & Farhi, 1979; Sannerstedt et al. 1970; Vargas et al., 1986), although both Lee et al. (1966) and Matzen et al (1990) reported smaller decrements.

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37 The changes with posture in older individuals are generally of a smaller magnitude. On an absolute basis, HR increments during tilt are less than in young persons, although at least one study found no difference in the response (Lipsitz, Mietus, Moody, & Goldberger, 1990). Increases of only 10-15 beatsmin1 are common (Kenny et al., 1987; Lee et al., 1966; Lye et al., 1990; Shannon et al., 1991; Vargas et al., 1986). However, one investigation (Ecoffey, Edouard, Pruszczynski, Taly and Samii, 1985) found that HR did not increase in elderly men during 30 tilt. Although this may be due to the low angle of tilt used, another investigation (Dambrink and Wieling, 1987) also found small HR increments (0-5 beatsmin1 ) in 60 to 90 year-olds during a 70 tilt. Even on a relative basis, HR increments during tilt are smaller in older individuals. Jansen et al. (1989) reported that elderly normotensives had a 1015% increases in HR compared with 20-25% increments in young normotensives. Several investigators (Dambrink & Wieling, 1987; Norris, Shock, & Yiengst, 1953; Smith, Barney, Groban, Stadnicka, & Ebert, 1985) have also found that the peak steady state HR response to orthostatic changes or to neck suction took longer to achieve in older individuals. Stroke volume during tilt decreases approximately 25-40% in older individuals (Lee et al. 1966; Lye et al., 1990; Shannon et al., 1991; Vargas et a l. 1986). Shannon et al. (1991) found that the greater reduction in SV in older, as compared with younger, individuals was related to their inability to decrease ESV despite similar reductions in EDV. It was hypothesized that the inability to decrease ESV was due to aging changes in the vascular system. The data comparing postural changes in Qin young and old subjects are contradictory. Vargas et al. (1986) found equivalent resting and tilt Q values in both young (x = 29.9 yrs) and old (x = 70.4 yrs) subjects. On the other hand, Shannon et al. (1991) found similar resting Q values in old and

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38 young subjects, but found that young subjects increased Q by 19 % during a 60 tilt while old subjects experienced an 18% decrease Finally, Lee et al. (1966) found that older subjects had a 12% fall in cardiac index while young subjects saw only a 3 % drop. A comparison of the BP responses of old and young subjects during tilt reveals a variety of response patterns. Most investigations have found that SBP remains unchanged, both in young (Beetham & Buskirk, 1958; Convertino et al., 1984; Davies et al., 1976; Huber et al., 1988; Matzen et al., 1990; Williams et al., 1988) and elderly (Kenny et al 1987; Lee et al., 1966; Lye et al., 1990) subjects. Two cross-sectional studies comparing the BP response to head-up tilt in young, middle-aged, and elderly subjects also did not find age-related differences Kaijser and Sachs (1985) evaluated the SBP and DBP response to 8 minutes of 60 tilt and found no difference in response among the groups Similarly, Smith et al (1984) found that the MAP response did not differ among different age groups in response to tilt. However, Vargas et al. (1986) found that SBP decreased and DBP increased during 70 head-up tilt in both old and young subjects, with young subjects showing greater increases in DBP. Peripheral resistance increased equally for young and old subjects. In contrast, Dambrink and Wieling (1987) found that SBP decreased in older subjects but remained stable in young subjects during an upright tilt. However, the age-related DBP response was in agreement with Vargas et al. (1986) Similarly Lipsitz, Maddens, Pluchino, Schmitt, and Wei (1986) found that the peripheral resistance response to standing was greater in young, as compared with old subjects, after one minute of standing. Equivalent responses after three minutes suggested a delay in the vasoconstrictor response in older subjects. Other studies (Ebert et al 1982; Frey & Hoffler, 1988; Jansen et al., 1989; Shannon et al., 1991) finding that DBP and/or

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39 peripheral resistance increases more in older subjects have attributed the enhanced response to a compensatory mechanism for the decreased HR and Q response. Few longitudinal studies document the cardiovascular responses to tilt after a period of physical training but several have addressed the issue of training-induced responses to tilt by comparing trained and untrained subjects in a cross-sectional design. Diaz and Rivera (1986) showed that trained subjects had a significantly lower HR both during supine rest and during a 30-minute tilt. During the tilt, trained subjects increased HR by 17 beatsmin1 while untrained subjects increased HR by 24 beatsmin 1 This may be related to training-induced hypervolemia. Klein, Wegmann, Bruner and Vogt (1969) and Klein, Bruner, Jovy, Vogt, and Wegmann (1969) also found that trained subjects had lower HRs under both rest and tilt conditions While the magnitude of the change from rest to tilt reported by Klein, Wegmann, Bruner and Vogt (1969) was 6.2 beatsmin1 lower in the trained subjects, the relative increases were nearly identical (33 7 % vs 32 3 % beats min1 for trained and untrained subjects, respectively). Similarly, Harma and Lansimies (1985) did not find a difference between fit and untrained men in the relative magnitude of the HR response to tilt. In an early longitudinal study, Beetham and Buskirk (1958) found that physical conditioning did not change the HR or BP response to 70 tilt in young subjects. On the other hand, Shvartz et al (1981) found a lower HR and better maintenance of BP during tilt table testing in 5 of 10 subjects after training and/ or heat acclimation However, the lack of a true control (non exercising) group in this study does not permit definitive conclusions to be made regarding the effects of training alone. Improved responses to 60 tilt were also found by Convertino et al. (1984) after 8 days of cycle ergometer

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40 training at 65% of V0 2 max. Mean tilt duration to syncope increased by 6 minutes, associated with an increase in PV and a decrease of 9 beatsmin1 in the HR response to tilt. However, the heart rate acceleration from supine to tilt positions only declined 4 beatsmin1 due to a 5 beatsmin1 reduction in resting HR. The BP response to tilt was unchanged by training. The HR response to tilt after training in elderly individuals has not been characterized. However, there are some animal data to suggest that exercise training increases NE content in the heart (Gwathmey et al., 1990); this may indicate an increased adrenergic responsiveness. Whether this would result in an increased HR response during tilt is not known; confounding factors might include increases in SV and/or BV, which would tend to offset any increase in HR. Blood/Plasma Volume Hagan, Diaz, and Horvath (1978) studied the effect of 35 minutes of supine posture, followed by 35 minutes of standing, on Hct, Hb concentrat i on, plasma PROT, and PV in young subjects. After 35 minutes in the supine posture, PV increased by 440 ml, representing an increase of 11.7%. Assumption of the standing position resulted in an increase of 10.3% and 10.8% for Hct and Hb, respectively, and an increase of 20 8% in plasma proteins. Hydrostatic pressure produced a fluid efflux of 593 ml and reduced BV and PV by 9.5 and 16.2%, respectively. Red cell mass was unchanged by posture. Davies et al. (1976) found similar results in a 45-minute, 85 tilt. After 45 minutes, PV had decreased 16.8%, with a corresponding increase in Hct of 11 %, from 41.0 to 45.5. A 2-hour, 45 head up tilt induced a significant increase in Hct from 42.5 to 44.0, resulting in a calculated decrease in PV of 7.2% in young subjects

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41 (Williams et al., 1988). Tarazi, Melsher, Dustan, and Frohlich (1970), however, found somewhat smaller PV decreases during a 20-minute, 50 tilt. Their subjects experienced a PV decrease of 113 ml, corresponding to a 3.9% decrement. Data from studies with the elderly demonstrate results similar to the majority of studies with young subjects. Lye et al. (1990) found that a 10minute, 70 head-up tilt elicited a 10.8% decrease in PV in healthy elderly subjects. Physical training does not appear to affect the magnitude of the PV decrement during tilt. Convertino et al. (1984) found that although the absolute PV decrease during a 60 tilt was greater after 8 days of training (544 ml vs. 479 ml), the relative decrement remained the same (13.9% vs 13.6%) Similar results were found by Greenleaf et al. (1988) who studied the response to a 60 head-up tilt before and after a 6-hour water immersion protocol both prior to and after 6 months of exercise training in young to middle-aged men. Plasma volume decreases ranged from 9.0% to 12.6% during the four tilt procedures. In addition, neither prenor post-tilt Hb and Hct values were changed with training. Hemoglobin increased from 14.5 to 15.8 while Hct increased from approximately 37 0 to 39 9 during tilt both preand post training. Vasoactive Hormones Vasopressin (AVP). Upright posture translocates approximately 500 ml of blood to the lower extremities while another 200-300 ml may be transferred to the veins in the buttocks and pelvis (Blomqvist & Stone, 1983); prolonged tilt further reduces BV by filtration of plasma from the capillaries in the legs. This decrease in central BV and CVP may promote A VP secretion through stimulation of cardiopulmonary receptors (Harrison et al., 1986).

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42 That AVP secretion during tilt is stimulated by volume receptors is supported by research showing that dehydration results in greater resting and tilt AVP concentrations. Harrison et al. (1986) found that resting levels of AVP were five times higher, while tilt values were approximately 6.5-7 times higher in dehydrated subjects. Similarly, Greenleaf et al. (1988) found that AVP levels were increased in response to tilt after, but not before, a 6 hour water immersion which reduced body weight by 1.12 kg Vasopressin secretion during head-up tilt may also be affected by increases in the renin-AII axis resulting from generalized sympathetic stimulation, decreased renal blood flow and/ or pressure, or decreased osmolar load at the juxtaglomerular cells (Mouw, Bonjour, Malvin, & Vander, 1971; Ramsay, Keil, Sharpe, & Shinsako, 1978) Hypotension is also a potent stimulator of A VP secretion (Share, 1976). Vasopressin promotes homeostasis during orthostasis by increasing the permeability of cells in the collecting ducts to water, thus increasing the reabsorption of fluid in the kidney. Vasopressin also limits filtration of plasma into the interstitial space by the selective vasoconstriction of skeletal muscle and skin arterioles. The result is both a redistribution of vascular volume to critical tissues (e.g., the brain), and a lowering of capillary pressure which favors net reabsorption of fluid from the interstitial space. The increased peripheral resistance induced by A VP does not usually increase BP because of baroreceptor-induced compensatory changes in HR and Q. In addition, A VP may cause a reduction in cardiac contractility as a result of coronary arteriolar constriction (Goodman & Frey, 1988) Many researchers have documented the expected increase in A VP during tilt. However, increases from basal values appear to vary widely, ranging from 25 to 175% (Davies et al., 1976; Huber et al., 1988; Lye et al 1990;

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43 Sander-Jensen et al., 1986; Williams et al., 1988). Davies et al. (1976) found that tilt values were approximately 1.6-1.9 times higher than basal values up to a tilt duration of 30 minutes, after which time AVP increased strikingly to 3-4.5 times basal values This occurred when HR and BP were stable but when PV had reached its nadir (-17%). These data support the role of volume receptors in regulating AVP during postural stress. Davies, Forsling and Slater (1977) also documented large increases (approximately 700%) in AVP release only after 30 minutes of tilt and hypothesized that the delayed increase was due to the increase in renin and All. Basal values of AVP may be higher in the elderly but the magnitude of increase during tilt may not differ between young and old (Vargas et al., 1986) The increase in A VP secretion is most likely due to volume receptors since osmolality generally remains constant (Greenleaf et al., 1988; Harrison et al., 1986; Sander-Jensen et al., 1986); however, hyperosmolality cannot be disregarded since it has been shown to increase (Vargas et al., 1986) Differences among studies attempting to document the AVP response of elderly and young subjects may be due to the existence of "responders" and "nonresponders" Rowe, Minaker, Sparrow, and Robertson (1982) found that some subjects did not increase A VP during 8 minutes of quiet standing, and that the prevalence of "nonresponders" increased with age from 8.3% (1 of 12) in young subjects to 46.7% (7 of 15) in elderly subjects. Despite the presence of appropriate stimuli and the apparent beneficial effects of A VP in maintaining BP homeostasis, not all studies have documented AVP increases during tilt. Mohanty et al. (1985) found that AVP did not increase in young to middle-aged subjects during a 5-minute, 80 head-up tilt. These authors suggested that AVP is not secreted in response to LBNP or tilt unless significant hypotension occurs. Indirect support for this

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44 hypothesis is offered by Ecoffey et al. (1985) who found that A VP did not change in elderly men during tilt when MAP remained constant. However, the low angle of tilt (30) may be responsible for the nonresponsivenss of the neurohumoral system Bie, Secher, Astrup, and Warberg (1986) found unchanged A VP during 20 and 40 tilts associated with unchanged or increased MAP Although MAPs were not reported, both Banner et al (1990) and Greenleaf et al. (1988) also found no change in A VP during tilt protocols utilizing 45 and 60 angles, respectively. The data regarding the AVP response to tilt after physical training are not entirely consistent. Greenleaf et al. (1985) found that A VP increased during tilt before but not after, a 12-day heat acclimation/ exercise program. Convertino et al. (1984) also found a decrease in the AVP response to a 60 tilt after 8 days of training. Compared with the response prior to training, the peak A VP response declined 37.7%; however, this was not found to be statistically significant. A decline in the AVP response to tilt after training is consistent with the hypothesis that a training-induced increase in PV better maintains central BV and pressure (Convertino et al., 1984) In contrast, Greenleaf et al (1988) found that A VP levels did not increase during a 60 tilt either before or after 6 months of training. However, both preand post-training values of A VP were significantly increased by an identical tilt protocol after 6 hours of water immersion, lending support to the hypothesis that AVP secretion is not stimulated by reductions in central BV until PV losses reach approximately 20%. Renin (PRA) Renin release from the JG cells in the kidney is stimulated by decreases in arterial pressure and the All-mediated increase in arteriolar vasoconstriction and peripheral resistance raise arterial pressure back to normal. All also excites sympathetic vasomotor outflow, thus

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45 reinforcing its own vasoconstrictor action. In addition, AIi increases cardiac contractility by increasing calcium influx in cardiac myocytes. The combination of these effects markedly increases BP and makes All a potent pressor agent. All also contributes to maintenance of salt and water balance through the stimulation of both ALDO and AVP secretion (Davies et al., 1977; Goodman & Frey, 1988) Because of its indirect role in BP and fluid volume homeostasis, renin is increased during tilt, stimulated by highand low-pressure baroreceptors and through P-receptor-mediated mechanisms (Grassi et al., 1988; Kiowski & Julius, 1978) Upright PRA values average 1.9 ng AIml1 hr1 compared with 1.1 ng AIml-lhr-1 for resting values (Thomas, 1985). Like AVP, however, the increments during tilt appear to vary widely In general, it appears that longer tilt durations elicit greater PRA concentrations, even when the tilt angle is low. A 74% increase was shown by Banner et al. (1990) after a 60-minute, 45 tilt, while Davies et al. (1976, 1977) found increases of 60-80% during 30 minutes of 85 tilt. Increases of 110-120% were found with a 2 hour, 45 protocol (Williams et al., 1988) and with a 25 minute upright protocol (Solomon et al., 1986) In contrast, Mohanty et al. (1985) found only a 44% increase in young to middle-aged subjects during a 5-minute, 80 tilt while Lye et al. (1990) saw a 50% increase in PRA in elderly subjects during a 10-minute, 70 head-up tilt. One exception to this generalization was the 110120% increase shown by Huber et al. (1988) with a 10 minute upright tilt. Most authors have found that supine and orthostatic PRA values decline with age (Cleroux et al., 1989; Crane & Harris, 1976; Hayduk et al., 1973; Saruta et al., 1980). The relative increases during tilt, however, may be similar between young and old subjects, averaging 100% across the age range (Hayduk et al., 1973). The decrease in renin release with age may be due to a

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46 decrease in cardiopulmonary baroreceptor sensitivity. Cleroux et al. (1989) found that elderly subjects did not increase renin activity during LBNP despite significant decreases in CVP, while young and middle-aged subjects demonstrated significant increases in PRA with equivalent changes in CVP Ecoffey et al. (1985) and Kenny et al. (1987) also found that PRA did not increase in elderly individuals during tilt. However, the low tilt angles used in these studies may have affected the results: Ecoffey et al. (1985) used a 15minute, 30 head-up tilt in elderly men, while Kenny et al. (1987) utilized a 2hour, 40 tilt in asymptomatic elderly men and women Gender differences may also have affected the renin response to orthostasis in the Kenny et al. (1987) study Gregerman and Bierman (1981) state that in one-third of females over the age of 70, renin activity levels are not only low but fail to rise with postural change. The use of a combined sample of males and females may have masked a possible tilt-induced increase in the elderly males The PRA response to tilt after training is potentially important since it may be a primary mechanism for the increase of peripheral resistance through All formation. A decrease in the peripheral resistance response to orthostasis as a result of endurance training has been proposed as a mechanism of reduced orthostatic tolerance in trained subjects (Goldwater, DeLada, Polese, Keil, & Luetscher, 1980; Mangseth & Bernauer, 1980). However, the data are scant and contradictory On the one hand, Greenleaf et al. (1988) found that PRA increased in response to a 60 tilt prior to, but not after 6 months of exercise training in young and middle-aged men. In contrast, Convertino et al. (1984) found that 8 days of training did not change the peak PRA response to a 60 tilt. Catecholamines Increases in SNS activity and plasma NE levels as a result of orthostasis are well-documented (Cryer, 1980; Jansen et al 1989;

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47 Mohanty et al., 1985; Vargas et al., 1986; Williams et al., 1988; Zerbe, Henry, & Robertson, 1983) Increases can range from a low of 60-80% (Banner et al., 1990; Jensen et al., 1989; Sander-Jensen et al., 1986; Williams et al 1988) to 150170% (Cleroux et al., 1989; Huber et al 1988) Although some researchers have found that NE levels are greater at rest (Gregerman & Bierman, 1981; Jensen et al., 1989; Vargas et al., 1986) and during tilt (Vargas et al., 1986) in elderly subjects when compared to young subjects, Cleroux et al. (1989) found similar resting NE levels in young (16-30 years), middle-aged (37-49 years) and elderly (61-73 years) subjects. However, Cleroux et al. (1989) found that the NE response to an equivalent drop in CVP induced by LBNP was significantly less in elderly subjects, and attributed this decline to a reduction in the sensitivity of the cardiopulmonary baroreceptors A reduction in NE secretion in response to tilt in the elderly is also suggested by comparing the results of Sander-Jensen et al. (1986) and Ecoffey et al. (1985) In the former study, a significant increase in NE was found in response to a 30 tilt in young subjects, while in the latter study, no increase in NE was found in 58 to 82 year old men during a 15-minute tilt at the same angle. The basal function of the adrenal medulla does not appear to change with age; thus resting levels of EPI remain constant (Gregerman & Bierman, 1981) Low angles of tilt (e g 30) do not appear to stimulate EPI secretion either in young (Sander-Jensen et al., 1986) or old (Ecoffey et al., 1985) subjects In contrast, greater angles of tilt (e.g., 45 and 60) stimulated EPI secretion in young subjects (Banner et al., 1990; Sander-Jensen et al., 1986). The effect of tilt duration is less clear. Although some researchers using protocols of 5 and 10 minutes (Mohanty et al., 1985; Huber et al., 1988) did not find significant changes in EPI, Jansen et al. (1989) found similar increases (approximately 85%) in young and old subjects in a 10-minute, 45 head-up tilt.

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48 There are scant data characterizing the catecholamine response to tilt after training The only data appear to be from a heat acclimation/ exercise study by Greenleaf and coworkers (1985); it was found that EPI and NE did not increase in response to a 70 head-up tilt test prior to 12 days of heat acclimation and exercise However, increases were noted during the tilt test at the end of the 12-day study. The response of elderly individuals after training has not been studied. Summary. Vasopressin, renin, and NE all act to maintain BP homeostasis during orthostasis via a variety of mechanisms Although increases in these hormones during head-up tilt have not been universally documented, differences in protocols may account for some of the discrepancies. Hormones Associated with Fluid Volume Control: Aldosterone (ALDO) Increased ALDO causes an increase in the reabsorption of Na+ and water and an increase in the excretion of K+ in the renal collecting ducts. Because of its role in defending BV head-up tilt increases, while supine posture inhibits, ALDO Upright ALDO levels average 30-280 pgmI-1 (Loriaux & Cutler, 1986), compared with 20-100 pgml-1 for supine values (Labhart, 1986) While some investigators have indeed found an increase in ALDO during head-up tilt (Bie et al., 1986; Mohanty et al., 1985; Sander-Jensen et al 1986; Vargas et al., 1986), other investigators have found increases in ALDO during tilt only under pathological conditions For example, Harrison and coworkers (1986) found that tilt-induced ALDO secretion occurred only during dehydration. Similarly, neither Sander-Jensen and coworkers (1986) nor Huber et al. (1988) found ALDO increases during head-up tilt until pre syncopal symptoms became evident.

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49 Although some authors have found that aging decreases resting plasma levels of ALDO due to a concomitant decrease in PRA (Crane & Harris, 1976; Saruta et al., 1980), Vargas et al. (1986) found that there was no age difference between young and elderly subjects in resting ALDO values. In addition, both age groups increased ALDO secretion to the same extent during a IO-minute, 70 head-up tilt. Both resting and tilt findings are consistent with their data on the renin response. In contrast, Lye et al. (1990) did not find a significant increase in plasma ALDO concentration in elderly subjects as a result of an identical tilt protocol. Data on the tilt response of ALDO after training are scarce. However, data from a cross-sectional study (Skipka et al., 1979) indicate that the response of ALDO to water immersion may be higher (i.e., less suppressed) in trained subjects, suggesting a decreased sensitivity of cardiopulmonary receptors. There may also be an uncoupling of the renin and ALDO responses with training: Skipka et al. (1979) found that the responsiveness of ALDO secretion did not correspond to renin activity levels, which were not significantly different between trained and untrained subjects at rest and which declined at a similar rate during immersion. Adrenocorticotropic Hormone (ACTH) Because almost any type of physical or mental stress can lead to greatly enhanced ACTH secretion, ACTH levels would be expected to increase during head-up tilt. In addition, ACTH secretion is sensitive to atrial stretch (Cryer & Gann, 1974) so that a decrease in right atrial volume would result in an increased secretion. Several training-induced adaptations would favor a decrease in ACTH secretion during head-up tilt after training. First, an increased PV would favor a greater fluid volume reserve and a better

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maintenance of central BV during orthostasis (Convertino et al., 1984). In addition, a training-induced increase in muscle mass may facilitate venous return and enhance CVP during orthostasis and thus contribute to CVP maintenance. 50 Only two studies have noted the response of ACTH to orthostasis: one found that there were no changes (Galen, Louisy, Habrioux, Lartigue, & Guezennec, 1988) while the other found an approximate 100% increase (Huber et al., 1988). Both studies utilized an upright tilt position; interestingly, it was the shorter of the two protocols (Huber et al., 1988; 10 minutes vs 25 minutes) which produced the significant increase in ACTH No studies have recorded the ACTH response to tilt after a program of physical training in either young or elderly subjects Protein (PROT), Sodium (Na+) and Potassium (K+) Researchers who have measured Na+, K+, and/or osmolality during a variety of head-up tilt protocols have generally reported no change (Davies et al., 1977; Harrison et al., 1986; Huber et al., 1988; Mohanty et al., 1985; Sander Jensen et al., 1986) Mohanty et al. (1985) attribute the constancy of K+ to the secretion of NE which, via a ~2-adrenoreceptor-mediated activation of adenylate cyclase, stimulates the Na+ /K+-ATP-ase that pumps K+ into skeletal muscle When NE secretion during tilt was prevented by bromocriptine administration, there was a significant increase in plasma K+ concentration Sander-Jensen et al. (1986) found small increases in PROT during both 30 (from 8.27 to 8.63 gdl-1, 4 3%) and a 60 (8.15 to 8.30 g /dl-1, 1.8%) head up tilts Hagan et al (1978) found larger increases (20.8%; from approximately 6.0 to 7.5 g/ dl) in the erect posture, compared with resting, supine values

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51 Training does not appear to affect the PROT or electrolyte response to tilt in young persons. Greenleaf et al. (1985) did not find that Na+ or K+ changed during 70 head-up tilt, either before or after a 12-day heat acclimation program Greenleaf et al. (1988) also found similar electrolyte responses during a 60 tilt to tolerance before and after a 6-month training program; the only exception appeared to be a significant increase in K+ during tilt prior to training. Although Greenleaf and coworkers (1985; 1988) found that PROT increased during tilt both before and after training and/ or heat acclimation, no direct comparisons were made on whether the magnitude of increase was similar at the two time points. Data on the PROT or electrolyte response to tilt after training in older persons are lacking. Mechanisms Potentially Responsible for Changes in Orthostatic Responses Plasma Volume Changes One hypothesis regarding improvements in orthostatic responses after training postulates that an increased BV helps in maintaining orthostatic integrity by providing a larger fluid volume reserve against which fixed gravitational forces act (Blomqvist and Stone, 1983, Bungo, Charles, & Johnson, 1985; Convertino et al., 1984; Hyatt and West, 1977; Shvartz et al., 1981) Convertino et al. (1984) and Shvartz et al. (1981) both document that decreases in orthostatic HR were related to increases in BV Conversely, Harrison, Kravik, Geelen, Keil, & Greenleaf (1985) documented a relationship between a smaller BV and a tendency to faint during orthostatic maneuvers However, two studies provide evidence against this hypothesis Convertino, Sather, Goldwater, and Alford (1986) studied the effect of various

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52 physical and physiological variables on peak LBNP tolerance. Blood volume contributed to LBNP tolerance in a multiple regression model but the slope was negative, indicating that a high BV was associated with a lower LBNP tolerance. Levine et al. (1991) also found that the subjects with the lowest LBNP tolerance had the greatest resting PV. They speculated that the mechanism responsible for this apparent anomaly might involve a training induced increase in left ventricular compliance; this would result in greater decreases in EDV and SV for a given reduction in EDP during orthostasis and negate the advantage of an increase in BV Paradoxically, the increase in BV together with the parallel increase in CVP (Convertino et al., 1991) may serve to produce a resetting of the low pressure cardiopulmonary baroreceptors. This allows an increased fluid volume at equivalent hormonal levels. There may also be an attenuation of the cardiopulmonary receptor stimulus-response mechanism leading to a reduction in A VP or renin secretion for an equivalent CVP decrement during orthostasis (Convertino et al., 1984; Greenleaf et al., 1988). An attenuated hormonal response may result in a reduction in the cardiac output or peripheral resistance response to orthostasis. Since higher levels of PRA and A VP during orthostasis appear to play a major role in maintaining tolerance (Harrison et al., 1985; Sather et al., 1985; Sather, Goldwater, Montgomery, & Convertino, 1986; Shvartz et al., 1981), a reduced response would be counterproductive. Muscle Mass Changes An increased muscle mass, particularly of the lower body, may help improve orthostatic tolerance due to the enhancement of venous return (Convertino, 1987; Greenleaf et al., 1975). This, in turn, may help to maintain

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53 Q and arterial pressure during orthostasis. Postural hypotension in response to simulated microgravity has been associated with decreased musculature, particularly in the lower extremities, and increased compliance in the leg vasculature (Convertino et al., 1989; Duvoisin et al. 1989). Early training studies (Shvartz, 1968a; Shvartz, 1969) suggested that resistance training improved chronotropic responsiveness to standing or head-up tilt. However, it could not be determined whether the improved responses were due to increases in muscle mass or changes in baroreceptor sensitivity Changes in Baroreceptor Sensitivity High-pressure baroreceptors in the carotid sinus and aortic arch are mechanoreceptors sensitive to changes in arterial pressure A fall in arterial pressure, such as is induced during orthostasis, decreases afferent nerve activity and releases inhibitory activity in the cardiovascular centers of the central nervous system. A series of reflexes ensue which act to maintain arterial pressure by increasing Q and/ or peripheral resistance The end result is an increase in HR and contractility, increased venoand vasoconstriction, and reduced blood flow to the skin, skeletal muscles, kidney and splanchnic area (Convertino, 1987) The effect of physical conditioning on baroreflex sensitivity is a controversial issue, partially due to the use of different experimental designs (cross-sectional vs longitudinal) An early cross-sectional study by Stegemann, Busert, and Brock (1974) found that the HR and BP responses to both neck suction and neck pressure were less in trained runners than in sedentary controls In later studies, endurance athletes were found to have a lesser baroreflex sensitivity during LBNP compared with resistance trained athletes (Smith et al., 1988; Smith & Raven, 1986) or untrained subjects

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54 (Raven, Graitzer, Smith, & Hudson, 1985; Raven, Rohm-Young, & Blomqvist, 1984). In contrast, Barney et al. (1985) found that young endurance trained men had increased baroreceptor responses to neck suction when compared to untrained men. Finally, some cross-sectional stud i es provide evidence that training does not affect the baroreflex Falsetti, Burke, and Tracy (1982) found that the HR responses of trained swimmers and untrained controls to neck suction and neck pressure were similar In addition, MAP responses of the two groups to LBNP were not significantly different. Hudson, Smith and Raven (1987) also found that baroreflex sensitivity at -50 mmHg of LBNP was similar for trained and untrained women Levine et al. (1991) found similar baroreflex responses in high-, mid, and low-fit young men in response to neck suction and neck pressure. Finally, Fiocchi, Fagard, Vanhees, Grauwels, and Amery (1985) found that baroreflex sensitivity did not correlate with V0 2 max in trained cyclists However the low correlation (r = 0.05) may be partly due to the homogeneity in the V0 2 max values (54 1 1.4 mlkg-lmin 1). Longitudinal animal data provide equally equivocal results. Tipton, Matthes, and Bedford (1982) and Bedford and Tipton (1987) provide animal data in support of the hypothesis that endurance training attenuates baroreflex control of BP, particularly during hypotensive ep i sodes. In their experiments, trained rats experienced greater and faster falls in arterial pressure during LBNP than untrained controls; the group differences were abolished with baroreceptor denervation The data from Gwirtz, Brandt, Mass, & Jones (1990), using a dog model, support this conclusion However, in an earlier study, this group of investigators (Mass, Gwirtz, Smith, & Umeakunne 1986) found that baroreceptor sensitivity in dogs was not affected by 10 weeks of daily exercise training

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55 Longitudinal training data in humans is scarce Somers, Conway, Johnson, & Sleight (1991) reported that 6 months of endurance training in middle-aged hypertensives resulted in an increase in baroreceptor sensitivity as measured during phenylephrine infusions This was accompanied by decreases of 9.7 and 6.8 mmHg in systolic and diastolic pressures, respectively, a prolongation of the R-R interval, and an increase in the R-R variability. They noted, however, that hypertension is associated with a decrease in baroreceptor sensitivity and a decrease in the R-R variability, and that these appeared to normalize with training. Whether normotensive individuals would see the same changes was not investigated. In contrast, Seals and Chase (1989) suggest that training has no effect on baroreceptor responsiveness. They found that 11 weeks of endurance training in middle-aged and older men did not alter the baroreflex control of HR in response to neck suction, neck pressure, or LBNP. Similarly, Vroman, Hea l y, & Kertzer (1988) report that 12 weeks of endurance training in young men produced no change in the baroreflex sensitivity (as measured by ~HR/ ~SBP) during LBNP at -40 mmHg. While baroreflex sensitivity decreases with age (Gribbin et al., 1971; Lipsitz, 1989), the effect of training on this parameter has not been investigated. Altered Hormonal Response The response of vasoactive hormones to orthostasis may be affected by training if lowand/ or high-pressure baroreflex sensitivity is altered. Although basal A VP secretion does not appear to change with training (Convertino et al., 1980a; Convertino et al., 1983; Convertino et al., 1991), it is possible that training attenuates the response of the cardiopulmonary receptors to acute changes in CVP (Boning & Skipka, 1979; Claybaugh et al.,

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1986; Skipka et al., 1979). A reduction in resting (Hagberg et al., 1989b; Kiyonaga et al., 1985) and orthostatically-induced (Goldwater et al., 1980) NE secretion after training may be a mechanisms for reducing renin secretion after training (Davies et al., 1977). Changes in vascular sensitivity to pressor hormones may also play a role in altering responses to orthostasis Wiegman et al. (1981) found decreases in vasoconstrictor, and possibly venoconstrictor, response to NE after 6 weeks of endurance training in rats, and hypothesized (Wiegman, 1981) that ~-adrenergic sensitivity was increased. This could play a role in altered BP and peripheral resistance responses during orthostasis Summary 56 Physiological responses hypothesized to contribute to the maintenance of arterial pressure during orthostasis are altered by physical training. The direction of change, however, is not always consistent with an improvement in the orthostatic responses when each mechanism is considered separately Blood volume increases may provide a larger fluid volume reserve to offset fluid translocation during orthostasis; however, the effect of this larger volume may be to reduce cardiopulmonary baroreceptor sensitivity and vasoactive hormone release. The chronotropic responsiveness of the high pressure baroreceptors may also be attenuated; this may be offset somewhat by a larger BV and an improved SV Finally training may improve muscle mass and tone and thus improve responses to orthostasis via an improved venous return.

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CHAPTER3 METHODOLOGY Subjects Eighty-three subjects, ranging in age from 60 to 82 years, volunteered to participate in this study. An initial screening by telephone was used to identify subjects who were within the desired age range, had been sedentary for at least one year, and who had no overt history of cardiovascular or pulmonary disease, or any orthopedic limitations to exercise testing and training. Subjects meeting these criteria reported to the laboratory where the entire study protocol, the inherent risks and hazards of the study, and the necessary time commitment were explained. Subjects were also asked to complete demographic, medical history, and activity questionnaires (Appendix A) These forms were reviewed by the investigator; subjects not meeting the physical and health requirements for the investigation were notified and excluded from the study Subjects meeting the requirements were scheduled for a further screening visit. Written informed consent was obtained from each subject who wished to continue (Appendix B) Based on this orientation, eight subjects were disqualified due to prior cardiac disease (n. = 5) or other medical or orthopedic problems (n. = 3). Ten subjects elected not to continue. All procedures were approved by the University of Florida College of Medicine Institutional Review Board (Appendix C) In a separate screening visit, the subject's medical history questionnaire was reviewed by a physician; the physician then administered a 57

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58 cardiovascular physical examination, including a resting 12-lead electrocardiogram (ECG). If any clinically significant findings such as hypertension (blood pressure [BP] exceeding 160/100 mmHg at rest), angina pectoris, or an abnormal resting ECG (ST segment depression or elevation that is horizontal or downsloping greater than 1 mm, 0 08 seconds from the point, or the presence of abnormal Q waves) were found, the subject was referred to his/her personal physician and excluded from participation in the study Subjects that were deemed suitable were then administered a graded treadmill exercise test (GXT) according to the Naughton protocol (Naughton & Haider, 1973). The protocol used a constant speed of 2 mileshour1 ; the grade was 0% initially and increased 3.5% every 2 minutes. The test continued until the subject reached voluntary maximal exertion or became symptomatic with positive hemodynamic or medical indices Heart Rate (HR) and ECG were monitored continuously throughout the exercise and recovery periods. A 12-lead ECG was recorded at the end of each stage of exertion, at peak exercise, and at each minute for 7 minutes of recovery; a 3-lead ECG rhythm strip was recorded at the intermediate minute of each exercise stage. Blood pressure was measured by auscultation at rest prior to exercise, at the end of each stage of exercise, immediately post-exercise, and at minutes 1, 3, 5, and 7 of recovery. Rating of perceived exertion (RPE) using the Borg scale (Borg, 1982) was determined during each minute of exercise. For subjects to continue in the study, the test must have been terminated by the subject because of fatigue with no significant evidence of hemodynamic or cardiorespiratory problems The test was terminated by the investigators and/ or attending physician if any of the following occurred : angina pectoris, ataxia or pallor, symptomatic supraventricular tachycardia,

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59 horizontal or downsloping ST segment depression that was greater than 3 mm at 0.08 seconds after the J-point, second or third degree heart block, onset of bundle branch block, ventricular couplets (> 2/min), ventricular tachycardia (~ 3 consecutive PVC's), Ron T premature ventricular contractions (PVCs), frequent unifocal PCVs (>10/min), frequent multifocal PVCs (>4/min), a BP in excess of 250/110, or a drop in systolic BP (American College of Sports Medicine, 1991). All GXTs were supervised by a physician trained in cardiovascular exercise testing. A crash cart with all necessary emergency medications and a defibrillator was immediately adjacent to the treadmill during every GXT Based on the physical examination and GXT, 21 subjects were disqualified from further participation in the study. Reasons for disqualification included elevated resting BP (n = 5), other resting ECG abnormalities (n_ = 2), abnormal HR or BP response to exercise (n = 4), and ST segment depression during exercise (n = 10). Thus, 44 subjects (14 males, 30 females) were accepted into the study. Type of Data Needed The criterion measures indicative of the cardiovascular response to an orthostatic stress were the HR, stroke volume (SV), cardiac output (Q) and BP responses during a 30-minute supine rest; a 15-minute, 70 head-up tilt; and a 15-minute supine recovery. These responses were recorded during initial (Tl) testing and also at the midpoint (13 weeks; T2) and end (26 weeks; T3) of a physical training program (Appendix D). Several mechanisms have been proposed to explain improvements in the cardiovascular response to an orthostatic stress after training These mechanisms include a) an increased blood volume (BV), b) improved

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60 baroreflex function, c) increased muscle mass, and d) improved hormonal response. An appropriate analysis of each mechanism was needed to determine which factor, if any, contributed to improved orthostatic responses. Blood volume was measured at Tl and T3 using the Evan s Blue dye technique (Greenleaf et al., 1979) while baroreflex responsiveness was assessed by analyzing the HR response to coughing in the supine and 70 tilt positions (Cardone et al., 1987; Maddens, Lipsitz, Wei, Pluchino, & Mark, 1987; Wei & Harris, 1982) Lower body muscle mass was assessed using dual x-ray absorptiometry (Haarbo, Gotfredsen, Hassager, & Christiansen, 1991). Increases in vasoactive hormones in response to upright tilt act to maintain blood pressure. Therefore, the levels of vasopressin (A VP), plasma renin activity (PRA), norepinephrine (NE) and epinephrine (EPI) were assessed at rest and during upright tilt. Other hormones and electrolytes instrumental in fluid volume control and the stress response (adrenocorticotropic hormone [ACTH], aldosterone [ALDO], sodium [Na+], potassium [K+], and protein [PROT]) were also measured at rest and during tilt. Finally, data from a maximal oxygen uptake test and strength tests were used to assess the presence and magnitude of the training response. Methods of Data Collection Maximal Oxygen Uptake ( V0 2 max) Test Prior to testing, a 20 or 22 gauge, 1 1 /2 inch venous catheter was placed under aseptic conditions in an antecubital vein for blood sampling to determine plasma hormones (ACTH, AVP, PRA, ALDO, EPI, NE), plasma PROT, and electrolytes (Na+ and K+) at rest and at maximal exercise. The catheter was kept patent during the test with sterile heparinized saline

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61 Subjects rested in the supine position for 20 minutes after catheter placement before a 24-26 ml blood sample was drawn for determination of resting hormones, PROT, and electrolyte values. The blood sample was divided among pre-chilled vacuum-type collection tubes (Vacutainer, Becton Dickinson, Rutherford, NJ) containing ethylenediaminetetracetic acid (EDTA) (for ACTH, AVP, PRA, ALDO), or heparin/EGTA/ glutathione (for PROT, electrolytes, EPI, NE). The samples were centrifuged at 3500 rpm for 15 minutes at 2-4 C. The plasma was placed into separate polypropylene tubes and kept frozen at -20 C (ACTH, A VP, PRA, ALDO, PROT, electrolytes) or -80 C (NE, EPI) until analysis. The subject then performed a symptom limited maximal treadmill test to determine peak oxygen consumption. The test consisted of the Naughton protocol; however, if the subject walked for longer than 12 minutes during the initial screening GXT, the initial speed during the VO2max test was 3 mileshr1 rather than 2 mileshr1 During the V02max test, the subject breathed through a mouthpiece attached to a low-resistance breathing valve and had a nose clip in place; expired air was collected in meteorological balloons. The expired air was analyzed for fractional oxygen and carbon dioxide concentrations using gas analyzers (Ametek-Thermox, Pittsburgh, PA) calibrated with precision gases. Expired gas volumes were measured with a 120 liter Tissot spirometer (Collins, Braintree, MA). During the VO 2 max test, the subject's HR, ECG, BP, and RPE were monitored in the same manner as during the screening GXT, and the same signs and symptoms used for stopping the GXT prior to the subject's achieving volitional maximal exertion were also used. Immediately upon cessation of exercise, another 24-26 ml venous blood sample was drawn and treated as for the resting sample. Testing at T2 and T3 was identical to the

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initial V0 2 max protocol except that blood samples were not taken at T2. Ambient temperature during the test was kept at 23-24C. Tilt Table Test 62 Preparation for testing included the placement of ECG electrodes (for monitoring standard and augmented limb leads), and mylar-coated aluminum electrode tapes around the neck and thorax (for monitoring HR, SV and Q). A 20 or 22 gauge, 1 1 /2 inch venous catheter was placed under aseptic conditions in an antecubital vein for a) PV measurement, and b) blood sampling to determine plasma hormones, PROT, electrolytes, Hb and Hct before and after the tilt procedure. The catheter was kept patent during the entire test period with sterile heparinized saline. A small (approximately 1 ml) venous blood sample was taken at the time of the catheter insertion for the determination of Hct, which was necessary for the calculation of SV with the impedance cardiograph. The subject assumed a supine position on the motorized tilt table (Model 720, Tri W-G, Inc., Valley City, ND) and was connected to ECG (Quinton, Seattle, WA) and cardiac impedance (Minnesota Impedance Cardiograph, Model 304B, Surcom, Inc., Minneapolis, MN) monitoring devices. A BP cuff was fitted around the upper arm for manual BP measurement. Heart rate, SV, and BP were measured during a 30-minute supine control period after 15, 20, 25 and 30 minutes. Stroke volume was measured with the impedance cardiograph using three representative waveforms during the first 15-20 seconds of each measurement period. Heart rate was measured as the instantaneous rate obtained from the same R-R intervals as the SV measurements. The mean of the three measurements was taken as the representative value for each measurement period. Cardiac

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63 output was calculated by the impedance cardiograph as the product of HR and SV. Systolic and diastolic BP were measured manually with a mercury sphygmomanometer (PyMoh, Somerville, NJ) and stethoscope after the impedance measurements were made. A digital readout of the HR was continually available on the ECG monitor and a 6-second rhythm strip was recorded along with the cardiac impedance measurements A 24-26 ml venous blood sample was drawn after approximately 28 minutes of supine rest for the duplicate determinations of plasma hormones, PROT, and electrolytes; blood samples were treated as described for the VO2max test. The blood sample for triplicate measurements of Hct and Hb was placed in a pre chilled EDTA-treated vacuum-type collection tube and placed on ice or refrigerated until analysis. At the end of 30 minutes of supine rest, baroreflex responsiveness was assessed by the response to coughing (Cardone et al., 1987; Wei & Harris, 1982). A 1-minute baseline period commenced and the BP was measured during the final 30 seconds of this period The subject was then instructed to cough by inhaling deeply and coughing forcefully 3 times in rapid succession. Blood pressure was measured immediately on cessation of the cough. An ECG strip was recorded continually beginning 10 seconds prior to the cough to provide the baseline R-R interval, and ending 1 minute after cough cessation. The sequence was repeated two more times. Plasma volume (PV) measurement was then made. For this measurement, a 23 gauge butterfly infusion set was inserted into an antecubital, wrist or hand vein on the arm opposite the one in which the venous catheter was inserted. A known quantity (approximately 2 2.5 ml) of a 0 5% aqueous T-1824 (Evan's blue dye) solution was injected over a 90 second interval and a 5 ml blood sample taken via the venous catheter 10

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64 minutes after the injection (Greenleaf et al., 1979) The blood was placed in a heparin-treated vacuum-type collection tube and centrifuged at 3500 rpm for 15 minutes at 2-4 C. The plasma was placed in a polypropylene tube and kept frozen at -20 C until analysis After PV determination, the fixed-speed motorized tilt table was brought from supine to the 70 head-up position, taking approximately 15-20 seconds. The 15-minute tilt period began once the subject was in the 70 head-up position (To) A HR rhythm strip was recorded every minute during the first 6 seconds of each minute. Impedance measurements were made during the first 15-20 seconds of each minute. Blood pressures were recorded 30 seconds after To and after impedance measurements at minutes 1, 2, 3, 4, 5, 10, and 15. A 24-26 ml venous blood sample was drawn between minutes 1315 of the tilt procedure and analyzed for Hct, Hb, plasma hormones, PROT, and electrolytes At the end of the 15 minute tilt, the subject again repeated the cough sequence while in the 70 head-up position. The tilt test was discontinued if any of the following occurred: a) the subject reached the predetermined time limit for the tilt portion of the test; b) presyncopal symptoms such as a fall in systolic BP greater than 15 mmHg between adjacent 1 minute measurements and/ or a sudden bradycardia greater than 15 beatsmin1 occurred; c) the systolic BP fell below 80 mmHg; or d) the subject requested to stop due to dizziness, nausea, or discomfort (Sather et al., 1986) Following completion or discontinuance of the tilt portion of the test, the subject was returned to the supine position in approximately 15-20 seconds The 15-minute recovery period began upon reaching the supine position. Measurements (HR, SV, Q, BP) were made along the same time schedule as during the tilt. During the entire test, the subject was asked to

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65 refrain from conversation, aside from answering any questions from the investigators regarding their status, and from unnecessary movement Temperature during the test was kept at 23-24C. The tilt test was repeated at T2 and T3 and was identical to the initial test except that PV was not measured and blood samples were not taken at T2 Strength Testing One repetition maximum (1-RM) leg strength was assessed using the Nautilus (Dallas, TX) Leg Press machine. Arm strength was assessed with the Nautilus Biceps Curl machine and the Nautilus Triceps Extension machine. Subjects with range-of-motion limitations in the hip, knee, or shoulder were tested by either adjusting the seat position on the machine or by double pinning the weight stack. Thus subjects were tested through the pain-free part of their range-of-motion. These variations were recorded so that subjects were tested in the same manner at T2 and T3 Subjects began by warming up with 4-5 submaximal repetitions. The resistance on any subsequent single lift was increased by 5-10 pounds according to the difficulty with which the subject executed the previous lift; a one minute rest was allowed between trials. The 1-RM was considered to be the maximum amount of weight that could be lifted through the subject's pre-determined full range-of-motion. Lumbar extension strength was assessed with a MedX (Ocala, FL) Lumbar Extension machine. Subjects underwent a multiple joint angle test consisting of maximum voluntary isometric contractions at seven angles (0, 12, 24, 36, 48, 60, 72 of lumbar flexion; where 0 represented full extension and 72 represented full flexion). Subjects with range-of-motion limitations were tested only at angles consistent with their capabilities

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Testing always proceeded consecutively from 72 to 0 of flexion. The criterion measure consisted of the maximum strength averaged over the number of angles tested. Body Composition 66 Muscle mass was assessed noninvasively using a Dual-Energy X-ray Absorptiometer (Lunar Radiation, Madison, WI). The subject lay in a supine position while the X-ray scanner performed a series of transverse scans moving from head to toe at 1 cm intervals. Measurements of total and regional bone mineral content, fat mass and fat free mass were obtained. Measurements of skinfold thickness were made with Lange calipers (Cambridge, MA) at the triceps, chest, axilla, subscapula, abdomen, suprailium, and thigh, following the procedures outlined by Pollock and Wilmore (1990). Measurements from the seven sites were summed (I,7) Body circumferences were measured with a steel tape at the shoulder, abdomen, waist, gluteus, right thigh, and right upper arm following the procedures outlined by Pollock and Wilmore (1990). Blood Sample Analyses Plasma volume analysis. T-1824 (Evan's blue) dye analysis was based on the methods of Greenleaf et al. (1979). The dye from the plasma sample was extracted onto a wood-cellulose powder (Solka Floe SW-40A) chromatographic column after it had been separated from the albumin by the action of a detergent (Teepol 610 in 2% Na2HPO4). Interfering substances such as pigments, proteins, and chylomicrons were washed from the column with 2% Na2HPO4. The dye was then eluted from the column with an 1:1 acetone

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water mixture. The addition of KH2PO4 buffered the pH of the eluate to 7.0; the absorbance of the eluate was read at 615 nm. Plasma volume was calculated from the formula: where PV = (VXD)(STXv) 1.03(T) V = volume (ml) of T-1824 dye injected (22.6 mg/5 ml) D = dilution of standard (1:250) St = absorbance of standard v = volume of sample extracted (1.0 ml) T = absorbance of plasma sample 1.03 = correction factor for dye uptake by tissues BV was calculated as PV /(1 0.91Hct). 67 Hemoglobin; hematocrit. Hemoglobin (Hb) concentration was determined with triplicate measurements using the cyanmethemoglobin method (Sigma Diagnostics, St. Louis, MO) and a Spectronic 20D spectrophotometer (Milton Roy Company, Rochester, NY). Hematocrit (Hct) was measured in triplicate with a microhematocrit centrifuge (IEC, Model MB, Needham Heights, MA) and a Fisher Micro-capillary Tube Reader. Hematocrit measurements were not corrected for trapped plasma or for whole body hematocrit. Percent changes in PV, BV and red cell volume (RCV) during the tilt procedure were calculated from Hb and Hct measurements according to the formulas of Dill and Costill (1974): BVA = BVB (HbB/HbA) RCV A = BV A (HctA) /100 PV A = BV A CV A ~BV,% = 100 (BVA BVB)/BVB ~CV,%= 100 (CVA CVB)/CVB ~PV,% = 100 (PVA PVB)/PVB where the subscripts B and A refer to measurements taken before and after the tilt procedure, respectively.

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68 Hormone analyses. Vasopressin was extracted from 0.5 ml plasma samples by adsorption to bentonite and was eluted from the bentonite with a 4:1 (volume to volume) mixture of acetone and 1.0 N HCI. Average recovery was 80%; results were not corrected for recovery. Dried extracts were reconstituted to 0.25 ml with assay buffer (0 05 M phosphate buffer containing 0.01 M EDTA and 0.2% bovine serum albumin; pH= 7 4) Vasopressin was measured by radioimmunoassay (RIA) using a highly specific anti-A VP polyclonal antibody (raised in the laboratory of Dr. Charles Wood, University of Florida). 12 51-labeled AVP (DuPont, Welmington, DE) was used as tracer, and A VP (Sigma) was used as standard. The range of the standard curve was from 0.05 to 10 pg per tube. The detection limit of the assay (90% of maximal binding) was 0.078 pg per tube, which translated to 0.39 pgml1 after extraction of 0.5 ml of plasma. Values below 0.39 pgml1 were assigned a value of 0.39 pgml1 for statistical purposes. The intra-assay coefficient of variation for a low pool (0.40 pg per tube) was 4% (n. = 10) and for a high pool (4 0 pg per tube) was 14% (n = 10). Interassay coefficient of variation was 7% (0.35 pg per tube; n. = 13) (Raff, Kane, & Wood, 1991). For ACTH analysis, plasma samples and standard (0.5 ml) were extracted on powdered Corning glass (0.35mg per 0.5 ml of plasma, 100-200 mesh in double-distilled water, Corning Glass Works, Corning, NY) and eluted from the glass with a 1:1 (volume to volume) mixture of 0.25 N HCl and acetone. Dried extracts were reconstituted to 0.5 ml in assay buffer (0.5 M phosphate buffer, pH 7.4) Adrenocortocotropic hormone was measured by RIA using an antibody specific to 1-39 hACTH raised in rabbits in the laboratories of Dr. Charles Wood and Dr. Maureen Keller-Wood (University of Florida) Standard (synthetic human 1-39 ACTH) was a gift of the National Hormone and Pituitary Program, NIDDK (University of Maryland School of

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69 Medicine); 12 51-labeled ACTH was used as tracer Values for extracted plasma samples were corrected for recovery using extracted standard. The lowest standard used in the assay was 20 pgmI1 ; values below this were assigned the value of 20 pgmI1 for statistical purposes. Interassay coefficients of variation were 19.2% and 9.8% from samples of mean concentrations of 33 pgml1 (n = 24) and 76 pgml1 (n = 24), respectively (Bell, Wood, & Keller Wood, 1991) Aldosterone was measured using a RIA kit from Diagnostic Products Corporation (Los Angeles, CA). Unextracted plasma samples were placed in ALDO antibody-coated tubes to which 12 51-ALDO was added; samples were then incubated for 3 hours at 37 C. The range of the standard curve was from 25 to 1200 pgmI1 Values below 25 pgml1 were assigned the value of 25 pgml1 for statistical purposes Intraassay coefficients of variation (provided by Diagnostic Products) ranged from 2.7% for samples with a mean concentration of 803 pgml1 to 8.3% for samples with a mean concentration of 52 pgml1 Interassay coefficients of variation (provided by Diagnostic Products) ranged from 3.9% for samples with a mean concentration of 468 pgml1 to 10.4% for samples with a mean concentration of 51 pgml-1. Due to inadequate storage the plasma samples for PRA were damaged and the data is not presented. Epinephrine (EPI) and norepinephrine (NE) were analyzed using high performance liquid chromotography (HPLC) using a Waters (Millipore Corporation, Milford, MA) HPLC system consisting of an injector unit (WISP TM Model 712B), pump (Model 510), and electrochemical detector (Model 460). The pH of 1 ml plasma samples was adjusted to 8.7 with 2 M Tris/EDTA buffer; 50 ml of internal standard (3,4, dihydroxybenzylamine; manufacturer supplied) was then added. Norepinephrine, EPI and the standard were

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70 extracted from this solution by adsorption onto alumina and were eluted from the alumina with a 2:1:1 (volume) mixture of glacial acetic acid, 10% sodium disulfide, and 5% EDTA. A 20 ml sample of extract was injected onto a reverse-phase C1s column and EPI and NE were measured by electrochemical detection of the column effluent. Values were corrected for recovery using the internal standard. The intraassay coefficient of variation for NE was 1.4% while the interassay coefficient of variation was 3.8% (Convertino et al., 1991). Total plasma PROT was determined using refractometry. This method is based on refraction and change in velocity of light waves as they cross an air /fluid interface. The higher the solute content, the greater the refraction (Raphael, 1976). Using this method, a 20 l drop of plasma was placed on the refractometer glass; light was admitted through a prism and PROT determination made to the nearest 0.2 gdl1 Both Na+ and K+ were determined to the nearest 0.1 mEqL1 from plasma samples using a Nova I ion-specific electrode system (Nova Biomedical, Waltham, MA) Training The 44 subjects who comple t ed the initial testing were randomly assigned to one of two experimental (exercising) groups, or to a non exercising control group. The experimental groups undertook endurance training on a treadmill (Trackmaster, Model TM 200E, JAS Mfg., Carrollton, TX) (TREAD; n = 16), or endurance-plus-resistance (Nautilus plus MedX ) training (TREAD/RESIST; n = 17) The remaining 11 subjects were assigned to the control (CONT) group All subjects were asked not to change their lifestyle (e.g., diet and exercise habits) over the 6-month duration of the study

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71 Training for TREAD and TREAD /RESIST consisted of three sessions per week for 26 weeks. All training sessions began with 5 to 10 minutes of warm-up exercises and ended with a 5 minute cool-down walk. Initially all subjects exercised for 20 minutes at 40 to 50% of their maximal heart rate reserve (HRRmax) (Pollock & Wilmore, 1990). Exercise duration was increased by 5 minutes every 2 weeks until exercise time was 40 minutes After the fifth week, exercise intensity was gradually increased to 60-70% HRRmax Intensity was increased first by increasing the walking speed until the subject reached a comfortable, brisk pace; further increases in intensity were accomplished by raising the treadmill grade Once subjects reached 40 minutes of exercise duration and 60-70% HRRmax, the intensity and duration were maintained through the 14th week. Rating of perceived exertion (RPE) during these sessions averaged approximately 12-13 initially (light/ somewhat hard) and progressed to 13-14 (somewhat hard/hard, heavy). The average training intensity for weeks 1-13 was 62.6 4.2% HRRmax A VO2max test was administered at T2 and training heart rates were adjusted for the latter half of the study based on the results of this test. Beginning in the 15th week, subjects gradually increased their intensity to 75-85% HRRmax while duration was increased to 45 minutes. The average training intensity and RPE for weeks 15-26 was 78.7 4.6% HRRmax and 14-15 (hard), respectively. The subjects in TREAD/RESIST additionally performed selected resistance training exercises during the 26 weeks of the study. One set each of 8-15 repetitions of biceps curl, triceps extension and leg press was performed 3 times per week, while one set of 8-12 repetitions of lumbar extensions was performed once a week. In the initial weeks of training, subjects were taught the proper lifting form and were required to exercise to moderate fatigue. After 13 weeks of training, subjects were encouraged to train at an intensity

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that produced volitional muscle fatigue in 12-20 repetitions. When subjects could consistently complete 12-15 repetitions for the arm exercises, 15-20 repetitions for the leg exercise, or 10-15 repetitions for the lumbar extension exercise, resistance was increased by approximately 5%. 72 Based on a comparison to the Tl 1-RM values, training intensity for the first 13 weeks averaged 67.9, 85.4, and 99.6% 1-RM for the leg press, biceps curl and triceps extension exercises, respectively. Intensity for the final 13 weeks averaged 73.7, 80 7, and 97.5% of the T2 1-RM for the leg press, biceps curl, and triceps extension, respectively. Training intensity for the lumbar extension averaged 61.5% of the Tl peak torque during weeks 1-13, and 66.4% of the T2 peak torque during weeks 14-26. Data Analysis Dependent Measures The dependent measures consisted of the HR, SV, and BP measurements taken at successive time intervals during the tilt test. Calculated variables, such as mean arterial pressure (MAP = DBP + 0.33 [SBP DBP]), TPR (MAP IQ) and Q were also dependent measures during the test. Due to the assessment of several potential contributing mechanisms to any possible improvements in orthostatic response, other variables assumed dependent status in the various analyses. These variables included PV, total body and regional muscle mass, maximal strength, hormonal response to tilt, V0 2 max, and the response to cough.

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73 Statistical Analyses Forty-one of the original 44 subjects completed training and/ or their obligations as control subjects. Of these 41, 8 were eliminated from statistical analyses due to ~-blockade medication (n = 3), the presence of advanced cancer (n = 1), or pre-syncopal symptoms during T1 tilt testing (n = 4) Data from the subjects experiencing pre-syncopal symptoms during T1 tilt testing were analyzed separately. Therefore, the sample size used for all analyses, unless otherwise indicated, is 33. Group characteristics, V0 2 max, strength, and body composition. In order to determine whether initial group characteristics were similar, the T1 age, height, weight, I,7, and relative V0 2 max (mlkg1 min1 ) were each analyzed using a one-way anlaysis of variance (ANOV A) with Duncan's multiple range test. The change in I,7 and relative V0 2 max values over 26 weeks was analyzed in a 2 X 3 (time X group) repeated measures ANOV A design A one-way ANOV A and a Duncan s multiple range post-hoc test performed on lower body lean mass measurement, and on the T1 maximum strength values for leg press (LP), biceps curl (BI), and triceps extension (TRI) values, and lumbar extension (LE) indicated that there were initial group differences that could be accounted for by including gender in the T1 ANOV A. Therefore, the analyses of the strength and lean mass changes were done in a 2 X 3 (time X group) analysis of covariance (ANCOVA) design using the T1 score as the covariate. Cardiovascular responses. Means and standard deviations for HR, SV, Q, SBP, DBP, MAP, and TPR were calculated. An inspection of the raw data

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74 suggested that the multiple time measurements for each variable could be collapsed in order to provide a smaller number of representative values Therefore a one-way repeated measures ANOV A using the four resting supine measurements was performed for each of the dependent measures. High type I error rates indicated that differences among the four values were due to random variation; the four values for each variable were therefore averaged to provide a single resting measurement. Similarly, a series of repeated measures analyses for HR, SV, Q, SBP, DBP, MAP, and TPR were performed on the measurements made during tilt (TILT) and supine recovery (REC). Separate analyses for HR, SV, and Q were done on the measurements from minutes 2-5, 6-10 and 11-15 for both TILT and REC. Analyses of the BP variables and TPR were done on measurements from minutes 2-5 during both TILT and REC. An a priori decision was made not to include the raw data from TILTo, TILT1, RECo, and REC1 in these analyses since these time points represented transitional periods where values were rapidly changing. The T1 resting values of HR, SV, Q, SBP, DBP, MAP, and TPR were compared among the three groups using a one-way ANOV A. The effect of training on the resting variables was investigated in a 2 X 3 (test X group) repeated measures ANOV A. Using the collapsed resting, tilt and recovery values, a 2 X 3 X 11 (test X group X time) repeated measures ANOV A was used to compare rest, tilt and recovery values for each dependent variable. A significant test effect for a particular variable was further evaluated by creating a mean value (collapsed over time and group) for each test. A significant test X group interaction was further analyzed in a 2 X 3 (test X group) repeated measures ANOV A using the mean value for a particular variable (collapsed over time) for each group

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and test A significant time effect for a particular variable was evaluated by comparing the TILT and REC values, collapsed over group and test, to the resting value in a one-way ANOV A with 11 levels of time 75 Plasma volume and hormone/ electrolyte responses Plasma volume measurements were obtained successfully at both Tl and T3 in only 18 of 33 subjects. Because of the small number of subjects with duplicate PV measurements in each of the training groups, subjects in TREAD and TREAD/RESIST were combined into a single group (TRAIN) for PV statistical analyses. In order to determine whether initial group values were similar, the Tl pretilt PV BV, RCV, Hb, and Hct were each analyzed using a one-way ANOV A with Duncan's multiple range post-hoc test. To determine whether tilt and/or training affected these variables, PV, BV, RCV, Hb, and Hct were each analyzed in a 2 X 4 (group X time) repeated measures ANOV A design The time levels represented pretilt and tilt at both Tl and T3. The percent change in PV, BV, and RCV during tilt at Tl and T3 were analyzed in a 2 X 2 (group X time) repeated measures ANOV A. Because of the necessity of combining TREAD and TREAD /RESIST into a single group for the various BV analyses, the hormonal responses were similarly analyzed in 2 X 4 (group X time) repeated measures ANOV A designs The time levels represented pretilt and tilt at both Tl and T3 Cough test. The parameters measured during the cough test represented the reflex responses in the presumed baroreceptor-mediated event; no direct measure of the reflex stimulus (e g ., intra-arterial pressure measurements) was available The resting R-R interval for each cough test was calculated as the mean of five intervals occurring prior to the onset of coughing In the minute following the cessation of coughing, the following parameters were identified : the minimum R-R interval the time (in seconds)

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76 after cough cessation at which the minimum R-R interval occurred, and the number of R-R intervals occurring between the cessation of coughing and the minimum R-R. From these parameters, the difference between the resting and minimum R-R was calculated(~ R-R). Means and standard deviations of the first 40 intervals after the cough were calculated and transformed to HR values with the formula: HR = 60/R-R. To determine whether values from the three supine and three tilt cough trials were comparable, the resting R-R, minimum R-R, R-R, time of minimum R-R, and interval of minimum R-R were each analyzed in a one way repeated measures ANOV A. Based on the results of these tests, the three supine and three tilt values were each averaged. Using the averaged values, group differences at Tl were assessed using a one-way ANOV A and Duncan's multiple range test. The effect of training was analyzed with an ANCOV A design with the Tl values as the covariate. Analysis of the 40 beats after the cessation of coughing was done on HR values averaged every five beats. A one-way ANOV A with nine levels of time was used to compare the resting HR with the eight averaged post-cough HRs for each test and group To assess the effect of tilt and training, a 4 X 3 (test X group) respeated measures ANOV A was performed for each of the nine time points The four tests were Tl supine, Tl tilt, T3 supine and T3 tilt. In all cases, statistical probabilities are presented as the chances of concluding wrongly that the mean values obtained during the tilt test were due to true differences and did not arise from random variability given the sample size of this experiment. A p 0.05 was required for statistical significance.

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CHAPTER4 RESULTS Subject Characteristics Descriptive data on age, height, weight, and sum of seven skinfolds (I,7) at the start of training are presented for the control (CONT), treadmill (TREAD), and treadmill plus resistance (TREAD/RESIST) groups in Table 4-1. The results of the ANOVA performed to assess differences in initial subject characteristics indicated a large type I error rate for weight~= 0.15), height~ = 0.14) and I,7 = 0.49). Thus, any differences in these three variables at the start of the training program were due to random variation However, the probability of a type I error for the age analysis was small = 0.01). Post hoc analysis using Duncan's multiple range test indicated that TREAD was older than CONT at the start of the program. Table 4-1. Characteristics of Control, Treadmill, and Treadmill/Resistance Training Groups at the Start of 6 Months of Exercise Training. Group Age Height Weight I,7 (yrs) (cm) (kg) (mm) CONT (n= 9) 65.8 6 7 164 9 8.5 71.0 12 7 186 54 TREAD (n. = 14) 72.4 4.5* 161.4 6.6 61.8 14 2 173 57 TREAD /RESIST (n = 10) 68.7 3 8 168.8 11.4 73.4 17.8 150 73 Values are mean S.D. CONT = Control; TREAD = Treadmill; TREAD /RESIST = Treadmill/Resistance; I,7 = Sum of 7 skinfolds (triceps, chest, subscapula, axilla, abdomen, suprailium, thigh) 0.01, greater than CONT 77

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78 Training Responses Maximal Oxygen Uptake The Tl and T3 VO 2 max (mlkg1 min1 ) values for CONT, TREAD, and TREAD /RESIST are listed in Table 4-2. The results of the ANOV A to assess differences in Tl values indicated that any differences among groups in initial VO 2 max were due to random variation (12 = 0.32). The 2 X 3 ( test X group) repeated measures analysis used to assess the effects of training resulted in a type I error rate of< 0.01 for detecting a test X group interaction. Follow up analyses showed that after 26 weeks of training, TREAD and TREAD/RESIST increased VO2max by 16.4% and 13.7%, respectively (12 0.01). The 5.3% decline in the VO2max of CONT during the 26 week study period could be ascribed to random variation (12 = 0.11) Table 4-2. VO 2 max (ml kg-1 min-1) Responses of Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training. Group CONT TREAD TREAD /RESIST Values are mean S.D. n 9 14 10 Tl 22.8.7 22.0 .4 24.8.0 T3 21.6 1 25.6 5.6* 28 2 5.4* CONT= Control; TREAD= Treadmill; TREAD/RESIST= Treadmill/Resistance 12 0 01, greater than corresponding Tl value

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79 Strength In strength testing, there were 10 subjects who did not complete T3 leg press (LP) testing. Seven subjects had sustained back or knee injuries over the 6 month interval which precluded LP testing and/ or training; three subjects did not complete their strength testing obligations at T3 Four subjects did not complete T3 biceps curl (BI) and triceps extension (TRI) testing ; two of these subjects had sustained injuries which precluded testing and/ or training, while the other two subjects did not complete their T3 testing obligations. Therefore, the sample size for LP 1-RM strength testing was 23, while for BI and TRI testing it was 29 The sample size for lumbar extension (LE) testing was 19. The Tl and T3 values for LP, BI, TRI, and LE strength are listed in Table 4-3. The results of the ANOVA used to assess differences in Tl values indicated a low probability of a type I error in the detection of group differences for LP (i2 < 0.01), BI (i2 < 0 01), TRI (i2 = 0 05) and LE (i2 = 0 03) The results of Duncan's post hoc test indicated that TREAD/RESIST had higher strength scores than TREAD in LP, BI, and TRI and had higher scores than both TREAD and CONT in LE. However, when gender was used as a covariate in the Tl analysis, the resulting high p-values (12 = 0.71, 0.74 0.58, 0.67 for LP, BI, TRI, and LE respectively) indicated that once gender was accounted for, any differences among groups were due to random variation The effect of training on all strength measures was therefore analyzed with an analysis of covariance (ANCOVA) design using the Tl strength scores as the covariate. Table 4-3 lists the T3 group means adjusted for the Tl scores. ANCOV A results indicated that differences in adjusted T3 LP scores could be

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80 accounted for by random variation (12. = 0.55) Thus, strength training by TREAD /RESIST did not improve leg/buttocks strength to a greater extent than the changes seen in TREAD and CONT. Using absolute strength scores, TREAD/RESIST increased strength in LP by 16.5 % after 26 weeks of training However, TREAD and CONT also increased LP strength by 18 9 % and 8 2 %, respectively Table 4-3 Strength Testing Scores of Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training Variable Group n LP (lbs) CONT 5 TREAD 11 TREAD /RESIST 7 BI (lbs) CONT 6 TREAD 14 TREAD /RESIST 9 TRI (lbs) CONT 6 TREAD 14 TREAD /RESIST 9 LE (Nm)a CONT 6 TREAD 7 TREAD /RESIST 6 Tl T3 114 0 49 9 123.3 37 6 108.1 63.2 128.5 75.4 216.3 127.5** 251.9 149.8 47.1 7 46.3 21.5 35.9 14 1 36 6 16 1 57 2 22 8** 71.9 32.5 36.7 16 9 35 8 16.6 28.2 8.9 29.3 10.1 43 1 17.3** 55 8 24.1 145 1 39 8 149.4 33.9 142 4 52.8 147 8 71.9 269 9 3* 274 8 170 8 Adjusted T3 154.6 .8 166.7 6 9 170.0 9 5 43 8 2.3 46 5 1 6 58.2 2 0+ 33.4 2.5 36.7 1.6 46 0 1.9+ 190.6 12 8 191.9 11.9 182.1 14 2 Tl and T3 values are mean S D.; Adjusted T3 values are mean S.E. CONT = Control; TREAD = Treadmill; TREAD /RESIST = Treadmill/Resistance; LP = Leg press; BI = Biceps curl; TRI = Triceps extension; LE = Lumbar extension Adjusted for Tl strength scores p $ 0.05, greater than TREAD and CONT at Tl * p $ 0 05, greater than TREAD at Tl t adjusted T3 score greater than CONT and TREAD a Newton-meters averaged over the number of angles tested

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81 Analysis of covariance results indicated that the adjusted T3 BI scores of TREAD/RESIST were greater than those of either TREAD (l! < 0 01) or CONT (l! < 0.01) The adjusted TRI scores for TREAD /RESIST were also greater than those for both TREAD (12< 0.01) and CONT (l! < 0.01). Using absolute strength scores, TREAD /RESIST increased strength in BI and TRI by 25 7% and 29.5%, respectively, while both TREAD and CONT showed changes of less than 5% in these exercises. Analysis of covariance results for LE strength indicated that differences among groups in adjusted T3 LE scores could be accounted for by random variation (l! = 0.88). Thus, lumbar extension training by TREAD /RESIST did not improve lower back strength to a greater extent than the changes seen in TREAD and CONT. Using absolute strength scores, TREAD /RESIST increased strength in LE by 1.8% after 26 weeks of training. However, TREAD and CONT also increased LE strength by 3.8% and 3.0%, respectively. Body Composition Two control subjects did not complete testing obligations at T3; therefore, calculation of muscle mass data was based on a sample size of 32, while sum of seven skinfold (I7) and girth data were based on a sample size of 31. Means and standard deviations for CONT, TREAD, and TREAD/RESIST for body weight, I7, arm and leg girths, and lean mass measures are listed in Table 4-4. The results of the ANOVA used to assess group differences in Tl values indicated a low probability of a type I error for lower body lean mass (l2. = 0.04) and for arm lean mass (l2. = 0.04) The results of Duncan's post hoc test indicated that TREAD/RESIST had greater arm and lower body lean mass than TREAD. The probability levels for type I errors in detecting group differences at Tl for arm girth, leg girth, I7, body

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82 Table 4-4 Body Composition Measurements for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training. CONT I,7 (mm) (n = 7) Body weight (kg) (n = 11) Arm girth ( cm) (n = 7) Leg girth ( cm) (n = 7) Arm lean mass (kg) (n=8) Trunk lean mass (kg) (n=8) Total body lean mass (kg) (n = 8) Lower body lean mass (kg) (n = 8) TREAD (n = 14) I,7 (mm) Body weight (kg) Arm girth ( cm) Leg girth (cm) Arm lean mass (kg) Trunk lean mass (kg) Total body lean mass (kg) Lower body lean mass (kg) TREAD/RESIST (n = 10) I,7 (mm) Body weight (kg) Arm girth ( cm) Leg girth (cm) Arm lean mass (kg) Trunk lean mass (kg) Total body lean mass (kg) Lower body lean mass (kg) Tl 186 54 71.0 12.7 31.0 4.0 54.8 5.5 3 8 1.3 18.9 4.5 40.7 10.7 14.0 3.5 173 57 61.8 14 2 28.8 3.7 49 7 4.0 3.2 1.3 18.9 4.7 37.0 8.5 12.5 2.7 150 73 73.4 17 8 31.5 5.0 52 7 5.4 4.9 2.1 23.0 6.7 47.1 13 8 16.4 4.St T3 191 62 72.4 14.2 31.9 3.6 54.9 5.0 3.9 1.3 19.2 5 2 41.3 10 6 14.6 3.4 159 60.8 14.6 28.5 3 7 48.3 3.9 3.4 1.3 18 7 4.4 37.1 8.5 12.7 2.8 146 73.7 17.9 32.2 4.5 51.5 5.4 5.1 1.9 22.5 6.4 46.8 13 1 16.7 4.3 Adjusted T3* 4.0 1.2 20 4 0.5 41.7 0 3 14.7 0.2 4.1 0.9 20.0 0.3 41.0 0.3 14.3 0.2 4.1 1.1 19.8 0.4 41.0 0.3 14.4 0 2 Tl and T3 values are mean S.D.; adjusted T3 values are mean S.E. CONT= Control; TREAD= Treadmill; TREAD/RESIST= Treadmill/Resistance; I,7 = Sum of seven skinfolds (triceps, chest, subscapula, axilla, abdomen, suprailium, thigh) Adjusted for Tl lean mass values t p $ 0.05, TREAD/RESIST> TREAD at Tl Change from the respective Tl value

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weight, total body lean mass, and trunk lean mass were 0.07, 0.27, 0 49, 0 15, 0 10, 0.49 respectively 83 When gender was used as a covariate in the Tl analyses for arm and lower body lean mass, the resulting high p-values = 0 35 and 0.52, respectively) indicated that, once gender was accounted for, any initial differences among groups were due to random variation. The effect of training on all lean mass measures was therefore analyzed with an ANCOV A design using the Tl measure as the covariate The results indicated that the changes with training for total body lean mass, lower body lean mass, arm lean mass, and trunk lean mass could be ascribed to random variation (12. = 0 27, 0.32, 0 75, and 0.64, respectively). Analyses of the effect of training on I,7, body weight, arm girth and leg girth were each done in a 2 X 3 (time X group) repeated measures ANOVA The type I error rates for detecting a time X group interaction for I,7, body weight, arm girth, and leg girth were 0.03, 0.05, 0 01, and 0 37 respectively. Follow up analyses indicated that there was a decrease in the I,7 (12. = 0 01) and body weight = 0.02) for TREAD. Differences in I,7 and body weight between Tl and T3 for CONT (12. = 0.41 and 0.23, respectively) and TREAD/RESIST (12. = 0 32 0.62, respectively) were due to random variation. The follow up analysis for arm girth indicated that TREAD/RESIST had an increase in arm girth (12. = 0.03), while changes in arm girth for TREAD and CONT from Tl to T3 were due to random variation~ =.16 and 0.10, respectively)

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84 Cardiovascular Responses to Tilt Analyses to Average Data Means and standard deviations for the overall (averaged over tests and groups) heart rate (HR), stroke volume (SV), cardiac output (Q), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and total peripheral resistance (TPR) responses to tilt were calculated for minutes 15, 20, 25, and 30 of rest, minutes O through 15 of tilt (TILT) and minutes O through 15 of recovery (REC) (Table 4-5). Inspection of these data suggested that the multiple time measurements for each variable could be averaged in order to provide a smaller number of representative values A repeated measures ANOV A using the four resting supine measurements (i.e., minutes 15, 20, 25, and 30) showed that differences among the four time points for SV, Q, SBP, DBP, MAP, and TPR were due to random variation (Table 4-6). Therefore, the four values for each variable were averaged to provide a single resting measurement. The results of the test for HR indicated a low probability of a type I error (J2 = 0.05). Although this suggests that differences among the four resting HR measurements were due to some factor associated with time, inspection of the raw data (Table 4-5) shows that the four HR values ranged from 63 0 to 64.1 bmin1 Since this difference is not physiologically meaningful, the four resting HR values were also averaged to provide a single resting value. Similar repeated measures analyses were performed on the measurements from minutes 2-5, 6-10 and 11-15 for HR, SV, and Q for both

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85 Table 4-5. Overall Heart Rate, Stroke Volume, Cardiac Output, Blood Pressure and Peripheral Resistance Response to Tilt, Averaged Over Groups and Tests. Time HR sv Q SBP DBP MAP TPR (bmin1 ) (ml) (Lmin1 ) (mmHg) (mmHg) (mmHg) Rest (min) 15 64.1 9.4 50.9.8 3.24.76 126.4.2 77.0.3 93.3.9 2483 20 63.2 9.2 52.2.4 3.26.76 125.4.3 76.6 7 92.7.9 2469 25 63.0 9.3 52.1 6 3.26 80 126.8.9 77.0.4 93.4.8 2507 30 63.5 8 9 51.8.2 3 26.75 127.7.2 77.6.5 94.1.2 2454 Tilt (min) 0 68.9 1 38.6 8.5 2.61.54 124.1.2 80.5.9 94.9.9 3052 1 71.2 6 37 0 7.5 2 61.51 124.9.5 81.2.2 95 6.4 3041 2 71.4 3 36 6 7.3 2.58.50 127.1 1 81.8.7 96.7.2 3096 3 70 7 9.7 36 8 7.8 2.57.52 127.6 3 82.1.4 97.1.0 3144 4 70.4.1 37.2 8.2 2.59.53 126.7 7 82.4.3 97.0.0 3127 5 70.7.6 37.0 8.0 2.58.52 128.2.4 82.3.1 97.5 8 3160 6 71.2.5 37 0 7.8 2.60.50 7 71.4.4 37.0 8.0 2.61.50 8 71.8.8 37.3 8.2 2.65 48 9 72.1.8 37.4 8.5 2.66.55 10 72 0.5 37.4 8.9 2.65.51 128.6.8 82.2.3 97.5.4 3015 11 72 7.4 37.6 8.4 2.67.48 12 73.5.4 36.7 8.0 2.65.48 13 73.2.7 37.4 9.0 2.68.54 14 73.8.1 37.2 9 1 2 69 49 15 74.1.9 36.9 9.3 2 66.47 126.2.1 81.5.2 96 2.9 2913 Recovery (min) 0 67.5.1 51.1.4 3.40.81 128.2.5 77.5 9 94.1.9 2413 1 64.2.5 52.1.0 3.29 71 128 6.1 78.3.9 94.9.9 2445 2 62 9.5 50.4.4 3.12.67 128.4 2 78.6 8 95.1 5 2589 3 62.6.2 50.2.8 3.07.68 128.3.3 78.6.9 95.1.1 2707 4 62.3 0 49.2.4 3.00.65 128.5.8 79.1 3 95 4 6 2725 5 62.5 2 48.7.6 2 99.66 128.4.6 78.7.4 95.1.7 2733 6 62 2 9.9 48 8.9 2.97.66 7 62.5 9.7 48.3.9 2 97 69 8 62.3 9.7 47.8.9 2.93.69 9 62 0 9.2 48 2.2 2.94.66 10 62.1 9.3 48 0.4 2 94 69 127.5.2 78.3.5 94.5.3 2751

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86 Table 4-5--continued. Time HR sv Q SBP DBP MAP TPR (bmin-1) (ml) (Lmin-1) (mmHg) (mmHg) (mmHg) Recovery (min) 11 62 5 9 3 48 2.3 2 96.72 12 62.5 8.9 47 9.5 2.96.69 13 62 5 9.6 47.7.2 2.93 70 14 62.4 8.7 48.4.1 2.97.69 15 62 0 8.6 47 5.9 2.93.69 126.8 1 78.6.2 94.5 6 2758 dyne seccm5 Values are mean S D.; HR= Heart rate; SV = Stroke volume, Q = Cardiac output, SBP = Systolic blood pressure; DBP = Diastolic blood pressure; MAP = Mean arterial pressure; TPR = Total peripheral resistance. tilt (TILT) and recovery (REC). Analyses of SBP, DBP, MAP, and TPR were done on measurements from minutes 2-5 for both TILT and REC. An a priori decision was made not to include the raw data from TILTo, TILT1, RECo and REC1 in these analyses since these time points represent periods of transition. The probability of a type I error in detecting a time effect in each of these analyses is presented in Table 4-6 Where the probability levels were high, it was concluded that any differences among the measurements were due to random variation, and that the measurements could be averaged to provide a single representative value However, several of the analyses produced low probability levels, leading to an initial conclusion that the differences were due to some factor associated with time In these cases, inspection of the raw data presented in one minute intervals (Table 4-5) showed that these differences were physiologically small F or example, the range of HR values at TILT6-10 was from 71.2 to 72 1 bmin-1 (range= 0.9 bmin 1 ). Similarly the ranges for the HR values at TILT11-1s and REC6-10

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87 Table 4-6. Analyses to Average Data: Type I Error Rates for Detecting a Time Effect Within Each Time Period for Heart Rate, Stroke Volume, Cardiac Output, Blood Pressure, and Total Peripheral Resistance. HR sv Rest 0.05 0.58 TILT 2-5 0.28 0.13 TILT 6-10 0.02 0.11 TILT 11-15 <0.01 0.03 REC 2-5 0.30 0.01 REC 6-10 <0.01 <0 01 REC 11-15 0.71 0.45 Q 0.91 0.55 0.66 0.85 0.01 <0 01 0.67 SBP 0 .13 0.78 0 91 DBP 0.61 0.74 0.71 MAP 0 22 0.52 0.91 TPR 0.73 0.26 0.01 HR = Heart rate; SV = Stroke volume, Q = Cardiac output, SBP = Systolic blood pressure; DBP = Diastolic blood pressure; MAP= Mean arterial pressure; TPR = Total peripheral resistance; REC= Recovery were 1.4 and 0.3 bmin1 respectively For the values of SV at TILT11-1s, REC2-s, and REC6-10, the ranges were 0.9, 1.7, and 1.0 ml, respectively. The ranges for the values at REC2-s and REC6-10 were 0.13 and 0 04 Lmin1 respectively. Finally, the range of values for TPR during REC2-s was 194 dyne seccm-5 Therefore, because of the small differences among the values during each of the pre-determined time periods, the raw data within each time period were averaged. These data are presented in Tables 4-7--4-10 Effect of Training on Resting Variables Resting values of HR, SV, Q, SBP, DBP, MAP, and TPR at Tl and T3 are shown in Table 4-11. The probability levels for a type I error in detecting a group difference in resting measurements at Tl (HR, 12 = 0.14; SV, 12 = 0.40; Q, 12 = 0 96; SBP, 12 = 0.58; DBP, 12 = 0.63; MAP, 12 = 0.55; TPR, 12 = 0 99) indicate that

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88 Table 4-7. Averaged Heart Rate and Stroke Volume Responses to 70 Head up Tilt for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training. Time Control (n = 9) Tl T3 Heart Rate (b min-1) Rest 61.6 6.0 61.0.2 Tilt 0 66.6.5 66.4.7 1 67.8 7.8 69.2.4 2-5 67.6 7.7 68.1.6 6-10 67.9 8.2 69.3.3 11-15 69 2 9.2 70.3.8 Recovery 0 62.1 5.9 64.4.4 1 60.0 5.6 60.3.5 2-5 59.0 4.7 58.0.8 6-10 59.0 5.3 58.7.4 11-15 59.8 4.8 59.9.9 Stroke Volume (ml) Rest 50.1.4 51.2.2 Tilt 0 36.1.2 37.1 9.0 1 36.4 9.2 35.2 7.4 2-5 34.7 8.0 35.5 6.4 6-10 35.5 8.3 36.2 7.3 11-15 36.0 8 6 36.7 8.1 Recovery 0 50.3 8.7 52.4.5 1 50.5.1 53.5.0 2-5 47.8 8.9 52.4.1 6-10 46.8.4 48.8.8 11-15 44.9 9.3 49.5.2 Values are mean S.D. Treadmill (n = 14) Tl T3 68.5.0 64.8 9.5 74.0.4 70.6.6 75.9.7 71.7.5 74.3.8 71.8.0 75.6.1 73.3.2 78.5.9 75 1.1 73.8.3 69.4.8 70.4.5 66 8.7 68.3.5 64.2.5 67.6.4 62.2 8.9 67.2.6 62.4 7.9 45.7.3 55.1.4 34.2.9 38.5 8.7 33.7.6 37.5 6.3 33.9.4 36.9 6.8 33.5.7 36.8 6.6 33.2.7 37.9 6.9 44.0.0 54.0.0 45.0.0 54.3.1 44.0.0 51.8.4 43.0.8 51.4 9.5 42.4.0 51.9.5 Treadmill/Resistance (n. = 10) Tl T3 61.7.7 60.4.6 66.4.8 65.5.3 68.8.3 68.1.0 70.3.3 67.4.6 71.1.9 68.5.6 72.4.2 69 9.1 67.7.3 64.0.2 63.6.7 60.1 9.7 61.6.0 58.9 9.6 62.0 9.9 58.7.1 62.0.1 58.5.5 50.9.0 47.3.3 43.6 7.0 41.0 8.9 40.4 9.3 39.1 8.8 39.6 9.7 39.0 8.4 41.1.9 38.4 8.5 40.7.6 39.3.1 51.7.3 46.7.1 55.6.4 48 8.6 49.9.3 45.4.8 48.8.4 44.1.8 47.8.8 45.3.1

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89 Table 4-8 Averaged Cardiac Output Responses to 70 Head-up Tilt for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training Time Control (n = 9) Tl T3 Cardiac Output (Lmin-1) Rest 3 05.57 3 09 65 Tilt 0 2.30.52 2.41.42 1 2.54 59 2 39.36 2-5 2.32.43 2.40.32 6-10 2.36.45 2 49.39 11-15 2 44 44 2.55.42 Recovery 0 3.12.52 3 35 75 1 3 00.51 3.15 70 2-5 2 81.48 3.00 64 6-10 2.74.54 2 81 66 11-15 2 67.51 2 92.72 Values are mean S.D Treadmill (n = 14) Tl T3 3.13 69 3.55.88 2.50.58 2 70 67 2.56.60 2 70.50 2.51 52 2.62.51 2.53.45 2 66.46 2.57.43 2.79 46 3.21.67 3 69 90 3.05 67 3 65.74 2 97.59 3.27 65 2.89 59 3 17 75 2.84 62 3 20.82 Treadmill/Resistance
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90 Table 4-9. Averaged Systolic and Diastolic Blood Pressure Responses to 70 Head-up Tilt for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training. Time Control (n =9) Tl T3 Systolic Blood Pressure (mmHg) Rest 124 9 122 11 Tilt 0 120 14 123 15 1 120 13 126 15 2-5 126 12 127 13 6-10 127 15 127 13 11-15 126 16 125 12 Recovery 0 124 15 127 15 1 126 12 131 11 2-5 126 12 131 11 6-10 126 13 128 12 11-15 127 13 130 13 Treadmill (n = 14) Tl T3 127 12 135 20 124 13 128 20 125 14 125 19 126 13 130 16 125 13 134 22 123 12 129 127 18 135 17 127 14 135 16 126 14 133 17 124 12 132 19 123 12 129 18 Diastolic Blood Pressure (mmHg) Rest 77 8 78 7 79 75 Tilt 0 83 9 79 11 79 80 1 83 12 80 10 79 81 2-5 83 11 82 9 81 80 6-10 83 9 82 9 83 79 11-15 81 12 83 9 81 81 Recovery 0 76 9 77 8 78 77 1 79 10 80 8 80 77 2-5 79 11 79 8 79 77 6-10 77 10 79 8 78 75 11-15 78 12 79 9 78 76 Values are mean S.D. Treadmill/Resistance
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91 Table 4-10. Averaged Mean Arterial Blood Pressures and Total Peripheral Resistance Responses to 70 Head-up Tilt for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 Months of Exercise Training. Time Control (n = 9) Tl T3 Mean Arterial Pressure (mmHg) Rest Tilt 0 1 2-5 6-10 11-15 Recovery 0 1 2-5 6-10 11-15 92 8 92 8 95 10 94 12 96 12 95 11 97 10 97 9 97 11 97 9 96 13 96 9 92 11 94 10 94 11 97 9 94 11 96 9 93 11 96 9 94 12 96 10 Treadmill (n = 14) Tl T3 95 95 10 94 96 94 96 96 96 10 97 97 95 97 13 94 96 9 95 96 7 94 95 9 93 94 9 93 93 9 Total Peripheral Resistance (dyne seccm-5) Rest 2616 2508 594 2527 2252 Tilt 0 3436 3231 902 3139 2963 1 3128 3281 782 3152 2918 2-5 3454 3315 721 3176 2990 6-10 3323 3142 831 3181 2885 11-15 3161 3136 703 3092 2683 Recovery 0 2424 2389 890 2397 2146 1 2579 2628 867 2584 2150 2-5 2762 2733 914 2626 2384 6-10 2954 2715 2710 2444 11-15 3034 2909 2762 2418 Values are mean S.D. Treadmill/ Resistance
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92 Table 4-11. Effect of Training on Supine Resting Heart Rate, Stroke Volume, Cardiac Output, Blood Pressure, and Total Peripheral Resistance Measurements for Control, Treadmill, and Treadmill/Resistance Groups Before (Tl) and After (T3) 6 months of Exercise Training. Q SBP DBP MAP Test HR (b min1 ) sv (ml) (L minl) (mmHg) (mmHg) (mmHg) CONT (n=9) Tl 61.6 6.0 50.1.4 T3 61.0 5.2 51.3.2 TREAD (n = 14) Tl 68.5 0 45 7 7.3 T3 64 8 9.5 55.1.5t TREAD /RESIST (n = 10) Tl 61.7 7 50.9 0 T3 60 4.6 47.3.3 3.05.57 3.09 65 3.13 69 3.55.88t 3.08.69 2.80.53t 124 9 122 127 135 122 9 126 77 78 79 75 77 77 *dyne seccm-5; + 12 $ 0.05, change from respective Tl value Values are mean S.D 92 8 92 8 95 6 95 92 6 93 7 TPR 2561 2508 2528 2252t 2504 2769t HR= Heart rate; SV = Stroke volume; Q = Cardiac output; SBP = Systolic blood pressure; DBP = Diastolic blood pressure; MAP = Mean arterial pressure; TPR = Total peripheral resistance CONT = Control; TREAD = Treadmill; TREAD /RESIST = Treadmill/Resistance. The effect of training on resting SV and Q was also investigated using 2 X 3 (test X group) ANOV A. The probability of a type I error in detecting a test X group interaction for resting SV was very low <12 < 0.01), indicating that group assignment affected resting SV Further analysis using a one-way ANOVA for each group showed that TREAD increased resting SV by 9.4 ml (20.6%) as a result of training <12 < 0.01) (Table 4-11). The type I error rate for detecting a change in SV from Tl to T3 in TREAD/RESIST was 9.4%. In absolute terms, resting SV of TREAD /RESIST decreased by 3 6 ml (7.1 %). The

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differences between Tl and T3 resting SV values for CONT were due to random variation (12. = 0.73). 93 Analysis of resting Q data from Tl and T3 showed that there was a test X group interaction (I2. < 0 01). Further analysis using a one-way repeated measures ANOV A for each group indicated that TREAD increased resting Q by 0.42 Lmin 1 (13.4%) after 6 months of training (I2. = 0.01) while TREAD/RESIST showed a decline of 0.28 Lmin 1 (9 1%; 12 = 0 03) (Table 4-11) Any differences between the Tl and T3 resting Q values for CONT were due to random variation (12. = 0.81). The greater Q for TREAD was due to the increase in SV since resting HR was decreased by 3 7 bmin1 On the other hand, the decline in resting Qin TREAD/RESIST was due to a 7 1 % decrease in SV as well as a 2.2% decrease in HR The probability of a type I error in detecting a test X group interaction in TPR was 0.02 Further analysis indicated that TREAD decreased resting TPR by 10.9% (276 dyne seccm-5; 12 = 0 05) while TREAD/RESIST increased resting TPR by 10 6% (265 dyne seccm-5, 12 = 0 04) (Table 4-11). Any differences between the Tl and T3 resting TPR values for CONT were due to random variation (12 = 0.96). The decrease in resting TPR for TREAD was associated with a greater resting Q, while the increase in resting TPR for TREAD/RESIST was associated with a decline in resting Q The repeated measures analyses for the resting BP variables indicated that training did not affect these measurements. Type I error rates in detecting t e st X group interactions were 12 = 0.37, 0.14, and 0.89 for resting SBP, DBP, and MAP, respectively

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94 Effect of Training on the Cardiovascular Responses to Tilt Using the averaged resting, tilt and recovery values, a 2 X 3 X 11 (test X group X time) repeated measures ANOV A was used to compare the rest, TILT and REC HR, SV, Q, SBP, DBP, MAP, and TPR values. The overall Wilks' Lambda type I error rate generated for each effect and interaction is listed in Table 4-12. The ~-value for a test effect for HR = 0.03) suggested that there was a systematic difference between Tl and T3 in this variable; further analysis showed that the mean HR at Tl was 68.0 11.0 bmin1 while it decreased 2.9% (2.0 bmin1 ) to 66.0 9.7 bmin1 at T3. This is similar in magnitude to the change seen in resting HR. Table 4-12. Wilks' Lambda Values for 2 X 3 X 11 (Test X Group X Time) Repeated Measures Analysis for Heart Rate, Stroke Volume, Cardiac Output, Blood Pressure, and Peripheral Resistance Responses to 70 Head-up Tilt. Effectt HR sv Q SBP DBP MAP TPR Tst 0.03 0.13 0.53 0.08 0.30 0.49 0.81 TstXG 0.29 0.02 0.02 0.76 0.66 0.96 0.01 Tm <0.01 <0.01 <0.01 0.02 0.06 0.12 <0.01 TmXG 0.75 0.87 0.89 0.08 0.15 0.25 0.81 Tst X Tm 0.56 0.39 0.33 0.94 0.38 0.86 0.75 TstXTmXG 0.48 0.16 0.26 0.38 0.56 0.99 0.42 t Tst = Test; Tm = Time; G = Group HR= Heart rate; SV = Stroke volume, Q = Cardiac output, SBP = Systolic blood pressure; DBP = Diastolic blood pressure; MAP = Mean arterial pressure; TPR = Total peripheral resistance. The p-values for test X group interactions for SV and Q < 0.01 and~ < 0.01, respectively) suggest an effect of training on these variables. Further

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95 analysis using a one-way repeated measures ANOV A for each group showed that TREAD increased average test SV 5.9 ml (15.0%) from 39 3 5 1 ml at Tl to 45.2 9.0 ml at T3 (12 = 0 01). The 3.1 ml (6.7 % ) decrease in the average SV measurement of TREAD /RESIST was due to random variation (g = 0 15): the Tl and T3 values were 46 2 12 1 ml and 43 1 9.3 ml, respectively. Changes in the average SV of CONT were also due to random variation (g = 0.47) : the Tl and T3 values were 42 6 7.4 ml at Tl and 44.4 8.5 ml, respectively (Figure 4-1) The post hoc analysis of the Q data (one-way ANOV A by group) showed that TREAD increased average test Q after 6 months of training: the Tl mean test value was 2 80 0.52 Lmin1 while the mean T3 value increased to 3.06 0.63 Lmin1 (~ = 0.26 Lmin1 +9.3 % ; 12 = 0.04). Average test Q decreased in TREAD/RESIST from 2 95 0.54 Lmin 1 at Tl to 2.66 0 32 Lmin 1 at T3 (~ = 0.29 Lmin 1 -9.8%, 12 = 0 05) The changes from Tl to T3 in average Q for CONT were due to random variation. The control group had a Tl value of 2 67 0 34 Lmin 1 while the T3 value was 2 78 0.39 Lmin1 (g = 0.48) (Figure 4-1). The percent changes in average test SV and Q are illustrated in Figure 4-2. A further analysis of the change in SV and Q from rest to tilt was done in a 2 X 3 (test X group) repeated measures ANOVA using both the absolute and relative differences between the mean resting value and the mean tilt value Results of these analyses are listed in Table 4-13. The decline in SV from rest to tilt in TREAD increased from 12 0 7 6 ml at Tl to 17 7 6.6 ml at T3; the relative decline was also increased from 25 0 14 3 % at Tl to 31.5 7.6 % at T3. Any changes for CONT and TREAD/RESIST in the relative (12 = 0 79 and 0.37, respectively) or absolute (12 = 0 73 and 0.25 respectively) declines in SV could be accounted for by random variation.

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a) 50 45 ]40 > CJ) 35 30 b) 3.5 3 a 2 1.5 Tl Tl CONT (n=9) .....QTREAD* (n=14) --TREAD/RESIST (n=10) *p=0.01, T3> Tl T3 Test CONT (n=9) -QTREAD (n=14) -TREAD/RESIST (n=10) *p=0 04, T3 > Tl; tp=0.05, T3 < Tl T3 Test 96 Figure 4-1. Mean test responses of control (CONT), treadmill (TREAD), and treadmill/resistance (TREAD/RESIST) groups to 70 head-up tilt before (Tl) and after (T3) 6 months of exercise training: a) stroke volume (SV); b) cardiac output (Q). A similar change took place for the absolute decline in Q. The decline in Q at Tl for TREAD was 0.59 0.52 L min 1 ; this increased to 0.86 0.51 L min1 at T3 The type I error rate for detecting a t i me X group interaction in the relative change in Q was 0 11. The relative changes in Q shown by

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97 a) 20 10 ---CONT ,,....._ '&'-' 0 TREAD :> Cl) <] TREAD /RESIST -10 -20 Tl T3 Test b) 20 10 __.__ CONT ,,....._ '&'-' 0 .o TREAD <] -10 TREAD /RESIST -20 Tl Test T3 Figure 4-2 Percent change (,1) in mean test response from prior to exercise training (Tl) to after (T3) 6 months of exercise training in control (CONT), treadmill (TREAD), and treadmill/resistance (TREAD/RESIST) exercise groups: a) mean test stroke volume (SV) and b) mean test cardiac output ( Q) TREAD at Tl and T3 were 17 3 15.1 % and 23.1 9.6%, respectively (}2 = 0.08). Any changes for CONT and TREAD/RESIST in the relative (}2 = 0.70 and 0.24, respectively) or absolute (~ = 0.90 and 0.21, respectively) declines in Q could be accounted for by random variation.

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Table 4-13. Analysis of the Effect of 6 Months of Exercise Training on the Relative and Absolute Change in Stroke Volume and Cardiac Output from Rest to 70 Head-up Tilt for Control, Treadmill, and Treadmill/Resistance Groups 98 Variable Test X Group* CONTt TREADt TREAD /RESISTt (n = 9) (n=14) (n=l0) .1SV 0 01 0.73 <0 01 0 25 % .1SV 3 0.07 0.79 0.03 0 37 .1Q 0.05 0.90 0.04 0 21 % .1Qa 0 11 0 70 0.08 0.24 CONT = Control; TREAD = Treadmill; TREAD /RESIST = Treadmill/Resistance. Wilks' Lambda t Single degree-of-freedom contrast, analysis of mean difference (Tl-T3) L1 values calculated as (mean resting value mean tilt value) a % -1 values calculated as (-1 value/mean resting value) The p-value for t e st X group interaction for TPR = 0 01; Table 4-12) suggested an effect of training on this variable However, further analysis using a one-way repeated measures ANOV A for each group resulted in a high probability of a type I error in detecting a test effect for all groups (12. = 0 83, 0.20, and 0 25 for CONT, TREAD, and TREAD/RESIST, respectively) The raw data show that TREAD decreased average test TPR by 199 dyne seccm-5 (7 0 % ) from 2843 466 dyne sec cm-5 at Tl to 2644 637 dyne sec cm-5 at T3. Average test TPR increased in TREAD/RESIST by 240 dyne sec cm 5 (8.7 % ) : the Tl and T3 values were 2749 645 dyne sec cm 5 and 2989 446 dyne sec cm 5, respectively. The change in average TPR of CONT was from 2973 448 dyne sec cm 5 at Tl to 2926 617 dyne seccm 5 at T3 (47 dyne sec cm 5, 1.6 % ) To test the probability that changes during TILT and REC (time effect) in HR, SV, and Q could be attributed to random experimental variation a

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99 repeated measures analysis comparing all levels of time to rest was performed for each variable. At each time point, values were averaged over tests and groups. The results of these analyses are shown in Table 4-14. For the HR analysis, there was a very low type I error rate for all time points during TILT; it was concluded that TILT caused an increase in HR. Heart rate initially accelerated 5 3 bmin1 (8.3%), from a resting value of 63.5 9 3 bmin1 to a value at TILTo of 68 8 12 7 bmin 1 There were further increases during TILT; the final HR value (TILT11-1s) was elevated 9 7 bmin1 (15 2%) above the resting value A further analysis of the trend during TILT showed that the HR increase, while slight, was progressive A comparison of each level of time to the mean of subsequent levels yielded the following type I error rates: rest, I,!< 0 01; To 12 < 0 01, T1, I,!= 0.06, T2-s, 12 < 0 01, and T6-10, I,!< 0 01. The HR at RECo was elevated 6.5% (4 1 bmin1 ) above the resting value, but the large typ e I error rate at REC1 indicated that the difference from rest at this time point could be accounted for by random variation The HR fell below resting (1.2-1.6 bmin1 ; 1.9-2.5%) during the remainder of REC. The analysis comparing all time levels of SV to rest showed that there was a very low type I error rate for all time points during TILT (Table 4-14); it was concluded that TILT caused an decrease in SV Decreases in SV during TILT ranged from 11.9 ml (23 8%) to 13.6 ml (27.1 % ). The large typ e I error rate at RECo and REC1 indicate that the differences from rest at these points could be due to random variation. However, the small type I error rates during the remainder of the time points during REC indicate that further supine rest (up to 15 minutes) caused a decrease in SV. Stroke volume declined 1.7 to 3.2 ml (3 3 to 6.4%) between minutes 2 and 15 of REC. The low type I error rate during TILT for the Q analysis comparing all time points to rest suggest that upright tilt caused a decrease in Q; decreases

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Table 4-14. Post Hoc Analysis for Time Effect to Detect Changes in Heart Rate, Stroke Volume, and Cardiac Output as a Result of 70 Head-up Tilt (Means Averaged Over Tests and Groups) Time Rest Tilt 0 1 2-5 6-10 11-15 Recovery 0 1 2-5 6-10 11-15 MeanSD (b min1 ) Heart Rate t %~ p 63.5 9 3 68 8 12.7 +5.3 +8 3 <0.01 70.7 11.0 +7 2 +11 3 <0 01 70.4.3 +6.9 +10.9 <0 01 71.4 1 +7 9 +12.4 <0 01 73 2 12 0 +9 7 +15.2 <0.01 67 6 11.9 +4.1 +6.5 <0.01 64.2 10 9 +0 7 +1.1 0 27 62 3 10.2 -1.2 -1.9 0.04 61.9 9 7 -1.6 -2 5 0.01 62 3 9 1 -1.2 -1.9 0 03 Comparison to resting value + = Change from rest % ~ = Percent change from rest Stroke Volume MeanSD ~+ %~ p* (ml) 50 1 10.6 -38 2 8 8 -11.9 -23.8 <0.01 36 9 7 7 -13 2 -26.3 <0.01 36.5 7.4 -13.6 -27.1 <0.01 36.8 8.0 -13 3 -26.5 <0 01 37.1 8 9 -13.0 -25.9 <0 01 49.6 11.8 -0.5 -1.0 0.55 51.0 11.9 +0.9 +1 8 0.25 48.4 11.5 -1.7 -3.3 0 02 47.0 11.5 -3.1 -6 2 <0.01 46.9 12.0 -3.2 -6.4 <0 01 Cardiac Output MeanSD ~+ %~ p* (L min-1) 3 15 0 71 2.56 0.52 -0.59 -18.7 <0 01 2 60 0.51 -0.55 -17.5 <0.01 2 54 0.47 -0.61 -19 4 <0.01 2.59 0.46 -0.56 -17.8 <0.01 2 64 0.45 -0.51 -16 2 <0 01 3 29 0 77 +0 14 +4.4 0.03 3 22 0.70 +0 12 +3.8 0 18 2.95 0.61 -0.20 -6.3 <0.01 2 85 0 64 0.30 -9.5 <0 01 2.86 0 67 -0 29 -9 2 <0.01 ...... 0 0

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101 during TILT ranged from 0.51 to 0 61 Lmin-1 (16 2 to 19.4 % ) At RECo, Q was elevated by 0.14 Lmin1 (4 4%), but the large type I error rate at REC1 = 0 18) indicated that the difference from rest at this time point could be due to random variation Decline in Q during the remainder of REC ranged from 0 20 to 0.30 Lmin1 (6 3 % to 9 5%) (Table 4-14) The overall multivariate analysis for both SBP and DBP showed a small probability of a type I error in detecting a time effect = 0 02, and 0 06, respectively) (Table 4-15). In the post-hoc analyses comparing all time points to rest, the small p-value for SBP at TILTo indicated that initiation of tilt caused a reduction in SBP. However, the reduction was small (3 mmHg, 2.3 % ) (Table 4-15). The large type I error rates generated for the other time points during TILT indicate that any differences from rest in SBP was due to random variation It can be concluded that SBP is well maintained during TILT in healthy older persons The small type I error rates generated for SBP at RECo, REC1, and REC2 s indicated that SBP was slightly {1-2 mmHg, 12 % ) elevated for up to 5 minutes after upright tilt. However, it should be noted that the mean values at these time points were similar to the value at TILT10, for which a large probability of a type I error rate was obtained. The post hoc time analysis for DBP showed a small probability for a type I error at all time points during TILT (Table 4-15) It can be concluded, therefore, that upright tilt caused an increase in DBP Increases during tilt averaged 4-5 mmHg (5-7 % ). The large p-values generated for DBP during REC suggest that any differences from rest were due to random variation. Therefore, after upright tilt, DBP rapidly recovers to near resting values. The overall multivariate test for MAP indicated an 11 9 % probability o f a type I error in detecting a time effect (Table 4-12) Therefore, further analyses were not done Inspection of the raw data (Table 4-15) show that upright tilt

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Table 4-15. Post Hoc Analysis for Time Effect to Detect Changes in Systolic, Diastolic, and Mean Arterial Pressure as a Result of 70 Head-up Tilt (Means Averaged Over Tests and Groups) Systolic Blood Pressure Diastolic Blood Pressure Mean Arterial Pressure Time MeanSD ~t %~ p* MeanSD ~t %~ p* MeanSD ~t %~ p* (mmHg) (mmHg) (mmHg) Rest 127 14 -77 93 8 Tilt 0 124 16 -3 -2.4 0.06 81 +4 +5.2 0.02 95 10 +2 +2.2 NC 1 125 17 -2 -1.6 0 18 81 +4 +5 2 0 01 96 10 +3 +3 2 NC 2-5 128 15 +1 +0.8 0 41 82 +5 +6 5 <0 01 97 9 +4 +4 3 NC 10 129 17 +2 +1.6 0 20 82 +5 +6.5 <0.01 98 9 +5 +5.4 NC 15 126 17 -1 -0.8 0 74 81 +4 +5 2 <0 01 96 +3 +3.2 NC Recovery 0 128 16 +1 +0.8 0 03 78 +1 +1.3 1.00 94 9 +1 +1.1 NC 1 129 14 +2 +1.6 <0 01 78 +1 +1.3 0.29 95 8 +2 +2.2 NC 2-5 129 14 +2 +1.6 0 02 79 +2 +2.6 0 18 95 8 +2 +2.2 NC 10 128 16 +1 +0.8 0.40 78 +1 +1.3 0.47 95 8 +2 +2 2 NC 15 127 15 +0 +0 0 0.59 79 +2 +2 6 0 24 95 9 +2 +2 2 NC tValue rest (Value rest)/rest *Comparison to resting ,-..I NC = Not calculated (see text) 0 N

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103 caused a slight increase in MAP which was 2 mmHg (2 2%) initially, with further small increases to 5 mmHg (5 4%) during the remainder of TILT The decreases in SBP at TILTo and TILT1 are responsible for the slightly attenuated initial response of MAP. Differences from rest during REC were less than 2 2% (1-2 mmHg). Table 4-16 Post Hoc Analysis for Time Effect to Detect Changes in Total Peripheral Resistance as a Result of 70 Head-up Tilt (Means Averaged Over Tests and Groups) Time Rest TILT 0 TILT 1 TILT 2-5 TILT 10 TILT 15 RECD REC1 REC 2-5 REC10 REC15 Value rest Mean S.D. (dyne seccm-5) 2478 3052 761 3041 718 3140 665 3015 622 2913 599 2413 689 2445 603 2688 667 2851 858 2757 816 t (Value rest)/rest ** Comparison to rest +574 +563 +662 +537 +435 -65 -33 +210 +373 +279 %~t 12.** +23 2 <0 01 +22.7 <0.01 +26.7 <0.01 +21.7 <0.01 +17.6 <0.01 -2 6 0.07 -1.3 0.44 +8 5 <0.01 +15 1 <0.01 +11.3 <0.01 The analysis comparing all time levels of TPR to rest showed that there was a very low type I error rate for all time points during TILT (Table 4-16); it was concluded that TILT caused an increase in TPR. Increases in TPR during TILT ranged from 435 dyne seccm-5 (17 6%) to 662 dyne seccm 5 (26.7%) The typ e I error rate at RECo was 0.07; however, the difference from rest was small at this point (65 dyne seccm 5, 2 6%). The large type I error rate at REC1

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104 indicates that the difference from rest at this point was due to random variation. The small type I error rates generated for remainder of the time points during REC indicate that further supine rest (up to 15 minutes) caused an increase in TPR. Resistance was elevated between 212 and 373 dyne sec cm-5 (8.5 to 15.1 %) between minutes 2 and 15 of REC. The elevation in TPR was associated with a decline in Q during this period. Hormonal and Plasma Volume Response to Training and Tilt Plasma volume measurements were obtained in 18 subjects (CONT n = 7; TREAD !l = 4; TREAD /RESIST !l = 7) from the main sample of 33. A repeated measures analysis with four levels of time (pre-tilt and tilt at both Tl and T3) showed no time X group interaction for either PV (p, = 0.72) or BV (0.84). Therefore, data from TREAD and TREAD/RESIST were combined into a single group (TRAIN) An initial analysis of resting PV and BV was done in a 2 X 2 (group X time) repeated measures ANOVA. The time measurements represented only the pre-tilt measurements at Tl and T3. Therefore, subjects who were eliminated from the main sample of 33 because they fainted during the Tl tilt test or because of medical conditions which may have affected their cardiovascular responses to tilt were included in this analysis of resting PV and BV responses. The results indicated that TRAIN (n = 15) increased PV by 300ml(11.0%) from 2731 674 ml at Tl to 3031 939 ml at T3 (p, = 0.04), while BV increased 501 ml (12.2%) from 4114 1050 ml at Tl to 4616 1499 ml at T3 (p, = 0 07). The Tl and T3 measurements of PV for CONT (n = 9) were 2734 510 ml and 2723 652 ml, respectively, while the respective BV measurements were 4164 900 ml and 4248 1149 ml.

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105 For the remainder of the analyses, the sample of 18 was used The responses of plasma volume and related variables to training and tilt for this sample are shown in Table 4-17. The type I error rate generated by a one-way ANOV A indicated that group differences in Tl pre-tilt values for PV (12 = 0 86), BV (0 91), and RCV (0.99) were due to random variation. Table 4-17. Responses of Plasma Volume, Blood Volume, and Red Cell Volume to 70 Head-up Tilt Before (Tl) and After (T3) 6 Months of Exercise Training in the Control and Exercise Training Groups (n. = 18). Tl T3 Pre-tilt Tilt Pre-tilt Tilt CONT (n. = 7) PV (ml) 2752 586 2128 2704 750 2162 532 BV (ml) 4166 1039 3643 805 4229 1323 3791 1108 RCV (ml) 1415 474 1514 413 1524 591 1630 613 TRAIN (n. = 11) PV (ml) 2691 742 2165 558 2947 957 2434 972 BV (ml) 4107 1149 3649 960 4499 1498 4177 1625 RCV (ml) 1415 421 1484 1552 552 1743 673 Overall (n. = 18) PV (ml) 2715 668 2151 491 2853 867 2328 821 BV (ml) 4130 1077 3647 878 4394 1399 4027 1423 RCV (ml) 1415 429 1496 415 1541 550 1699 634 Values are mean S.D CONT= Control; TRAIN = Exercise-training (Treadmill+ Treadmill/Resistance Groups); PV = Plasma volume; BV = Blood volume; RCV = Red cell volume. Analyses of changes in PV, BV, and RCV were done in a 4 X 2 (time X group) repeated measures ANOV A where the four time points used were pre-tilt and tilt at both Tl and T3. The results of these analyses are shown in Table 4-18. The analysis for PV indicated that there was a decrease in PV

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106 during tilt at both Tl and T3 (l2 < 0.01) that was not affected by group assignment (12. = 0.41 for time X group interaction). Decreases averaged 20.8% and 18.4% for Tl and T3, respectively. Table 4-18. Probabilities for Type I Error in Detecting a Change in Plasma Volume, Blood Volume and Red Cell Volume as a Result of 70 Head-up Tilt or Exercise Training. PV BV RCV Group by Time* 0.41 0.58 0.58 Wilks' Lambda Time* Pre-tilt Tl Tilt Tl Pre-tilt Tl Pre-tilt T3 <0.01 <0.01 <0 01 to to to to Pre-tilt T3t Tilt T3t Tilt Tlt Tilt T3t 0.31 0.15 0.05 0 21 0.09 0.03 <0 01 <0 01 <0.01 <0.01 <0 01 <0.01 t Single-degree-of-freedom contrast, analysis of mean difference PV = Plasma volume; BV = Blood volume; RCV = Red cell volume. Differences between the Tl and T3 pre-tilt (12. = 0.31) or tilt (l2 = 0.21) PV values were due to random variation Although TRAIN increased resting PV by 9.5% (256 ml), the type I error rate for the time X group interaction indicated this change was not different from the 1.7% (48 ml) decrease seen in CONT. Despite the increase by TRAIN, the decreases in PV during tilt for TRAIN were nearly identical on an absolute basis (526 and 513 ml for Tl and T3, respectively). The absolute PV during tilt at T3 was 269 ml (12.4%) greater than the Tl tilt measurement and only 9 6% lower than the resting Tl value. The analysis of BV showed similar results (Table 4-18). There were decreases in BV during tilt at both Tl (483 ml, 11.7%) and T3 (367 ml, 8.3%) (12. < 0.01), while differences between the two pre-tilt BV values were due to

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107 random variation (12 = 0.15). The type I error rate of 0 09 for the relationship between the Tl and T3 tilt values indicates that there may have been a systematic increase in the BV measurements during tilt. The average Tl tilt measurement was 3647 878 ml while the T3 measurement was increased 10.4% to 4027 1423 ml Group assignment did not appear to affect BV changes, as evidenced by the large type I error rate generated for the group X time interaction (I?, = 0.58) Although TRAIN increased resting BV by 9.5% (392 ml), the type I error rate for the time X group interaction indicated this change was not different from the 1.5% (63 ml) increase seen in CONT. The absolute BV during tilt for TRAIN at T3 was 528 ml (14.5%) greater than the Tl tilt BV and 70 ml greater than the resting Tl BV. Red cell volume increased during tilt at both Tl (12 < 0 01) and T3 (12 < 0.01) (Table 4-18). There were increases in both resting (I?,= 0 05) and tilt (12 = 0 03) RCV from Tl to T3; however, these were not related to group assignment (I?,= 0.58 for overall t i m e X gro u p interaction). The responses of Hb and Hct to training and tilt are shown in Table 419 A one-way ANOVA on the Tl pre-tilt values indicate that any initial group differences were due to random variation (12 = 0 72 and 0.50 for Hb and Hct, respectively) Analyses of the Hb and Hct responses to tilt and training were done in a 4 X 2 (time X group) repeated measures ANOV A where the measures of time were pre-tilt and tilt at both Tl and T3 The results of these analyses are shown in Table 4-20 Both Hb and Hct increased during tilt at Tl and T3 (12 < 0 01); the changes were not group related (12 = 0.24 and 12. = 0.39 for Hb and Hct, respectively, for overall time X group interaction) Differences between the Tl and T3 resting Hct values were due to random variation (I?,= 0.12) However, the type I error rate for the differences between the Tl and T3

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108 tilt Hct values = 0.07) indicated a systematic change in the tilt Hct values; the average tilt value at Tl was 40.2 3.8% while the average T3 tilt value was 41.5 3.2% Table 4-19. Hemoglobin and Hematocrit Measurements at Rest and During 70 Head-up Tilt Before (Tl) and After (T3) 6 Months of Exercise Training in Control and Exercise Training Groups (n = 18) Group CONT (n = 7) TRAIN (n = 11) Tl T3 Tl T3 Values are mean S.D. Hematocrit Pre-tilt Tilt 36 8.3 38.6.2 37 7.4 37.8.4 41.1 7 42.1 7 40.4.5 41.7.4 Hemoglobin Pre-tilt Tilt 13.2.7 13.4.6 13 0 8 14.2.8 15.0.3 14 9.8 14.6.3 15.5 9 CONT= Control; TRAIN= Combined (Treadmill+ Treadmill/Resistance) training group The low type I error rate associated with the change in resting Hb from Tl to T3 < 0 01) indicated a systematic change between these two time points. Mean resting values of Hb increased from Tl (12 9 1.4 mg/ dl) to T3 (13.9 1.1 mg/ dl); this change was not group related (12 = 0 24 for overall tim e X group interaction). However, changes in Hb during tilt from Tl to T3 were due to random variation = 0.21). The percent change in PV, BV, and RCV during tilt at Tl and T3 was calculated and is shown for each group in Table 4-21. The large type I error rate for a test X group interaction generated by the 2 X 2 (test X group) ANOVA indicated that any group differences in the percent change in PV between Tl and T3 were due to random variation (12 = 0.53). Similarly, values for t e st X group interactions in the percent change in BV = 0 99) and

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RCV (12. = 0 10) during tilt at Tl and T3 indicated random variation could account for group differences. 109 Table 4-20. Probabilities for Type I Error in Detecting a Change in Hemoglobin and Hematocrit as a Result of 70 Head-up Tilt Before (Tl) or After (T3) 6 Months of Exercise Training. Hb Hct Group by Time* 0.24 0.39 Wilks' Lambda Time* Pre-tilt Tl Tilt Tl Pre-tilt Tl Pre-tilt T3 <0.01 <0.01 to to to to Pre-tilt T3t Tilt T3t Tilt Tl t Tilt T3t <0 01 0.12 0 21 0.07 <0.01 <0 01 <0.01 <0.01 t Single-degree-of-freedom contrast, analysis of mean difference Hb = Hemoglobin; Hct = Hematocrit. Table 4-21. Percent Change in Plasma Volume, Blood Volume, and Red Cell Volume During 70 Head-up Tilt Before (Tl) and After (T3) 6 months of Exercise Training in the Control and Exercise Training Groups (n = 18) Group CONT (n= 7) Tl T3 TRAIN ( n = 11) Tl T3 Values are mean S D. APV (%) -22.2 .2 -19.4 4 2 -18.9 6.5 -18.6 7.3 A BV (%) -11.9 4.4 -9.7 4.3 -10.6 5 2 -8.4 5.6 ARCV (%) 9.8 13 1 7 7 7.1 5 1 6.1 11.4 6.9 CONT = Control; TRAIN = Combined training group (Treadmill + Treadmill/ Resistance. APV = Change in plasma volume from supine rest to 70 head-up tilt. ABV = Change in blood volume from supine rest to 70 head-up tilt ARCV = Change in red cell volume from supine rest to 70 head-up tilt

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110 Hormone/ electrolyte analyses were done on a sample of 27 Analyses were initially performed using a 4 X 3 (time X group) repeated measures design in order to determine if group assignment affected the response to tilt or training The four levels of time consisted of the measurements at pre-tilt and tilt at both Tl and T3 Time X group interactions for the various analyses were as follows: ALOO = 0.53; A VP,~= 0.43; K+, I?.= 0.86; Na+,~= 0.30; PRO,~ = 0 99 ; NE, I?. = 0.50; and EPI, I?. = 0.46. It can be concluded that any differences among the groups across the four levels of time were due to random variation Therefore, because of the necessity for combining the training groups for PV analyses and because of the relationship between hormones/ electrolytes and fluid volume control, data for TREAD and TREAD/RESIST were combined into a single group (TRAIN) for these hormone/ electrolyte analyses However, the time X group interaction for the ACTH analysis yielded a type I error rate of 0 03. Follow up analyses indicated that there were group differences in the response to tilt at T3: CONT had an increase in ACTH during tilt at T3 from a resting value of 57.5 47.5 pgml1 to a tilt value of 84.5 52.8 pgml1 (~ = 0 01) The change in ACTH from rest to tilt at T3 for TREAD was from 69.6 36.2 pgml 1 to 49 3 31.2 pgml1 respectively~= 0.07) while the change from rest to tilt for TREAD/RESIST was from 44 1 24 8 pgml 1 to 58.7 32 6 pgml1 respectively~= 0 20). The type I error rate for detection of a change in ACTH as a result of tilt at Tl was 0.54, while comparisons of the Tl and T3 resting values, and of the Tl and T3 tilt values yielded a type I error rates of 0 28 and 0.17, respectively

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111 Table 4-22. Hormonal/Electrolyte Response to 70 Head-up Tilt Before and After 6 Months of Exercise Training in the Control and Exercise Training Groups (n = 27). Pre-training Post-training Rest Tilt Rest Tilt ACTH (pgml-1) CONT (n = 7) 35.1 12.4 46.8 26.5 57.5 .5 84.5 52.8 TRAIN (n. = 20) 54.8.4 54.6.7 56.9 .9 53.9 .9 Overall (n. = 27) 50.2 .0 52.8 .0 57.1 .7 61.0 38.2 ALDO (pgml-1) CONT (n. = 7) 57.4 29.1 72.2 28.6 61.5 43.4 69.4.3 TRAIN (n = 20) 57.3 31.3 67.9 42.4 58.5 36.4 70.8 53.5 Overall (n = 27) 57.3.2 69 0 38.8 59.3 .5 70.5 53 6 AVP (pgml-1) CONT (n. = 7) 2.5.0 2.5.6 2.3 1.9 3.1 .0 TRAIN (n = 20) 2 5.8 4.3 2.5 1.6 1.2 1.8 2 0 Overall (n. = 27) 2 5.8 3.9.8 1.7 1.4 2.2.6 K+ (mEqL1 ) CONT (n. = 4) 4 2 0.2 4.4 0.3 4.3 0.3 4.4 2 TRAIN (n. = 13) 4.1 0.4 4.3 0.3 4.3 0.5 4 4 0.4 Overall (n = 17) 4.1 0.3 4.3 0 3 4 2 0.4 4.4 0.3 Na+ (mEqL-1) CONT (n = 7) 141.5 2.2 141.3 2.9 141.7 3.5 141.9 2 6 TRAIN (n. = 20) 140 0 1.8 140.5 2.9 140.8 3.2 141.4 3 0 Overall (n = 27) 140.4 2.0 140.7 2.9 141.1 3.2 141.5 2 8 PROT (mgdl-1) CONT (n. = 7) 8.2.7 9.0 0.7 8.6.4 9.5 0.3 TRAIN (n. = 20) 8.2 0.7 9.0.7 8 6.4 9.5 0.5 Overall (n = 27) 8 2 0.7 9.0 0.7 8.6 .4 9.5 0.5 NE (pgml-1) CONT (n =6) 436 140 636 300 112 585 191 TRAIN (n = 20) 517 186 780 389 139 712 213 Overall (n = 26) 498 178 747 297 368 136 683 212 EPI (pgml-1) CONT (n. = 6) 6.3 15.5 21.7 36 3 0 0 0 0 17.3 26.9 TRAIN (n. = 20) 29.7 56.4 11.9 30.2 9 1 19.6 22.4 38.2 Overall (n. = 26) 24 3 50 6 14.1 31.2 7 0 17.5 21.2 35.5 Values are mean S.D. CONT= Controls; TRAIN= Combined (Treadmill+ Treadmill/Resistance) training group; ACTH = Adrenocorticotropic hormone; ALDO = Aldosterone; AVP = Vasopressin; K+ = Potassium, Na+ = Sodium; PROT = Protein; NE = Norepinephrine; EPI = Epinephrine.

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Table 4-23 Probabilities for Type I Error in Detecting a Change in Hormone Concentration as a Result of 70 Head-up Tilt Before (Tl) or After (T3) 6 Months of Exercise Training. 112 Group by Time* Time* Pre-tilt Tl Tilt Tl Pre-tilt Tl Pre-tilt T3 ACTH 0.05 0.07 ALDO 0 91 0.08 AVP 0.14 0.29 K+ 0 69 <0.01 Na+ 0 81 0 48 PROT 0.99 <0.01 NE 0.88 <0.01 EPI 0.59 0 19 Wilks' Lambda to to Pre-tilt T3t Tilt T3t 0.20 0.07 0.78 0.99 0 37 0.16 0.10 0 46 0.47 0.31 0 01 <0.01 0.01 0.34 0.26 0 72 to Tilt Tlt 0 42 0.03 0.09 <0.01 0 75 <0.01 <0.01 0.92 to Tilt T3t 0 13 0.05 0.21 0.15 0 38 <0.01 <0 01 0.05 t Single-degree-of-freedom contrast, analysis of mean difference ACTH = Adrenocorticotropic hormone; ALDO = Aldosterone; A VP = Vasopressin; K+ = Potassium, Na+= Sodium; PROT = Protein; NE= Norepinephrine; EPI = Epinephrine Means and standard deviations for each hormone/ electrolyte analysis are presented in Table 4-22. Values for ACTH are included for reference. The type I error rates for detecting a time X group interaction and a time effect, as well as the error rates associated with detecting a mean difference between two time points are presented in Table 4-23 In the repeated measures ANOV A for ALDO, the p-value for the time effect was 0.08, while the value for the time X group interaction was 0 91 (Table 4-23). This suggests that ALDO secretion changed as a result of tilt but was not affected by training. Follow up analyses indicated that changes in resting and tilt concentrations of ALDO from Tl to T3 were due to random variation (}2 = 0.78 and 0 99 for resting and tilt, respectively). However, ALDO increased during tilt at both Tl (12 = 0.03) and T3 (12 = 0 05) Aldosterone

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113 increased 20.4% at Tl from an average at rest of 57.3 30.2 pgml 1 to a tilt average of 69 0 38.8 pgml1 Increases at T3 averaged 18 9%, from 59 3 37.5 pgml-1 at rest to 70.5 53.6 pgml1 during tilt (Table 4-22). An initial analysis for AVP indicated that there was no effect of training on AVP levels (12 = 0.14 for time X group interaction, Table 4-23) In addition, the high type I error probability level for a time effect (J2 = 0 29) indicated that there was no increase in A VP secretion as a result of tilt at either Tl or T3 Increases during tilt averaged 56% at Tl and 29% at T3 (Table 4-22). However, because these data did not appear normally distributed, a log transformation of the data was made. Analysis of the transformed data indicated that there was an increase in AVP during tilt at Tl (12 = 0 02); there was no increase at T3 (J2 = 0 83) due to a decrease in A VP secretion by TRAIN (J2 < 0 01). Changes in resting and tilt plasma Na+ from Tl to T3 as well as changes in plasma Na+ during tilt at each test were due to random variation (J2 = 0 48 for overall t i me effect) Changes during tilt at Tl and T3 were less than 1 % Plasma K+ increased during tilt at Tl (J2 < 0.01) in all groups; the increase averaged 0 2 mEqL1 (4.9%). However, the probability of a type I error for detecting a time effect during tilt at T3 was 14.8%, despite the fact that the increase (0.2 mEqL 1 4 8%) was nearly identical to the Tl change. Changes in resting and tilt plasma K+ from Tl to T3 were due to random variation (J2 = 0.10 and 0.46 for resting and tilt, respectively) There was an increase in PROT during tilt at both Tl (9.8%, 12 < 0 01) and T3 (10.5%, 12 < 0 01). In addition, there was an increase in both resting (4.9%, 12 = 0.01) and tilt (5.6%, 12 < 0.01) PROT at T3 These changes were not different between groups (J2 = 0 99 for time X group interaction)

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114 Norepinephrine increased during tilt at Tl (50%, 12< 0 01) and at T3 (86%, 12< 0.01) Resting NE decreased 26% from Tl to T3 (J2_ = 0 01); however, this was not due to training as indicated by the overall time X group interaction (12= 0.88) The high p-values for a time effect and a time X group interaction for the EPI response indicate that EPI did not change as a result of either tilt or training. Responses of Subject Experiencing Presyncopal Symptoms Four subjects (2 males, 2 females) did not complete the 15 minute tilt portion of the test at Tl ("fainters") One subject experienced syncope while three others experienced presyncopal symptoms (nausea, sweating, lowered BP) and requested test termination. At T2, three of the original four fainters were able to complete the tilt portion of the test, while at T3 all four subjects successfully completed the 15 minute tilt. Because all of fainters had been assigned to either TREAD (n = 1) or TREAD/RESIST (n = 3), and since there was an effect of training on the SV and Q responses to the tilt test, the cardiovascular responses from these subjects were calculated and compared with those of the 24 subjects in TREAD and TREAD /RESIST who completed the test ("nonfainters") The HR, SV, Q, BP, and TPR responses are listed in Tables 4-24--4-28 For each variable, a 3 X 2 (test X group) repeated measures ANOV A was performed at each time point during the test However, because of the small number of fainters and the variability of their data, the analyses indicated that differences between fainters and nonfainters at all points for all variables could be ascribed to random variation Therefore, only descriptive data are offered below.

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115 Table 4-24 Heart Rate Responses of Fainters (F; n = 4) and Nonfainters (NF; n = 24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training. Tl T2 T3 Time F NF F NF F NF Rest 59 7 6 4 65 6 6 61.5.0 63 4 8 0 56 9 6 3 63 0 0 TO 70.8 4 70 8.6 72.5.4 69 4.5 66 6 0 68.4 9 Tl 71.8 6 72 9.4 75 6.9 72 4 9.6 69.4 2 70 2.6 T2 73 6.8 73 0.7 75 5 0 73 0 0 70 0 2 70.5.2 T3 74 2 8 72.4.8 75.5.9 71.6 8.9 68 9.0 70.1.4 T4 74 1 8 72 4.5 77 5 2 71.7 9 0 68 8 9 69 7.6 TS 71.6 7.9 72 8.5 77.1.2 71.4 9.9 69.5.4 69.7.5 T6 69 7 9.6 72.4.7 79.0.0 72.0 9.1 69.2 0 71.2.9 T7 68.4 7.9 73.4.2 76.0.9 72.2 8.9 73.2 3 70 9 0 TB 73.6.6 74.0.9 79 8 0 72.6 9.0 69 8.9 71.0 5 T9 73 0 6 74 4.9 80.3 0 73 7 2 73 3 8 71.1.2 T10 73 3.1 74.4 7 77 5 7 72.3 9.8 70 3 0 71.7.9 T11 90.2 75.7 3 81.4.4 72.8 9 6 71.6.3 72.1.4 T12 84 1 76.2 7 83.2.4 74.5 9 7 73.4 9 73.0 3 T13 46 2 75 7.3 85 9 6 74.0.7 70 7 0 71.9 5 T14 76.3 8 85 4.2 74.9 9 70 7.4 73 4.4 T15 76.5.6 85 1.5 74.6 3 71.2.8 74 1 6 RO 56 2 5 71.2 1 62 0.5 67 3 8.6 59 6.5 67.1 4 Rl 48.4.6 67.6 3 60.0.8 64 1 9.4 55.5 7 0 64 0.6 R2 53 6.5 65 6 9 57 9.9 64 3.4 51 4 4.4 62.3 4 R3 57 8 0 65.7.5 56.6.6 63 4 9.5 52 7 5 3 62.0 1 R4 55 7 9 6 65.4.1 58 0.4 62.4 9.3 51.1 3.2 62.0.1 RS 55 9 7.7 65 2.2 58 3 8 62 9 9 7 54 3 4 8 61.8.8 R6 59.0 8.0 65 4 2 59 1 8 62 3 9.7 52 1 6.1 60 9 9 3 R7 56 7 4.8 65.3.6 59.5 9.0 63 6 9.4 52 0 4.9 60.9 9 5 RB 55 5 5.9 65 6 1 58.5.2 63 2 8.9 52.4 4.5 60.8 9.6 R9 56 6 6.3 64 9.1 58.4.4 62 9 8 3 53 6 6 1 60.5 9.4 RIO 58.9 4.8 65 1.1 59 5.5 63 0 8 2 52 8 3.8 60 4 9.8 R11 55 5 5.3 65 2.2 58.7 3 63.1 9.0 52.4 3.4 61.3 9.5 R12 56.1 5 2 65 2.9 59 9 9.8 63 3 8 6 55.3 8.1 60.6 8 9 R13 56 4 5.9 65.4 2 58.2.6 63.4 9.3 52 7 5 1 60.8 8.9 R14 56 2 6 0 64 2.3 57.3.0 63.6 9.1 54.8 4.1 61 4 8.7 R15 55.2 3.5 64 9.8 58.9.1 62.9 8 6 55.5 7 7 61.6 8 7 Values are mean S D T = Tilt; R = Recovery

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116 Table 4-25. Stroke Volume Responses of Fainters (F; n = 4) and Nonfainters (NF; n = 24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training. Tl T2 T3 Time F NF F NF F NF Rest 43.3 7.3 47.8 1 44 5 4.2 56.7.0 50.7 4.7 51.9.9 TO 30.1 7.8 37.9 7.8 33.1 7.5 40.0 7.5 36.4 2.1 39.6 8.7 Tl 30.8 5.6 36.5 7 9 30.3 5.5 37.1 7.0 36.2 5.0 38.2 7.3 T2 31.7 6 0 36.1 7.0 29.8 7.7 37.4 7.6 33.8 3 8 37.5 7.6 T3 32.8 5.3 36 0 8 1 31.5 7.5 38.2 8.3 37.3 6.7 37.8 7.7 T4 31.2 4.2 36.6 9.1 29.8 8.2 38.2 8.5 36.6 8.4 38.4 7.7 TS 33.5 6.2 36.5 8.1 29 9 8.4 38.2 9.1 36.6 4.9 37.5 7.4 T6 36.1 6.6 36.4 8.5 32 8 9.0 38.1 8 .1 37.3 7.1 37.4 7.2 T7 36.3 5.6 36.6 8.5 31.7 7.9 38.5 8.7 36.5 6.4 37.3 6.7 TB 32.9 6.9 37.4.0 32 7 7.8 37.8 7.9 36.0 4.7 37.5 7.5 T9 32.0 4.7 36.9 9 7 30 6 9.3 38.7 8.6 34.0 4.8 37.9 7 7 T10 31.8 3 1 36.2 9.4 34 1.7 38 9 8 9 35 7 5 3 38.2 9.0 T11 39 0 37 0 9 5 33.9 4.7 38 2 7 0 35 8 6.0 38.4 8.6 T12 33.3 35 8 9.3 32.3 6.0 36 7 7 2 33 9 5 8 37 8 7.7 T13 44.8 36 1.1 34.0 7.0 38 1 8.4 35 7 8.3 39.5 9.0 T14 36.4 2 33.7 8.4 37.2 8.7 35.6 5.6 39.0 9 .1 T15 35.6.6 37.4.2 37.4 8 0 35.5 6.7 38.1 .1 RO 50.9 6 6 47.2 6 49.0 9.4 55 4.4 49.0 4.8 50.8.0 Rl 50.8 8 8 49.4.0 47.3.1 55.2.0 47.4 7.4 52 1 8 R2 44.5 7.3 47.0.1 48 2.4 54.1.8 51.2.7 49 7.2 R3 47.3.4 47.5.9 44.9 2 54.2.6 49.4 8.3 49.2.0 R4 48 7.3 45.8.8 46 8.3 52.1 9 49 9 8.5 48.5.3 RS 42.8 3 45 6 7 47.5.7 51.8.8 46.7 6.4 48 6.8 R6 44 6 8.4 45 1.8 45 3.0 51.5.4 51.6 4 6 49.8.3 R7 46 1 6 6 45.3.1 42 7 5.8 51.0.2 49 2 9.3 48.2.7 RB 48.3.2 45.7.5 44.8 9.6 51.5.9 49.2.1 46 7.3 R9 49 0 9 0 45.5.4 44.3 9.0 51.2 8.9 48.0 7.5 48.2.0 R10 46.5.4 45.5.4 44.3 6 7 51.7 7 47 6 5.5 47.6.5 R11 48.3.2 45.9 8 44.7 7.2 52.9.2 47.2 7.5 47.2.8 R12 51.1 7.3 44.4.7 45.9 6.0 50 6.0 47 9 6.2 48.7.2 R13 48 5 8 9 44 2.0 43.7 6.4 49.9.0 49.9 3.8 49.5.3 R14 49.1 9 8 44.8 0 43.4 8.8 50.1.2 49 7 9 1 50.1.7 R15 46.7 0 44.0.8 43.7 6.1 50.5 9 1 48 2.0 49.0.0 Values are mean S.D T = Tilt; R = Recovery

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117 Table 4-26. Cardiac Output Responses of Fainters (F; n = 4) and Nonfainters (NF; !l = 24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training. Tl T2 T3 Time F NF F NF F NF Rest 2.57.44 3.10 68 2.71.35 3.57.75 2 89.38 3.24 83 TO 2.07.44 2.62.50 2.36.57 2.74.59 2.43.46 2.66.55 Tl 2.19.40 2.62.57 2.28.50 2.67.52 2.54 76 2.67.47 T2 2.28.31 2.59.50 2.26.70 2.71.56 2.38.57 2.60.50 T3 2.38.36 2.57.53 2 37.62 2.72.56 2.59.78 2.61.51 T4 2.26 28 2.62.57 2.33.79 2.72 60 2 53.90 2.63.47 TS 2.41.64 2.61.53 2.33.79 2 69.58 2 57.70 2.60.51 T6 2.54 78 2.58 45 2.60.88 2 72.58 2.65.88 2.64.49 T7 2.46.53 2.62.49 2.41.69 2 74.54 2.71 87 2.63.47 TB 2.46.98 2 73.55 2.60.76 2.67.45 2.54.73 2.64.47 T9 2.37.81 2.68.55 2.48.89 2 83 60 2 53 80 2.69.48 Tl0 2.35.71 2.63.49 2.65.98 2.78.62 2.55 78 2.66 .44 Tll 3.53 2 72.46 2.75.41 2.76.53 2.61.82 2.69.46 T12 2.79 2.66.49 2.66.56 2.72.52 2.51.85 2 70 44 T13 2.07 2.66.50 2.91.69 2.79.59 2.58.00 2 76.57 T14 2.70.49 2.87.92 2.75.56 2.53.73 2.76.45 T15 2.63.47 2.78.45 2.75.53 2.56.82 2.72.46 RO 2.86.84 3.28.78 3.04.84 3 72 86 2 96 86 3.34.87 Rl 2.51 94 3 22.76 2.81.70 3.50.71 2.67.76 3.33 72 R2 2.39.70 2.99.61 2.76.60 3.41.76 2 63.67 3.09.61 R3 2.63.82 3.03.72 2 51.66 3.37.68 2.62.61 2.96.63 R4 2.47 57 2.94 69 2.69.63 3 21 63 2 61 52 2.93.66 RS 2 20.55 2 91 68 2.70.40 3 21 68 2.56.56 2 93.67 R6 2 64.62 2.87.62 2.64.58 3.20.65 2.69.42 2.96.74 R7 2.61.44 2.89.69 2.53.48 3.21.69 2.54.54 2.87.73 RB 2.66.41 2.94.71 2.59.53 3.17.71 2.57.53 2.79.66 R9 2.66.59 2.90 67 2 57.54 3 19.55 2.59 63 2.84 72 Rl0 2.78.72 2.89.64 2.62.47 3.24 73 2.52.46 2.83.71 R11 2.82 75 2.92.67 2 61.48 3.32 76 2.49.52 2.82 74 R12 2.88 55 2.86.70 2.67.59 3.17 66 2 65.49 2.91.76 R13 2.66.56 2.84.75 2.52.48 3.12.67 2.64.38 2.95 70 R14 2.75.61 2.82.70 2.47.51 3.15.63 2 73.62 3.02.77 R15 2.67.59 2.81.69 2.56.54 3.17 61 2.70.74 2.95.74 Values are mean S.D. T = Tilt; R = Recovery

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118 Table 4-27 Systolic and Diastolic Blood Pressure Responses of Fainters (F; n. = 4) and Nonfainters (NF; n. = 24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training Time F SBP (mmHg) Rest 125 19 TO 131 23 Tl 140 T2 134 T3 132 20 T4 130 20 TS 134 T10 131 27 T15 RO 111 11 Rl 117 18 R2 119 19 R3 120 21 R4 124 RS 126 R10 126 21 R15 125 21 DBP (mmHg) Rest 79 7 TO 84 9 Tl 87 13 T2 84 8 T3 85 9 T4 82 10 TS 85 12 T10 84 20 T15 RO R1 R2 R3 R4 RS R10 R15 74 9 78 9 78 9 78 11 79 12 78 11 76 9 76 10 Tl NF 125 11 123 13 125 13 125 12 125 13 124 12 126 14 126 12 123 14 125 16 124 13 124 14 124 12 125 13 125 13 125 12 123 12 78 80 81 82 82 83 83 84 81 78 79 80 79 80 79 79 79 Values are mean S.D. T = Tilt; R = Recovery F 131 18 131 17 134 12 133 13 139 13 135 16 137 16 132 25 138 24 129 13 130 16 132 15 133 16 130 15 129 22 131 26 134 20 78 8 86 6 87 7 88 7 88 6 88 5 87 4 84 11 87 8 80 6 81 9 82 7 80 10 81 11 81 12 82 10 81 11 T2 NF 127 14 117 18 122 16 120 17 122 15 121 15 121 18 124 16 123 16 126 12 129 13 127 15 128 13 126 12 126 14 126 15 127 16 77 5 79 11 81 8 81 8 81 8 79 8 81 9 81 7 80 8 78 7 78 6 79 5 78 6 79 6 79 6 78 6 79 6 F 126 14 131 18 125 16 134 15 133 13 139 13 135 15 130 15 136 4 133 6 128 21 132 16 138 11 135 10 125 21 127 17 129 16 77 4 80 10 79 8 85 6 84 6 84 8 84 5 83 6 84 6 80 2 75 7 76 6 79 4 78 3 76 6 78 6 77 5 T3 NF 131 18 127 21 127 22 130 22 133 22 130 15 131 19 133 22 130 22 133 15 133 16 132 17 133 17 133 18 132 18 131 22 130 19 76 6 81 11 81 10 81 8 82 8 82 9 81 9 81 9 82 8 77 6 77 6 78 5 78 6 78 7 78 7 78 6 78 6

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119 Table 4-28. Mean Arterial Blood Pressure and Total Peripheral Resistance Responses of Fainters (F; n = 4) and Nonfainters (NF; n = 24) to 70 Head-up Tilt Before (Tl), After 3 Months (T2), and After 6 Months (T3) of Exercise Training. Tl T2 T3 Time F NF F NF F NF MAP (mmHg) Rest 94 11 93 96 11 94 7 93 7 94 9 TO 99 13 94 100 10 92 11 97 12 96 12 Tl 105 21 95 103 9 94 9 94 11 96 T2 100 12 96 103 9 93 10 101 9 97 T3 100 12 96 104 8 94 9 100 8 98 11 T4 98 13 97 104 8 93 9 102 9 98 10 TS 101 15 97 103 8 94 11 100 8 98 10 TIO 100 22 98 100 15 95 9 96 8 98 11 TIS 95 104 13 94 10 101 3 98 11 RO 86 10 94 96 9 94 7 98 1 96 8 Rl 91 12 94 97 11 95 7 92 12 96 7 R2 91 12 94 98 95 7 95 9 96 8 R3 92 14 94 98 95 6 98 6 96 8 R4 93 16 95 97 95 6 97 5 96 9 RS 93 15 94 97 94 7 92 11 96 9 RIO 92 13 94 98 15 94 8 94 9 95 9 R15 92 14 94 99 95 8 94 8 95 9 TPR (dyne seccm-5) Rest 3030 863 2518 2866 566 2214 2649 503 2467 TO 3947 867 2987 3538 811 2759 3227 453 2979 Tl 3434 151 3067 3677 532 2935 3119 779 2939 T2 3528 281 3089 3947 2875 3500 720 3001 T3 3397 294 3112 3721 2905 3245 733 3089 T4 3484 474 3110 3889 2809 3517 3042 TS 3277 755 3084 3873 2925 3290 851 3095 TIO 3428 278 3069 3311 2873 3281 907 2965 TIS 3006 2994 281 2837 3426 2812 RO 2570 828 2386 2729 2137 2776 740 2423 Rl 3188 2456 2931 922 2296 3087 872 2371 R2 3254 2611 2979 806 2366 3063 991 2569 R3 3132 842 2655 3308 2368 3343 923 2677 R4 3109 913 2695 3034 910 2454 3038 726 2727 RS 3551 2724 2924 622 2467 3016 841 2711 RIO 2752 627 2730 3090 845 2444 3070 654 2825 R15 2496 262 2852 3192 840 2491 2986 960 2696 Values are mean S.D.; T = Tilt; R = Recovery

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a) 100 80 rl I i:::: 60 ..0 '-" 40 ::r: 20 b) 60 > Cf) 40 20 0 c) 4 3 rl I i:::: ..... S 2 -.a 1 0 0 RTilt 0 RTilt 0 0 5 10 5 10 5 10 1 15 0 Minutes 15 0 Minutes 15 0 Minutes ---Fainters (n=4) Nonfainters (n=24) 5 10 15 ---Fainters (n=4) Nonfainters (n=24) 5 10 15 Fainters (n=4) Nonfainters (n=24) 5 10 15 120 Figure 4-3. Responses of fainters vs. nonfainters to 70 head-up tilt prior to exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output ( Q). (R = Rest; Numbers above data points are number of fainters used in calculation of means at all times up to next marked point.)

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121 The HR responses of the two groups at Tl are shown in Figure 4-3 The numbers above the time points in the graph represent the number of fainters used in calculating that mean and all subsequent means prior to the next marked point. Thus, all four fainters were used in calculating the means at rest and through TILT5; three fainters were used for calculations for TILT6 and TILT7 Two fainters were represented at TILTs through TILT10, while one fainter was used at TILTn through TILT13 All four fainters were used in calculation of REC data The HR responses of the fainters appear nearly identical to those of the nonfainters through TILT10. The response after minute 10 (one subject) shows a sharp increase, followed by a precipitous drop The RECo and REC1 HRs for the fainters were approximately 12-13 bmin 1 below that of the nonfainters HR for the fainters remained approximately 6-8 bmin1 below that of the nonfainters throughout the remainder of REC The resting SV of the fainters at Tl was approximately 5 ml below that of the nonfainters (Figure 4-3). Although the response during TILT was erratic, at most time points through TILT10 the SV rema i ned approximately 5 ml below that of nonfainters The response after minute 10 (one subject) shows an erratic pattern with a tendency to be elevated above the nonfainters response Stroke volume during REC continued an irregular pattern but appeared similar to the nonfainters' response throughout most REC. The Q response of the fainters at Tl was approximately 0.50 Lmin 1 lower than that of nonfainters at rest (Figure 4-3). The erratic pattern during tilt mirrored that of the SV response. The response after minute 10 (one subject) showed a large increase prior to a precipitous drop Cardiac output during REC was initially depressed between 0.33 and 0.68 Lmin1 through REC5 It recovered somewhat between REC6 and REC9 and was only

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a) 100 80 -I i::: 60 .... s ,.0 40 '-' ::r:: 20 0 b) 60 40 20 0 c) 4 3 -I i::: 2 '-' .a 1 0 Tilt 0 5 10 RTilt 0 5 10 4 RTilt ---Fainters (n=4) .....g..._ Nonfainters (n=24) 'Recoverx 15 0 Minutes ,4 5 10 15 ---Fainters (n=4) ---0Nonfainters (n=24) 15 0 Minutes 4 5 10 15 Fainters (n=4) .....g..._ Nonfainters (n=24) 0 5 10 15 0 5 10 15 Minutes Figure 4-4. Responses of fainters vs nonfainters to 70 head-up tilt after 3 months of exercise training : a) heart rate (HR); b) stroke volume (SV); c) cardiac output ( Q) (R = Rest; Numbers above data points are number of fainters used in calculation of means at all times up to next marked point.) 122

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a) 100 80 ,....._ ...... I i:: 60 ..... E ,.0 40 ......, 20 0 b) 60 > Cf) 40 20 0 c) 4 3 ,....._ ...... I .s E 2 ..J ......, .a 1 0 R Tilt 0 5 10 R Tilt 0 5 10 _._ Fainters (n=4) ....o.... Nonfainters (n=24) 15 0 Minutes 5 10 15 15 0 Minutes _._ Fainters (n=4) ....o.... Nonfainters (n=24) 5 10 15 _._ Fainters (n=4) ......oNonfainters (n=24) 0 5 10 15 0 5 10 15 Minutes Figure 4-5 Responses of fainters vs. nonfainters to 70 head-up tilt after 6 months of exercise training: a) heart rate (HR); b) stroke volume (SV); c) 123 cardiac output ( Q). (R = Rest; All four fainters used in calculation of means at all time points )

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a) 160 140 __ 120 t),O ::C 100 s 80 s ........ 60 CJ) 40 20 0 b) 100 80 -t),O ::r: 60 s s ........ 40 Cl 20 0 c) 120 100 -t),O 80 s 60 ........ 40 20 0 5 0 5 10 2 10 15 0 Minutes _._ Fainters (n=4) Nonfainters (n=24) 10 15 _._ Fainters (n=4) Nonfainters (n=24) 5 10 15 _._ Fainters (n=4) Nonfainters (n=24) 0 5 10 15 0 5 10 15 Minutes 124 Figure 4-6 Responses of fainters vs nonfainters to 70 head-up tilt before exercise training: a) systolic blood pressure (SBP); b) diastolic blood pressure (DBP); c) mean arterial pressure (MAP). (R = Rest; Numbers above data points are number of fainters used in calculation of means at all times up to next marked point.)

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a) 160 140 ,....._ 120 bO 100 80 '--' 60 (/) 40 20 0 b) 100 80 bO 60 s s '--' 40 Cl 20 0 c) 120 100 bO 80 1 60 '--' 40 20 0 I Tilt 0 5 10 0 5 10 I R. Tilt 0 5 10 15 0 Minutes 15 0 Minutes I ---Fainters (n=4) Nonfainters (n=24) 5 10 15 _._ Fainters (n=4) Nonfainters (n=24) 5 10 15 _._ Fainters (n=4) Nonfainters (n=24) ,Recovery 15 0 5 10 15 Minutes 125 Figure 4-7. Responses of fainters vs. nonfainters to 70 head-up tilt after 3 months of exercise training: a) systolic blood pressure (SBP); b) diastolic blood pressure (DBP); c) mean arterial pressure (MAP). (R = Rest; Numbers above data points are number of fainters used in calculation of means at all times up to next marked point.)

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a) 160 140 120 oO ::C 100 E: 80 E: .._ P-4 60 i:o CJ) 40 20 0 b) 100 80 oO ::r: 60 E: E: .._ P-4 40 i:o Q 20 0 c) 120 100 oO 80 ::r: E: E: 60 .._ 40 20 0 R Tilt 0 5 10 I Tilt 0 5 10 I RI Tilt 0 15 0 Minutes I _._ Fainters (n=4) Nonfainters (n=24) 5 10 15 _._ Fainters (n=4) Nonfainters (n=24) Recovery 15 0 Minutes 5 10 15 _._ Fainters (n=4) Nonfainters (n=24) 15 0 15 Minutes 126 Figure 4-8 Responses of fainters vs nonfainters to 70 head-up tilt after 6 months of exercise training : a) systolic blood pressure (SBP); b) diastolic blood pressure (DBP); c) mean arterial pressure (MAP) (R = Rest; All four fainters used in calculation of means at all time points )

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a) 5000 ,....._ l.f') 4000 I s u u 3000 Q) c,i Q) 2000 '"O ......., 1000 0 b) 5000 ,....._ l.f') 4000 I s u u 3000 Q) c,i Q) 2000 '"O ......., iz 1000 0 c) 5000 ,....._ i 4000 u 3000 c,i Q) 2000 '"O ......., 1000 0 127 --Fainters (n=4) --0Nonfainters (n=24) I R! Tilt 0 5 10 15 0 5 10 15 Minutes --Fainters (n=4) --0Nonfainters (n=24) I ,Recovery 0 5 10 15 0 5 10 15 Minutes --Fainters (n=4) --ONonfainters (n=24) 0 5 10 15 0 5 10 15 Minutes Figure 4-9 Total peripheral resistance response of fainters vs nonfainters t o 70 head-up tilt : a) before exercise training; b) after 3 months of exercise training; c) after 6 months of exercise training (R = Rest; Numbers above data points are number of fainters used in calculation of means at all times up to next marked point.)

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128 depressed 0 21 to 0 28 Lmin1 below that of nonfainters. Differences between nonfainters and fainters were negligible after that point. Three of the four subjects who were unable to complete the tilt portion of the test at Tl were able complete the tilt at T2. The HR, SV, and Q comparisons at T2 of these subjects and the 24 nonfainters are shown in Figure 4-4 At rest, the HR response is nearly equal However, in contrast to Tl, the HR response of the fainters shows a steady increase throughout TILT and is approximately 10-11 bmin1 higher than nonfainters toward the end of TILT The HR of fainters is slightly below that of nonfainters throughout REC. The SV response of the fainters is consistently below that of the nonfainters throughout rest, TILT and REC. The Q response, while initially depressed, approximates that of the nonfainters toward the end of TILT in response to the higher HR. The Q of fainters during REC is consistently depressed between 0.51 and 0.86 Lmin1 when compared to the nonfainters' response. The T3 HR, SV, and Q comparisons between the two groups are shown in Figure 4-5 The HR response of the two groups during TILT is nearly identical; however, the response of the fainters during REC is still somewhat lower The SV response of the two groups is nearly identical throughout the entire test, reflecting predominantly an increased response by the fainters The Q responses during TILT are similar, reflecting slight increases by the fainters and slight decreases by the nonfainters During REC, the response of the fainters is still below that of the nonfainters but by a smaller margin than at T2 At Tl, fainters had similar BP responses to nonfainters during supine rest prior to tilt (Tables 4-27--4-28; figure 4-6). However, at the initiation of tilt

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129 fainters had increases of 6 and 5 mmHg in SBP and DBP, respectively, while nonfainters showed a 2 mmHg decrease in SBP and a 2 mmHg increase in DBP. During tilt prior to the onset of symptoms, the SBP of fainters was 6 to 15 mmHg higher than that of nonfainters, while the DBP was up to 6 mmHg higher The SBP for fainters at RECo was 14 mmHg below that of the nonfainters, but gradually recovered by REC4 The DBP for fainters at RECo was 4 mmHg below that of nonfainters but recovered by REC1 At T2, the BP responses of the fainters were consistently higher than those of nonfainters (Tables 4-27--4-28; Figure 4-7) This appears to be due to both a decrease in the nonfainters' response and an increase in the fainters' response. The fainters' response may be due to apprehension regarding the test. At T3, the responses of fainters and nonfainters appear similar. Total peripheral resistance responses are shown in Table 4-28 and Figure 4-9. Fainters had higher resting TPR values, reflective of a lower Q (Table 4-26). The greater TPR values during tilt for fainters at Tl and at T2 were associated with generally higher MAP and the generally lower Q. TPR values for the two groups are more similar during tilt at T3. The absolute and percentage change data for HR, SV, Q, SBP, DBP, MAP, and TPR at Tl, T2, and T3 are presented for each fainter in Appendix E. Initial characteristics of the fainters and nonf ainters are listed in Table 4-29 Sample sizes for the nonfainters are as listed earlier under each respective analysis section. Analyses (one-way ANOV A) of differences between the fainters and nonfainters at Tl for each characteristic or test showed that any group differences could be ascribed to random variation (Table 4-29). However, the small number of fainters limits the power of the analyses. Even so, a visual inspection of the data shows no obvious differences between the two groups that could help explain the lack of initial

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130 Table 4-29 Comparison of Subject Characteristics, Aerobic Capacity, Strength, and Body Composition of Nonfainters (n. = 24) vs. Fainters (n. = 4) Prior to Exercise Training. Age (yrs) Height (cm) Weight (kg) Strength Leg press (kg) Biceps curl (kg) Triceps extension (kg) Lumbar extension (Nm) Body Composition Sum of 7 skinfolds (mm) Lean mass (kg) Lower body lean mass (kg) Values are mean S.D. Nonfainters 69.5 5.6 164 6 9.1 67.8 15.5 23.0 4.4 155.8 103 9 44.8 21.9 34.6 14.8 936 521 168.3 61.4 41 1 11.4 14.1 3.8 Fainters 70.3 6 5 168 4 11 7 75.3 7.6 23.0 7 2 175.0 75 2 47.5 17.7 40 0 12.7 954 197 0 .2 44.3 8 5 15.5 3.8 0.82 0 47 0.31 0 97 0 62 0 82 0.49 0 98 0.41 0.59 0.48 tolerance of the fainters for the tilt test. Differences between the two groups in age, height, and weight were not striking Initial aerobic power measurements of the two groups were nearly identical. Fainters were somewhat stronger than nonfainters, particularly in the LP In body composition measures, fainters had greater lean mass than nonfainters ; however, when lean mass and lower body lean mass were calculated as a percentage of total mass and lower body mass, respectively, the groups were nearly equal Lean mass as a percentage of total mass was 63.7% and 61.3 % for nonfainters and fainters respectively, while lower body lean mass as a percentage of lower body mass was 60.4% an 59 9% for nonfainters and fainters, respectively. Although it appeared that fainters tended to have a

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131 larger I.7 skinfold measurement, these data were somewhat skewed since one subject in the fainters group had one of the largest measurements. Measurements of blood volume variables and hormone concentrations at rest and in response to tilt are listed for nonfainters and fainters in Table 4-30. Sample size for the nonfainters is n = 18 for plasma and blood volume and n = 27 for hormone analyses. Blood volume was measured successfully in only two of the fainters, while hormone concentrations were measured in three of the fainters Although statistical comparisons between the two groups were made, the small sample size for the fainters limits the power of the analyses. Therefore, primarily qualitative observations will be made Fainters appeared to have a slightly higher PV than nonfainters at Tl but a greater decline during tilt (720 ml, 24.6% vs. 564 ml, 20.8%). This is despite the fact that the fainters were tilted for a shorter time interval than the nonfainters. Both groups had smaller absolute and relative declines at T3 : 642 ml, 20.0% for fainters and 525 ml 18.4% for nonfainters. Fainters had larger relative increases in ALDO during tilt: at Tl, ALDO increased 94.5% in the fainters while the increase in nonfainters was 20.4%. This disparity remained at T3, when all of the fainters were able to complete the tilt portion of the test. Fainters had a greater baseline PROT concentration at Tl; however, while the PROT concentration of the fainters decreased 4.4% from Tl to T3, that of the nonfainters increased by 4.9%. A striking difference between the two groups was in the A VP and ACTH responses to tilt (Figure 4-10). Nonfainters had a 56% increase in AVP as a result of tilt. Fainters, on the other hand, had a 1526% increase despite a shorter tilt interval. After 6 months of training, fainters still had a large relative increase in AVP (1258%), although the absolute resting and tilt

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132 Table 4-30. Comparison of Blood Volume and Hormone Responses of Nonfainters (n. = 24) vs. Fainters (!! = 4) to 70 Head-up Tilt Before and After 6 Months of Exercise Training. Pre-training Post-training Rest Tilt Rest Tilt PV (ml) Nonfainters (n = 18) 2715 668 2151 491 2853 867 2328 821 Fainters (n = 2) 2928 339 2208 182 3202 687 2560 528 BV (ml) Nonfainters (n = 18) 4130 1077 3647 4394 1399 4027 1423 Fainters (n. = 2) 3994 215 3657 430 4746 1076 4421 1116 RCV (ml) Nonfainters (n = 18) 1415 429 1496 415 1541 550 1699 634 Fainters (n = 2) 1466 1449 247 1544 389 1861 588 ACTH (pgml-1) Nonfainters (n = 27) 50.2 .0 52.8 .0 57.0 .7 61.0 38 2 Fainters (n = 3) 51.8 18.3 183.4 173.1 49.1 .8 148.4 149.5 ALDO (pgml-1) Nonfainters (n = 27) 57.3 30.2 69.0 38.8 59.3 .5 70.5 53.6 Fainters (n = 3) 43.7 5.3 85.0 25.6 51.9 42.9 97 0 22.9 AVP (pgml-1) Nonfainters (n = 27) 2.5 2.8 3.9 3.8 1.7 1.4 2.2 2.6 Fainters (n = 3) 3.9 .7 63.4.0 1.2 0.4 16.3 11.4 K+ (mEqL-1) Nonfainters (n = 17) 4 1 .3 4.3 0.3 4.2 .4 4.4 0 3 Fainters (n. = 3) 4.1 0.2 4.3 0.2 4.1 0.2 4.5 0.2 Na+ (mEqL-1) Nonfainters (n = 27) 140.4 2.0 140.7 2.9 141.1 3 2 141.5 2.8 Fainters (n = 3) 141.2 0.3 140.8 0.6 141.2 0.4 142.6 1.3 PROT (mgdl-1) Nonfainters (n = 27) 8.2 0 7 9.0 0.7 8 6 0.4 9.5 0.5 Fainters (n = 3) 9.1 .4 9.9 0.6 8 7 0 3 9.9 0.5 NE (pgml-1) Nonfainters (n = 26) 498 178 747 368 136 683 212 Fainters (n_ = 3) 658 858 520 469 187 918 417

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Table 4-30--continued. Pre-training Rest Tilt EPI (pgml-1) Nonfainters (n = 26) 24.3 50.6 Fainters (n = 3) 28.0 48.5 14.1 31.2 140.3 27.0 Values are mean S.D. 133 Post-training Rest Tilt 7.0 17.5 17.3 30.0 21.2 35.5 21.0 36.4 PV = Plasma Volume; BV = Blood volume; RCV = Red cell volume; ACTH= Adrenocorticotropic hormone; ALDO= Aldosterone; AVP = Vasopressin, K+ = Potassium; Na+= Sodium; PROT = Protein; NE= Norepinephrine; EPI = Epinephrine. concentrations declined substantially. Similarly, fainters had larger increases in ACTH than nonfainters during tilt at Tl (11 < 0.01) and T3 (I1 < 0 01). At Tl, the correlations between the percentage change in HR during tilt and the percentage change in ACTH and AVP were -0.88 (I1 = 0.31) and -0.93 (I1 = 0 23), respectively. Similarly, the correlations between the percentage change in SBP during tilt and the percentage change in ACTH and A VP were -1.0 (11 = 0.06) and -1.0 (I1 = 0.02), respectively. Another difference between the fainters and the nonfainters was in the EPI response to tilt. Fainters increased EPI during tilt at Tl by 401 % (12 = 0 09) while the change in EPI secretion in the nonfainters could be ascribed to random variation (12 = 0 36). The EPI response of fainters during tilt was decreased at T3 (J2 = 0.06)

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a) 80 60 ..!. s ge40 '-" < 20 0 b) 200 ,_ 160 ..... I ...... 120 00 0.. '-" i5 80 40 0 Preti! t Tilt Pretilt Tilt _._ Fainters, Tl (n=3) --0Fainters, T3 (n=3) _._ Nonfainters, Tl (n=27) --9Nonfainters, T3 (n=27) _._ Fainters, Tl (n=3) --0Fainters, T3 (n=3) _._ Nonfainters, Tl (n=27) --9Nonfainters, T3 (n=27) Figure 4-10. Hormonal responses of fainters and nonfainters to supine rest (pretilt) and 70 head-up tilt before (Tl) and after (T3) 6 months of exercise training: a) vasopressin (AVP); b) adrenocorticotropic hormone (ACTH). Responses to the Cough Test Analyses to Average Data 134 The overall responses to the cough test (averaged over tests and groups) were calculated and are shown in Table 4-31. In order to determine whether the values from the three cough trials conducted during both supine rest and during tilt could be combined to yield representative values for

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135 supine and tilt, a repeated measures ANOV A was performed. The probability of a type I error in detecting a time effect among the three cough trials during both rest and tilt is listed in Table 4-32 Where the type I error probabilities were high, it was concluded that any differences among the three trials were due to random variation. Table 4-31. Overall Responses to Three Supine and Three Tilt Cough Trials Values Averaged Over Tests and Groups (n = 24) Supine 1 2 3 Mean Tilt 1 2 3 Mean Rest R-R (sec) 0.96 0 14 0.95 0.13 0.96 0.14 0 96 0.14 0.83 0.15 0 81 0.14 0.81 0 15 0.82 0.14 Values are mean S.D. Min R-R (sec) 0.78 0.11 0.79 0 11 0.81 0.11 0 79 0 11 0 70 0 12 0 70 0 14 0.70 0.12 0 70 0.12 R-R (Rest Min ) (sec) 0.18 0 08 0.15 0.05 0 15 0 07 0 16 0.07 0 13 0.06 0 10 0 05 0.11 0 06 0.11 0.05 Time to Min R-R (sec) 3 33 1.53 3.43 1.82 3.13 1.54 3.13 1.26 4.64 27 5 11 7.02 4 03 2.30 4.15 1.61 Interval of Min R-R 4.15 1.73 4.11 2 14 3 79 1.93 3 83 1 46 6.40 3 07 5 15 1.96 5 79 3.40 5 80 2.24 Several of the tests, however, produced low typ e I error rates An inspection of the raw data showed that the detected differences were usually small and physiologically not important. For example, the difference among the three supine resting R-R intervals was 0.01 seconds. The difference in the HRs calculated from these intervals was 0.7 bmin-1. The difference between the highest and lowest resting R-R during tilt was 0 02 seconds, resulting in a HR difference of 1.8 bmin1 The minimum R-R interval values during

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136 Table 4-32. Analyses to Average Cough Data: Type I Error Rates for Detecting a Difference Among the Three Cough Trials for Supine and Tilt Cough Tests (n = 24). Supine Tilt Rest R-R 0 08 <0.01 Min. R-R .1 R-R <0.01 0.53 (Rest Min.) 0.41 0.05 Time to Min R-R 0.45 0.41 Interval of Min. R-R <0.01 <0.01 supine rest ranged from 0 78 to 0 81 seconds, which resulted in a HR difference of 2.8 bmin 1. The .1 R-R during tilt ranged from 0 10 to 0.13 seconds When the HRs for the respective resting and minimum R-R values were calculated and the HR difference calculated, the values varied from 11.6 to 13.4 bmin-1 (range = 1.8 bmin-1). Both supine and tilt cough trials resulted in a low probability of a type I error in detecting a time effect for the variable "interval of minimum R-R". This represents the interval after the cessation of coughing during which the minimum R-R interval occurred. Due to the method of measuring this variable, the accuracy of measurement was at best within 1 interval. The difference between the largest and smallest intervals for the supine trials was 0 36 intervals, while the difference for the tilt trials was 1.25 intervals. This latter value would calculate to a difference of approximately 1 second. Therefore, because of the relatively minor differences among trials for the five major cough test variables, the values for the supine and tilt trials were each averaged to yield a single representative value. These values are shown in Table 4-33.

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137 Table 4-33 Mean Supine and Tilt Cough Variable Values for Control, Treadmill, and Treadmill/Resistance Training Groups Averaged Over Three Supine and Three 70 Head-up Tilt Cough Trials Before (Tl) and After (T3) 6 Months of Training (n = 24). Control (n = 6) Tl Supine T3 Supine Tl Tilt T3 Tilt Treadmill (n = 9) Tl Supine T3 Supine Tl Tilt T3 Tilt Rest R-R (sec) 0.98.11 1.00.09 0.84.11 0 83.11 0.84 12 0.92.10 0 74.10 0.79.11 Treadmill/Resistance (n = 9) Tl Supine 1 00 18 T3 Supine 1 02 18 Tl Tilt 0 84.20 T3 Tilt 0.87 21 Values are mean S D. Anal}'.:ses of Cough Res12onses Min R-R (sec) 0.81 13 0.83 10 0 71.12 0 72.08 0 71 09 0.77.09 0 64.08 0.69.08 0.82.16 0 83 13 0 71.17 0 76.18 R-R Time to (Rest-Min) Min R-R (sec) (sec) 0 18 06 3 27 67 0.16 08 3 76.49 0 13 04 3.61.13 0.11 05 4.16.48 0.14 05 2.52.44 0 15 06 2.95.71 0.10 04 3 17.38 0.10.05 4.16.96 0.18.10 2.57.82 0 19 10 3 99 33 0.13 08 4.06.73 0 11 06 5 68.40 Interval of Min R-R 4 1.6 4.3.5 5.3 5 5.6 2 3.5.9 3 8.4 4.9. 1 6.0.9 3.1.0 4.5.5 5.5 2 7 5 6 The results of the ANOV A performed to assess group differences in initial values indicated a large type I error rate for the supine values of minimum R-R (~ = 0 32), R-R (~ = 0.13), time to minimum R-R = 0.25), and interval of minimum R-R = 0.27) Large type I error rates were also generated for the tilt values of resting R-R = 0.29), minimum R-R = 0.41) R-R = 0.48) time to minimum R-R (~ = 0.45), and interval of minimum R R = 0.83). Thus any differences in these two variables at the start of the

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138 training program were due to random variation. However, the probability of a type I error for the supine resting R-R analysis was small (12. = 0.04). Post hoc analysis using Duncan's multiple range test indicated that TREAD/RESIST had a higher mean resting R-R (lower HR) than TREAD at the start of the program. When gender was used as a covariate in the Tl analysis, the resulting high p-value (12. = 0.30) indicated that once gender was accounted for any difference among groups was due to random variation. The effect of training on all cough variables was therefore analyzed with an ANCOV A design using the Tl measure as the covariate. The ANCOV A results indicated that the changes with training for all cough variables could be ascribed to random variation Type I error rates generated in the analyses for supine variables are as follows: resting R-R, 12. = 0.26; minimum R-R, 12. = 0.71; R-R, 12. = 0.76; time to minimum R-R, 12. = 0.64; and interval of minimum R-R, 12. = 0.79. Type I error rates generated in the analyses for tilt variables are as follows: resting R-R, 12. = 0.42; minimum R-R, 12. = 0.66; R-R, 12. = 0.52; time to minimum R-R, 12. = 0.55; and interval of minimum R-R, 12. = 0.62. Inspection of the raw data (Table 4-33) shows that TREAD increased supine resting R-R by 0 09 seconds (10 5%). This calculates to a 6.6 bmin1 decrease in the supine resting HR, from 69.8 to 63 2 bmin1 Increases in supine resting R-R for TREAD/RESIST and CONT were 3 0% and 1.0%, respectively. Increases exhibited by TREAD, TREAD/RESIST, and CONT in the minimum supine R-R were 8.1 % (0.06 seconds, 6.1 bmin1 decrease), 1.2% (0.01 seconds, 0.9 bmin1 decrease) and 1.2% (0.01 seconds, 0 9 bmin-1 decrease), respectively. Increases in resting and minimum R-R during tilt for TREAD were 0.05 seconds (6.8%, 5.2 bmin1 decrease) and 0.04 (6.3%, 5.6 bmin1 decrease)

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139 seconds, respectively. There was a small increase in resting R-R during tilt for TREAD/RESIST (0.03 seconds, 3.6%, 1.4 bmin1 decrease) but a somewhat larger increase for the minimum R-R (0.05 seconds, 7.0%, 5.6 bmin1 decrease) The control group had small increases in both resting and minimum R-R during tilt: 0 02 seconds (2.5%, 1.8 bmin 1 decrease) and 0.1 seconds (1.4%, 1.2 bmin1 decrease), respectively Because training did not affect resting R-R, minimum R-R, L1 R-R, time to minimum R-R and interval of minimum R-R, analysis of the effect of tilt on these variables was performed in a repeated measures analysis using mean values averaged over tests and groups. Results indicated that tilt resulted in a decrease in resting R-R (i:2 < 0.01), minimum R-R (I2 < 0.01), and L1 R-R (I2 < 0.01), while time to minimum R-R (I2 < 0 01) and interval of minimum R-R (12. < 0 01) increased It must be noted, however, that that the decrease in the L1 R-R with tilt is due entirely to the decrease in the resting R-R, since a given L1R-R at a lower baseline translates to a greater change in HR. The average change in supine HR from resting to minimum was 13.4 bmin1 while the average change in tilt HR from resting to minimum was 12.5 bmin 1 In addition, the higher interval of minimum R-R during tilt is due partially to the faster HR. A summary of the effect of tilt and exercise training on the responses to the cough test is presented in Table 4-34

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140 Table 4-34. Summary of the Effect of Tilt and Training on the Responses to the Cough Test. Variable Response to Tilt Resting R-R ,!, Minimum R-R ,!, .1 R-R ,!, Time to Minimum R-R t Interval of Minimum R-R t ,!, = p $ 0.05, decrease in response as a result of tilt t = p $ 0.05, increase in response as a result of tilt Response to Training = p $ 0.05, no change in response after 6 months of exercise training Analyses of Beat by Beat Data R-R intervals were recorded for one minute after the cessation of cough; a maximum of 40 post-cough beats were measured. R-R interval measurements were converted to HR measurements using the formula HR= 60/R-R. Due to the large number of variables (40 beats/position, 2 positions/test [supine, tilt], and 2 tests [T1,T3]), multivariate analyses could not be performed. Therefore, every group of five beats was averaged to provide a representative value; these values are shown in Table 4-35. A repeated measures analysis comparing each of these averaged values to the resting value was performed for each group and test. This analysis was designed to indicate the recovery to resting heart rate levels after coughing. The results are indicated in Table 4-35 and illustrated in Figures 4-11 through 4-13 The inconsistent results from CONT are most likely due to the

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141 Table 4-35 Heart Rate Values Averaged Every Five Beats for 40 Beats Post Cough for Control, Treadmill, and Treadmill/Resistance Groups for Supine and 70 Head-up Tilt Cough Tests Before (Tl) and After (T3) 6 Months of Training (n = 24). Tl T3 Group/Beats Supine Tilt Supine Tilt Control (n = 6) Rest 61.2 6.2 71.4 8.2 60.1 0 72.3 5 1-5 74 1.2* 84 0.3* 70.1 0* 80 9.4* 6-10 71.3.9* 84.0.7* 66.9 7* 81.3 1 11-15 65.8.5 80.7.7* 64.2 1* 78.2.2* 16-20 63 1 9 2 77 0 6 62 8 2* 74 8.1* 21-25 62.0 7.5 75.2 1 62.0 5 74 1.3 26-30 61.6 7.8 74.9.4 61.8.4 74.3.8 31-35 62 6 7.4 74.5.3 61.0 1 74.4.3 36-40 61.9 7.1 73 6.5 60 7 5 74.5.0 Treadmill (n = 9) Rest 71 4 8.9 81.1 9 7 65.2.4 75.9 9 2 1-5 83.8 0* 92.7.4* 76 0.1* 85.3 9* 6-10 80.4.8* 92.6.6* 72.5.8* 86 0 2* 11-15 74.5.7* 89.1 2* 68.1.4* 83 7.3* 16-20 73.0.4 85.9.7* 65.2 5 79 7.6* 21-25 72.3.4 84.6 4 66.2 8 78.0 1 26-30 72 2.8 84.0.3 65.9.8 78 6.9 31-35 71.6.5 84.8.3 66 1.4 78.6.8 36-40 71.6.2 84.4 3 66 1 0 78 9.8 Treadmill/Resistance (n = 9) Rest 60.2 9.2 71.4.7 58.8 8 8 69 0.4 1-5 73.3.9* 83.8 5* 71.0 8* 78 6.8* 6-10 70.9.6* 85.4 2* 69.6.7* 79.2.5* 11-15 67.3.6* 82.4.9* 64 3.2* 76 8.3* 16-20 65.2 9* 78 1.0* 61.9 6* 73.6 6 21-25 64.0 2* 76.4.5 61.2.1 73.4.7 26-30 62.2 9.5 76.6.5 60.9.8 72.9.7 31-35 62 4 9.8 76 5.5 60.8 5 73 8 7 36-40 61.2 1 76.1.1 60.5 1 73.5 2 Values are mean S.D. n. 0.05, greater than rest

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142 100 * t 80 ,....._ ,....., I 60 i::: ..... s __._ Tl supine ,.0 .._, 40 ---0T3 supine :r: 20 _._ Tl tilt ----0.T3 tilt 0 15 20 25 Beats Post-Cough Figure 4-11. Heart rate (HR) response to cough test in supine and 70 head-up tilt positions by control group before (Tl) and after (T3) 6 month training protocol. Data points represent the average HR calculated every 5 beats after cessation of coughing. (R = Rest, n = 6) 12.::; 0 05, greater than rest in all tests t 12. ::; 0.05, greater than rest for T3 supine, Tl tilt, and T3 tilt tests 12. ::; 0.05, greater than rest for T3 supine and T3 tilt tests variability at Tl. However, the results for TREAD are similar for Tl and T3 and show that recovery to resting HR was achieved by beat 16-20 in the supine position and by beat 21-25 in the 70 head-up tilt position. The results for TREAD/RESIST are somewhat different in that they show a faster recovery in the 70 head-up position at both Tl and T3 In addition, recovery is faster by approximately five beats in both the supine and tilt positions at T3. A 4 X 3 (test X group) repeated measures analysis was performed at each time point; the four tests were Tl supine, Tl tilt, T3 supine, and T3 tilt. Results are presented in Table 4-36. The high error rates for a test X group interaction at all points indicates that the relationship among the HR values for supine and tilt cough tests at Tl and T3 was similar for all groups The low

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100 80 60 s 8 40 20 0 R 5 10 15 20 25 Beats Post-Cough _._ T1 supine ---0T3 supine -11T1 tilt -0T3 tilt 30 35 143 40 Figure 4-12. Heart rate (HR) response to cough test in supine and 70 head-up tilt positions by treadmill exercise group before (Tl) and after (T3) 6 month training protocol. Data points represent the average HR calculated every 5 beats after cessation of coughing. (R = Rest, n = 9) 12 $ 0.05, greater than rest in all tests t 12 $ 0.05, greater than rest in Tl tilt and T3 tilt tests type I error rates at all points in the "Supine Tl to Tilt Tl" and "Supine T3 to Tilt T3" columns indicates that the HR at each point during the tilt cough test was greater than the HR during the respective supine cough test (Table 4-37) In the comparison of the supine Tl and supine T3 tests and of the tilt Tl and tilt T3 tests, the low type I error rates through beats 16-20 indicate that the initial response to cough was greater at Tl than T3 (Table 4-37) for both the supine and tilt cough tests. With the exception of the supine HR value at beats 31-35, the HR responses between the two tests (Tl and T3) were similar for both the supine and cough tests after beat 20.

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144 Table 4-36 Probabilities for Type I Error for Detecting a Difference in Heart Rate Values at Each Time Point Post-Cough During Supine and 70 Head-up Tilt Cough Tests Before (Tl) and After (T3) 6 months of Exercise Training (n = 24). Test Time* Supine Tl Supine T3 Supine Tl Tilt Tl X to to to to Group* Tilt Tlt Tilt T3t Supine T3t Tilt T3t Rest 0.48 <0 01 <0 01 <0 01 0.02 0 07 Beat 0-5 0.55 <0 01 <0.01 <0 01 <0.01 <0.01 6-10 0 46 <0.01 <0.01 <0 01 0.02 0 01 11-15 0.90 <0.01 <0 01 <0 01 0.07 0 04 16-20 0.70 <0 01 <0 01 <0.01 0 05 0 06 21-25 0.87 <0 01 <0 01 <0 01 0 11 0 12 26-30 0 77 <0.01 <0.01 <0.01 0 11 0 11 31-35 0.93 <0 01 <0.01 <0 01 0 05 0 10 36-40 0.66 <0 01 <0 01 <0 01 0 15 0.24 Wilks' Lambda t Single-degree-of-freedom contrast, analysis of mean difference Table 4-37 Heart Rate Response to Supine and 70 Head-up Tilt Cough Tests Before (Tl) and After (T3) 6 Months of Exercise Training, Values Averaged Over Groups for Every Five Beats for 40 Beats Post-Cough (n = 24). Rest Beat 0-5 6-10 11-15 16-20 21-25 26-30 31-35 36-40 Supine Tl 66.0.4 77 5.4 74.6 0 69.6.3 67 6 3 66.6.9 65.8.7 65.9.4 65.3.1 Values are mean S D Tilt Tl 77 1.4 87 2.2 87.8.8 84.5 2 80.7.0 79 2.8 79 0 3 79.1 7 78 6 4 Supine T3 62.5.2 72 7 2 70.0.4 65.7 0 63 4 5 63 3 0 63 0 7 62.8 9 62 7 3 Tilt T3 74 2.6 81.8.3 82.4 6 79.8.8 76 3.4 75.4 5 75 5 0 75 8.8 75.9.9

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100 80 ,-... ,-< I 60 ::: s ,!:I .....,,, 40 20 0 R 5 10 15 20 25 Beats Post-Cough 145 _._ Tl supine T3supine Tl tilt __Q..._ T3 tilt 30 35 40 Figure 4-13. Heart rate (HR) response to cough test in supine and 70 head-up tilt positions by treadmill/resistance exercise group before (Tl) and after (T3) 6 month training protocol. Data points represent the average HR calculated every 5 beats after cessation of coughing. (R = Rest, n = 9) 12. $ 0.05, greater than rest in all tests t 12. $ 0.05, greater than rest in Tl tilt and T3 supine tests 12. $ 0 05, greater than rest in Tl supine test

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CHAPTERS DISCUSSION AND CONCLUSIONS Introduction This investigation was the first longitudinal study to investigate the effect of exercise training on the cardiovascular and hormonal responses to orthostasis in the elderly. Cross-sectional and longitudinal studies in younger individuals have suggested that either weight training (Shvartz, 1968a, 1969; Smith et al., 1988; Smith & Raven, 1986) or endurance training with a resistive component (Convertino et al., 1984; Greenleaf et al., 1985; Shvartz et al., 1981) could provide better maintenance of blood pressure during an orthostatic challenge The present study used a) uphill treadmill walking and b) uphill treadmill walking in conjunction with selected resistance exercises, to determine if one of these types of programs could positively affect orthostatic responses in men and women over 60 years of age Proposed mechanisms for training-induced adaptations included increased plasma volume, increased muscle mass, increased baroreceptor responsiveness, and altered neuroendocrine responses. Maximal aerobic power was increased by 16 4% and 13 7% in the treadmill (TREAD) and the treadmill plus resistance (TREAD/RESIST) groups, respectively. TREAD /RESIST increased strength in biceps curl and triceps extension by 26% and 30%, respectively This is in agreement with data showing that improvements in aerobic power and strength average 1530% and 25-30%, respectively, in younger individuals (ACSM, 1990; Fleck & 146

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Kramer, 1987) and indicates that older individuals can make comparable relative gains in health and fitness parameters with appropriately designed programs. Exercise Training and Cardiovascular Responses to Head-up Tilt Heart Rate, Stroke Volume, and Cardiac Output 147 Changing from the supine to the upright position translocates approximately 800 ml of blood from the central circulation to the periphery (Blomqvist & Stone, 1983). In response to this venous pooling, central venous pressure, end-diastolic volume and stroke volume (SV) are sequentially reduced; in an attempt to maintain cardiac output (Q), heart rate (HR) increases. In the present study, the immediate HR response was a 5 3 bmin1 (8 3%) increase; HR then increased progressively to 9 7 bmin1 (15 2%) after 15 minutes These data are consistent with studies finding absolute and relative increases of 10 to 15 bmin-1, and 10% to 15%, respectively, in older individuals (Jansen et al., 1989; Kenny et al., 1987; Lee et al., 1966; Lye et al., 1990; Shannon et al., 1991; Vargas et al., 1986) This is less than the 10-30 bmin1 (20-25%) increases seen in younger individuals (Beetham & Buskirk, 1958; Convertino et al., 1984; Jansen et al., 1989; Shannon et al., 1991; Vargas et al., 1986). This decreased cardioacceleration capacity is commonly attributed to a reduction in the responsiveness of the high-pressure baroreflex system with age (Frey & Hoffler, 1988; Gribbin et al., 1971) due to arterial rigidity and a reduction in the afferent baroreflex signal, or to a reduction in efferent HR responsiveness (Lipsitz, 1990) The HR response to tilt was not altered by training: average HR increases at Tl for CONT, TREAD, and TREAD/RESIST were approximately

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148 6, 7, and 8 bmin1 respectively, while the increase at T3 was approximately 8 bmin1 for all groups. These data are in agreement with those of Shvartz (1968a, 1969), who did not see a difference between control and training groups in the HR response to standing or 90 tilt after 7 weeks of endurance or resistance training Convertino et al. (1984), on the other hand, found that 8 days of training (2 hd1 65% V0 2 max) decreased the HR response to 60 head-up tilt by 16 7%, from 24 to 20 bmin1 The percent change in average tilt HR was negatively correlated (r = -0.68) with the percent change in resting PV In the present study, the same inverse relationship between the percent change in resting PV and the percent change in the HR response to tilt existed (r = -0.50; Figure 5-1) 20 ..... ::8 0 10 ..... QJ Cl) s::: 8.. 0 Cl) QJ I-< -10 <] -20 y = 0.0054-0.3182x; r=-0.50, p = o ; 12 -10 0 10 20 30 40 %~ resting plasma volume Figure 5-1 Relationship between the relative change in resting plasma volume and the relative change in the HR response to tilt. In the present study, SV andQ were measured by impedance cardiography While the validity of absolute values measured by impedance has been questioned (Smith, Bush, Wiedmeier, & Tristani, 1970), impedance has been shown to reliably estimate relative changes in SV and Q (Ebert,

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149 Eckberg, Vetrovec, & Cowley, 1984; Gabriel, Atterhog, Oro, & Ekelund, 1976; Kubicek, Karnegis, Patterson, Witsoe, & Mattson, 1966; Smith et al., 1970) To test the reliability of the impedance technique, correlation coefficients between the Tl and the T3 measurements for resting SV and Q for CONT were calculated and were 0.67 (SEE= 8.5 ml, 17.0%) and 0.71 (SEE= 0.44 Lmin-1, 14 5%), respectively The correlations between Tl and T3 for the SV and Q measurements made during the remainder of the tilt test (TILT and REC) were 0 70 (SEE= 8 6 ml, 20 6%) and 0.54 (SEE= 0.50 Lmin1 18 9%), respectively Thus, in the present study, the impedance technique was moderately reliable in estimating SV and Q. An earlier study from our laboratory (Strzepek, 1990) found higher correlations (r = 0 97) and lower standard errors (8 7%) between repeated Q measurements in a sample of young and old subjects. This may be due to the fact that the repeated measurements in the earlier study were taken within 10 minutes while in the present study, they were taken 6 months apart. Stroke volume decreases during tilt in the present study (11.9 to 13 6 ml; 23 8% to 27 1 %) were consistent with the data from Lee et al. (1966) which showed a 25% decrease in SV in 47 to 82 year old men, but were somewhat less than the 30-40% decreases shown by other investigators (Lye et al., 1990; Shannon et al., 1991; Vargas et al., 1986). The 16-20% decrease in Q in the present study was similar to the 11 % to 20% decreases documented for older individuals (Lee et al., 1966; Lye et al., 1990; Shannon et al. 1991; Vargas et al., 1986). Training induced adaptations were found in both the SV and Q responses during tilt, with TREAD showing 15 0% and 9.3% increases, respectively, in the mean test responses At the same time, there was an increase in the magnitude of both the absolute and relative changes from rest

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150 to tilt in both SV and Q TREAD/RESIST, on the other hand, decreased average test Q by 9.8%; the magnitude of the both the absolute and relative change from rest to tilt in SV or Q was unaltered Possible Mechanisms Increases in SV during tilt may be due to increased preload (i.e., plasma volume [PV]) (Convertino et al., 1984; Shvartz et al., 1981) Due to technical difficulties, however, duplicate PV measurements were made in only four subjects in TREAD The correlation between the change in tilt SV (measured at the end of tilt) from Tl to T3 and the change in tilt PV was 0.50; the correlation between changes in resting SV and changes in resting PV from Tl to T3 in TREAD was 0 85. Therefore, increased preload was associated with and augmented SV at rest and during an orthostatic challenge in TREAD. Unexpectedly, TREAD/RESIST had a decrease in the both the resting and average test Q at T3. While PV also increased in this group, it appears that other training-induced adaptations occurred which may have masked the expected relation between hypervolemia and increased SV and Q. In addition to preload, alterations in cardiac contractility and afterload might explain the decrease in SV and Q It is not likely that a decrease in contractility is responsible for the decrease in Q in TREAD/RESIST. Such a negative inotropic effect would be associated with decreased sympathetic stimulation; although resting NE was decreased in the present study, the reduction was not related to group assignment (Table 4-23). In addition, there is no evidence in the literature to suggest that exercise training results in a decrease in contractility Previous studies in the elderly (Schocken et al., 1983) have shown that contractile

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151 function, as measured by left ventricular (L V) ejection fraction and L V end systolic volume, is not changed with training. A change in afterload is also an unlikely explanation for the decrease in 6 in TREAD /RESIST since the statistical analyses showed no test X group interaction for any of the BP responses (Table 4-12) Therefore, it appears that the decrease in Q in TREAD /RESIST is due to factors affecting venous return With venous return and Q compromised, there was an increased reliance on peripheral resistance for the maintenance of BP However, it is unclear from the present data what mechanism, or combination of mechanisms, is responsible for decreased venous return Exercise Training, Resting Plasma Volume and Resting Hormonal Responses Initial BV, normalized for body weight, was 59.5 8 6 mlkg1 for CONT, 68.2 7 6 mlkg-1 for TREAD, and 63.6 8.0 mlkg1 for TREAD /RESIST; this is comparable to the pre-training values of 60-80 ml kg1 found for younger subjects (Convertino et al 1980a; Convertino et al., 1980b; Convertino et al., 1991; Mack, Thompson, Doerr, Nadel, & Convertino, 1991) and indicates that healthy elderly individuals can maintain a relative BV comparable to younger individuals. While some researchers have shown that resting ALDO levels decrease with age (Crane & Harris, 1976; Gregerman & Bierman, 1981; Saruta et al., 1980) and may play a role in decreasing BV with age, others have shown that resting PRA and ALDO levels are similar for young and old subjects (Vargas et al., 1986) Resting ALDO values in the present sample were similar to values quoted for younger individuals (20-100 pgml1 ) (Labhart, 1986) and may be associated with the comparable BV values

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152 The capacity to increase BV with training also appears to be maintained in the healthy elderly individual. In the present sample, the combined training group (TRAIN) increased both PV and BV by 9 5% (256 ml and 392 ml, respectively) while CONT showed a 1.7% decrease (48 ml) in PV and a 1.5% increase (63 ml) in BV. The relative increases in PV and BV in TRAIN are similar to the 9-12% training-induced increases seen in younger individuals (Convertino et al., 1980a Convertino et al., 1980b; Convertino et al., 1991). The increase in BV normalized for body weight (5 7 mlkg1 8 7%) is similar to training induced increases (5 mlkg1 7%) quoted for younger individuals (Convertino, 1991). Increases in PV in TRAIN were associated with increases in total PROT content (+20 6 g; r = 0 99). If 1 g of protein distributes in 14-15 ml of water (Scatchard, Batchelder, & Brown, 1944), the expected increase in PV would be 288-309 ml, which agrees closely with the measured increase of 256 ml. The changes in PROT content in TRAIN are similar to the 28 g training-induced increase noted by Convertino, Brock, Keil, Bernauer, and Greenleaf (1980), and indicate the importance of plasma proteins in facilitating hypervolemia with training by providing an increased water binding capacity Resting levels of A VP, ALDO, and ACTH were not changed with training This result supports the hypothesis that chronic increases in BV reset the stimulus-response relation between BV (and CVP) and hormonal secretion via cardiopulmonary volume-sensitive receptors. While this relationship has been demonstrated in younger males (27 to 44 years; Convertino et al 1991), these are the first data from a longitudinal training study to suggest this mechanism in elderly males and females

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Exercise Training and the Hormonal and Plasma Volume Response to Head-up Tilt 153 In the present study, training did not affect the absolute or relative PV declines during tilt. The PV reductions during tilt at Tl and T3 were 564 ml and 525 ml, respectively, comparable to the preand post-training declines of 544 ml and 479 ml seen by Convertino et al. (1984) in an 8-day training regimen in young men The relative declines were similar at Tl and T3 (20 8 % and 18 4%, respectively) but were greater than the 9-13% decreases during tilt reported by Convertino et al. (1984) and Greenleaf et al (1988). This suggests that elderly individuals undergo a greater challenge during a given orthostatic maneuver than younger individuals While the decreases in PV during tilt for TRAIN were nearly identical at Tl and T3, the PV at the end of tilt at T3 was 269 ml greater than the respective Tl measurement because of PV expansion. Thus, an important functional benefit of an increased PV is an expanded reserve to buffer fluid shifts that take place during orthostatic challenges. Increases in AVP during tilt appear to vary widely (Davies et al., 1976; Huber et al 1988; Lye et al., 1990; Sander-Jensen et al., 1986; Williams et al., 1988) and may be due to interactions among various stimuli, such as lowered central blood volume (CBV) and pressure, increased sympathetic nervous system activity, and/or hyperosmolality, within each individual. This variability was suggested by Rowe et al. (1982) who postulated the existence of responders" and nonresponders" in regard to orthostatic AVP secretion and is reflected in the present data where only 10 of 27 subjects had increases in AVP of greater than 1.0 pgml1 during tilt. This suggests that atrial receptors are not sole controllers of A VP secretion, but require concomitant hypotension (Mohanty et al., 1985).

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154 A training-induced increase in PV would be expected to attenuate the AVP response to tilt because of better maintenance of CBV and pressure. The peak AVP response to head-up tilt in TRAIN decreased 58% from Tl to T3, while the peak response in CONT increased 24%. This is similar to the results reported by Convertino et al. (1984), where training induced a 38% decline in the A VP response to tilt after training, with a concomitant increase in PV of 12%. Responses of Fainters Four subjects were unable to complete the 15 minute tilt duration at Tl due to the onset of presyncopal or syncopal signs and symptoms; all four subjects were able to complete the test at T3. An important consideration when dealing with older individuals who faint or experience presyncopal symptoms during orthostatic maneuvers is whether medications may have contributed to the reaction. While some of the drug regimens of these subjects can cause nausea or fainting (Medical Economics Data, 1992), three of the fainters were under the same medication regimen throughout the study The fourth subject had the medication dosage (a.blocking agent) increased shortly after the Tl test. This suggests a limited effect of medication on the symptoms experienced at Tl. Thus, contributing factors must lie elsewhere. Stroke Volume and Cardiac Output Cardiac output appeared to be lower in the fainters, both at rest and consistently throughout the tilt. The lower resting Q for the fainters cannot be due to a lower PV since normalized PV measurements for fainters and nonfainters (TRAIN) were 41.9 mlkg-1 and 40.6 mlkg-1, respectively. A lower Q, coupled with a similar BV, suggests an impaired venous return

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155 capacity in the fainters. The mechanism for impaired venous return in the present study is unclear. Sather et al. (1986) also noted a lower resting Q and a smaller Q reserve in low tolerant subjects during LBNP. If, as has been hypothesized by Lye et al. (1990), there is a lower minimum limit for SV and Q during orthostasis, then the lower resting Q in the fainters resulted in a smaller Q reserve, which may have contributed to their intolerance. Plasma volume decreases during tilt at Tl were greater for the fainters (720 ml, 24.6%) than for the nonfainters (526 ml, 19.5%) despite a greater TPR and a shorter duration of tilt. The greater and faster decline in PV may be associated with the onset of presyncopal symptoms since Murray, Krog, Carlson, and Bowers (1967) estimated that presyncopal symptoms could be precipitated by losses of greater than 500 ml from the effective circulation. At T3, fainters had a 12.5% (0 32 Lmin1 ) increase in resting Qand an approximate 15% increase in the lowest Q during tilt Nonfainters increased resting Q by only 4 1% (0.13 Lmin1 ) while the Q during tilt was nearly identical. The larger increases in Q by the fainters cannot be accounted for by PV changes, since both groups increased PV by approximately 9.5% The augmented Q in the fainters may have been related to improved venous return and may have contributed to an increased tilt tolerance by helping to maintain cerebral perfusion and mean arterial pressure Blood Pressure In the present study, there were no obvious differences in the resting blood pressures of the fainters and nonfainters. Tilt initially induced larger increases in SBP, DBP and MAP in the fainters although the MAP increases (7-8 mmHg) were within the range defined as normal by Frohlich, Tarazi,

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Ulrych, Dustan, and Page (1967). Since the Q was lower in fainters, this suggests a greater reliance on TPR for MAP regulation. 156 It has been postulated that orthostatic intolerance in the elderly is inversely related to elevated supine SBP, and may be related more to decreases in SV or to impaired vasoconstriction than to impaired cardioacceleration (Lipsitz, Storch, Minaker, & Rowe, 1985; Smith & Fasler 1983; Williams, Caird, & Lennox, 1985) The present data do not support the hypothesis that orthostatic intolerance in the elderly is related to impaired vasoconstriction and inversely related to supine SBP. Only male A had a resting SBP > 140 mmHg and a decline in TPR during tilt; this is probably related to a-blockade medication. The other three fainters had supine SBP ranging from 100 to 125 mmHg and increases in TPR during tilt that were proportionally greater than those of the nonfainters. Hormonal Responses A higher A VP and ACTH response to tilt or LBNP protocols is a common finding in subjects who become intolerant (Davies et al., 1976; Greenleaf et al., 1988; Harrison et al., 1985; Harrison et al., 1986; Huber et al., 1988; Lee et al., 1966; Norsk et al., 1986; Sander-Jensen et al., 1986) The present data for fainters at Tl are in accord with this finding. Vasopressin secretion is stimulated by hypotension (Share, 1976); thus the heightened response in subjects who experience failure of blood pressure control mechanisms Fainters in the present study had greater and more rapid absolute and relative decreases in PV during tilt at Tl; this may also have augmented the A VP response The mechanism for the large increases in A VP and ACTH in the fainters appears to be related to hypotension and the stimulation of

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157 cardiopulmonary receptors. The primary defense against hypotension in the upright position involves the neural control of peripheral resistance Fainters in the present study had higher resting and orthostatic TPR responses. The higher resting response may be related to a decreased TPR reserve during orthostasis and may prompt failure of this system sooner than experienced in nonfainters. As this defense begins to fail, venous return and left ventricular end-diastolic volume drop, precipitating activation of ventricular stretch receptors. The stimulation of the cardiopulmonary receptors increases AVP secretion and a secondary line of defense is activated whereby there is an attempt to maintain blood pressure and peripheral resistance via hormonal secretion. Adrenocorticotropic hormone is also stimulated via cardiopulmonary receptors. This relationship between hypotension and increased hormonal secretion is supported by the data which show that correlations between the relative change in HR and the relative changes in ACTH and A VP during tilt for the fainters at Tl were -0 88 and -0.93, respectively, while the relation between the relative change in SBP and the relative changes in ACTH and AVP were -1.0 and-1.0, respectively. Responses to Cough Test The HR response to cough is a simple, noninvasive test used to assess the integrity of the reflex arc responsible for cardiac acceleration. Coughing produces increases in intrathoracic pressure ranging between 50 and 250 Torr, and decreases in pulse pressures (Sharpey-Schafer, 1953); the magnitude of the intrathoracic pressure change has been shown to be unrelated to the extent of cardioacceleration (Wei & Harris, 1982). On cessation of cough, there is a decrease in arterial and pulse pressures, and an increase in vasodilation which is associated with increases in right intracardiac pressures. Cardiac

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acceleration is thought to be a baroreceptor-mediated response to this hypotension (Wei & Harris, 1982; Sharpey-Schafer, 1953) 158 To evaluate the reliability of the cough test, correlat i on coefficients between the Tl and T3 measurements for CONT were calculated and were as follows : resting R-R, r = 0.80 (SEE= 0.08, 8.6%); minimum R-R r = 0.69 (SEE = 0 09, 11.4%); I). R-R, r = 0 55 (SEE= 0.06, 37.5%) Thus, the cough test showed a moderately reliable estimate of resting and minumum R-R measurement in this study. However, the data from TREAD and TREAD /RESIST indicate that there was no change in these parameters in response to cough as a result of training, suggesting that neither endurance nor endurance plus resistance training changes baroreceptor responsiveness in the elderly. This may be due either to age-related decreases in arterial compliance which attenuate afferent baroreceptor signals (Lipsitz, 1990), or to decreases in efferent HR responsiveness to hypotensive stimuli (Gribbin et al., 1971) Con cl us ions Twenty-six weeks of training in 60 to 82 year-old men and women produced significant training adaptations, as evidenced by the 16.4% and 13.7% increases in VO2max in TREAD and TREAD /RESIST, respectively. TREAD had small decreases in body weight and skinfold measurements while TREAD /RESIST increased strength in 1-RM BI and TRI testing and increased arm circumference. Endurance training alone produced increases in resting and mean test SV and Qin response to 70 head-up tilt. These adaptations may be related to an increased plasma volume and an augmented venous return Endurance plus resistance training decreased Q at rest and in response to 70 head-up tilt and may be related to reduced venous return Intolerance to tilt at Tl in four

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159 subjects was associated with a lower resting and tilt-induced Q, and greater AVP and ACTH secretion. Improved tolerance for the tilt test in these subjects appeared to be related to increases in SV and Q at rest and during tilt. Resting plasma volume was increased by training in the elderly but was not associated with changes in resting hormonal levels. This suggests a change in the stimulus-response relationship between BV and the hormone secretion mediated by volume-sensitive receptors The hormonal response to tilt was unchanged by training except for a decrease in the A VP response at T3; this may be related to increases in central blood volume Directions for Future Research While the finding of an increase in SV and Q in TREAD was not surprising, the finding of a reduced Qin TREAD/RESIST was unexpected Therefore, further research on the effect of strength training on cardiac parameters in the elderly is needed. This is particularly true considering the recent inclusion of resistance training in the ACSM s guidelines (1990) for the development and maintenance of fitness in healthy adults In addition, the recent increase i n interest in moderateto highintensity resistance training for older adults (Fiatarone et al., 1990; Frontera et al., 1988; Kauffman, 1985) presents an ideal opportunity for study The effect of resistance training on the cardiac parameters in different subgroups of the elderly (e g., hypertensive vs. healthy) also deserves study The four subjects who experienced pre-syncopal and syncopal symptoms during the tilt test prior to training were all able to complete the tilt test without symptoms after 6 months of training. The improved responses appeared related to increases in SV and Q An important avenue therefore, for future research is to study the training-induced cardiac,

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hormonal, and plasma volume adaptations in a larger group of orthostatically intolerant subjects. 160 This was the first longitudinal study to investigate the cardiovascular and hormonal responses to orthostasis in the elderly before and after exercise training. It was not possible to investigate all mechanisms potentially affecting the responses. Other areas for future investigation include a) measurement of central venous pressure and forearm vascular resistance to complement measurements of PV and hormonal responses to orthostasis and training, and to determine the influence of training on cardiopulmonary baroreflex control of vascular resistance in the elderly; b) inclusion of both young and elderly individuals in a longitudinal exercise training study to more fully identify the effect of aging on cardiovascular and hormonal adaptations to orthostasis. Investigation of these areas in different subgroups in the elderly (e.g., healthy elderly, hypertensives, elderly with orthostatic hypotension; elderly taking ~-blockers) is also important.

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APPENDIX A DEMOGRAPHIC, MEDICAL AND ACTIVITY QUESTIONNAIRES

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CENTER FOR EXERCISE SCIENCE UNIVERSITY OF FLORIDA, GAINESVILLE, FLORIDA 32611 392-9575 DEOMGRAPHIC INFORMATION NAME DATE __ / __ / __ Last First MI Month Day Year AGE DATE OF BIRTH __ / __ / __ Month Day Year SOCIAL SECURITY # -PHONE ____ HEIGHT _in ___ cm WEIGHT lb --___ kg RESIDENCE ____________________ City REFERRING PHYSICIAN Street State ZIP Country SURGEON (if applicable) _______________ HOME PHYSICIAN (if different from referring M.D.) _______ ADDRESS City Sex Male Female Race White Black Asian __ Hispanic Other: Street State --------162 ZIP Country

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Marital Status __ Single Married __ Divorced or separated Widowed Religion (optional) Catholic Protestant __ Jewish __ Jehovah Witness Education Completed __ 1-8 years __ 9-12 years __ 13-16 years __ 17-18 years __ more than 18 years Occupation (list) Present work status __ Working full time __ Working part time # years ____ # years ____ # years ____ Hindu Muslim None Other: __ High school graduate __ Bachelor's degree __ Master's degree __ Doctoral degree __ Not employed Reason: __ Medical Retired Other Indicate your family income before taxes (U.S. dollar equivalent) __ less than $10,000 $10,000 $25,000 $25,000 $50,000 more than $50,000 STATEMENT OF CONFIDENTIALITY 163 I understand that information contained on this questionnaire is regarded as confidential, and will not be released without my prior written permission. The information will not be used for the setting of fees The Center for Exercise Science may, however, use the information for statistical and other research purposes. Signature Date

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CENTER FOR EXERCISE SCIENCE UNIVERSITY OF FLORIDA, GAINESVILLE, FLORIDA 32611 392-9575 CARDIOVASCULAR HISTORY 164 NAME ID# DATE Answer the following questions, indicating the month and year of the event or diagnosis where appropriate. 1. 2. 3. 4 5. 6 7 8. 9. Has a doctor ever told you that you have heart disease? Have you ever had a heart attack? Have you ever had chest pain? Have you ever had cardiac catheterization? Have you ever had balloon angioplasty? Have you had coronary artery bypass graft surgery? If yes, list date and number of grafts: _/_ #grafts:_ 1 2 Mo Yr. Have you ever had a stroke? Do you have hypertension (high blood pressure)? 3 Yes No Month/Year 4+ --__ / __ __ / __ __ / __ __ / __ __ / __ I I If yes, how long have you had hypertension? less than 1 year 1-5 years 6-10 years more than 10 years Do you have diabetes mellitus? --I

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165 Yes No Month/Year 10. Do you take insulin for diabetes? --If yes, how long have you taken insulin? less than 1 year 1-5 years 6-10 years more than 10 years 11. Do you take oral hypoglycemics for diabetes? 12 Do you have a cardiac pacemaker? If yes, how long have you had a cardiac pacemaker? less than 1 year 1-5 years 6-10 years more than 10 years 13. Have you had a carotid endarterectomy? --I 14. Has your doctor ever told you that you have a heart valve problem? --I 15 Have you had heart valve replacement surgery? --I If yes, what heart valves were replaced? mitral aortic 16 Have you had cardiomyopathy? I 17 Have you had a heart aneurysm? I 18 Have you had heart failure? I 19. Have you ever suffered cardiac arrest? I

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20. OTHER MEDICAL PROBLEMS: Indicate if you have had any of the following medical problems: Past Now Alcoholism Allergies Anemia Arthritis Asthma Back injury or problem Blood clots Bronchitis Cirrhosis Claudication Elbow or shoulder problems Emotional disorder Eye problems Gall bladder disease Glaucoma Gout Headaches Hemorrhoids Hernia Hip, knee, or ankle problems Intestinal disorders Kidney disease Liver disease Lung disease Mental illness Neurologic disorder OB I GYN problems Obesity/ overweight Phlebitis Prostate trouble Rheumatic fever Seizure disorder Stomach disease Thyroid disease Tumors or cancer List type: ______ Ulcers Other specify: 21. Surgical Procedures: Indicate if you had had any of the following surgeries, and if so, the appropriate date. Adhesion repair Appendectomy Yes No Month/Year __ / __ __ / __ 166

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167 21. Surgical Procedures (continued) Back surgery Yes No Month/Year Bladder surgery Bowel surgery Breast surgery Cataract surgery Gall bladder surgery Hemorrhoid surgery Joint surgery Kidney surgery Lung surgery OB I GYN surgery Prostate surgery Stomach surgery Other specify: __ / __ __ / __ __ / __ __ __ __ / __ __ / __ __ / __ __ / __ __ / __ __ / __ __ / __ __ __ __ / __ __ / __ 22. Medications: Indicate the medicines you currently use on a regular basis. Yes No Allergy medicines/ antihistamines Antacids Antibiotics Anti-arrhythmics Anti-inflammatory agents Aspirin Asthma medicines Beta blockers Birth control pills (# years: --~> Blood pressure medicines Blood thinners Cortisone Diabetes medicines/ insulin Diuretics/"water pills" Gout medicines Heart medicines Hormones/ estrogen Laxatives Nitroglycerin Pain medicines Psychiatric medicines/ anti-depressants Sedatives/ sleeping pills Seizure medicines Thyroid medicines Tranquilizers Vi tam ins/ iron Other specify: ________

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NAME CENTER FOR EXERCISE SCIENCE UNIVERSITY OF FLORIDA, GAINESVILLE, FLORIDA 32611 392-9575 FAMILY HEALTH HISTORY ID# DATE 168 A If any members of you immediate family have or have had any of the following conditions, indicate their age at the time of the event: Father Mother Brother(s) Sister(s) Heart Attack yr yr yr yr Stroke yr yr yr yr Coronary Artery Disease yr yr yr yr If deceased, not age at time of death yr yr yr yr B Indicate if any members of you immediate family have or have had the following conditions by marking the appropriate lines : Father Mother Brother(s) Sister(s) High Blood Pressure yr yr yr yr High Cholesterol yr yr yr yr Diabetes yr yr yr yr Obesity yr yr yr yr

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NAME CENTER FOR EXERCISE SCIENCE UNIVERSITY OF FLORIDA, GAINESVILLE, FLORIDA 32611 392-9575 ACTIVITY ST A TUS ID# DATE 1. Please indicate your usual activities. 169 Frequency per month 1-4 5-8 9-12 13-16 17+ Minutes per session 0-20 20-40 40-60 60+ Badminton Baseball/ softball Boating Bowling Cycling (motor) Cycling (road) Cycling (stationary) Dancing (aerobic) Golf (ride) Gold (walk) Gymnastics Hiking Horseback riding Hunting/fishing Jogging/ running Martial arts Racquetball Handball Rope jumping Rowing, canoeing Sailing Skating Skiing (x-country) Skiing (downhill) Skiing (water) Soccer/ football Swimming Table tennis Tennis Volleyball Walking Weight training Yard work/ gardening Other specify:

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170 2. Does you usual job require sustained physical activity? __ Yes __ No __ Not employed __ Not applicable (retired) 3. How would you rate your physical fitness (endurance)? low medium high 1 2 3 4 5 6 7 4. How would you rate your strength? low medium 1 2 3 4 5 6 high 7

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CENTER FOR EXERCISE SCIENCE UNIVERSITY OF FLORIDA, GAINESVILLE, FLORIDA 32611 392-9575 TOBACCO HISTORY 171 NAME ID# DATE 1. Have you ever used any tobacco product on a regular basis? 2 Yes No IF YES : Continue If NO : Stop here What form(s) of tobacco do/did you regularly use? Past Now # years Cigarettes Cigars Pipe Chewing tobacco Snuff 3 Are you a former smoker? Yes No IF YES: a How long ago did you stop smoking? Less than 6 months -6-12 months --1-2 years __ 3-5 years __ 5-10 years __ more than 10 years b What was your reason for stopping? Doctor s advice -Concern about health --Heart surgery or cardiac event __ Family pressure __ Education program Amount/Day ___ packs ___ cigars pipefuls chaws --___ dips ___ Other specify: ___________

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APPENDIX B INFORMED CONSENT DOCUMENT

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CENTER FOR EXECISE SCIENCE UNIVERSITY OF FLORIDA, GAINESVILLE, FL 326 1 1 392-9575 Informed Consent to Participate in Research You are being i nvited to participate in a research study This form is designed to provide you with information about this study and answer any of your questions 1 TITLE OF RESEARCH STUDY Effects of 6 months of endurance and resistance exercise training on healthy men and women over 60 years of age 2. PRINCIPAL INVESTIGATOR Name: Michael L. Pollock, Ph.D. Telephone Number : 904-392-9575. 3. THE PURPOSE OF THE RESEARCH The purpose of the study is to determine if you as a healthy person between the ages of 70-89 can adapt to endurance and strength exercise training with improvements in cardiovascular function, strength, orthostatic tolerance (ability of blood pressure reflexes to quickly adapt to changes in posture), and body composition (reduction in body fat, increase in bone density and muscle weight). 4. PROCEDURES FOR THIS RESEARCH Visit 1: During your first visit to the Center for Exercise Science, the entire study protocol and the time commitment necessary will be explained An investigator will be available to answer any questions You will also be given a medical history form and a physical activity questionnaire to take home and complete (30 minutes) Visit 2: During your second visit, you will undergo an examination by a physician and have your blood pressure and electrocardiogram (ECG) recorded at rest. A 15 ml venous blood sample will be drawn for screening purposes This is equivalent to approximately 3 teaspoons of blood There will be a nominal fee of $45 75 for this blood chemistry screening. You will then take an exercise test on a treadmill while your ECG and blood pressure are monitored. Every two minutes during this test the exercise will become more difficult, until the physician stops the test because of certain signs or symptoms, or when you are unable to continue 173

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because of fatigue. If you have no cardiovascular or other significant medical abnormalities considered contra-indicative to exercise training, you will be included in the study (2 hours). 174 Visit 3 : Your blood pressure will be measured at rest after 15 minutes of quiet sitting ; you will then stand up and you blood pressure will be measured after 1 minute of quiet standing. You will then be familiarized with some o f the other equipment and procedures used in some of the later testing sessions These include a breathing valve used to collect your expired air (Visit 4), a tilt table test (Visit 5), and strength tests (Visit 6) (2 hours). Visit 4 : This visit includes a test of blood pressure reflex sensitivity and a maximal exercise test. The blood pressure reflex sensitivity test consists of a series of intravenous drug infusions which are designed to either slow or speed up the heart rate. The blood pressure response to this change in heart rate will be recorded. To make the drug infusions easier, a needle will be placed in a forearm vein before the test is begun This needle place ment will be done under sterile conditions and kept open with sterile saline for the duration of the test. This needle will also be used for blood sampling during the exercise test. You will then undergo a second exercise test; it will be similar to the test in Visit 2 except that you will have a rubber mouthpiece in your mouth and a clip on you nose so that your expired air can be collected. This test will be continued until certain signs or symptoms indicate the test should be stopped or you are unable to continue because of fatigue During this test measurements of hormones will be made at rest and at maximal exercise. For this it will be necessary to take two small blood samples of approximately 4 teaspoons each (2 hours). Visit 5 : This visit includes measurement of right heart pressure, plasma volume, and a tilt table test. To make all of the tests easier, a needle will be placed in a forearm vein before the first test is begun This needle placement will be done under sterile conditions and kept open with sterile saline for the duration of the test session This needle will also be used for plasma volume measurement and for blood sampling during the tilt test. For the indirect measure of the pressure in your right heart, a pressure gauge will be attached to the needle in your arm You will simply lie on your right side with your right arm hanging down while the pressure measurement is made. Measurement of plasma volume will also be made during this session. A special non-toxic dye will be injected into the arm opposite the one with the venous catheter (needle) and a blood sample of approximately 1 1 /2 teaspoons will be taken after 10 minutes. You will simply lie on on your back on a table during the test. The tilt test is performed on a special table which can be adjusted to various angles. The tilt test will consist of 30 minutes rest (lying on your back with the tilt table in a level position), 15 minutes of 70 head-up tilt,

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175 and 15 minutes recovery, again lying on your back with the tilt table level. You will have your pulse, blood pressure, cardiac output (amount of blood your heart pumps each minute), stroke volume (amount of blood your heart pumps each beat), and blood flow in the arm and leg made during the entire test. During this test, you will be asked simply to lie quietly and to refrain from conversation except to answer questions from the investigators. A physician will monitor all tests. In the head-up tilt test, some measurements of blood volume change and hormones will also be made. For this, it will be necessary to take two small blood samples, each less than 1/2 teaspoon, and two small blood samples, each about 4 teaspoons. The total amount of blood taken during the test is about 9 teaspoonfuls (2 1 /2 hours). Visit 6: Your resting blood pressure will again be measured as in Visit 3. Then your body fat and muscle mass will be assessed by measuring skinfold fat thicknesses and circumferences. Body fat and muscle will also be measured with the ultrasound technique which uses sound waves to measure muscle and fat layer thicknesses. The ultrasound technique is non-invasive and consists of putting a sound wave transducer up against the skin at various locations on the body. A 2-dimensional picture of the fat and muscle layers is then printed. Another body composition measurement technique will measure fat and muscle tissue using X-ray methods (DEXA). The DEXA method is non-invasive. You will need only to lie first on your back and then on your side for a total of 20-30 minutes while the scanner arm of the machine records your total and regional bone mineral, fat and lean body mass composition. Muscular strength will be measured by using maximum effort tests for the upper arm, lower back, and legs. Warm-up and gradual increase in workload will be used during strength testing (2 hours). Visit 7: The distensibility of the veins in your lower leg will be measured. This involves the placement of a thin gauge around your lower leg and the placement of a cuff similar to a blood pressure cuff around your leg just above the knee. Pressure in the cuff will be increased to 30 mmHg, which is much lower than the pressure of cuff inflation during a blood pressure reading (normally about 200 mmHg). The slight change in the size of your lower leg will then be measured. This is a non invasive test; you will simply need to lie quitely on a table for the test. You will then walk on the treadmill at 3 submaximal speeds. You will again be using the mouthpiece and nose clip as in Visit 4. At each of the 3 submaximal speeds, you will walk for approximately 6 minutes while your heart rate and expired gases are analyzed. Each 6 minute exercise session will be followed by a 2 minute slow walk (1 1/2 hours). Visit 8: Resting blood pressure will again be measured. During this visit, the muscle electrical activity in your arm will be recorded with surface electrodes at rest and in response to a light stimulus. The time it takes to respond to a light stimulus will also be recorded.

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176 During this visit, you will also ride a stationary bicycle at several submaximal speeds while the electrical activity in your legs is recorded Surface electrodes will be placed on your upper right leg You will pedal the bicycle at each speed for 2 minutes. In between work bouts, you will rest until your heart rate comes down to its resting level (2 hours) The total amount of blood drawn during all the testing sessions is about 22 teaspoons; this is approximately one-quarter the amount of blood that you would give if you donated a pint of blood. You will then be randomly assigned to an endurance training group, an endurance and strength training group, or a control group. The control group will not exercise during the study, but will be given the opportunity to train as soon as the study is over. Endurance exercise training by both exercise groups will be done 3 times per week for 6 months in the Center for Exercise Science on treadmills and/ or stair-stepping machines The exercise intensity will be individually prescribed based on your heart rate response to exercise The program will start at a very low intensity and short duration and will gradually progress up to 70-80% of your capacity for 40--50 minutes each session. The progression will be based on your response to the program One of the exercise groups will also do strength training for the arms and lower back Strength training for the arms will be done 3 times per week in a room adjacent to the Center for Exercise Science on the same days as the endurance exercise training Strength training for the lower back will be done 1 day each week on one of the endurance exercise training days Training will begin very slowly and gradually to allow for gradual adaptation For the arm training, you will perform 8-12 repetitions of 2 exercises on Nautilus exercise machines. For the lower back training, you will perform 8-12 repetitions on the MedX Lower Back Machine. The progression will be based on your adaptation, with initial intensity being set at a light weight for each machine The weight lifted will be slowly increased each week until you perceive the training to be moderately hard Continued increases will be based on your adaptation to training Retesting: After 3 months of training, and again at the end of the study, subjects in the exercise and control groups will repeat Visits 4-8 5 POTENTIAL RISKS OR DISCOMFORTS Endurance exercise testing and training is associated with a small risk of cardiovascular complications. The risk for exercise testing is about 3-4 non-fatal incidents (events) in 10,000 GXTs and 1 fatal event per 25,000 tests. The Cooper Clinic in Dallas, Texas has had 6 non-fatal and no fatal cardiovascular events in 80,000 exercise tests. Five of 6 events occurred

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177 with persons with known cardiovascular disease. The risks involved with exercise testing for older individuals may be higher than this. The risk will be minimized in this study because all the personnel involved with testing and training are experienced in working with older men and women In addition, a physician will monitor all of the exercise tests and your blood pressure, heart rate and ECG will be closely monitored during the exercise tests. You can expect some fatigue and breathlessness to accompany the exercise testing at the start, the middle, and end of the study. With regard to exercise training, only 1 fatal event has occurred over the past 15 years of exercise training at the Aerobics Activity Center in Dallas. Their event rate is less than one in over 1,000,000 miles of walking and jogging. Exercise training for older individuals may involve a higher risk. Thus, the risk of serious injury is considered extremely low for both exercise testing and training. In this study, your heart rate and level of exertion will be monitored frequently as you exercise in order to further assure your safety. However, there is the possibility of minor injury, such as pulling a muscle or twisting an ankle or knee, during the exercise training phase of the study. There is little data on the injury rate in strength training. Our previous experience with strength testing and training in older individuals indicates that the musculoskeletal injury rate is low during strength training. You may, however, experience some minor muscle soreness during training. The injury rate may be higher during strength testing, but the risk in the present study will be kept low by careful warm-up and slow progression. The risk of any cardiovascular complication during strength testing and training is low; studies of participants in recreation sports, which included some weight trainers, showed 1 cardiovascular complication per 495,000 participants. The risks of drawing blood from a vein include discomfort at the site of needle placement; possible bruising and swelling around the site of needle placement; rarely an infection; and uncommonly, faintness from the procedure. The risk is minimized by the use of sterile techniques and the infusion of sterile saline to keep the catheter open during the duration of their placement. The risk of serious injury with blood drawing and ca theteriza tion is therefore quite minimal. The risks involved in the drug infusions used to test baroreflex sensitivity are minimal. The drugs are used only to change the heart rate within the normal range and the blood pressure response to the change of heart rate will be recorded. A catheter will be in place for this test; aside from the risk of catheter placement, as noted above, there has been no recorded incidence of complications arising from use of this procedure. The safety of the test will be assured by the direct supervision of a physician, and by the availability of drugs to counteract the initial infusions if the need should arise. During the tilt test, the possibility exists that you may feel nausea, dizziness, lightheadedness, sweating, tunnel vision, or faintness before the

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178 15-minute limit of this test. If this happens, or if you heart rate of blood pressure drop too low, the test will be immediately ended and the table returned to a level position. This should quickly relieve these symptoms. In addition, you will be secured to the tilt table by a wide Velcro band across the hips so there is little danger of falling in the event that you do faint. A physician will monitor all head-up tilt tests There is a small X-ray dosage during the DEXA (X-ray) body composition procedure The dose during a total body scan is less than 0.5 mrem This exposure is far less than the average radiation exposure of 30 mrem from a chest X-ray and is approximately 0 3% of the average annual per capita exposure in the U S. This low dosage is due to the low current setting of the apparatus, and the speed of the procedure In addition, lead oxide shielding surrounds the X-ray tube within the machine and this reduces radiation levels outside the scan area on the body and around the scan table A quality control test is run every day the machine is used in order to assure that only low levels of radiation are emitted. 6 POTENTIAL BENEFITS TO YOU OR TO OTHERS You will receive a complete cardiovascular examination and a battery of tests at the start of the study The results of these studies will be available to your private physician. You will also receive an individualized exercise prescription based on your exercise capacity and the chance to complete a six month training program at no charge and under the close supervision of a highly-qualified research team. Society in general will learn whether endurance and strength exercise can elicit beneficial adaptations with respect to body composition, muscular strength, cardiovascular function, orthostatic tolerance, and blood pressure in healthy men and women over the age of 70. 7 ALTERNATIVE TREATMENT OR PROCEDURES, IF AVAILABLE You may choose not to participate in the study 8 GENERAL CONDITIONS I understand that I will __ / will not _x_ receive money for my participation in this study If I am compensated, I will receive I understand that I will x / will not __ be charged additional expenses for my participation in this study If I am charged additional expenses these will consist of $45.75 for a blood chemistry and blood lipid screening and for analysis of thyroid hormones.

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I understand that I am free to withdraw my /my child's consent and discontinue participation in this research project at any time without this decision affecting my /my child's medical care If you have any questions regarding your rights as a subject, you may phone 392-3063. 179 In the event of my /my child sustaining a physical injury which is proximately caused by this experiment, professional medical care received at the J Hillis Miller Health Center exclusive of hospital expenses will be provided me without charge. This exclusion of hospital expenses does not apply to patients at the Administration Medical Center (V AMC) who sustain physical injury during participation is VAMC-approved studies. It is understood that no form of compensation exists other than those described above I also understand that the University of Florida and the Veterans Administration Medical Center will protect the confidentiality of my records to the extent provided by Law The Study Sponsor, Food and Drug Administration or either Institutional Review Board may ask to review my records; however, the records will remain confidential as only a number and initial will be used 9 SIGNATURES I have fully explained to ____________ the nature and purpose of the above-described procedure and the benefits and risks that are involved in its performance. I have answered and will answer all questions to the best of my ability I may be contacted at telephone number 904-392-9575. Signature of Principal or Co-Principal Investigator Obtaining Consent Date I have been fully informed of the above-described procedure with its possible benefits and risks and I have receive a copy of this description. I have given permission for my /my child's participation in this study Signature of Patient or Subject of Relative or Parent or Guardian (specify) Signature of Child (7 to 17 years of age) Signature of Witness Date Date Date

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APPENDIXC INSTITUTIONAL REVIEW BOARD APPROVAL LETTER

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HEALTH CENTER INSTITUTIONAL REVIEW BOARD D11-22 UNIVERSITY OF FLORIDA VICE PRESIDENT FOR HEALTH AFFAIRS HEAL TH SCIENCE CENTER BOX J-14 C1inesville Flo, i d zip 32610-0014 July 19, 1991 TO: FROM: Michael L. Pollock, Ph.D., J-277 B. J. Wilder, M.D., J-14 Chairman, Institutional Review Board ~0.11.:: .. Vice Chair J-14 SUBJECT: Reapproval of Institutional Review Board Project I 26 7-90 --=--'--....._ ____ Your request to continue your research Project involving human subjects 1_.aa2..a.6 ..... 7_-.;..90"----title: Effects of 6 Months of Endurance Exercise Training on Healthy Men and Women 70-89 Years of Age is approved as recommended by the Institutional Review Board. You are reminded that a change in protocol in this project must be approved by resubmission of the project to the Board for approval. Also, the prin cipal investigator must report to the Chair of the Board promptly, and in writing, any unanticipated problems involving risks to subjects or others, such as adverse reactions to biologicals, drugs, radio-isotopes or to medical devices. If the project has not been completed by 8/24/92 please request renewed approval, which is necessary for continuation of this project. If it is anticipated that VA patients will be included in this project, or if the project is to be conducted in part on VA premises or performed by any VA employee during VA-compensated time, final approval should be cbtained by application to the Veterans Administration Hospital Research Office By a copy of this memorandum the chainnan of your department is reminded that he is responsible for being informed concerning research projects involving human subjects in his department. He should review the pro tocols of such investigations as often as he thinks necessary to insure that the experiment is being conducted in compliance with our institution and with DHHS regulations. cc: B. J. Wilder, M.D. James E. McGuigan, M.D. Rhonda Cooper, Pharm.D Edward Block, M.D. Clinical Research Center DSR J HILLIS MILLER HEALTH CENTER co-Pls: /Joan F. Carroll, M.A. James A. Graves, Ph.D. David Lowenthal, M.D., Ph.D. Marian Limacher, M.D. Scott R. Leggett, M.S. Victor Convertino, Ph.D. William Chen, Ph.D. Myron Miller, M.D. Charles E. Wood, Ph.D. Colleae of Med i c i ne Co ll eae o f Nun1n1 Collece of Phuma.cv Co ll eae o f Health Related Pro f ess i ons Colleae of Dfflt 1 stry Co ll eae o f Veterinary Med i c i ne Veterinuv Med i cal T each i n1 Hoip1ta l Shands Hoso1,a l Veterans Adm i n,s tr auon Medica.l Center (Q U A l (M,lO Y~ fS f Ql',Oltl U~I JY / A fflh,4ATI V f AC T IO N fMl't. O'ffR 181

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APPENDIXD DATA COLLECTION FORMS FOR TILT TEST

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Name: Age : CENTER FOR EXERCISE SCIENCE UNIVERSITY OF FLORIDA, GAINESVILLE, FLORIDA 32611 392-9575 CARDIOVASCULAR DATA, HEAD-UP TILT ____________ Date: ____ T1/T2/T3 Ht : ____ Wt.: ____ BSA: ____ Hct: Baseline Pre Post Hb: Pre Post HR sv Q 0 HI Suoine -15 -10 -5 0 Tilt 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 183

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184 Recoverx 0 7 I 7 I I T 1 2 J_ 4 5 6 7 B 9 10 11 12 ]3 14 15

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NAME: CENTER FOR EXERCISE SCIENCE UNIVERSITY OF FLORIDA, GAINESVILLE, FLORIDA 32611 392-9575 ARM BLOOD PRESSURE, TILT PROTOCOL DATE: TEST: Systolic Diastolic Su~ine -15 -10 -5 0 Tilt 0 1 2 3 4 5 10 15 Recoverv 0 1 2 3 4 5 10 15 185

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186 COUGH TEST DATA Pre-cough R-R: Min. R R: Cough #: L1 R-R: Time to min. R-R: Beat R-R Cum. time. Beat R R Cum. time. Beat R-R Cum. time 1 46 78 2 47 79 3 48 80 4 41 81 5 42 82 6 43 83 7 44 84 8 45 85 9 46 86 10 47 87 11 48 88 12 49 89 13 50 90 14 51 91 15 52 92 16 53 93 17 54 94 18 55 95 19 56 96 20 57 97 21 58 99 22 59 100 23 60 101 24 61 102 25 62 103 26 63 104 27 64 105 28 65 106 29 66 107 30 67 108 31 68 109 32 69 110 33 70 111 34 71 112 35 72 113 36 73 114 37 74 115 38 75 116 39 76 117 40 77 118

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APPENDIXE INDIVIDUAL FAINTERS' DATA

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a) 120 100 ......... 80 -~ 60 ..n 40 l: 20 0 b) 70 60 50 40 s _._ Tl --0T2 _._ T3 10 > 30 I C/) ''t::Allct; .... ~~L.g.'~ 20 10 15 0 Minutes 5 10 _._ Tl --0T2 _._ T3 15 Tilt Recovery 0 ....... ...-. ....... _._ ....................... _._ ....... ...-. ....... __..__.__......__.__._ ___ ....... ___ ___ c) 4 1 0 0 5 10 15 0 5 0 5 10 Minutes I _._Tl --0T2 _._T3 Recover 15 0 5 Minutes 10 15 10 15 Figure E-1. Responses of female fainter A to 70 head-up tilt before (Tl), a fter 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output (Q). Arrows mark time of occurrence of presyncopal symptoms at Tl. (R = Rest) 188

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189 a) 60 40 20 "fl:. '--' I 1Z 0 ::c: _._ Tl I <1 -20 --0-T2 -40 _._ T3 -60 0 5 10 15 0 5 1 0 15 M i nutes b) 80 _._ Tl 60 40 --0T2 20 --T3 "fl:. '--' 0 > CJ) <1 -20 -40 -60 -80 Tilt Rec o very 0 5 10 15 0 5 10 15 Minutes c) 80 _._ Tl 60 40 --0-T2 20 _._ T3 "fl:. '--' 0 .a <1 -20 -40 -60 t I Tilt Recovery 80 0 5 10 15 0 5 10 15 Minutes Figure E-2. Percent change(~) from supine rest in response to 70 head-up tilt in female fainter A before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output (Q). Arrows mark time of occurrence of presyncopal symptoms at Tl.

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a) 180 160 140 oe 120 100 E 80 :i 60 CJ) 40 20 R Tilt 0 b) 120 100 oe 80 r::. 60 ......... 20 0 c) 120 100 & 80 E: E: 60 ......... 20 0 0 I R Tilt 0 5 5 t 10 10 10 15 0 Minutes I Recover _._Tl ~T2 --T3 5 10 _._Tl ~T2 --T3 15 0 5 10 Minutes 15 0 Minutes _._Tl ~T2 -T3 5 10 190 15 15 15 Figure E-3. Blood pressure responses of female fainter A to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise traini n g: A) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure. Arrows mark time of occurrence of presyncopal symptoms at Tl. (R = Rest)

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a) 30 20 ,...._ 10 p.. 0 Cl)
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a) 6000 m 5000 I E 4000 u Q) 3000 s:::: >, 2000 1000 E-< R Tilt 0 0 b) 120 100 80 60 40 ........ 20 E-< <] 0 -20 -40 ilt -60 0 5 10 5 10 Recove 15 0 Minutes I ,RecoverY. 15 0 Minutes 5 5 192 --Tl --0-T2 -n 10 15 --Tl --0-T2 T3 10 15 Figure E-5. Total peripheral resistance (TPR) response of female fainter A to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) absolute resp o nse; b) percent change (.1) from supine rest. Arrows indicate time of occurrence of presyncopal symptoms at Tl.

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a) 120 10 0 ,-... ,..... 8 0 I i:; ... E 60 ...0 -4 0 20 0 b) 70 60 50 ,-... ] 40 -> 30 CJ) 2 0 10 0 c) 4 3 ,-... ,..... I i:; ... E 2 ...J -. a 1 0 RO 5 1 0 I _._ Tl -0T2 _._ T3 Tilt 0 5 _._ Tl -0-12 --T3 RTil 0 5 10 t 10 _._ Tl --T3 Min u tes 'Rec o very, 15 0 Minutes 1 5 0 Min u tes 5 5 10 15 10 15 Figure E-6 Responses of female fainter B to 70 head-up tilt before (Tl), a fter 3 months (T2), and after 6 months (T3) o f e xercise training : a) heart rate (HR); b) stroke volume (SV); c) cardiac o utput (Q). Arrows mark time of occurrence of presyncopal symptoms at Tl and T2. (R = Rest) 1 9 3

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a) 60 40 20 ..._,, 0 __________ l _____ : l: <] -20 -40 Tilt -60 0 5 10 15 0 Minutes b) 80 60 _._ Tl 40 -0T2 ~20 _._T3 ..._,, > 0 ---------------CJ)
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a) 180 160 140 i120 S 100 E 80 60 Cf} 40 20 R Tilt 0 0 b) 120 100 5 f 10 Recover _._ Tl ~T2 -T3 15 0 5 Minutes 10 15 80 ~-=l"'l~~~..-..LH:::====t~=I 60 f _._Tl 40 0 20 0 c) 120 100 r 80 s S 60 ..._, 40 20 I R Tilt 0 5 10 f 15 0 Minutes ~T2 -T3 _._Tl ~T2 -T3 15 0 ....... ....._ ........ ....._ ................................................................ _.__ .................... '-'-'-....._ ........ ....._ .................. ,__,__.__. 0 5 10 15 0 5 10 15 Minutes 195 Figure E-8 Blood pressure responses of female fainter B to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: A) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure. Arrows mark time of occurrence of presyncopal symptoms at Tl and T2. (R = Rest)

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196 a) 30 ---Tl 20 -0T2 ....... 10 -T3 ......,, P.. 0 o::i (/)
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a) 6000 G:;5000 s 4000 u Q) 3000 :9. 2000 1000 b) 120 100 80 .60 .._,, 40 2~ -20 -40 -60 0 0 Til 0 5 10 15 0 Minutes -1I I Recovery 5 10 15 0 5 Minutes 197 -Tl --0T2 -T3 5 10 15 -Tl --0-T2 -T3 10 15 Figure E-10 Total peripheral resistance (TPR) response of female fainter B to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) absolute response; b) percent change (.1) from supine rest. Arrows indicate time of occurrence of presyncopal symptoms at Tl and T2.

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a) 120 100 ,....._ 80 i:: -~ 60 .0 .._,, 40 20 0 b) 70 60 50 ,....._ ] 40 .._,, 30 20 10 0 c) 4 ,....._ ..... I i:: 3 2 ,-J .._,, .a 1 0 0 I R, Tilt 0 _._ Tl -O-T2 --11-T3 5 5 _._Tl -O-T2 --11-T3 5 10 10 10 15 0 Minutes 15 0 Minutes I Recover 15 0 Minutes 10 15 -0T2 T3 5 10 15 5 10 15 Figure E-11. Responses of male fainter A to 70 head-up tilt before (Tl), aft er 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output (Q) Arrows mark time of occurrence of presyncopal symptoms at Tl. (R = Rest) 198

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a) 60 40 -40 -60 b) 100 80 60 40 -,J2. 20 .._.., 0 -20 -40 -60 -80 c) 80 60 40 -.. 20 -,j2. .._.., 0 .a <1 -20 -40 Tilt 0 0 -60 Tilt -80 0 5 ~T2 -T3 5 ---Tl ---0-T2 _._T3 5 10 10 10 1 15 0 Minutes Recoverr, 5 15 0 5 Minutes t I Recover 15 0 5 Minutes _._ Tl ---0-T2 _._T3 10 10 10 199 15 15 15 Figure E-12. Percent change (.1) from supine rest in response to 70 head-up tilt in male fainter A before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training : a) heart rate (HR) ; b) stroke volume (SV); c) cardiac output (Q) Arrows mark time of occurrence of presyncopal symptoms at Tl.

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a) 180 160 140 & 120 6 100 s 80 .._, 60 i:ci CJ) 40 20 0 b) 120 100 & 80 E 6 60 .._, i:ci 40 Cl 20 0 c) 140 120 bb 100 :r:: 6 80 6 .._, 60 < ::E 40 20 0 Tilt 0 5 il 0 5 5 10 10 10 15 0 Minutes 15 0 Minutes 200 --Tl --0T2 -T3 10 15 ---Tl --0T2 -T3 5 15 ---Tl --O-T2 -T3 5 15 Figure E-13. Blood pressure responses of male fainter A to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: A) sys tolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure Arrows mark time of occurrence of presyncopal symptoms at T1. (R = Rest)

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a) 30 20 ........ 10 .._., 0 C/) <:J -10 -20 -30 b) 30 20 ........ 10 .._., 0 Q <:J -10 -20 -30 c) 30 20 ........ 10 .._., 0 <: ::E <:J -10 -20 -30 Tilt 0 Tilt 0 Til 0 5 _._ Tl ~T2 -T3 10 _._T3 5 _._ Tl ~T2 -T3 5 10 10 ,RecoverY. 15 0 Minutes Recover 15 0 Minutes :Recovery 5 5 15 0 5 Minutes 10 10 15 10 15 Figure E-14. Percent change(~) from supine rest in blood pressure response to 70 head-up tilt in male fainter A before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure. Arrows mark time of occurrence of presyncopal symptoms at TL 201

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a) 6000 rn 5000 I s u 4000 u (I) rJl 3000 (I) s:: >::9, 2000 1000 0 b) 120 100 80 ,......_ 60 40 .._, 20
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a) 120 ---Tl 100 --0--T2 ,....._ ,...... 80 -II-T3 I s:: 8 60 ..0 ..__., 40 20 I ,Recovery 0 0 5 10 15 0 5 10 15 Minutes b) 70 60 50 ,....._ ..40 8 ..__., _._ Tl > 30 ---0T2 Cl) 20 T3 10 I R Tilt 0 0 5 10 10 15 Minutes c) 4 3 ,....._ ,...... I s:: 8 2 ---Tl ,-..l ..__., .a ---0T2 1 -II-T3 0 5 10 15 0 5 10 15 Minutes Figure E-16 Responses of male fainter B to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: a) heart rate (HR); b) stroke volume (SV); c) cardiac output (Q) Arrows mark time of occurrence of presyncopal symptoms at Tl. (R = Rest) 203

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a) 60 40 20 0 -20 -40 -60 b) 80 60 40 20 ..._,, > 0 (/)
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a) 180 160 140 bb 120 ::r: S 100 E 80 :i 60 CJ) 40 20 iTilt 0 0 b) 120 100 f 80 S 60 20 0 c) 120 100 & 80 s S 60 40 20 0 il 0 I R Tilt 5 10 5 10 15 0 Minutes 15 0 Minutes _._Tl .....O-T2 -T3 5 10 _._Tl .....0-T2 -T3 5 10 _._Tl .....oT2 -T3 15 15 0 5 10 15 0 5 10 15 Minutes 205 Figure E-18 Blood pressure responses of male fainter B to 70 head-up tilt before (Tl), after 3 months (T2), and after 6 months (T3) of exercise training: A) systolic (SBP); b) diastolic (DBP); c) mean arterial (MAP) pressure. Arrows mark time of occurrence of presyncopal symptoms at Tl. (R = Rest)

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a) 30 20 ...-.. 10 '-" 0 CJ'}
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207 a) 6000 _._ Tl 5000 ---0-T2 I 4000 -T3 u Q) 3000 >... 2000 p.. 1000 E-< 0 5 10 15 0 5 10 15 Minutes b) 120 _._ Tl 100 80 ---0T2 60 -T3 40 ........ 20
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208 LIST OF REFERENCES Abrams, W. B & Berkow, R. (Eds.) (1990). The Merck manual of geriatrics Rahway, NJ: Merck & Co., Inc. Adams, G. M & deVries, H A (1973). Physiological effects of an exercise training regimen upon women aged 52-79 Journal of Gerontology,~ 5055 American College of Sports Medicine (1990). The recommended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness in healthy adults. Medicine and Science in Sports and Exercise,~ 265-274. American College of Sports Medicine. (1991) Guidelines for exercise testing and prescription (4th ed ) Philadelphia : Lea & Febiger. Aniansson, A., & Gustafsson, E (1981) Physical training in elderly men with special reference to quadriceps muscle strength and morphology. Clinical Physiology, L 87-98. Aniansson, A., Ljungberg, P., Rundgren, A., & Wetterqvist, H (1984) Effect of a training programme for pensioners on condition and muscular strength. Archives of Gerontological Geriatrics,~ 229-241. Atomi, Y., Ito, K., Iwasaski, H., & Miyashita, M. (1978). Effects of intensity and frequency of training on aerobic work capacity of young females Journal of Sports Medicine,~ 3-9. Banner, N R., Williams, M., Patel, N Chalmers, J., Lightman, S L., & Yacoub, M. H. (1990). Altered cardiovascular and neurohumoral responses to head-up tilt after heart-lung transplantation. Circulation,~ 863-871. Barney, J A., Ebert, T J Groban, L., & Smith, J. J. (1985). Vagal-cardiac activity and carotid-to-cardiac baroreflex responses in trained (T) and untrained (UT) men Federation Proceedings, 11, 818. Barry, A J., Daly, J W Pruett, E. D R., Steinmetz, J R., Page, H F, Birkhead, N C., & Rodahl, K. (1966) The effects of physical conditioning on older individuals. I. Work capacity, circulatory-respiratory function and work electrocardiogram Tournal of Gerontology, ll, 182-191.

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209 Barry, A. J Steinmetz, J. R., Page, H.F., & Rodahl, K. (1966) The effects of physical conditioning on older individuals. II Motor performance and cognitive function. Journal of Gerontology, ZL 192-199 Bass, D. E Buskirk, E R., lampietro, P. F., & Mager, M (1958). Comparison of blood volume during physical conditioning, heat acclimatization, and sedentary living. Journal of Applied Physiology, lb 186-188. Beck, J (1989). General principles of aging: Demography of aging. In J Beck (Ed ), Geriatrics review syllabus: A core curriculum in geriatric medicine .{pp 1-5). New York: American Geriatrics Society, Bedford, T G., & Tipton, C. M., (1987) Exercise training and the arterial baroreflex. Journal of Applied Physiology, fil, 1926-1932. Beetham, W. P., & Buskirk, E R. (1958) Effects of dehydration, physical conditioning and heat acclimatization on the response to passive tilting Journal of Applied Physiology, U, 465-468 Bell, M. E., Wood, C. E., & Keller-Wood, M (1991) Influence of reproductive state on pituitary-adrenal activity in the ewe Domestic Animal Endocrinology,~ 245-254. Bie, P., Secher, N H Astrup, A., & Warberg, J. (1986). Cardiovascular and endocrine responses to head-up tilt and vasopressin infusion in humans. American Journal of Physiology, 251, R735-R741. Bjorntorp, P. (1987). Effect of physical training on blood pressure in hypertension. European Heart Journal, 8 (Suppl B), 71-76. Blomqvist, C. G., & Stone, H. L. (1983) Cardiovascular adjustments to gravitational stress. In J. T Shephard & F. M Abboud (Eds.), Handbook of physiology The cardiovascular system. Peripheral circulation and organ blood flow (Section 2, volume 3, part 2, pp. 1025-1063). Bethesda, MD: American Physiology Society. Boileau, R. A., Buskirk, E R., Horstman, D. H Mendez, J & Nicholas, W C. (1971). Body composition changes in obese and lean men during physical conditioning Medicine and Science in Sports, a, 183-189. Boning, D & Skipka, W (1979) Renal blood volume in training and untrained subjects during immersion European Journal of Applied Physiological and Occupational Physiology, if, 247-254

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210 Borg, G. A V. (1982) Psychophysical bases of perceived exertion Medicine and Science in Sports and Exercise, H:, 377-381 Braith, R. W ., Lowenthal, D. T Graves, J. E., Leggett, S H Wilcox, C., & Pollock, M. L. (1990). The influence of exercise training on the renin aldosterone system of the elderly. Medicine and Science in Sports and Exercise, 22 (Suppl. 2), S33. Bungo, M. W Charles, J B & Johnson, P C. (1985) Cardiovascular deconditioning during space flight and the use of saline as a countermeasure to orthostatic intolerance Aviation, Space, and Environmental Medicine, 22., 985-990. Buskirk, E R. & Hodgson, J L. (1987) Age and aerobic power: The rate of change in men and women. Federation Proceedings, 1, 1824-1829 Cardone, C., Bellavere, F., Ferri, M & Fedele, D (1987) Autonomic mechanisms in the heart rate response to coughing Clinical Science, ll, 55-60. Carroll, J F Pollock, M. L., Graves, J E Leggett, S H., Spitler, D & Lowenthal, D. T. (in press) Incidence of injury during moderate-and high intensity walking training in 60-79 year old. Journal of Gerontology Chapman, E. A deVries, H A & Swezey, R. (1972) Joint stiffness : Effects of exercise on young and old men. Journal of Gerontology, 'IL 218-221. Chien, S., Usami, S Simmons, R. L., McAllister R. F., & Gregersen M I. (1966) Blood volume and age : Repeated measurements on normal men after 17 years Journal of Applied Physiology, ll 583 588 Clark, B. A. Wade, M G., Massey, B. H., & Van Dyke, (1975) Response of institutionalized geriatric mental patients to a twelve-week program of regular physical activity Journal of Gerontology, aQ., 565-573 Claybaugh, J R. Pendergass D R., Davis, J. E Akiba, C., Pazik, M ., & Hong, S K. (1986) Fluid conservation in athletes : Responses to water intake, supine posture, and immersion Journal of Applied Physiology, 7-15. Cleroux, J., Giannattasio, C., Bolla, G Cuspidi, C. Grassi, G., Mazzola, C., Sampieri L., Seravalle, G., Valsecchi M., & Mancia, G (1989). Decreased cardiopulmonary reflexes with aging in normotensive humans American Journal of Physiology, 257, H961-H968. Cononie, C. C., Graves J E., Pollock, M L., Phillips, M I., Sumners C. & Hagberg J.M (1991) Effect of exercise training on blood pressure in 70to

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211 79-yr-old men and women. Medicine and Science in Sports and Exercise, 505-511. Convertino, V. A (1987). Aerobic fitness, endurance training, and orthostatic intolerance. Exercise and Sport Sciences Reviews, 12, 223-259 Convertino, V A (1991). Blood volume: its adaptation to endurance training Medicine and Science in Sports and Exercise,~ 1338-1348. Convertino, V A., Brock, P. J., Keil, L. C., Bernauer, E M & Greenleaf, J E (1980a). Exercise training-induced hypervolemia: Role of plasma albumin, renin, and vasopressin Journal of Applied Physiology,~ 665-669 Convertino, V A Doerr, D F Mathes, K. L., Stein, S. L., & Buchanan, P. (1989) Changes in volume, muscle compartment, and compliance of the lower extremities in man following 30-days of exposure to simulated microgravity. Aviation, Space, and Environmental Medicine, 60, 653-658 Convertino, V. A., Greenleaf, J. E & Bernauer, E. M. (1980b). Role of thermal and exercise factors in the mechanism of hypervolemia Journal of Applied Physiology, 4:, 657-664 Convertino, V. A Keil, L. C., Bernauer, E. M & Greenleaf J. E (1981) Plasma volume, osmolality, vasopressin, and renin activity during graded exercise in man. Journal of Applied Physiology, 2-Q, 123-128. Convertino, V. A., Keil, L. C., & Greenleaf, J. E. (1983) Plasma volume renin, and vasopressin responses to graded exercise after training. Journal of Applied Physiology,~ 508-514. Convertino, V. A Mack, G. W & Nadel, E R. (1991) Elevated central venous pressure: A consequence of exercise training-induced hypervolemia? American Journal of Physiology, 260, R273-R277 Convertino, V A., Montgomery, L. D., & Greenleaf, J.E (1984). Cardiovascular responses during orthostasis: Effect of an increase in V0 2 max. Aviation, Space, and Environmental Medicine, .22, 702-708. Convertino, V A., Sather, T. M Goldwater, D. J., & Alford, W. R. (1986) Aerobic fitness does not contribute to prediction of orthostatic intolerance. Medicine and Science in Sports and Exercise,~ 551-556 Crane, H. G. & Harris, J J. (1976) Effect of aging on renin activity and aldosterone excretion Journal of Laboratory and Clinical Medicine,~ 947959

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212 Cress, M. E., Thomas, D. P., Johnson, J., Kasch, R. W., Cassens, R. G Smith, E L., & Agre, J C (1991). Effect of training on V02max, thigh strength, and muscle morphology in septuagenarian women. Medicine and Science in Sports and Exercise, 23, 752-758 Cryer, G. L., & Gann, D.S. (1974). Right atrail arceptors mediate the adrenocortical aresponse to small hemorrhage. American Journal of Physiology, 227, 325-328 Cryer, P. E. (1980). Physiology and pathophysiology of the human sympathoadrenal neuroendocrine system. The New England Journal of Medicine, 303, 436-444. Dambrink, J. H A & Wieling, W. (1987). Circulatory response to postural change in healthy male subjects in relation to age. Clinical Science, ll, 335341. Davies,, R., Forsling, M L., & Slater, J. D H (1977). The interrelationship between the release of renin and vasopressin as defined by orthostasis and propranolol. Journal of Clinical Investigations,~ 1438-1441. Davies, R., Slater, J. D H., Forsling, M L., & Payne, N. (1976). The response of arginine vasopressin and plasma renin to postural change in normal man, with observations on syncope Clinical Science and Molecular Medicine, 2.L267-274. deVries, H. A (1970). Physiological effects of an exercise training regimen upon men aged 52 to 88 Journal of Gerontology, 22, 325-336. Diaz, F J., & Rivera, A. E. (1986). Heart rate, blood pressure and plasma volume changes, related to posture and physical fitness. Medicine and Science in Sports and Exercise, S15 Dill, D B., & Costill, D. L. (1974). Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. Journal of Applied Physiology, JZ, 247-248 Dill, D B., Hall, F. G., Hall, K. D., Dawson, C & Newton, J. L. (1966) Blood, plasma, and red cell volumes: Age, exercise, and environment. Journal of Applied Physiology, 21, 597-602. Duvoisin, M R., Convertino, V A., Buchanan, P Gollnick, P. D & Dudley, G. A (1989). Characteristics and preliminary observations of the influence of electromyostimulation on the size and function of human skeletal

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Solomon, L. R., Atherton, J. C., Bobinski, H., & Green, R. (1986). Effect of posture on plasma immunoreactive atrial natriuretic peptide concentrations in man. Clinical Science, Z1, 299-305. Somers, V. K., Conway, J., Johnston, J., & Sleight, P. (1991). Effects of endurance training on baroreflex sensitivity and blood pressure in bor~erline hypertension. The Lancet, 337, 1363-1368 Sowers, J R. (1987) Hypertension in the elderly American Journal of Medicine, 82 (Suppl. 1B), 1-8. Sowers, J. R., Rubenstein, L. Z., & Stern, N (1983). Plasma norepinephrine responses to posture and isometric exercise increase with age in the absence of obesity. Journal of Gerontology,~ 315-317. 226 Stamford, B A (1972) Physiological effects of training upon institutionalized geriatric men Journal of Gerontology, 451-455. Stegemann, J., Busert, A., & Brock, D. (1974). Influence of fitness on the blood pressure control system in man. Aerospace Medicine,~ 45-48. Strzepek, L. A (1990). The noninvasive measurement of cardiac output in the young and elderly by electrical bioimpedance cardiography, acetylene rebreathing, and doppler ultrasound techniques Unpublished master's thesis, University of Florida, Gainesville. Tarazi, R. C Melsher, H. J Dustan, H. P & Frohlich, E. D., (1970). Plasma volume changes with upright tilt: Studies in hypertension and in syncope Journal of Applied Physiology,~ 121-126 Thomas, C. L. (1985). Taber's cyclopedic medical dictionary (15th ed.). Philadelphia: F. A Davis Company Thompson, C. A Tatro, D. L., Ludwig, D A., & Convertino, V A. (1990) Baroreflex responses to acute changes in blood volume in humans. American Journal of Physiology, 259, R792-R798. Tipton, C. M. (1991). Exercise, training and hypertension: An update In J 0. Holloszy (Ed.), Exercise and sport sciences reviews (pp. 447-505) Baltimore : Williams & Wilkins. Tipton, C. M., Matthes, R. D & Bedford, T. G (1982) Influence of training on the blood pressure changes during lower body negative pressure in rats. Medicine and Science in Sports and Exercise, H:, 81-90.

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227 Vargas, E., Lye, M., Faragher, E. B., Goddard, C., Moser, B., & Davies, J. (1986) Cardiovascular haemodynamics and the response of vasopressin, aldosterone, plasma renin activity and plasma catecholamines to head-up tilt in young and old healthy subjects Age and Ageing, 15., 17-28 Volpe, M Cuocolo, A., Vecchione, F., Lembo, G., Pignalosa, S Condorelli, M., & Trimarco, B. (1989). Influence of volume expansion on hemodynamic effects of atrial natriuretic factor in rabbits. American Journal of Physiology, 256, H852-H858. Vroman, N. B., Healy, J A., & Kertzer, R. (1988) Cardiovascular response to lower body negative pressure (LBNP) following endurance training Aviation, Space, and Environmental Medicine, .-22., 330-334 Wade, C. E Dressendorfer, R. H O'Brien, J C., & Claybaugh, J. R. (1981) Renal function, aldosterone, and vasopressin excretion following repeated long-distance running. Journal of Applied Physiology,~ 709-712 Wei, J. Y., & Harris, W S (1982). Heart rate response to cough Journal of Applied Physiology, 1039-1043 Wiegman, D. L., Harris, P D Joshua, I. G & Miller, F N. (1981) Decreased vascular sensitivity to norepinephrine following exercise training Journal of Applied Physiology, 21, 282-287. Wieling, W Borst, C., van Brederode, J. F. M., van Dongen Torman, M A ., van Montfrans, G A., & Dunning, A. J. (1983) Testing for autonomic neuropathy: Heart rate changes after orthostatic manoeuvres and static muscle contractions Clinical Science, ., 581-586. Williams, B 0 Caird, F. I., & Lennox, I. M (1985) Hemodynamic response to postural stress in the elderly with and without postural hypotension Age Ageing, .H, 193-201 Williams, T. D. M., Walsh, K. P Lightman, S L., & Sutton, R. (1988). Atrial natriuretic peptide inhibits postural release of renin and vasopressin in humans American Journal of Physiology, 255, R368-R372 Wilmore, J. H., Davis, J A., O'Brien, R. S., Vodak, P A., Walder, G R., & Amsterdam, E. A (1980). Physiological alterations consequent to 20-week conditioning programs of bicycling, tennis, and jogging. Medicine and Science in Sports and Exercise, 11, 1-8 Zerbe, R. L., Henry, D. P., & Robertson, G. L. (1983) Vasopressin responses to orthostatic hypotension. American Journal of Medicine, Z1, 265-271.

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BIOGRAPHICAL SKETCH Joan F. Carroll received a Bachelor of Arts degree from the State University of New York in Binghamton in 1975. She received her Master of Arts in Physical Education at the University of Florida in 1984. After four years of teaching at the University of Florida, she continued her studies toward a Ph.D. degree at the University of Florida. She will also earn a Certificate in Gerontology upon graduation During her four years of study for a Ph.D., she has worked on two research projects involving cardiovascular and strength training for elderly men and women. She has also been involved in research documenting injuries with training in the elderly and the use of ultrasound in the prediction of body composition. Upon graduation, she wishes to pursue a career in teaching and research in a university setting. 228

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I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree of ctor of Philo y; Michael L. Pollock, Chair an Professor of Exercise and Sport Sciences I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree f Doctor of Philosophy. --::, Jame E. Graves Assistant Scientist of Exercise and Sport Sciences I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degr ~~ YCharles E Wood Associate Professor of Physiology I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree of Doctor of Philosophy.

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I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree of Doctor of Philosophy. : kd ~~~ Victor A. Convertino Courtesy Associate Professor of Exercise and Sport Sciences This dissertation was submitted to the Graduate Faculty of the College of Health and Human Performance and to the Graduate School and was accepted as partial fulfillment of the requirements for the degree of Doctor of Philosophy. May, 1992 De Dean, Graduate School

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UNIVERSITY OF FLORIDA 111 1111111111111I IIIII IIIII II IIIIII IIII IIII IIII II IIII IIII IIIII I I 3 1262 08554 1836

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AN EXAMINATION OF SUPPLANTATION AND REDISTRIBUTION EFFECTS OF LOTTERY ALLOCATIONS TO A COMMUNITY COLLEGE SYSTEM By SUSAN ROBINSON SUMMERS A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 1993

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Copyright 1993 by Susan Robinson Summers

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For Gordon

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ACKNOWLEDGEMENTS I am grateful to my chair, Distinguished Service Professor Emeritus James L. Wattenbarger. Dr. Wattenbarger guided my doctoral experience at the University of Florida. He instilled in me an enduring desire to provide leadership in carrying forward his mission, that the Florida community college system provide access to higher education for all the citizens of Florida. Dr. Wattenbarger encouraged my writing, and gave me the opportunity to be his research assistant at the Institute of Higher Education. I thank my cochair, Dr. Davids. Honeyman, for the opportunity to work full time as his research assistant, for his endless support throughout this study, and for the countless hours spent with me pursuing the mysteries of higher education finance. I wish to thank my committee members: Dr. C. Arthur Sandeen, for his enthusiasm for my topic and belief in my ability to bring this dissertation to fruition, and Dr. James H. Pitts for his abiding faith in me. I extend special appreciation to Dr. M. David Miller for his kind instruction, and the many hours he shared with me developing the research design and regression models for this study, and reviewing my findings. I thank my colleague, Mr. Jeffrey Maiden, for his unflagging support and generosity, exploring iv

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with me the mysteries of educational finance, statistics, and the mainframe computer. This study was made possible through the help of many different people in the Florida Department of Education and the Florida Governor's Office. I would like to extend deepest appreciation to Dr. Edward L. Cisek, Deputy Executive Director, Department of Education, Division of Community Colleges. Dr. Cisek was supportive of my use of Divisional data to analyze the effect of the Florida Lottery on the community colleges. Dr. Cisek extended the assistance of his staff in collecting and verifying all the data used in this study; Mr. Kenneth E. Jarrett, Director of Financial Services, and Dr. Howard Campbell, Bureau Chief of Information Systems, were especially helpful. Mr. Jarrett lent several hours of his time during each visit I paid to the Division, and later answered my questions by telephone. Dr. Campbell provided enrollment data. At the Governor's Office of Budget and Management, Mr. Link Jarrett, Educational Policy Director, and Mr. Subhasis Das, analyst, Revenue and Economic Analysis Policy Unit, gave assistance with supplemental data. My colleagues at Lake City Community College supported my doctoral pursuit in many different ways. I extend special thanks to President Muriel Kay Heimer, Vice President Deborah Hecht, and Deans John Davis, Richard J. Jackson, and David Richards. I thank my assistant, Ms. Lynn Bodiford for V

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her loyalty and patience throughout the four years of doctoral study. I thank my father, Dr. John Robinson, for instilling in me perfectionism, a deep belief in the value of higher education, and a reverence for research. I thank my mother, Mrs. Hazel Floyd Robinson, for her enduring belief in my ability to succeed, and the time she spent caring for my children while I was involved in doctoral studies. I appreciate my parents for the examples they set by being literate, articulate, and meticulous in practicing their professions. Most especially, I wish to acknowledge the contributions of my husband, Gordon Summers, and children, Sam, Catherine, and Daniel. They sacrificed countless hours of time that would have been spent with me, had I not pursued this goal. They never asked me to quit this quest; and most of all, they always believed in me. vi

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TABLE OF CONTENTS ACKNOWLEDGEMENTS ABSTRACT CHAPTERS 1 2 3 INTRODUCTION . . ..... Impact . . . . . . . Supplantation. . . . . .. Redistribution . . . ...... Categorical Versus Noncategorical Allocations ............. The Florida Education Lotteries. Community College and K-12 Similarities Lottery Allocations as Noncategorical Awards . . . . . . Lottery as a Proportion of Operating Revenues ........ An Unstable Period in Community College Funding . . . . . . Definition of Terms ............ REVIEW OF THE LITERATURE ......... Twentieth Century American Lotteries The Impact of the Lottery on Community College Funding ..... The Florida Education Lotteries Lottery Revenues Viewed as an Excise Tax . . . . . . . . Supplantation ............ Redistribution ........ The Lottery as a Quasi-Business Monopoly ............ Earmarking Lottery Proceeds The Historical Context of Contemporary Lotteries . . . . . . . The Earliest Lotteries ........ Territorial Florida Lotteries .. Intercolonial and Interstate Lotteries. Early Examples of Supplantation and Redistribution ....... The Revocation of State Lotteries .. METHODOLOGY .............. Hypothetical Constructs. ...... Assumptions. . . ...... Data . . . . . . vii iv xi 1 2 2 3 3 4 6 7 10 11 13 17 17 20 28 37 43 46 50 54 56 57 58 59 61 63 66 67 68 69

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Procedures . . ....... Design ...... Impact . . . . . Supplantation .......... Redistribution .. The Effect of Categorical Lottery Allocations. . . ..... 4 RESULTS AND DISCUSSION . . .. Impact . . . . . . . . Supplantation. . . . .. Redistribution .............. The Effect of Categorical Lottery Allocations .. Summary of Findings .... Conclusions ......... 5 SUMMARY AND CONCLUSIONS Summary of Results ......... Impact . . . . . . Supplantation . . . .. Redistribution ........... Categorical versus noncategorical lottery awards .... Conclusions ............... Impact . . . . . . . Supplantation . . . . Redistribution. . . . ... The Effects of Categorical Awards Implications and Suggestions for Future Research . . . . . . 71 72 74 76 79 79 82 85 88 94 96 100 102 104 107 107 107 109 110 111 112 112 114 115 117 APPENDICES . . . . . . . 122 APPENDIX A THE FLORIDA COMMUNITY COLLEGES 123 APPENDIX B STATE-OPERATED LOTTERIES, CONSTITUTIONAL AND STATUTE CITATIONS, AND LOTTERY FUND BENEFICIARIES . . . . 124 APPENDIX C RAW DATA SETS. . . . . 129 Data Set C-I: The variables OBS, CC, YR, LT, CAT, GRF, TOTSTATE, FTE, and FTEX12 130 Data Set C-II: The variables OBS, LOT, LOTFTE, GRFFTE, STATFTE, and TOTAL E&G 143 REFERENCES BIOGRAPHICAL SKETCH. viii 156 166

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LIST OF TABLES Table 1. System differences in proportions of categorical and noncategorical funds in FY 1992-93 lottery allocations. . . . . . . . . . 9 Table 2. Florida Education Enhancement Trust Fund allocations to the K-12, cc, and SUS systems, shown as a percentage of total ...... Table 3. Per-student funding history of Florida's community colleges, FY 1981-1993, expressed in 30 current dollars. . . . . . . . . 32 Table 4. Descriptive statistics of all variables. 86 Table 5 ANOVA table and parameter estimates for the relationship between the lottery and the fiscal status of the Florida community colleges. . . 88 Table 6. ANOVA table and parameter estimates for the supplantation model GRF = B 0 + B 1 YR + B 2 LT + B 3 YR*LT. . . . . . . . . . . 90 Table 7. ANOVA table and parameter estimates for the supplantation model GRF = B 0 +B 1 YR+B 2 LT. . . . 91 Table 8. Stepwise analysis of supplantation. 93 Table 9. Stepwise regression for the dependent variable FTEX12. . . . . . . . . 95 Table 10. The effect of categorical lottery allocations, the model B 1 CAT + B 2 LT + B 3 CAT*LT. . . . . . vs. noncategorical TOTSTATE = B 0 + Table 11. The effect of categorical vs. restricted lottery allocations, the model TOTSTATE = B 1 CAT+B 2 LT. . . . . Table 12. Stepwise analysis of the effect of categorical versus noncategorical allocation of lottery funds. . . ....... ix 97 99 100

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LIST OF FIGURES Figure 1 The spread of lotteries across the United States, 1964 through 1993. . . . . 19 Figure 2 Florida Lottery allocations to education, FY 1987 FY 1993, shown in current dollars {Source: State of Florida Department of Education, 1992, 1993) ....................... 34 Figure 3. Percentages of FY 1992 lottery allocations, categorical & noncategorical {Source: State of Florida Department of Education, 1993, p. 4). 38 Figure 4. Parimutuel tax revenues rose from FY 1965 until the inception of the Florida Lottery, FY 1987 {Source: State of Florida Governor's Office of Planning and Budgeting, 1993).... . . . . . . . . 51 Figure 5. Supplantation of State of Florida general revenue dollars with Florida Lottery dollars allocated to the community college system. 92 Figure 6. Redistribution of funding sources for Florida's community college system, FY 1972 FY 1991. . . . . . . . . . . . 96 X

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Abstract of Dissertation Presented to the Graduate School of the University of Florida in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy AN EXAMINATION OF SUPPLANTATION AND REDISTRIBUTION EFFECTS OF LOTTERY ALLOCATIONS TO A COMMUNITY COLLEGE SYSTEM By Susan Robinson Summers December, 1993 Chairman: James L. Wattenbarger Cochair: David S. Honeyman Major Department: Educational Leadersh i p This dissertation was designed to determine whether an institution benefitted from being a designated recipient of a state-operated lottery. A state system of public community colleges was used for the analysis. The method was to determine whether there was any change since the inception of the Florida Education Lotteries in the available resources and actual expenditures of the 28 state-supported community colleges in Florida. Four basic questions investigated the effect of a state lottery as a revenue source for a public community college system: 1. Did the start of the Florida Lott e ry coincide with a change in the expenditure trends of the Florida commun i ty colleges? This study provided evidence of an inverse relationship between lottery dollars and total c ommun ity college expenditur e s; also, gen e r a l r e v e nu e allocat i ons to xi

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the Florida community colleges declined after the inception of the Florida Lottery. 2. Did Florida Lottery funds either supplant or enhance state general revenue funds expended in support of community college education? The lottery allocations were shown to have been too small, and too recent, to have exerted a significant effect on the magnitude of the state total allocation to community colleges. The results of this study indicated that supplantation effects were influenced by redistribution. 3. Did the addition of the lottery as a revenue source result in a redistribution in the proportion of community college expenditures funded through state sources? This study provided evidence of redistribution. The community colleges were shown to have been increasingly dependent on nonstate sources of revenue since the inception of the Florida Lottery in Fiscal Year 1987. 4. The fourth question concerned the proportion of lottery dollars that were released to community colleges in the form of a categorical allocation versus lottery dollars that were awarded without spending restrictions. There was evidence that the extent to which the lottery allocation was a categorical award was positively correlated with the size of the total state allocation. The issue of categorical awards was linked to redistribution and supplantation. xii

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CHAPTER 1 INTRODUCTION The latter third of the 20th century has been a time when, for politically expedient reasons, governments have experimented with the use of alternative, nontax methods to generate funds for social programs. One of the most pervasive methods over the past three decades was the implementation of state-sponsored lotteries as supplemental government revenue sources. While some lotteries were used to generate funds for the state treasury, state lottery revenues were often earmarked for a publicly-supported social system such as education, parks and recreation, or economic development. The purpose of this dissertation was to examine the fiscal results of earmarking lottery revenues for a public system of higher education. This study was designed to determine whether such a system benefitted from being a designated recipient of a portion of the profits from a state-operated lottery. A state system of public community colleges was used for the analysis. The method used to address this question was to determine whether there had been any change since the inception of the Florida Education Lotteries in the available resources and actual expenditures 1

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2 of the 28 state-supported community colleges in Florida. Did the Florida community colleges, in fact, benefit financially from being earmarked for a portion of the proceeds from the Florida Lottery? Impact The first issue addressed in this study concerned the use of a state lottery as a revenue source for a designated beneficiary. Did lottery dollars have an effect on the financial status of the beneficiary? Did the start of the lottery allocations coincide with a change in the expenditure patterns of the beneficiary? Did the addition of lottery revenues correlate with a significant change in the total funds available for expenditure by the beneficiary? Specifically, did the Florida community colleges incur greater expenditures after the Florida Lottery was added as a revenue source? Supplantation The second issue addressed in this study was whether or not the lottery had an effect on the amount of state nonlottery funds that were allocated to the beneficiary. Were lottery dollars in addition to, or a substitute for, nonlottery state funds? In other words, did the addition of lottery funds result in the enhancement or supplantation of nonlottery funds? Specifically, did the 1987 introduction of

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lottery dollars as a revenue source for Florida community colleges affect the total amount of state funds that were allocated to the 28 community colleges in Florida? Redistribution The third issue addressed in this study concerned the extent to which the annual, current expenditures by the beneficiary were derived from state funds. Did state all source allocations decline or increase relative to beneficiary current expenditures that were funded through all sources? In this analysis, the annual expenditures per weighted full time equivalent student (FTE} at each of the Florida community colleges were examined as a function of State of Florida general revenue fund allocations to the community colleges. Categorical Versus Noncategorical Allocations 3 The fourth and final issue addressed in this study was whether or not expenditure restrictions on lottery dol l ars affected the amount of nonlottery dollars allocated to the beneficiary (Appendix B). In Florida, lottery funds were initially allocated exclusively as categorical, restricted expenditure awards. The extent to which the lottery allocation was categorically restricted decreased each year. The FY 1993 lottery allocation to Florida community colleges was completely noncategorical. Did the percentage of each

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4 college's annual lottery allocation that bore categorical spending restrictions correlate with the supplantation, enhancement, or redistribution of state nonlottery funds? In this analysis, total state expenditures from all sources, including lottery funds, were examined as a function of the percentage to which the lottery allocation was categorical. The Florida Education Lotteries Between 1965 and 1993, voters in 35 states and the District of Columbia approved referenda to implement a government-operated lottery for the purpose of creating a new state revenue source. The Florida Lottery, like 24 other state lotteries, was earmarked to serve as a revenue stream to fund a designated beneficiary. In Florida, the three systems of public education were the designated beneficiaries. The Florida lottery currently in operation was initiated through a constitutional amendment that was approved by statewide referendum in 1986 for the expressed purpose of generating new dollars for the treasury that would be spent to enhance education. To underscore the purpose of the Florida lottery, it was named by statute the Florida Education Lotteries. The net proceeds were deposited to the State Education Lotteries Trust Fund (FL St. .15.c.1). To ensure that the citizens of Florida wou l d forever be reminded that the purchase of a lottery ticket

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5 contributed to the support of education, all advertising was required to "inform the public about the significance of lottery funding to the state's overall system of public education," (FL St. .1215). Florida is typical of other lottery states in the use of a lottery to attempt to forestall increasing the citizens' tax burden. All governments are required to generate funds for the operation of governmental functions. Most state governments generate revenue through a combination of personal and corporate income taxes, and sales and excise taxes. Florida is one of only seven states without a state income tax; the others are Texas, South Dakota, and Washington, which like Florida are lottery operating states; Alaska and Wyoming, where revenue is earned from taxes on the extraction of natural resources; and Nevada, where the bulk of state general revenue is generated through excise taxes on casinos and other forms of parimutuel gambling (Fisher, 1988). In Florida, the state sales, tourism, and corporate taxes and user fees are the primary sources of general revenue (Wood & Honeyman, 1992). Florida voters, like those in other states, had routinely rejected referenda that attempted to instigate new forms of state revenue, or new taxes. Floridians were protected through their state constitution from both a personal income tax and a lottery. Floridians voted to amend the

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6 constitution to permit a lottery but continued to resist the concept of a state income tax (Karcher, 1989). Stark (1991) and Stark, Honeyman, and Wood (1991) demonstrated that the lottery was associated with the supplantation of general revenue funds for elementary and secondary education in Florida. There is need to extend the question to the higher education sector in general, and community colleges in particular. Have community colleges benefitted from the addition of a state lottery as a revenue source? Specifically, have lottery proceeds either supplanted or enhanced general revenue funds? Have lottery funds correlated with the redistribution of community college funding sources? If so, to what extent? This study specifically addressed the community college system for four different reasons, which follow. Community College and K-12 Similarities The first reason for focussing on the community college system was based on the similarities between the school districts and community colleges. The elementary and secondary school (K-12) funding systems have been extensively examined for purposes of determining fiscal equity. The methods used to study K-12 may be extended to the community college system, as was done by Harrell (1992) and suggested by Breneman and Nelson (1981). Nelson (1982, p. 215) noted that the community colleges are the "sector of

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7 higher education with the closest kinship to elementary secondary schooling." The district organization and funding formulas of the community colleges in Florida are in many ways similar to the elementary and secondary school districts. Both community colleges and school districts are funded through weighted FTE formulas. Further, the community college system consists of 28 separate institutions that are each governed by a local board with a board-appointed president heading each college. The community college system's local governance is analogous to the K-12 system's district school boards and superintendents. The emphas i s on local governance of the K-12 and community college systems contrasts sharply with the central governance of the Florida State University System (SUS). Thus, this study extended the work of others who examined school district funding using the regression analysis across time of dollars expended per weighted FTE. The similarities that were identified between the K-12 and community college systems would underscore any concerns that would be raised if disparate fiscal treatment of the community colleges were observed. Lottery Allocations as Noncategorical Awards The second reason for focussing on the Florida community college system was because the community college system had the greatest degree of local control in determining how the lottery allocations were spent. With

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8 local governance, local discretion concerning the expenditure of the lottery funds should facilitate responsiveness to district needs, and result in a highly visible effect. Thus, the allocation of lottery dollars for noncategorical spending as opposed to categorical grants and aids may be perceived as beneficial to both the community college and K-12 systems. Florida's community college leaders have been successful in getting virtually all categorical spending restrictions lifted from the lottery allocation. Florida's school district superintendents continue to receive a significant portion of the K-12 lottery allocation as a categorical award. This study included an examination of whether the community colleges have experienced a greater degree of general revenue supplantation because the lottery funds began to flow into the Community College Program Fund (CCPF) without categorical spending restrictions. Table 1 shows the K-12, community college (CC) and SUS lottery allocations for FY 1992 by dollars allocated as either categorical or noncategorical awards, and the categorical and noncategorical percentages of each system's total lottery allocation. The trend toward a completely noncategorical lottery allocation to the Florida community colleges may be traced to the 1990 recommendation of Clark Maxwell, executive director of the State Board of Community Colleges (Maxwell,

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1990). The question must be asked: Did lifting the categorical restrictions on the lottery allocation exacerbate the supplantation of general revenue funds? Interestingly, the K-12 and SUS noncategorical fund lottery allocations of FY 1992 included the term "for enhancement," and carried specific accounting, auditing and reporting requirements to document all expenditures of lottery dollars; no similar requirement was made of the community college system in FY 1992 (Florida Senate Bill 278-H, .517; .524; .540; .544; .569; .579). As may be 9 Table I. System differences in proportions of categorical and noncategorical funds in FY 1992-93 lottery allocations. Categorical Unrestricted K-12 allocations 78,572,355 505,427,645 Total 584,000,000 Percentages 13.5% 86.5% cc allocations 3,550,000 121,650,000 Total 125,200,000 Percentages 2.8% 97.2% SUS allocations 11,558,579 113,641,421 Total 125,200,000 Percentages 9.2% 90.8% Source : State of Florida Department of Edu c a t ion 1 99 3 p. 4.

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10 seen in Table 1, the community college system received the lowest percentage of lottery funds as categorical awards in FY 1992: categoricals comprised less than 3% of all lottery dollars awarded to community colleges, while comprising nearly 10% for the SUS and about 14% for K-12. The 1993-94 Florida Senate Appropriations Act allocated all lottery dollars for the community college system as noncategorical awards. Additionally, $9 million in noncategorical, nonrecurring lottery funds allocated to the Community College Program Fund {CCPF} for FY 1992 were not restored in the FY 1993 allocation {State of Florida Board of Community Colleges, 1993). Lottery as a Proportion of Operating Revenues The third reason for focussing on the Florida community college system was that the community college system received the largest per-FTE lottery allocation, and the lowest per-FTE general revenue fund allocation. Both enrollment in the community college system and funding per FTE were lower than was true for K-12; therefore, the total state allocation to the community colleges was considerably less than the K-12 allocation. The SUS was awarded more dollars per FTE than were community colleges, and the SUS total operating budget exceeded that of the community college system even though the total community college enrollment exceeded the total SUS enrollment. In FY 1990,

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11 the Florida community colleges generated 62.6% of student postsecondary FTE, while the SUS earned 37.4%. The community college share of student headcount for FY 1990 was even greater: 72.7% of all postsecondary students attended the community colleges (Campbell, 1992). However, the community college system was awarded 15% of total net proceeds from the lottery, which was the same percentage allocated to the SUS. Because the financial needs of the community colleges were so great, the lottery has arguably had a substantially greater effect on the overall fiscal health of the community college system than either the K-12 or SUS system. In fact, lottery dollars comprised 29.4% of the per-FTE funding of community colleges in FY 1991 (State of Florida Board of Community Colleges, 1993). Any supplantation or redistribution that occurred may be a real cause for concern. An Unstable Period in Community College Funding The fourth reason for focussing on the Florida community colleges system was that the life span of the state lottery coincided with sharp peaks and valleys in the per-FTE level of state support for the community colleges. The Florida Lottery's few years of existence have occurred during a fiscally turbulent period of history. It was implemented during a time of fiscal growth and state progra m expansion. The lottery met with record success during its

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12 first year, FY 1987, exceeding the revenue projections. In the earliest years, all awards made to education were in the form of categorical allocations accompanied by specific reporting requirements to document the enhancements on which lottery dollars were expended. Then, this nation's economy declined into recession. In FY 1990, 30 state governments made midyear allocation reductions to their systems of higher education, and college presidents in 22 states reported FY 1991 allocations that were lower than the FY 1990 allocations (Sweeney, 1991). Florida was one of the recession states. Throughout FY 1990, Florida's revenues fell far short of projections. Florida's former Governor Bob Martinez, who by law was obligated to balance the state budget, took the unprecedented step of ordering three separate midyear FY 1990 reductions to the general revenue allocations of all systems of education. The Florida State Board for Community Colleges responded by recommending the lifting of categorical spending restrictions for the lottery allocation (Maxwell, 1990). In the ensuing years, the proportion of lottery funds that was allocated to the community colleges with categorical spending restrictions rapidly declined. In FY 1993, the community college lottery allocation was entirely noncategorical. Thus, a brief span of time presents a unique opportunity to study the impact of categorical versus noncategorical allocations to the community colleges.

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13 Definition of Terms The beneficiary is the designated recipient. Here, the term pertains to the agency, service or institution that is designated for receipt of earmarked lottery funds. Categorical grants and aids are restricted-expenditure allocations within the Community College Program Fund (CCPF) used by the legislature to fund new or existing programs in keeping with the Florida Master Plan (Judd, 1988). The source of these funds is primarily the Educational Enhancement Trust Fund (EETF) but they are also comprised of general revenue funds. Categorical allocations comprise the Restricted Current Fund. The Community College Program Fund (CCPF) consists of the funds allocated by the Legislature to operate the community colleges during the fiscal year (State of Florida Department of Education, 1992b). It is comprised of both noncategorical program funds, and restricted-expenditure categorical grants and aids. Earmarking is to set aside, or designate, funds for a specific use, as in earmarking 15% of lottery proceeds for allocation to the community college system. Educational and general operations (E&G) are the routine activities that are funded through the general current fund and the restricted current fund (State of Florida Department of Education, 1990b).

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14 Educational Enhancement Trust Fund (EETF} is the state of Florida treasury fund for receipt of lottery revenues, as established by the Florida Lottery Act in 1986. It is contained in Article X, Section 15.c.1 of the Florida Constitution and enacted by Florida Statute .120 and .121.2. Enhancement refers to lottery funds as they pertain to the state nonlottery allocation to the beneficiary. If lottery funds enhance the total allocation, they comprise new dollars, or an additional sum to the total state allocation. For example, if the nonlottery allocation were $100 per fiscal year, and the lottery allocations were enhancement dollars, the nonlottery allocation would continue to be $100 and the lottery allocation would be an additional sum, perhaps $2. Thus, the total state allocation would be $102 with the enhancement of lottery dollars. Full time equivalent (FTE) refers to student enrollment, as a function of student course load. FTE is computed by the total number of student credit hours divided by 40 for Advanced and Professional courses, and Postsecondary Vocational instruction. FTE is computed by the total number of student instructional clock hours divided by 900 for all other forms of postsecondary instruction (State of Florida Department of Education, 1992b}. Lottery is a scheme for the distribution of prizes by lot or chance (Gove, 1969). The legal definition of a

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15 lottery always includes three elements: a prize, an award by chance, and a consideration (Little River Theatre Corporation v. State ex rel. Hodge, 1939). In the Florida lottery these chances are purchased for one dollar each for the prospect of winning a much greater amount of money. The grand prize in the lotto game is often as high as several million dollars. The chance to win a great prize for a small investment constitutes the risk, or gamble. The purchaser may select numbers, which introduces an element of skill or strategy. Alternatively, one may purchase computer-generated numbers or scratch-off tickets; thus, no skill or special knowledge is required in order to play. Program funds are allocations within the CCPF used for general operating expenditures and cost-to-continue existing programs (Judd, 1988). The major source is the Florida general revenue fund, but program funds are also comprised of EETF, or lottery, revenues Redistribution is to reallocate, reapportion, or spread a specific quantity to other areas; redistribution is a new distribution of a given total (Lambert, 1989). In this study, redistribution pertains to the proportional weight of the revenue sources which fund a state-supported agency such as a community college. For example, consider that state taxes have historically funded 80% of the current expenditures of a community college. If the state share

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16 shifts to 60% of current expenditures, redistribution is said to have occurred. Restricted Current Fund is the accounting fund used to track the resources available for the operation and support of instructional programs that are restricted by donors or donor agencies as to the specific purpose for which they may be expended (State of Florida Department of Education, 1990b). Categorical funds are restricted funds. Supplantation is to take the place of, or substitute, one thing for another, as in to substitute lottery funds for general revenue funds. Supplantation is the opposite of revenue enhancement. For example, consider that a state supported agency has historically been awarded $100 per year. A state lottery is implemented with the profits earmarked for the agency. The lottery allocation is $2 per year. If the state nonlottery allocation drops to less than $100 when the lottery is added as a revenue stream, supplantation is said to have occurred.

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CHAPTER 2 REVIEW OF THE LITERATURE An extensive body of literature exists on the subject of American lotteries. Much of the literature in this review was found in the fields of economics, tax law, public finance, political science, and American history. A void was found to exist concerning the use of a state lottery to fund higher education in general, or community colleges in particular. Twentieth Century American Lotteries In FY 1993, lotteries existed in 35 states and the District of Columbia (Appendix B). In their popularity, 20th century American lotteries reflected the resurgence of lotteries worldwide. In 1986, 140 different countries permitted some form of legalized gambling; 100 of these countries had legalized lotteries (Clotfelter & Cook, 1989). Many nations operate a lottery as a consumer entertainment product as well as a national revenue source. For example, the Philippine government has operated a national lottery since 1933; the Chinese government, since 1988. The former Soviet Union operated a lottery with sales in excess of one 17

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18 billion tickets annually, and prizes that included such scarce consumer commodities as washing machines, cars, and cash (Clotfelter & Cook, 1989). Figure 1 displays the spread of lotteries across the United States, beginning with the New Hampshire lottery in the 1964. Note that the most recent lotteries, as well as a number of nonlottery states, are clustered in the so-called Bible Belt states of the Southeast. Twentieth century lotteries represent the revival of an old and honored way to raise funds for worthy activities (Clotfelter & Cook, 1990a). The revival of United States lotteries was a phenomenon that began in New England in the 1960s and spread rapidly across the continental United States. The birth of the Florida Lottery corresponded with the birth of four other state lotteries. On the general election day in 1986 when Florida voters approved a lottery referendum, voters in Idaho, Kansas, Montana, and South Dakota approved state lottery referenda as well (Mikesell & Zorn, 1987). After three-quarters of a century when lotteries were illegal in every state and territory, by 1993 lotteries were approved for operation by the governments of 35 of the United States as well as the District of Columbia (Appendix B). State lotteries in the 20th century appeared to be an expedient way to raise new revenues for a state treasury by providing a consumer entertainment commodity through a government-held monopoly (Brinner & Clotfelter,

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1960s 1 s 1 o s f::::::::::::::::l 1980s lltlWI l 990s f:: : : :-: :/: : :1 Copyright 1993 Brodsrbund S o ftwar e Inc. A ll Righ ts Reserv e d 19 Figure 1 The spread of lotteries across the United States, 1964 through 1993. (Created using the PC Globe copyright 1993 Brderbund Software. Reprinted with permission of the company.) 1975; Clotfelter & Cook, 1987, 1990b). When lottery profits were earmarked for public education or some other socially redeeming purpose, as they were in 23 states, a lottery was commonly held to be a morally legitimate form of recreational gambling. Despite their popularity, there existed an historic and extensive body of literature showing that government operated lotteries were regressiv e in nature, unstable as a res ource base, and used by expedient politicians to gen era te new monies while avoiding new or higher taxes (All e n, 1991; Brinner & Clot fel ter, 197 5 ; Karcher, 1989 ). Lotteries were

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20 been voted into states where other forms of gambling were illegal, sometimes under the guise of being a deterrent to illegal gambling. However, lotteries have been found to have no impact on the prevalence of illegal gambling (Thomas & Webb, 1984). At the same time, lotteries have been associated with a 3% rise in the crime rates of certain lottery states (Mikesell & Pirog-Good, 1990). Additionally, lotteries have been shown to have exerted a suppressing effect on parimutuel wagering (Vasche, 1990). Since parimutuel wagering generates excise tax revenues, the suppression of commercial gambling is also the suppression of a state revenue source. In fact, after 23 consecutive years of annual growth, parimutuel revenues in Florida declined by 19% from the lottery's inception in FY 1987 through FY 1991, the most recent fiscal year for which figures were available at the time of this study {State of Florida Governor's Office of Planning and Budgeting, 1993). The 19% decline constituted a revenue loss of $24.9 million to the State of Florida treasury. The Impact of the Lottery on Community College Funding While there was an extensive body of literature regarding the lottery, there was a real dearth of research concerning the lottery as a revenue source for higher education, whether community colleges, colleges, or universities. Clotfelter {1991) noted that "community

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21 colleges are worthy of special attention owing to their size and spectacular growth." The growing prevalence of state operated lotteries has coincided with swelling community college enrollments during an era of fiscal restraint. The result was that state lottery revenues have comprised an increasingly common source of community college funds. It was time to examine the state-sponsored lottery as a revenue source for community colleges. Voters prefer lotteries over new taxes Nationwide, the 1980s and 1990s have been decades of decentralization, fiscal restraint, and economic recession. In the 1980s, federal general revenue sharing came to an end along with a reorganization of the federal budget that put more responsibility to fund state operations on the individual states, and less on the federal government (Blackley & DeBoer, 1993; Hildred, 1991). The tax relief and tax reduction measures of the 1970s gave way in the 1980s to state tax increases. Legislators in 34 states raised taxes in 1981, in 25 states in 1982, and in 41 states at least one state tax was raised in 1983 (Swartz & Peck, 1990). In the political climate of the 1980s and 1990s, taxpayers simultaneously experienced stagnant wages and a growing tax burden. In such a climate, a lottery was viewed by many citizens as being an unmitigated good, a voluntary contribution made by only those persons who chose to wager a bet (Mcconkey & Warren, 1987). The passage of a state

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lottery was politically more popular than the passage of additional taxes (Allen, 1991; Borg & Mason, 1988, 1990; Clotfelter & Cook, 1989; Wyett, 1991). This viewpoint was reinforced with the commonly held contention that lottery dollars would only provide revenue enhancement for the beneficiaries, and would not supplant general revenue dollars. The lottery as a share of total state revenues 22 Even successful state lotteries generate revenues that comprise only a small percentage of the total state treasury. As a proportion of all state revenues, the lottery shares increased somewhat in the 1980s. This increase may reflect real growth in lottery revenues, but it may also reflect a decline in other state revenues relative to lottery revenues. Nationwide, state lotteries were reported to generate an average ranging from 2% (Mikesell & Zorn, 1988) to 4% (Clotfelter & Cook, 1991) of state-earned revenue. Year-to-year and state-to-state variations were considerable. For FY 1985, the range extended from a low of only 0.09% of own-source state revenues in Vermont, to a high of 3.72% of state revenues in Maryland (Mikesell & Zorn, 1988). In FY 1985, the lottery states earned an average of 3% of general revenue dollars from lottery profits, up from 1.7% in FY 1980 (Mikesell & Zorn, 1987). In FY 1986, lottery profits showed a slight increase over FY

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1985, rising to about 3.3% of own-source state revenues (Clotfelter & Cook, 1989). Allocating lottery profits to community colleges The actual allocation of state lottery profits to community colleges appears to have been a pervasive phenomenon, yet one that was difficult to quantify. The method of allocation varied from state to state. Fourteen state legislatures earmarked the lottery profits for education, while others earmarked the funds for other beneficiaries. Thirteen state lotteries generated general revenue funds for the state treasury (Appendix B). In FY 1993, about two-thirds of all state lotteries generated funds that flowed, in part, to the public community colleges. 23 It was not always clear from reading the legislation which state community college systems received lottery allocations, because the earmarking was often unspecific. For example, the beneficiary was generically termed "education'' in the lottery legislation from Connecticut, Ohio, Michigan, and New Hampshire (Appendix B). Sometimes the profits were earmarked in a way that could have been received by a community college through a categorical grant award. In Arizona and Iowa, for example, lottery dollars funded economic development, the Indiana lottery funded capital improvements, and the Oregon lottery funded sports programs. These were initiatives in which community colleges

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24 commonly participate. In 13 states the lottery profits flowed into the general revenue fund, where they may have been reallocated to the community colleges as a special appropriation. For these reasons it was useful to compare the information compiled from the state constitutional and statute citations found in Appendix B, with information collected over the years from a consistent source. National Community College Finance Surveys were conducted since the 1960s by Dr James L. Wattenbarger and his associates at the Institute for Higher Education, University of Florida. In the 1988 edition of the Community College Finance Survey, which collected data for FY 1986, only the California respondent reported receipt of lottery funds (Wattenbarger & Mercer, 1988). In the 1990 edition of the same study, 15 state respondents reported that state lottery dollars provided partial funding for community colleges: California was joined by Connecticut, Florida, Indiana, Iowa, Michigan, New Hampshire, New Jersey, New York, Oregon, Rhode Island, Virginia, Washington, West Virginia, and Puerto Rico (Honeyman, Williamson, & Wattenbarger, 1991). The total rose to 21 states with the subsequent edition of the study, when 6 additional state respondents reported lottery funding for community colleges: Arizona, Illinois, Kentucky, Missouri, Pennsylvania, and Vermont (Honeyman, Summers, & Wattenbarger, 1993). The Ohio lottery was earmarked for education, but Ohio was not a participant in

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25 the most recent editions of the survey. Idaho, Minnesota, and Montana were all lottery-operating states, where the proceeds were earmarked for various projects, but those state respondents did not specify that lottery dollars were expended on community college education. Georgia voters approved a lottery referendum in 1992 which was earmarked for public education. Thus, the 21 state respondents who reported that lottery dollars were expended on community college education supported the estimate that two-thirds of all 35 state lotteries provided funds for public community colleges in FY 1993. Do lottery beneficiaries receive less state money? Hines (1992) compared FY 1993 with FY 1991 allocations to higher education. When Hines' results were overlaid with the results of the findings described above, some interesting patterns appeared. Hines grouped states into four quartiles based on their allocations for higher education in FY 1993 relative to FY 1991. Those classed as "lowest" had the lowest increase for the biennium--in fact, these states reported allocation decreases ranging from 12.51% to 3.34% Those classed as "highest" had allocation increases of 27.09% to 7.90%. The next-highest were classed "second;" the next lowest, "third" (Hines, 1992). If lottery funds were intended to enhance the total revenues available to a beneficiary, then a state lottery which was earmarked for education should have correlated

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26 with better state funding for education. However, Hines' analysis of state funding for higher education indicated that the higher education systems with the greatest gains in funding were found among the group of 15 states where there was no state lottery. The most lucrative state lotteries were found in states which budgeted funding reductions for higher education. In Hines' analysis, the two states showing the greatest funding gains for higher education were Nevada and Arkansas, neither of which had a state lottery. Of the entire "highest" quartile, 8 of the 13 states did not operate a state lottery. Only 3 states in the "highest" group had a lottery that was earmarked for education (Oregon, New Jersey, and Montana). Conversely, of the states in the "lowest" grouping, only Alaska was a nonlottery state. The other 12 "lowest" states had a state-operated lottery; of these, 5 state lotteries were earmarked for education (New York, Ohio, Connecticut, Florida, and California). Thus, there appeared to have been an inverse relationship during the early 1990s between the existence of a state lottery and the size of the state allocation to higher education. Interestingly, the lotteries in California, Florida, and New York were the highest-grossing state lotteries in FY 1990, with net receipts of $924 to $809 million dollars per state. The Ohio lottery produced gross receipts of $1.5 billion, compared with a gross of $1.9 billion each for the

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27 Florida and New York lotteries (Calkins, 1992). The drop in FY 1993 funding after a highly successful FY 1990 lottery may have indicated a plateau or erosion of lottery profits, combined with a reliance by those state legislators on the lottery as a funding source for higher education. Perhaps in the states where lottery revenues were earmarked for education, legislators developed a reliance on the lottery as an education funding source, diverting general revenue funds to other projects. When lottery revenues plateau or decline When the funding of an agency is tied to a state lottery, there is cause for concern about the stability of that funding. The expansion of the use of a state lottery as a revenue source for a designated beneficiary had coincided with a national trend for state lottery revenues to plateau, and even decline. In studying the New York lottery, DeBoer (1990) noted that gross sales and net revenue were stagnant over a 3-year period in the mid-1980s. In a separate study, DeBoer (1986) used regression analysis to predict that lottery sales growth nationwide would slow before 1995. In both of his studies, DeBoer established that the phenomenally rapid growth of state lotteries in the early 1980s was not present in the early 1990s. DeBoer's work was supported by Mikesell (1987) and Calkins (1992). Mikesell concluded, The potential lottery market in a state will fade as time passes and competition comes ... These

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findings should temper enthusiastic portraits of ever-increasing revenue. (p. 252) Calkins found that on-going state lotteries generated an annual revenue increase of 26% to 31% in the years 1981 to 1985. By 1990, the rate of growth over the prior year had sharply declined to only 6%. The Florida Education Lotteries 28 A ccording to the advertising campaign used to lobby for passage of the amendment, and written into the enabling legislation, the citizens were told that the Florida lottery would generate enhancement funds for improvements in education {Clotfelter & Cook, 1989; FL St. .102.1 ) The enabling legislation stated, further, that the lottery would not be used to substitute, or replace, general revenue funds (.102.2.a) While the actual wording of the constitutional amendment was vague and, therefore, flexible in interpretation, the enabling legislation specifically addressed the appropriate and allowable uses for lottery profits. In accordance with Article X, Section 15.c.1 of the Florida Constitution, N et proceeds derived from the lotteries shall be d eposited to a state trust fund to be designated t he State Education Lotteries Trust Fund, to be a ppropriated by the Legislature. Significantly, the amendment did not specify for what purposes the fund was to be appropriated. However, Florida

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29 Statute .102.2.a, the enabling legislation for the lotteries, specified That the net proceeds of the lottery games conducted pursuant to this act be used to support improvements in public education and that such proceeds not be used as a substitute for existing resources for public education. The legislation further stipulated that the funds were to be distributed among the three systems of publicly-funded education in Florida. Section 24.121.5.b specified, The Legislature shall equitably apportion monies in the trust fund among public schools, community colleges and universities. The allowable uses of the lottery profits, described in .121.5.a, May include, but are not limited to, endowment, scholarship, matching funds, direct grants, research and economic development related to education, salary enhancement, contracts with independent institutions to conduct programs consistent with the state master plan for postsecondary education, or any other educational program or purpose deemed desirable by the Legislature. The Florida lottery was required to retain at least 38% of the gross revenue from the sale of lottery tickets and other earned revenue for deposit in the Educational Enhancement Trust Fund, as specified in .121.2. Florida lottery allocation to community colleges Since FY 1991, lottery profits have been allocated so that 70% flow to the school districts, and the community college system and the SUS each receive a 15% share. Table 2 shows the percentages of lottery profits allocated to the K

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30 12, community college, and SUS systems for FY 1987 through FY 1992. Prior to the FY 1991 allocation, the proportional allocations varied. For example, in FY 1987, community colleges received 14.4% of the Florida Education Trust Fund receipts, while the SUS received 23.1%; in FY 1989, community colleges received 8.5%, and the SUS was awarded 15.1% (State of Florida Department of Education, 1992). The Florida and California lotteries were unique in that specific percentages of the profits were earmarked to fund higher education as well as school districts. A l though 14 of the 35 lottery states earmarked at least a portion of Table 2. Florida Education Enhancement Trust Fund allocations to the K-12, CC, and SUS systems, shown as a percentage of total. Fiscal Year K-12 cc SUS 1987 60.8% 14.4% 23.1% 1988 78.9% 11.6% 7 6% 1989 72.2% 8.5% 15.1 % 1990 75 2% 8 9% 1 4 .3 % 1991 70.0% 15.0 % 1 5 .0 % 1992 70.0% 15.0% 1 5 .0 % So ur c e: S tate o f Flo ri d a D e p artment of Education 1992, pp 3 5.

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31 the lottery profits for education, the earmarking was almost always limited to the school districts (Appendix B). Although the Illinois lottery profits were initially earmarked for all levels of public education, the Illinois legislature in 1985 suspended the allocation of lottery proceeds to higher education (Borg & Mason, 1988). Table 3 shows the funding history of the Florida community colleges since FY 1981, reflecting the erosion of the general revenue allocation as the lottery gained momentum, and the overall decline in the funding per FTE despite the increasing size of the lottery allocations. Despite the additional support of lottery funds since FY 1987, Jones and Brinkman (1990) noted that the Florida community colleges were under-funded and over-stressed: Florida's community colleges ... have comparatively few resources ... An analysis of expenditures per FTE student ... indicates that only two Florida institutions are above the national median on this measure. We consider this prima facie evidence of inadequate funding for the level of services being rendered. Because Florida enrollments are generally increasing faster than enrollments in other states and because funding has not kept pace in recent years, it is probable that more recent data would reveal a worse, not a better, picture. (p. A-6) Funding public education with the Florida Lottery In Florida, the proportion of each year's total educational support comprised of lottery funds has been essentially constant since the first two years following the inception of the lottery. As lottery funds increased, general revenue funds expended on education began to

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32 decline. D uring the first three years of lottery funding, the Florida general revenue allocation to education dropped Table 3. Per-student funding history of Florida's community colleges, FY 1981-1993, expressed in current dollars. STU LOT AS% FY GRF LOTTERY FEES TOTAL OF TOTAL 1981 2,027 0 632 2,659 1982 2,036 0 650 2,685 1983 2,348 0 662 3,010 1984 2,572 0 708 3,280 1985 2,678 0 721 3,398 1986 2,826 0 761 3,587 1987 2,893 137 798 3,829 3.6 1988 2,936 242 807 3,984 8.2 1989 2,816 448 807 4,071 11.0 1990 2,640 468 847 3,956 17.7 1991 2,262 667 994 3,924 29.5 1992 2,249 638 1,084 3,971 16.1 1993 2,302 620 1,124 4,046 15.3 Source : State of Florida Board of Communit y Colleges 1993 p 1 7. Notes: All sums e x pressed per FTE FY 1981-1991 represents a c tual data. FY 1992 represents estimated data based on appropriations and the most current reductions to General Revenue at time of press. FY 1993 represents estimated data based on Legisla t ive Appropriations as of 7/01/93 and estimated student fee revenues

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33 by 5% (Karl, 1991 ) Meanwhile, as a proportional source, lottery revenues at first rose, then declined The proportion of total state educational support comprised of lottery dollars more than doubled from FY 1988 to FY 1989; lottery dollars comprised less than 4% of the total FY 1988 state allocation to education (Allen, 1991) and comprised 9.5% of the total educational allocation in FY 1989 (State of Florida Department of Education, 1990b). In FY 1992, about 8% of the state's total allocation for education at all levels was comprised of lottery dollars (State of Florida Department of Education, 1992, 1993) As a proportion of total budget, these percentages approximated the projections made by former Florida Commissioner of Education Ralph Turlington Turlington lobbied hard for the lottery's passage, linking the lottery to enhancement dollars for education. Turlington's pro lottery campaign emphasized that passage of the lottery was crucial to the fiscal health of education. However, in 1986 Turlington projected annual lottery revenues of $350 million, an amount that would have comprised only about 7% of the FY 1986 total state allocation for education (Clotfelter & Cook, 1989). The future of Florida Lottery revenues The instability of the lottery as a revenue stream gives cause for concern. As the Florida Lottery revenues continue to plateau or decline, will the educational system

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34 1.. :I 1..2 1..1 1 ff 0,9 j_ i o,e ..... :1 0,7 .. 0 .,S E< ., ~ ., 0 5 0.4 0 3 0.2 0 1 1.987 1.988 1..989 1.990 1.991. 1..992 PlBce.1 Year ID f!IUJ.ion Figure 2 Florida Lottery allocations to education, FY 1987 FY 1993, shown in current dollars (Source: State of Florida Department of Education, 1992, 1993). absorb the weight of the effect? For the lottery has long been noted to be an unreliable source of income, "subject to major year-to-year swings," (Mikesell & Zorn, 1988). By FY 1993, the Florida Lottery allocation to education had never regained the FY 1989 level (State of Florida Department of Education, 1992, 1993). The fluctuations in the size of the Florida Lottery allocations to all systems of education are shown in Figure 2. Florida's lottery profits may be expected to fall in the mid-1990s based on two different factors: the maturity

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35 of the Florida lottery and the implementation of the Georgia lottery. One probable contributing factor in the success of the Florida lottery is that, prior to 1993, none of the states contiguous to Florida operated a lottery. The presence of contiguous co-lottery states was found to be negatively correlated with lottery revenues (Mikesell & Zorn, 1987). However, a contiguous state lottery has also been reported to facilitate ticket sales: Stover (1990) found that a lottery in a neighboring state could improve sales by increasing enthusiasm and consumer awareness. ~ Georgia voters approved a lottery referendum in 1992. The following year, in the first seven days' operation of the Georgia Lottery, $52 million dollars were wagered, a sum that represented $7.80 per capita for the state. With this feat the Georgia Lottery surpassed a six-year-old, unbroken national record for first-week lottery sales set by the Florida Lottery, where first-week gross receipts were equivalent to $7.70 per capita. Interestingly, the Georgia Lottery is headed by Rebecca Paul, who was the founding chief executive officer of the Florida Lottery (Florida's lottery record falls, 1993). In FY 1993, Florida Lottery revenues should reflect an effect from the Georgia Lottery, which may well be suppression of sales. Second, as the newness of the Florida lottery gives way to maturity, sales may be expected to decline. Mikesell's {1987) regression

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analysis suggested a revenue peak at a lottery age of 10 years, which the Florida Lottery will reach in 1997: Maturing lotteries at first sell more, then less; the presence of a neighboring state's lottery also hurts sales .... The forces of lottery age have the second strongest effect on sales ... with only the influence of a neighboring lottery having a stronger effect. (p. 252) Enhancement dollars or subsistence? 36 The Florida lottery's seven years of existence have coincided with a general recession, a devastating hurricane, and a drop in tourism, the state's major industry. Lottery dollars were used in FY 1990 for subsistence at the community colleges during the three mid-year reductions in the state allocation. While the community college system had initially used lottery dollars for such tangible enhancement projects as system-wide library automation and expanded library collections at the individual colleges, by FY 1990 the college presidents supported the lifting of categorical restrictions on lottery funds in order to fund basic current expenses. In FY 1991, the Florida legislature implemented a policy to permit the governing bodies of the K-12 school districts, community colleges, and state university system (SUS) to decide internally the method with which most of the lottery allocation would be awarded (State of Florida Department of Education, 1992). The K-12 system differed from both systems of Florida higher education in that the Florida legislature placed categorical spending restrictions

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37 on about 14% of the K-12 lottery allocation In comparison, the legislature reserved for categorical awards about 10% of the SUS lottery allocation, and less than 3% of the community college allocation. Each year since FY 1990, the legislature had placed a declining proportion of the community college lottery allocation under categorical spending restrictions. In FY 1993, the lottery allocation to community colleges was entirely noncategorical. Figure 3 graphically depicts the proportional differences between the K-12, community college (CC), and SUS educational systems in the lottery allocations for FY 1992 that were categorical, as opposed to noncategorical, awards. Lottery Revenues Viewed as an Excise Tax ( One reason for the lottery's popularity was that it was commonly considered to be a nontax public revenue (Berry & Berry, 1990; Clotfelter & Cook, 1989; Hersch & McDougall, 1989). However, many different researchers have argued that lottery revenues should be viewed as an excise tax, even though the participation in lottery games is voluntary. Contemporary American lotteries began in New Hampshire in 1964, where a state lottery was implemented in order to raise funds for education and to relieve the tax burden on property owners. It was viewed by the citizens of New Hampshire as "an acceptable, voluntary revenue source for a state that has neither a sales nor an income tax," (Thomas &

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l.l.0 1.00 90 &O 70 .. II ~o ,, i 0 50 14 II, ,o 30 20 1.0 0 IC 1.2 oc SUS Figure 3. Percentages of FY 1992 lottery categorical & noncategorical (Source: State Department of Education, 1993, p. 4). 38 allocations, of Florida Webb, 1984, p. 297). New York voters followed by approving a state lottery in 1967; the New Jersey voters, in 1970. In the 1970s, voters in 12 states approved lottery referenda. In the 1980s, 18 states were added to the lottery-operating list. A lottery was implemented in Wisconsin in 1988 explicitly for property tax relief (WI St. .10). In the 1990s, four more state lotteries were approved, in Georgia, Louisiana, Minnesota, and Texas. The general popularity of the lottery was reflected in the 65% approval rate averaged by 20th century state lottery

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39 referenda (Clotfelter & Cook, 1989). However, the trend to rely on a state lottery for needed revenues may have come full circle. Garland (1992) conducted a survey of New Hampshire voters' attitudes toward implementing a state income or sales tax to equalize the funding of the states' public schools. His findings suggested that the voters were ready to approve higher taxes, if those taxes were earmarked to benefit public education. Is the lottery regressive? Regardless of the prevalence and popularity of the 20th-century state lottery, a strong case may be made that the state lotteries are, in fact, excise taxes that are far more regressive than the excise taxes on liquor or tobacco. Several different researchers have used regression techniques to measure the economic regressivity of the lottery as a tax, as well as the prevalence of lottery play among different demographic groups (Mcconkey & Warren 1988). The most comprehensive analysis of the state-operated lottery as a public revenue source was written by Clotfelter and his associates (Brinner & Clotfelter, 1975; Clotfelter & Cook, 1987, 1989, 1990a, 1990b, 1991). As early as 1975, Brinner and Clotfelter argued that lottery revenues might be analyzed using the techniques used to study tax and public policy: A state lottery simultaneously creates a consumption good and taxes that good comparison to a situation in which a lottery exists but is not taxed the In similar implicit

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40 lottery tax imposes a burden which may properly be judged within the framework of traditional tax analysis. (p. 395) As more states implemented lotteries, Clotfelter and Cook (1987) extended the analogy: Not only is it appropriate to label the resulting net revenue an implicit tax, it is interesting to note that this implicit tax is closely analogous to a corporate tax on net income, but with a tax rate of 100 percent. (p. 534) The emotional intensity of Clotfelter and Cook's publications was evident. They described a lottery wager as a "sucker bet," (1989, p. 70), then a "lousy bet," (1990b, p. 104), and finally a "crummy bet," (1991, p. 228). Karcher (1989), an attorney and former New Jersey legislator, used an emotional tone to describe the lottery as a regressive tax: The end result is a system that, as tax policy, is regressive and rapacious, that uses promotions that target the poor, and that markets tickets in a manner that is often abusive and exploitative. These, indeed, are the three "sins" of the states: avarice, conscious oppression of the poor, and hypocrisy." (p. 7) Thomas and Webb (1984) supported the Clotfelter and Cook argument, that the lottery should be viewed as a regressive tax: That portion represented as "state share" or profit serves in practice as an excise tax. Regardless of whether the revenue is considered a tax or a profit, the result is the same; the contribution to the state treasury is in proportion to the quantity/price of the purchased product, and the burden of financing state services is apportioned among income groups in proportion to their demand. (pp. 306-307)

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41 Predictor variables of lottery participation Mikesell and Zorn (1988) argued that a state lottery was an excise tax that was also highly regressive because of the demographic descriptions of the persons who have the greatest participation rates: Lotteries bear a high implicit excise tax rate and, because of the pattern of play across income classes, appear to worsen the overall equity of the revenue system. (p. 38) Clotfelter and Cook (1989) concluded that the lottery was regressive for many reasons, including the demographic descriptions of the players. These researchers found the strongest predictor variable of lottery participation to be level of formal education. They found education to be negatively correlated with lottery play, which is the inverse of the positive correlation found to exist between casino gambling and education. Thus, in the United States, the people who are the most educated are most likely to gamble in casinos; the least educated people are most likely to play the state lottery. Clotfelter and Cook (1989) also found that ethnicity is a predictor variable of lottery play, with Blacks and Hispanics having greater participation rates than whites. Further, while income per se was not found to be predictive, frequent participants from the lowest income groups were shown to commit a greater percentage of their household wealth to the lottery; similarly, frequent participants from the highest income groups were shown to commit the lowest

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percentage of household wealth. Therefore, Clotfelter and Cook concluded that the lottery was regressive. Does earmarking exacerbate regressivity? 42 Borg and Mason (1988, 1990) examined the uses to which lottery revenues were put as well as the demographics of the players. Using regression analysis, they showed first, that the lottery had become more regressive over time; second, that the people who played the lottery most were those who received the least direct benefit from the state's expenditure of lottery profits. Borg and Mason cocncluded that the demographic disproportion of benefits received versus participation rates increased the regressivity of the lottery. Wyett (1991) argued that lotteries were regressive taxes whose regressivity was exacerbated when state legislators earmarked the proceeds for any recipients other than the state general revenue fund. Like Borg and Mason, Wyett found that lottery-funded projects were not heavily used by low-income citizens. Further, Wyett found that low income citizens disproportionately constituted the pool of lottery players. Lotteries are regressive taxes whose incidence of taxation falls most heavily on low-income families. In fact, lotteries are the most regressive tax in existence in the United States today ... Not only are these lotteries imp l icit taxes, but the directed use of the lottery revenues may affect the regressive nature of the tax. (p. 15)

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43 Type of lottery game versus regressivity All lottery games are not equally regressive; some games are more regressive than others. The on-line lotto games were found to be the least regressive, because they were played most heavily by higher-income persons, and were less favored by members of the lower-income groups (Clotfelter & Cook, 1989; Mikesell, 1989). On-line games also generated the most excitement and earned state treasuries the highest revenues because they sometimes incurred huge jackpots, often many millions of dollars (Masters & Gaines, 1993). Supplantation The tendency of lottery dollars to supplant general revenue funds was recognized by Weinstein and Deitch (1974) nearly two decades ago, using data collected from five different states from 1968 through 19 7 3. These researchers concluded that the supplantation of general revenue funds with lottery dollars was a more probable outcome than the enhancement of available resources for any given beneficiary. Wyett (1991) noted that earmarking the lottery proceeds for a speci f ic beneficiary was most l ikely to lead to supplantation of general revenue dollars. Wyett vi e wed supplantation a s b e ing p a rticular l y p r ob le mat i c w i th l ot ter y f unds, b ec au se th e lott er y had h is to ric ally be e n elas t ic,

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44 unstable, and unpredictable when used as a source of revenue. When lottery revenues plateaued or actually declined, as they did in Colorado, Illinois, Missouri, West Virginia, and the District of Columbia in FY 1988, the supplanted general revenue funds typically were not immediately restored to the lottery beneficiaries. Is supplantation inevitable? Clotfelter and Cook (1989) argued that supplantation was inevitable, despite measures like earmarking which were designed to control the use of revenues, because of the fungible nature of the state budget process. Even if state law does earmark lottery income to a particular purpose, there is reason to believe that the budget process nullifies the intended effect. Despite efforts to segregate lottery revenues, it is impossible to prevent the legislature from taking that source of revenue into account when voting on appropriations for an agency receiving earmarked funds. (p. 228) The Illinois lottery profits were earmarked for public education. Using trend analysis, Borg and Mason (1988) determined that supplantation of general revenue funds did, in fact, occur in Illinois, concluding that The evidence overwhelmingly suggests that it has. The problem extends beyond legislative redirecting. There has been no way to guarantee that the funds truly go to education since there has been no policy to prevent funds that would otherwise have gone to education from being diverted away to other programs. (p. 81} Supplantation in Florida It was demonstrated that supplanting K-12 general revenue funds with lottery dollars occurred in the state of

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45 Florida. Stark, Honeyman, and Wood (1991) found that lottery funds were used to substitute for a portion of general revenue funds in support of elementary and secondary education in FY 1989. According to MacManus and Spindler (1989), In Florida, there is no legal prohibition against legislative substitution of lottery revenues for other revenues that have supported education in the past. There is no guarantee that a new revenue source creates a net gain to the education funding base. (p. 1) MacManus and Spindler predicted that the true beneficiary of an earmarked lottery would not be the designated beneficiary, which in the case of Florida was education. They predicted that, in Florida, the benefits would accrue to city and county governments, because the supplanted state education funds might then be redistributed for expenditure on transportation, social services, health care, law enforcement, and other services that often burdened city and county governments. In the Florida Supreme Court opinion concerning the legality of Article X, which amended the Florida Constitution to permit a lottery, Justice Boyd wrote, The amendment itself makes clear that revenue realized by operation of the lottery will be placed in a state trust fund but that there is no absolute requirement that the funds be spent only on education. Even if it is all used for education this would not necessarily increase the level of state resources devoted to education since the legislature is free to reduce the funding of education from other sources. (Carroll v. Firestone, 1986, p. 1207)

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46 Redistribution The issue of the supplantation of general revenue funds is linked to the separate issue of fiscal redistribution. The concept of redistribution applies to the manner in which a finite quantity is divided. If the proportional division changes over time, the quantity is said to have been redistributed. The distribution and redistribution of goods is a problem that is extensively addressed in economic theory, often using regression analysis. The politics of redistribution The redistribution of income has long been a function of government. According to Tullock (1983, p. 1), "Redistribution is probably the most important single function of most modern governments." Further, according to Lucas (1992, p. 246), "The study of distribution is, over a long enough time period, the study of social mobility.'' On a microeconomic level, taxes paid by one citizen are collected by the government to be redistributed to other citizens. A referendum approving a state lottery may be approved because the citizens of the state desire to raise money for a common good, such as education (in Florida, California, and 12 other states), public parks and recreation (in Arizona and Colorado), or senior citizen aid (in New Jersey and Pennsylvania). Alternatively, the voters may want the recreational opportunity provided by playing the lottery, or they may plan to save their money while their fellow

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47 citizens purchase lottery tickets (Hersch & McDougall, 1989) Redistribution of personal income Clotfelter and Cook (1989) used the redistribution of personal income in their arguments against the lottery. They argued that the effect of the lottery on individuals was always redistributional: "Many lose so that a few might win," (p. 134). If one considers the category of players having the most frequent participation, those in the lowest economic group commit a greater percentage of their household wealth to lottery consumption, while the wealthiest commit the smallest percentage. If dollars spent by those at lower incomes are given more weight than dollars spent by those with higher incomes, an increase in the rate of implicit tax on lotteries is less desirable than an increase in the rate of tax on most other state taxes on distributional grounds alone. (Clotfelter & Cook, 1989, p. 227) Redistributional effects on institutional support Macroeconomically, a state treasury contains a finite amount of money that may be distributed to all the institutions which the legislature elects to fund in a fiscal year. One method used in this study to consider the redistribution of general revenue funds was to look at the percentage sources of the community colleges' fiscal support. A source of archival data concerning redistribution is the series of the Community College Finance Surveys

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48 conducted at the University of Florida, of which the most recent included information about state lotteries (Honeyman, Summers, & Wattenbarger, 1993; Honeyman, Williamson, & Wattenbarger, 1990; Wattenbarger & Mercer, 1985, 1988). The information collected from the Florida respondent indicated that the state's share of the Florida community college operating budgets had eroded over time, while the local share had grown, and the federal and "other'' categories had been unstable. A redistribution of inputs leads to a redistribution of outputs, a fact which has often been overlooked in fiscal planning. Clotfelter (1992) noted that a shift in an institution's sources of financial support leads to a redistribution in the array of services provided. This redistribution effect was readily apparent in Florida's community colleges, which were the primary point of entry for disadvantaged students into Florida's system of higher education. Federal support to these colleges was mainly in the form of grants for specific demographic groups and specific academic programs. For example, there were need based Pell grants to individual students, and Carl Perkins scholarship funds for disadvantaged students in high-wage vocational programs. When scholarship funds were unavailable or inadequate to meet the students' needs, these demographic groups were less likely to be consumers of higher education. For a second example, federal grants became available to

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49 assist with implementation of the Americans with Disabilities Act. The funds for these grants were obtained by the redistribution of funds from other federal projects. Redistribution of state own-source revenues One final aspect of redistribution is that of one revenue source supplanting, or suppressing, another. Borg, Mason, and Shapiro (1993) extended the work of Clotfelter and Cook (1989) in modeling the extent to which lottery ticket purchases suppressed revenues from other state tax sources. For example, a dollar that was spent on a lottery ticket was not subject to sales tax, and may have supplanted a dollar that would have been spent on a sales-taxable item. Also, an out-of-state lottery jackpot winner would have resulted in the redistribution of in-state dollars to the winner's home state. Using regression analysis, Borg et al. determined that for every dollar of state lottery revenue generated, from 15 to 23 of other tax revenue was lost. Even though this extreme still implies that the state receives 77 cents more tax revenue than before the lottery was imposed, those states that earmark their lottery dollars likely see significant reductions in their nonlottery revenue sources that need to be accounted for in their budgets. Otherwise, a bonanza in one area of the budget causes a sizable and likely unexpected shortfall elsewhere. (p. 123) Borg et al. found the strongest effects for states without a state income tax, with a relatively great reliance on sales and excise tax revenues, and with a high-revenue state lottery. Further, when a state had earmarked the lottery

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50 proceeds for a designated beneficiary, redistribution occurred among the state-supported agencies as a consequence of the rising or falling tides of the lottery fortunes. Redistribution of Florida revenues While the states studied by Borg et al. did not include Florida, their findings suggested a strong suppression effect by Florida's lottery profits on own-source revenues, and a redistribution of expenditures from the general revenue fund. The suppression of Florida parimutuel taxes that corresponded with the Florida Lottery years of operation was readily apparent. Parimutuel tax revenues in Florida commenced in FY 1965 and increased every year until FY 1987, which was the year of the start of the Florida Lottery. After FY 1987, parimutuel revenues declined each year, for a total decrease of 19% from FY 1987 to FY 1991, or a revenue decline of $24.9 million (State of Florida Governor's Office of Planning and Budgeting, 1993). Figure 4 illustrates the rise and fall of Florida's parimutuel tax revenues. The Lottery as a Quasi-Business Monopoly Twentieth-century state lotteries were operated somewhat like a business. The chief executive officer of the lottery was a government agent whose explicit duty was to encourage ever-expanding consumption by the public in order to generate public revenue (Clotfelter, 1991; Clotfelter &

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51 1.,0 1.)0 1.20 1.1.0 1.00 ,o 80 70 410 so ,o 30 1.,,5 1975 1985 1,,0 1970 1980 1~87 D l:n II M1l.l.1ona Figure 4. Parimutuel tax revenues rose from FY 1965 until the inception of the Florida Lottery, FY 1987 (Source: State of Florida Governor's Office of Planning and Budgeting, 1993). Cook, 1989; Fisher, 1988; Karcher, 1989; Karl, 1991). The quasi-business, profit-generating function of the lottery department was often specified in the legislation, as it was in Florida: That the lottery games be operated by a department of state government that functions as much as possible in the manner of an entrepreneurial business enterprise. (FL St. .102.2.b} The purpose of this department is to operate the state lottery ... so as to maximize revenues. (FL St. .104.2)

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52 An interesting analogy between higher education and the lottery as a state-produced consumer good was drawn by Clotfelter and Cook (1989): States seldom promote the liquor or utilities they sell, but both lotteries and higher education are marketed, publicized, and implicitly endorsed by the states, each in its own way. Far from being an insignificant appendage to state government, lotteries have become a highly visible enterprise. (p. 31) Ethical considerations Although much effort was expended by lottery directors to promote the sales of their product, Gulley and Scott (1993) questioned whether promotion were appropriate: One ... issue is whether states should set as their goal the maximization of net revenue accruing from the lottery. States that run liquor monopolies do not glamorize alcohol and exhort citizens to drink more, as is done in the marketing of lottery products. (p. 21) Karl (1991) objected as much to the content of the advertisements, as to the fact of promoting state lotteries: Lottery promotion amounts to publicly financing aggressive advertising that is often misleading and pernicious ... These government funded ads are big on promoting the lottery as a better investment than saving or education or hard work . Another popular lottery marketing technique elevates gambling to the level of civic responsibility. Touting lotteries as a boon to social programs from education to prison construction attracts new players and convinces reluctant state legislatures to adopt lotteries. (p. 14) Allen (1991) expressed concern that the lottery funds have been used by politicians to man i pulate the public into thinking that education were better funded than it really

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53 was; further, that lottery dollars were diverted from their intended, expressed, purpose. The budget suppression effect of education lottery revenues flies directly in the face of the legitimacy of the lottery itself, which has been negotiated between the state's public and its government. (pp. 302-303) Allen noted that lotteries had been implemented in low tax states, and also in states without a personal income tax such as New Hampshire, Connecticut, and Florida, where the lottery was viewed as an expedient nontax revenue source. High-tax states such as New York and New Jersey implemented lotteries to offset the revenue losses that resulted from a shrinking industrial revenue base. The popularity and "moral legitimacy" of state lotteries was viewed by Allen as a form of public naivete "as a function of having no recent exposure to lottery corruption," (Allen, pp. 300-301). Allen and others argued that the rapid expansion in the prevalence of state lotteries was a reaction to three interrelated elements: first, the federal cutbacks of the Carter, Reagan, and Bush administrations (Clotfelter, 1991; Hildred, 1991); second, the political mantra "no new taxes,'' (Berry & Berry, 1990, p. 396); and third, the growing demand for new and expanded social and health-care services (Swartz & Peck, 1990). Wyett (1991) called for the abolition of state lotteries, arguing that lotteries enabled legislators to

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shirk responsibility for finding adequate revenue sources through levying explicit taxes: "Political accountability" and "tax honesty" should replace "lip reading" and "tax amnesty" as the "buzzwords" in state finance in the 1990's Perhaps as a matter of public policy state lotteries should be abolished ... state legislators should be held to a new level of accountability. By abolishing lotteries, politicians will have to find other revenue sources to supplement their tax bases. They will have to raise taxes and actually say the word "tax," rather than resorting to such deceptive practices as ... promoting lotteries. (pp. 1415) 54 A separate but related problem was the fact that lottery revenues usually accounted for a much smaller proportion of a beneficiary's operating funds than the public was encouraged to believe. In the most successful lottery states, proceeds were roughly equivalent to a 1% increase in the state sales tax (Clotfelter & Cook, 1989). At the height of the Florida Education Lotteries campaign, a newspaper poll conducted in August of 1986 "found that over half of the respondents believed that the lottery would pay for a 'major portion' of the total state budget for education," yet the state Commissioner of Education projected enhancement revenues equal to only one-fifteenth of his total budget (Clotfelter & Cook, 1989, p. 155). Earmarking Lottery Proceeds The issue of earmarking should be examined in light of the actual benefits that accrued to the beneficiary.

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55 Are lottery beneficiaries better funded? Borg and Mason (1990) found that earmarking actual l y led to a decline in fiscal support for the beneficiaries, accompanied by a rise in the erroneous perception by the general public that these agencies were being well funded. In fact, Borg and Mason reported that earmarking lottery proceeds, whether for education or any other designated purpose, led to demonstrated supplanting in all states studied since 1968. They found that only two of the five lottery states incurred actual growth in nominal total allocations to education, while the other three states experienced declines in the absolute growth of education expenditures. The only states that showed an upward trend in total allocation per FTE were states with a simultaneous drop in enrollment coinciding with growth in the general revenue fund. Borg and Mason determined that What is driving support for education in the earmarking states is not the lottery, but rather the status of total revenues for the state in question. This provides early evidence that the lotteries have not been boons for their statutory beneficiaries because the advent of lottery revenues is not enough to avert trends in general revenues as they affect the funding of education. (p. 295) Supplantation versus economic recession Borg and Mason {1990) concluded that the lottery itsel f did not hurt educational funding; rather, ''What can be inferred is that the downward trends in the states' tota l revenues are the culprits," (p.297).

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Have the lotteries improved the conditions of the educational systems in the states where they exist? ... the answer is a resounding no .. it is more likely that those additional funds raised have supplanted alternative sources. Therefore, the general conclusion is that earmarked lotteries have not benefitted the statutory recipients. In fact, the recipients do not even achieve the relative benefit of neutrality. Earmarking has been concurrent with the decline in education expenditures in nominal terms in some of the states, and in real terms in all. This occurs because lottery revenues provide the legislators of each of the states with a procedure that camouflages their inability to raise sufficient tax revenue to adequately provide for the public school systems in their states. (pp. 299-301) Political expedience of earmarking 56 One reason that so many state lotteries were earmarked for a specific beneficiary was that it helped to get the referendum passed, as it did in Florida. A second reason was that an advertising campaign that linked the beneficiary with the lottery was believed to increase ticket sales (Clotfelter & Cook, 1989; Karl, 1991). Earmarking had the greatest effect where the lottery funds constituted a large portion of an agency's total budget; otherwise, because of the inherent fungibility of the budgeting process, earmarking had little real effect on the beneficiary's financial status (Clotfelter & Cook, 1989). The Historical Context of Contemporary Lotteries The state-operated lotteries of the 20th century were a departure from those that were described for the Greek,

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Roman, Biblical, and even Colonial American times. Nevertheless, a review of the history of the lottery lends perspective to the discussion at hand. The Earliest Lotteries 57 The lottery as a form of entertainment or a method of allocating resources has a very long and well-documented history. Lotteries were used by the Romans for entertainment and the Greeks to facilitate the democratic government process (Karcher, 1989). Lotteries were mentioned in both the Old and New Testaments of the Bible. In the Old Testament, in the Book of Numbers, the Lord God instructed Moses to use a lottery to divide the Promised Land among the 12 tribes of Israel: The land ... shall be apportioned by lot; the lots shall be cast for the properties by families in the father's line. Properties shall be apportioned by lot between the larger families and the smaller. (The New English Bible, Old Testament, Numbers 26:55-56, p. 182) In Proverbs, the outcome of a lottery was mentioned as being determined by Divine providence rather than fate: The lots may be cast into the lap, but the issue depends wholly on the Lord. (Proverbs 16:33, p. 767) Because of their belief in divine intervention into the lottery's outcome, Colonial Quakers opposed the lottery in Pennsylvania, believing that betting on a raffle or lottery was impious and a frivolous use of God's providence.

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58 Increase Mather wrote in his 1687 Testimony against Several Prophane and Superstitious Customs, He that makes use of a Lot wholly commits his affair to a superior Cause than either nature or art, therefore unto God. But this ought not to be done in a Sportful Lusory way. (Ezell, p. 17) In the New Testament, in the Book of Acts of the Apostles, the remaining apostles of Christ used lots to determine which disciple should become an apostle, replacing Judas Iscariot: They drew lots and the lot fell on Matthias, who was then assigned a place among the twelve apostles. (New Testament, Acts 1:26, p. 148) The first lottery to offer cash prizes while raising funds for the state was held in Florence, Italy in 1530. The Italians brought lotteries to France around 1533. In England, the first government lottery was chartered by Queen Elizabeth I in 1566. The English brought lotteries into Colonial America with an authorized drawing to support the Jamestown settlement in 1612 (Clotfelter & Cook, 1989). Territorial Florida Lotteries The first Florida lottery was cited as occurring in 1766, when Nathaniel Thompson was authorized by the Council of West Florida to sell his house by lottery (Ezell, 1960). The first Florida education lottery was launched when the trustees of Union Academy in Jacksonville, Florida, were authorized by the territorial legislature in 1828 to conduct a $1,000 lottery to endow the academy. Only four years later, in 1832, the Florida legislature banned all gaming,

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59 including lotteries (Greater Loretta Improvement Association v. State ex rel. Boone, 1970). Intercolonial and Interstate Lotteries The first Colonial lottery to be earmarked for education was held in 1746, when a lottery was used as a fund-raiser for the founding of King's College, later to be called Columbia University. In 1747, Yale College was approved a ,500 lottery to raise funds for housing; Harvard was approved a similar lottery for housing funds in 1765 (Ezell, 1960). In early American times, the population was sparsely distributed; therefore, fund raisers devised intercolonial lotteries in order to maximize revenue. Princeton, then called the College of New Jersey, was the recipient of proceeds from a lottery held simultaneously in Connecticut, Delaware, and Pennsylvania in 1753, setting the earliest recorded example of an intercolonial lottery (Ezell, 1960). The example was followed in the 20th century, when the smallest and most sparsely populated states formed lottery consortiums in the 1980s and 1990s. The first contemporary example was the signing of the Tri-State Lotto Contract by legislators in Maine, New Hampshire, and Vermont in 1985; Delaware was added in 1988. The Lotto America consortium began in 1988 and included the District of Columb i a and five states (Clotfelter & Cook, 1989; Appendix B) Lotto America

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60 was replaced in 1992 by the Powerball lottery, a lucrative consortium which included 14 small or sparsely-populated states (Delaware, Idaho, Indiana, Iowa, Kansas, Kentucky, Minnesota, Mississippi, Montana, Oregon, Rhode Island, South Dakota, West Virginia, and Wisconsin) and the District of Columbia ($110 million lottery prize not yet claimed, 1993). In Kansas, where a lottery was approved in 1987, legislators with foresight wrote into the enabling legislation that interstate lotteries could be operated between Kansas and any other state or the District of Columbia (KS St. 8731). Expedience of the lottery in Colonial America Thomas Jefferson was said to have originally opposed the government operation of lotteries (Karcher, 1989). He later supported the practice because of its expedience in Colonial America, where currency was scarce: An article of property, insusceptible of division at all, or not without great diminution of its worth, is sometimes of so large a value as that no purchaser can be found while the owner owes debts, has no other means of payment, and his creditors no other chance of obtaining it but by its sale at a full and fair price. The lottery is here a salutary instrument for disposing of it, where men run small risks for the chance of obtaining a high prize. (in Ezell, p. 13) Thomas and Webb (1984) responded to this quotation by saying that, Although not all colonists supported the use of lotteries to the degree exemplified by Jefferson, it was felt by many to be an acceptable device for raising funds. Most settlers had experienced the lottery in Europe and considered it to be a tax

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voluntarily paid, regardless of its regressive nature and in spite of its corrupt history. (p. 292) Early American education lotteries 61 In Colonial America, a lottery for the good of education was considered morally acceptable by citizens for whom gambling for sport was not permissible. The Quakers of Pennsylvania generally prevented the authorization of lotteries for civic or general purposes, but approved lotteries to benefit Princeton (then the College of New Jersey) in 1749, 1750 and 1761. The College, Academy and Charitable School of Philadelphia, later to become the University of Pennsylvania, was endowed with lotteries that dated to 1755 (Ezell). Early Examples of Supplantation and Redistribution An early version of the struggle over lottery funds that were earmarked for higher education was found in Colonial New York in 1753, concerning a lottery for King's College {Columbia). The enabling legislation Bore testimony to the growing feud between the Presbyterians, who opposed the school, and the Anglicans, who sponsored it. To keep the former from diverting the funds, an unusual clause in the statute declared that any representative who voted or consented to a diversion of this money would be ineligible to sit or vote in that or succeeding assemblies. An identical scheme again was approved in the following December. (Ezell, p. 37) Despite the "unusual clause," funds for higher education were diverted to corrections and health care. In 1756

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Action was taken to restore harmony between the Anglicans and Presbyterians when the New York legislature gave half the funds raised for King's College to the City of New York for a jail and "Pest house" for persons with "contagious Distempers." Mindful of the penalty for such action, the legislators first had taken the precaution of repealing that section of the law of 1753. (Ezell, p. 38) 62 Early attempts to divert lottery funds earmarked for higher education into the general treasury were also recorded during the Confederate period following the Revolutionary War, and preceding the War Between the States. In Delaware, In 1835 a $100,000 project to benefit education included $25,000 for the general treasury; and on February 17, 1852, an additional $100,000 was sought for governmental needs. New Jersey used this same approach in 1812 and 1823 by requiring the managers for lotteries approved for Queens College (later Rutgers) to obtain an additional $5,000 for the state. (Ezell, p. 109) Competition for state funds One justification for the Confederate-period diversion of lottery funds was that state governments of the early 19th century were becoming more involved in providing social and public health services, a province that formerly was funded predominantly by churches and private charities. Thus, even in the Confederate days, social services, law enforcement, and health care were competitors with education for receipt of state lottery profits. As was true in the 20th century, the competition among state-supported institutions and services was especially intense in the most populous states, where the demand for services was greatest.

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63 An elastic source of revenue After the Revolutionary War, lotteries earmarked for higher education were authorized to fund Harvard College in Massachusetts and Dartmouth College in New Hampshire (Ezell, 1960). Lottery revenues of the Colonial period sometimes fell below projections, just as they did in the 20th century, and for the same reasons: partially from saturation of the public's interest, but also because of the economic depression of the period. The Dartmouth College lottery of 1787, expected to raise ,800, brought in only despite the tactics of adding new games, special twists, and an extension of the sales period. The percentage of lottery proceeds that actually benefitted the colleges was sometimes much lower in those days than was true of the Florida lottery of 1993: a Harvard lottery of 1806 paid out $1,250,000 in prizes and overhead expenses, for a net proceed to Harvard of only $29,000. The Revocation of State Lotteries Lotteries remained popular in Confederate-period America. Between 1790 and 1860, 24 of 33 states used the lottery to finance internal improvements. However, anti lottery sentiment was growing: Important factors in the decisions of various assemblies to regulate lotteries included corruption, complaints of merchants that such unorthodox business methods diverted large sums from commercial channels and made competition

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difficult, and the harmful effects on lower classes. (Thomas & Webb, 1984, p. 293) Constitutional revocation of state lotteries 64 The lottery was outlawed by constitutional amendment in a number of states during the 18th century, beginning in Massachusetts in 1719, and extending to Pennsylvania in 1720, New York in 1721, Connecticut in 1728, Rhode Island in 1733, and New Jersey in 1748. By 1840, 12 of the 26 states had temporarily banned lotteries. At the start of the Civil War, all the remaining states except for Delaware, Missouri and Kentucky had banned the lottery (Thomas & Webb, 1984). This action was taken because the administration of state supported lotteries had evolved to the point that corruption was rife among the brokerage houses that sold lottery tickets, the promotion of lottery sales invoked concerns about the state governments' encouragement of public immorality, and the actual returns to the beneficiaries began to decline while the proportion expended on overhead greatly increased. Public backlash against the lottery was well summarized in this excerpt from a United State Supreme Court case of 1850: The suppression of nuisances injurious to public health or morality is among the most important duties of government. Experience has shown that the common forms of gambling are comparatively innocuous when placed in contrast with the wide-spread pestilence of lotteries. The former are confined to a few persons and places, but the latter infests the whole community; it enters every dwelling; it reaches every class; it preys upon the hard earnings of the poor; it plunders

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the ignorant and simple. (Phalen v. Virginia, 1850, p. 168) The last of the early American lotteries 65 The Louisiana Lottery was the most infamous and long lasting state lottery of the 19th century. It was finally halted by federal intervention, a result of the fact that 93% of all tickets were purchased through the U.S. Mail by citizens of other states or foreign countries. In 1895 Congress outlawed the importation and interstate carriage of lottery-related materials, an act which the Supreme Court upheld in 1903. The Louisiana Lottery was dissolved soon thereafter (Thomas & Webb, 1984). No 20th-century state lottery existed until the New Hampshire Lottery was approved in 1964.

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CHAPTER 3 METHODOLOGY The purpose of this study was to determine whether a state-supported agency benefitted fiscally from being a designated recipient of a portion of the profits from a state-operated lottery. The Florida Lottery and the Florida system of 28 community colleges were used to explore the issue. The analysis was divided into four separate questions. Regression models were constructed to examine each of the four questions proposed. Impact. The first question was whether the start of the Florida Lottery coincided with a change in the expenditure trends of the Florida community colleges. Supplantation. The second question was whether Florida Lottery funds either supplanted or enhanced state general revenue funds expended in support of community college education. Redistribution. The third question was whether the addition of the lottery as a revenue source resulted in a change, or redistribution, in the proportion of community college expenditures funded through state sources. Categorical/noncategorical. The fourth question concerned the proportion of lottery dollars that were 66

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67 released to community colleges in the form of a categorical allocation versus lottery dollars that flowed without spending restrictions into the Community College Program Fund (CCPF). The goal was to determine whether the percentage of categorical restrictions correlated with the total amount of state funds allocated to the community colleges. The method used to address these four questions was an archival study that analyzed three conditions using regression over time (Chatterjee & Price, 1991; Cook & Campbell, 1979). The first condition was the expenditure trends of the 28 state-supported community colleges in Florida. The second condition was the allocation of State of Florida general revenue and lottery funds to community colleges. The third condition was the percentage of each year's lottery allocation that was categorical, rather than noncategorical. Hypothetical Constructs The statistical models of this study were designed to test four basic hypothetical constructs: 1. A relationship exists between the Florida Lottery and the fiscal condition of the community colleges in Florida. This relationship may be reasonably known. 2. The relationship between the Florida Lottery and the Florida community colleges is plausibly causal.

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3. If the relationship is plausibly causal and reasonably known, then cause-and-effect constructs may be involved between the Florida Lottery and the fiscal status of the colleges. 68 4. If there is a probable, causal relationship between the Florida Lottery and the fiscal condition of the colleges, then this relationship may be generalized across other state lotteries, state community college systems, state educational systems, and other state-supported agencies that are earmarked for lottery funding. Also, this relationship may be generalized across other time periods (Cook & Campbell, 1979). Assumptions Each of the proposed models assumed linearity. Scatter plots and residual plots were constructed to assist in testing the five basic assumptions that concern the dependent (Y) variable in linear regression models: 1. A Y distribution exists for the X variables studied, with a finite mean and variance. 2. The Y observations are statistically independent of one another. 3. The Y values are a linear function of the X values. 4. The Y variance is homoscedastic for any fixed combination of X 1 X 2 , Xk.

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69 5. The Y distribution is normal for any fixed combination of X 1 X 2 , Xk (Kleinbaum, Kupper, & Muller, 1988) Where indicated by the residual and scatter plots, other versions of the models were tested with the introduction of a quadratic term. In every instance, the linear model was found to be the model which best fit the data. There were two assumptions made of the explanatory (X) variables: 1. The explanatory variables were nonstochastic; the X values were fixed and selected in advance of this study. 2. The X values were measured without error (Chatterjee & Price, 1991). The values of the data used for this study were robust to both of these assumptions. Did the Florida community colleges benefit from being earmarked for a portion of the proceeds from the Florida Lottery? This archival study used fiscal expenditure and enrollment data for each of the 28 Florida community colleges, and general revenue and lottery allocation data from the State of Florida Department of Education {State of Florida Department of Education 1990a, pp. 3, 6; 1990b, pp. 3-4, 25; 1991, pp. 3-4, 7; 1992, pp. 3-5, 8; 1993, p. l;

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70 State of Florida Department of Education Division of Community Colleges 1974, pp. 48, 70-74; 1975, pp. 32, 61-65; 1976, pp. 30, 56, 58-61; 1977, pp. 34, 63, 65-72; 1978, pp. 34, 62, 64-71; 1979, pp. 32, 60, 62-69; 1980, pp. 33, 63, 65-74; 1981, pp. 11, 42, 44-53; 1982, pp. 11, 42, 44-53; 1983, pp. 44-53; 1984, pp. 11, 42, 44-48; 1985, pp. 11, 39, 41-45; 1986, pp. 14, 52, 54-58; 1987, pp. 13, 73, 75-79; 1988a, 1988b, pp. 15, 75, 77-81; 1989, pp. 15, 77, 79-83; 1990a, 1990b, pp. 13, 79, 81-85; 1991a, 1991b, 1991c; 1992a, pp. 28-29, 76-77; 1992b; 1993a, 1993b). The State of Florida Commissioner of Education mandated a sophisticated, uniform system of data collection to track the 28 institutions of the Florida public community college system. Therefore, data concerning each of the 28 community colleges for each of the fiscal years under study were available from a central source, and the data were objectively considered to be uniform and reliable (Cook & Campbell, 1979; Mason & Bramble, 1989). Additionally, the Florida Department of Education, Division of Community Colleges staff persons who were responsible for compiling and reporting the community college data assisted with the data collection for this study. Indeed, one staff person was directly responsible for data management throughout the entire 22 fiscal years included in this study, and indicated a change in the method of reporting community college expenditures that occurred in FY 1974. This information

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71 resulted in a modification in the definition of one independent variable, TOTAL E&G (Total Education and General expenditures), and thus reduced a potential instrumentation threat to validity of the statistics. The data were comprised of State of Florida lottery and nonlottery allocations to the community colleges, TOTAL E&G, and weighted FTE for each of the 28 Florida community colleges for every fiscal year under study. Expenditure data was shown by Harrell and others to be appropriate to the study of community college finance (Harrell, 1992; Harrell, Honeyman, Wattenbarger, & Wood, 1993). Data for each institution, rather than the system as a whole, was used to increase the total number of data points, and, therefore, the power of the statistics (Mason & Bramble, 1989). Procedures Regression analysis over time was the statistical method used in this study. The community college fiscal status was operationalized as fiscal and enrollment data consistently collected over a 22-fiscal-year period. The data series was divided into two segments, which were comprised of lottery and nonlottery years (McCain & McCleary, 1979; McDowell, McCleary, Medinger, & Hay, 1980). Regression analysis over time was found throughout the review of the literature to be a method commonly selected

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72 for analyzing the outcome when state lottery profits were introduced as a revenue source. In order to increase the power of the regression analyses, data points were reported for each of the 22 fiscal years of the study, from each of the 28 community colleges, rather than for the community college system as a whole. As a result, this study included 616 data points. Population data, rather than sample data, were used for all computations. The population consisted of 28 separate community colleges throughout the period under study. Fiscal Years (FY) 1972 through 1993 were selected for all calculations except those involving community college year end expenditures. For community college expenditure data, FYs 1972 through 1991 were used, because data from subsequent years were unavailable at the time of this study. Fiscal Year 1972 was chosen as the starting year for the data used in this study, because FY 1972 was the first full year of completion of the State of Florida Master Plan, which implemented the full system of 28 community colleges (State of Florida Department of Education, 1990). Design The basic research design was a simple regression analysis over time. The design for observations (0) from 1972 through 1993, and the introduction of the intervening variable (X), the Florida Lottery:

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73 0 n 073 074 s 0 86 X 0 a1 aa 0 a9 093 For every O there were 28 entries, one for each community college, identified as CC=l, CC=2, ... CC=28 (Appendix A). The X was the term of introduction of the lottery as a revenue source. Selected indicators of lottery effect were variations around the X in the regression equation intercept, slope, and variance, as well as indications of cyclical variation, which were reflected in the scatter plots. Linear regression models were constructed to examine the four central questions concerning the effect of the Florida lottery on community college finance. Forward selection stepwise regression was used to isolate the variables which were correlated with the fiscal effect that lottery dollars have had on the Florida community college system. Tolerance and the variance inflation factor (VIF) were used to detect data redundancy, or collinearity of the independent variables (Chatterjee & Price, 1991). A Type I error probability level (a) of less than or equal to .05 was selected to support each decision to reject or fail to reject the null hypothesis (Blalock, 1972). Nondirectional hypotheses were used because the goal was to detect any change in trend, whether positive or negative. There was no initial assumption that the lottery had resulted in either

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an improved, or worsened, fiscal status at the community colleges. When the data met the criteria established for statistical significance, the squared multiple correlation 74 2 coefficient (R) was used to further assess the adequacy of fit of the regression models. To interpret the magnitude of effect size as reflected in the multiple correlation coefficient, the following parameters were used: 1 2 A large effect was an R greater than or equal to 15. 2 A medium effect was an R 2 greater than or equal to 06. 3 2 A small effect was an R greater than or equal to 01. 4. An R 2 less than .01 was not significant (Cohen, 1977, pp. 284-288). Each regression was summarized in tabular form detailing the partial and model squared multiple correlation coefficients (R 2 ), sums of squares and mean squares for the model, the values of the regression coefficients, T and F test values, and significance levels. Impact The first question addressed in this study was whether there was a relationship between the fiscal status of the Florida community colleges and the use of the Florida

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75 Lottery as a revenue source. The variables used in this model controlled for differences in FTE, because of fluctuating enrollments within each community college over the 22 years of this study, as well as the major differences in annual FTE across the 28 community colleges. The model used to detect the impact of lottery dollars on community college expenditures was FTEX12 = B 0 + B 1 GRFFTE + B 2 STATFTE + u, where FTEX12 = the dependent variable for Funds I and II (Total Education and General, E&G) expenditures per FTE by the individual community college, B 0 = the Y intercept of the B 1 regression equation, B 1 = the regression coefficient for the slope of the variable GRFFTE, GRFFTE = the independent variable for general revenue fund dollars per FTE, B the regression coefficient for the variable 2 STATFTE, STATFTE = the independent variable for the sum of general revenue and lottery dollars, expressed per FTE, and u = the random error term. The null (H 0 ) and alternative (H 8 ) hypotheses were

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76 The null hypothesis stated that there was no difference between nonlottery and lottery years in community college Funds I and II (E&G) expenditures per weighted FTE (McDowall, McCleary, Medinger, & Hay, 1980). Supplantation State of Florida nonlottery, general revenue allocations to each community college (GRF) for FY 1972 through FY 1993 were regressed against two independent variables, and an interaction term: the continuous variable fiscal year (YR), the dummy variable LT, denoting whether or not lottery funds were a community college revenue source for that year, and YR*LT, the interaction term. In regression analysis, interaction refers to the condition where the relationship of interest--here, YR and GRF--is different at different levels of an extraneous variablehere, LT (Kleinbaum, Kupper, & Muller, 1988). where The model proposed for the supplantation question was GRF = B 0 + B 1 YR + B 2 LT + B 3 YR*LT + u, GRF = the dependent variable for total state general revenue expenditures per community college for each fiscal year, B 0 = the Y intercept of the B 1 regression equat i on,

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77 B 1 = the regression coefficient for the slope of the variable YR, YR= the continuous independent variable Fiscal Year for any year, 1972-73 through 1993-94, B 2 = the regression coefficient for the variable LT, LT= a dummy variable coded O if no lottery allocation, 1 if lottery allocation, for any year; B 3 = the regression coefficient for the interaction term for the variables YR and LT; YR*LT = the interaction term for the variables YR and LT, and u = the random error term. The null (H 0 } and alternative (Ha} hypotheses to test for supplantation were H 0 : B 3 = O ; Ha : B 3 O The null hypothesis stated that the existence of the Florida Lottery had no effect on GRF allocations to the community colleges. The alternative hypothesis stated that the Lottery had an effect on GRF, which would be interpreted in one of two ways, depending on whether the coefficient B 3 were positive or negative. If B 3 were not zero, it would indicate a change in GRF because of a change in LT. Thus, the alternative hypothesis stated that the simple existence of the lottery corresponded with a change in GRF. If GRF

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dollars were supplanted, B 3 would be less than O; if GRF dollars were enhanced, B 3 would be greater than o. A second analysis of supplantation used forward selection stepwise linear regression. The purpose was to learn which variables were predictive of State of Florida all-source allocations to community colleges (TOTSTATE). Predictor (X) variables used for this analysis were LOT, GRF, CAT, and LT, where TOTSTATE = the continuous dependent variable for all state expenditures per community college per fiscal year, LOT= the continuous independent variable for the college's annual lottery allocation, expressed in dollars, GRF = the continuous independent variable for total state general revenue expenditures per community college for each fiscal year, expressed in dollars, CAT= the continuous independent variable for the percentage of lottery expenditure per community college that was a categorical, rather than noncategorical, award, and LT= a dummy independent variable coded O if there was no lottery allocation, 1 if there was a lottery allocation, for any fiscal year. 78

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79 Redistribution A forward-selection stepwise linear regression approach was used to examine the question of the redistribution of funding sources for the community colleges. The dependent (Y) variable was FTEX12. The predictor (X) variables were GRFFTE, LOTFTE, and STATFTE, where FTEX12 = the continuous dependent variable for total Funds I and II (E&G) year-end expenditures per FTE for each community college, GRFFTE = the continuous independent variable for general revenue fund dollars per weighted FTE, LOTFTE = the continuous independent variable for lottery dollars per weighted FTE, and STATFTE = the continuous independent variable for the sum of general revenue and lottery dollars, expressed per weighted FTE. The Effect of Categorical Lottery Allocations The final question concerned whether the proportion of the lottery allocation that was a categorical, as opposed to a noncategorical, award, could be correlated with a change in the all-source state allocation to the community colleges. The annual state allocations from both lottery and nonlottery funds (TOTSTATE) per community college were regressed against the percentage of each year's lottery allocation that was categorical (CAT), rather than

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80 noncategorical, and the dummy variable LT, denoting whether or not lottery funds were a community college revenue source for that year. The model for this equation was TOTSTATE =Bo+ B,CAT + BzLT + B3CAT*LT + u, where TOTSTATE = the continuous dependent variable for all state expenditures per community college per fiscal year, B 0 = the Y intercept of the B 1 regression equation, B 1 = the regression coefficient for the slope of the variable CAT, CAT= the continuous independent variable for percentage of lottery expenditure per community college that was categorical, rather than noncategorical, B 2 = the regression coefficient for the variable LT, LT= a dummy independent variable coded o if there was no lottery allocation, 1 if there was a lottery allocation, for any fiscal year; B 3 = the regression coefficient for the interaction term for the variables CAT and LT; CAT*LT = the interaction term; and u = the random error term. The null and alternative hypotheses:

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81 The null hypothesis {H 0 ) stated that CAT was not predictive of TOTSTATE. The alternative hypothesis {H 8 ) stated that CAT was predictive of TOTSTATE. If H 0 were rejected, the interpretation would depend on the sign of B 3 A positive B 3 would indicate a positive correlation between CAT and TOTSTATE; higher values of CAT were associated with more state funds. Likewise, a negative B 3 would indicate a negative correlation between TOTSTATE and CAT; higher values of CAT were associated with lower state allocations.

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CHAPTER 4 RESULTS AND DISCUSSION This study examined State of Florida fiscal and enrollment data for the 28 state-supported community colleges to answer four basic questions. Impact. The first question was whether the start of the Florida Lottery coincided with a change in the expenditure trends of the Florida community colleges. Supplantation. The second question was whether Florida Lottery funds either supplanted or enhanced state general revenue funds that were allocated for the support of the community college system. Redistribution. The third question was whether the addition of the lottery as a revenue source resulted in a change, or redistribution, in the proportion of community college expenditures that were funded through state sources. Categorical/noncategorical. The fourth question concerned the proportion of lottery dollars that were released to community colleges in the form of a categorical allocation versus lottery dollars that flowed without spending restrictions into the Community College Program Fund (CCPF). The goal was to determine whether the percentage of categorical restrictions correlated with the 82

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83 total amount of state funds allocated to the community colleges. Fiscal and enrollment data for each of the 28 community colleges were obtained from the State of Florida Department of Education, Division of Community Colleges. Fiscal Years (FY) 1972 through 1993 were used for all models except those involving year-end Funds I and II expenditure data (TOTAL E&G and FTEX12), data subsets which were only available through FY 1991 at the time of this study. The data were examined for outliers, or data points which were overly influential, using Cook's Distance, DFITS, and standardized residual statistical methods, and scatter and residual plots (Chatterjee & Price, 1991). No outlying data points were found that were excessively influential; therefore, none were removed The scatter and residual plots supported the five assumptions of linearity of each of the regression models; hence, no higher-order terms were used. Following is a listing of the abbreviations and definitions of each of the variables included in this study. CAT the percentage of the lottery allocation that was categorical, as opposed to noncategorical. CC community college a categorical variable ranging from 1 to 28, corresponding to the alphabetical listing of the community colleges and used to identify the community college that constituted each data point; e.g. Brevard

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84 Community College was identified as 1, while Valencia Community College was 28 (Appendix A}. FTE full time equivalent, a continuous variable referring to the weighted unit of measure used to describe community college enrollment. FTEX12 all-source Funds I and II (Total E&G} expenditures per FTE. This figure included state and nonstate sources of revenue. GRF general revenue fund allocation, in dollars. GRFFTE general revenue fund dollars per FTE. LOT the college's annual lottery allocation, in dollars. LOTFTE lottery dollars per FTE. LT a nominal, dummy variable coded o for nonlottery years, 1 for lottery years. STATFTE the sum of general revenue fund and lottery dollars, expressed per FTE. TOTAL E&G all-source Education and General (Funds I and II) expenditures. TOTSTATE the sum of state general revenue fund and lottery dollars. YR fiscal year, a continuous variable ranging from 72 (FY 1972-73) to 93 (FY 1993-94). Descriptive statistics for all the variables studied are shown in Table 4. The smallest variance, as reflected in the standard deviation scores, was found for the variables

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85 which controlled for differences in FTE: LOTFTE, GRFFTE, STATFTE, and FTEX12. There was a considerable range in the values for FTE, TOTSTATE, and TOTAL E&G, a fact which reflected the considerable variation in the size and relative wealth of the 28 community colleges. In general, the smallest colleges tended to have the highest expenditures per FTE (FTEX12), while the largest colleges had the lowest FTEX12 values. This reflected the economies of scale that were present in large, urban institutions, and the greater operating costs per student served for the smallest, rural colleges. Impact The first question addressed in this study was whether a correlation existed between the fiscal status of the community colleges and the use of a state lottery as a revenue source. Could the Florida Lottery be shown to have had an effect on community college finance? The variables used in this model controlled for FTE in an attempt to minimize the influence of the size of the institution on its relative wealth. GRFFTE contained only general revenue funds per FTE, while STATFTE included both general revenue and lottery dollars. The model proposed to test for impact, and the null and alternative hypotheses, were

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86 FTEX12 = 8 0 + B 1 GRFFTE + B 2 STATFTE + u The null hypothesis stated that there was no difference between nonlottery and lottery years in community college Funds I and II (E&G) expenditures per weighted FTE. The results of the analysis supported the decision to reject the null hypothesis at the chosen a= .05 level of significance. There was evidence that the addition of lottery funds as a revenue source correlated with a change Table 4. Descriptive statistics of all variables. VARIABLE COUNT MEAN MINIMUM MAXIMUM STAND DEV VALUE VALUE cc 616 n/a 1 28 n/a YR 616 n/a 72 93 n/a FTE 616 5720 391 35828 6042 LT 616 n/a 0 1 n/a LOT 616 968761 0 22241388 2426117 LOTFTE 616 150 0 786 246 CAT 616 0 0 94% 22% GRF 616 10816104 395244 87941772 12464390 GRFFTE 616 2029 784 4787 924 TOTSTATE 616 11784866 395244 103538111 14139740 STATFTE 616 2179 784 5177 1057 FTEX12 560 3160 966 7410 1410 TOTAL 560 16969650 527304 164546530 20711470 E&G

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87 in community college expenditures. Further, the sign of B 2 was negative, meaning that community college expenditures were negatively correlated with lottery dollars. In other words, larger lottery allocations were associated with lower community college expenditures. The allocation of F l orida Lottery dollars to community colleges coincided with a decline in the all-source E&G expenditures by the Florida community colleges. The model multiple correlation coefficient (R 2 ) was .42, indicating that 42% of the variance in FTEX12 was explained by the model that included both GRFFTE and STATFTE (Blalock, 1972, p. 464). This was a large effect size (Cohen, 1977, pp. 284-288). The Y intercept, B 0 was not interpretable because there was no probable case when the independent variable, GRFFTE, would equal O. All stat i stics had large F values; the F for the model was 302.04. The ANOVA source table and parameter estimates are shown in Table 5. Thus, the first test met with a statistically significant response. The addition of the Florida Lottery as a revenue source was shown to have coincided with a downturn in the expenditures of the Florida community colleges. The next step was to determine the nature of the effects that occurred in the fiscal status of the community co l leges following the introduction of the lottery as a revenue source. The issues of general revenue supplantat i on college

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revenue redistribution, and the percentage of each lottery allocation that was categorical rather than noncategorical were examined. Supplantation 88 The second question concerned whether the existence of the Florida Lottery correlated with either the supplantationor enhancement of general revenue fund allocations to community colleges. Table 5. ANOVA table and parameter estimates for the relationship between the lottery and the fiscal status of the Florida community colleges. FTEX12 = B 0 + B 1 GRFFTE + B 2 STATFTE + u H 0 : B 2 = 0 ; Ha : B 2 ,;, 0 Analysis of Variance Source Degrees of Sum of Mean sguare F Value freedom sguares Model 2 800781497 400390749 302.04 Error 608 805968428 1325606 Total 610 1606749925 Parameter Estimates Parameter Estimate Standard P>F error Intercept 380.90 114.53 11.06 .0009 B, 3.46 .24 205.12 .0001 Bz -2.08 .21 96.73 .0001 R2 = .42

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89 The model proposed for the supplantation question, and the null and alternative hypotheses, were GRF = Bo + B, YR + BzLT + B3YR*LT + 0 H 0 : B 3 = 0 ; H 8 : B 3 0 The null and alternative hypotheses tested for the existence of an interaction between the continuous variable YR and the dummy variable LT. An interaction would indicate that the relationship between YR and GRF was different for different levels of LT; in other words, that the simple presence of the lottery corresponded with a change in GRF. B 3 was the difference in the slopes of the lines for the two conditions of LT. A B 3 that was nonzero would provide evidence of an interactive effect. If either supplantation or enhancement had occurred, B 3 would not be O. The results of the analysis supported the decision to not reject H 0 ; there was no evidence of an interaction effect. The B 3 term was not significant at the selected a= .05 level. The results are shown in the supplantation ANOVA source table and parameter estimates contained in Table 6. A decision was made to test the data with an alternative version of the model, without the interaction term (Chatterjee & Price, 1991; Kerlinger & Pedhazur, 1973). An alternative, additive model was developed: GRF = B 0 + B 1 YR + B 2 LT + o

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90 The hypotheses tested for a change in the Y intercept over the two conditions of LT, which would provide an indication that GRF was either supplanted or enhanced. Again, the data supported the decision to not reject the null hypothesis. The regression coefficient B 2 was not significant at the a= .05 level. This study did not find evidence that either supplantation or enhancement of general revenue dollars had occurred to a statistically significant Table 6. ANOVA table and parameter estimates for the supplantation model GRF = 8 0 + B 1 YR + B 2 LT + B 3 YR*LT. GRF = Bo + B, YR + BzLT + B3YR*LT + U Source Model Error Total Parameter Intercept B, Bz B3 R2 = .13 H 0 : 8 3 = 0 ; H 8 : 8 3 0 Analysis of Variance Degrees of freedom 3 612 615 Sum of Mean square squares 1.26 4.20 8.29 9.55 1.36 Parameter Estimates Estimate Standard T for Hc. error Parameter=0 -48456339 10402320 -4.66 718059 131478 5.46 56166165 38847308 1.45 -622930 436064 -1.43 F Value 31.00 P> I TI .0001 .0001 .1487 .1537

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91 extent. The results are shown in the supplantation ANOVA source table and parameter estimates contained in Table 7. Over the period of the lottery years, FY 1987 through FY 1993, there was graphic evidence that supplantation had occurred in the community college allocation, as shown in Figure 5. The dark area represents lottery dollars (LOT). Also, supplantation of general revenue funds with lottery dollars was reported for the Florida K-12 system (Stark, 1991; Stark, Honeyman, & Wood, 1991). It was thus concluded Table 7. ANOVA table and parameter estimates for the supplantation model GRF = B 0 +B 1 YR+B 2 LT. Source Model Error Total Parameter Intercept B1 Bz R 2 = 13 GRF = Bo + B1 YR + BzLT + U H 0 : B 2 = 0 ; Ha : B 2 0 Analysis of Variance Degrees of Sum of Mean sguare freedom sguares 2 1.23 6.16 613 8.32 1.36 615 9.55 Parameter Estimates Estimate Standard T for Halerror Parameter=0 -43982570 9928119 -4.43 661429 125466 5.27 725410 1708982 .42 F Value 45.41 P>IT I 0001 .0001 .67 1 4

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92 that the issue of general revenue fund supplantation warranted further examination. Stepwise regression involving additional variables was used as another method to investigate supplantation, using the dependent variable TOTSTATE, and the independent variables LOT, GRF, CAT, and LT. At the a= .05 level of significance selected for this study, three variables entered the model: GRF, LOT, and CAT; however, CAT contributed nothing to the R 2 The model selected: YE.AR ~ GRF LOT Fioure 5. Supplantation of State of Florida general revenue dollars with Florida Lottery dollars allocated to the community college system.

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93 TOTSTATE = B 0 + B 1 GRF + B 2 LOT + B 3 CAT + u The partial R 2 for GRF was .98, indicating that a full 98% of TOTSTATE variance was explained by GRF alone. This statistic reflected the almost total reliance of the State of Florida on the general revenue fund to finance community colleges. The partial R 2 of LOT rounded to 2%. Despite the high gross revenues of the Florida Lottery, it was nonetheless a new and relatively minor revenue source. When viewed against the 22 years of the completed Florida system of community colleges, the share of lottery profits that was awarded to community colleges accounted for, at best, 2% of Table 8. Stepwise analysis of supplantation. Summary of Forward Selection Procedure for Y = TOTSTATE, X = LOT, GRF, CAT and LT SteQ Variable entered Number in Partial R 2 Model R 2 F Value P>IFI Model selected: 1 GRF 1 .98 .98 34551 .0001 2 LOT 2 .02 1.00 .0001 3 CAT 3 .oo 1.00 TOTSTATE = B 0 + B 1 GRF + B 2 LOT + B 3 CAT + u

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94 the variation in the total state allocation. General revenue dollars continued to comprise, by far, the greatest share of the state allocation; in comparison, the magnitude of the lottery allocation was essentially insignificant. The parameter estimates are shown in Table 8. Redistribution The third question concerned the varying proportions of total community college expenditures that were comprised of state general revenue funds. The goal was to determine whether the community colleges had been either better or less well funded by the State of Florida since the introduction of the Florida Lottery as a revenue source. To explore the redistribution issue, a forward selection stepwise regression was conducted using FTEX12 as the dependent variable. The independent variables were three variables that were controlled for differences in FTE: GRFFTE, LOTFTE, and STATFTE. The model selected: FTEX12 =Bo+ B,GRFFTE + BzSTATFTE + B3LOTFTE + u The R 2 was a large .50, of which .42 was explained by GRFFTE. The partial R 2 for STATFTE was .08, which was a medium effect size. The partial R 2 for LOTFTE was .005, which was not a statistically significant effect size. The model F value was 6.6, which met the a= .05 test of significance. The results of the analysis are displayed in Table 9.

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95 Figure 6 is a visual illustration of redistribution, using aggregate data for the community college system. Figure 6 shows that the difference between Total Education and General (Total E&G, or Funds I and II) funds expended by the community colleges, and state general revenue allocations, had increased over time. The gap widened as GRF plateaued and, later, declined after the introduction of the Florida Lottery in FY 1987, while Total E&G increased. The colleges thus appear to have been increasingly reliant on nonstate sources of revenue from FY 1987 through FY 1991. Table 9. Stepwise regression for the dependent variable FTEX12. Summary of Forward Selection Procedure for Y = FTEX12, X = GRFFTE, LOTFTE and STATFTE. Steg 1 2 3 Variable entered GRFFTE STATFTE LOTFTE Number in 1 2 3 Partial R 2 .419 .080 .005 Model R 2 .419 .498 .504 F Value 438.4 96.7 6.6 P>IFI .0001 .0001 .0103 Model selected: FTEX12 = Bo + B,GRFFTE + BzSTATFTE + B3LOTFTE + u

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96 The Effect of Categorical Lottery Allocations The fourth and final question was whether the extent to which lottery funds were allocated as categorical awards, with funding restrictions, was correlated with the total extent of state support for community colleges. Again, the dummy variable LT was used to denote lottery versus nonlottery years. CAT was a continuous variable expressed as the percentage of the total lottery allocation that was 1000 ,oo 800 700 coo I a 0 ., 500 ... ... iii: 11 ,oo 300 aoo 100 0 72 ?3 .,, ?!' 7 .,., 78 '7:t ao ai. 12 a3 M e!' a, ..., ~o :tj, .TOTAL E&.G Figure 6. Redistribution of funding sources for Florida's community college system, FY 1972 FY 1991.

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97 categorical. LT was a dummy variable coded o for nonlottery years, and 1 for lottery years. The model for this equation: TOTSTATE = Bo + B,CAT + BzLT + B3CAT*LT + U The null hypothesis {H 0 ) stated that the percentage of the lottery allocation that was categorical {CAT), rather than noncategorical, was not predictive of state support. The alternative hypothesis (Ha) stated that CAT was predictive of TOTSTATE. Table 10. The effect of categorical vs. noncategorical lottery allocations, the model TOTSTATE = B 0 + B 1 CAT + B 2 LT + B 3 CAT*LT. TOTSTATE = Bo + B,CAT + BzLT +B3CAT*LT + U H 0 : B 3 = 0 ; Ha : B 3 0 Source Model Error Total Parameter Intercept B, Bz B3 Rz = 13 Analysis of Variance Degrees of freedom 2 608 610 Sum of Mean square F Value squares 1.65 8.23 47.13 1.06 1.23 1.75 Parameter Estimates Estimate Standard T for He. P> ITI error Parameter=0 8329775 648594 12.84 .0001 65424 44160 1.48 .14 8143599 2235030 3.64 .0003 0 *

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98 It was not possible to obtain a parameter estimate for B 3 because CAT and LT were confounded variables: if LT equaled O, then CAT equaled O (Kleinbaum, Kupper, & Muller, 1988). The results of the analysis are shown in Table 10. The model was significant at the a= .05 level. The F value 2 was a large 47.13, and the R was .13. A decision was made to remove the interaction term and recalculate the statistics. The adjusted model and hypotheses were TOTSTATE =Bo+ B1CAT + BzLT + U The data for this second analysis supported the decision to reject H 0 at the a= .05 level of significance. The model using CAT and LT was found to be predictive of TOTSTATE. In this model, the Y intercept (B 0 = $8,370,292) represented the value of TOTSTATE when LT= CAT= O. B 2 was found to equal $8,203,082, the amount that the Y intercept increased when LT= 1. The sign of B 1 was positive; therefore, the greater the value of CAT, the greater the value of TOTSTATE The F for the model was moderately large (48.13). The R 2 was .14, which was a medium effect size (Cohen, 1977, pp. 284-288). The ANOVA source table and parameter estimates are shown in Table 11. Clearly, GRF was highly predictive of TOTSTATE; general revenue dollars were shown in the supplantation stepwise analysis to explain 98% of the total variance of TOTSTATE.

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For a more sensitive review of the other predictor variables, a stepwise analysis was conducted that did not include GRF as an independent variable. The model that was selected: 99 The strength of the association between LOT and TOTSTATE became more pronounced, as shown in Table 12. The F value for the model containing only LOT as an independent 2 variable was a huge 724.0. The full model R was a large Table 11. The effect of categorical vs. restricted lottery allocations, the model TOTSTATE = B 1 CAT+B 2 LT. Source Model Error Total Parameter Intercept B1 Bz R 2 = .14 TOTSTATE = Bo + B 1 CAT + B 2 LT + \) Ho: Bz = 0. I Ha: Bz 0 Analysis of Variance Degrees of Sum of Mean sguare freedom sguares 2 1.67 8.35 613 1.06 1.73 615 1. 23 Parameter Estimates Estimate Standard T for Holerror Parameter=0 8370292 642559 12.87 65424 44011 1.49 8203082 2226415 3.68 F Value 48.13 P> I TI .0001 .14 .0002

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100 .59, of which the partial R 2 for LOT was .54. The partial R 2 for CAT was .04; and for LT, .01. These are both small, but significant, effect sizes {Cohen, 1977, pp. 284-288). Thus, when used in conjunction with LOT, CAT was predictive of TOTSTATE at the a= .05 level of significance. Summary of Findings Answers to all four questions addressed in this study were supported by the results of the analyses at the a= .05 level of significance. Table 12. Stepwise analysis of the effect of categorical versus noncategorical allocation of lottery funds. Summary of Forward Selection Procedure for y = TOTSTATE, X = LOT, CAT and LT Steg 1 2 3 Variable LOT CAT LT entered Number in 1 2 3 Partial R 2 .54 .04 .01 Model R 2 .54 .58 .59 F Value 724.0 54.7 17.9 P>IFI .0001 .0001 .0001 Model selected: TOTSTATE = 13 0 + B 1 LOT + B 2 CAT + B 3 LT u

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101 Impact. The lottery was shown to have corresponded with a decline in the state funds available for community college expenditure. The F was a large 302.04, the regression coefficient B 2 was -2.08, and the correlation coefficient R 2 was a large .42. Supplantation. The data from the linear regression models supported the decision to not reject the null hypothesis. For the two models using GRF as the dependent variable, the highest-order regression coefficients, B 3 and B 2 were not significant at the a= .05 level. However, a stepwise analysis was conducted using TOTSTATE as the dependent variable. A model including GRF, LOT and CAT as predictor variables was selected, having a correlation coefficient which rounded to 1.00. The partial R 2 for GRF was .98. The partial R 2 for LOT was .02, a small, but significant, effect size. For CAT, the partial R 2 was .00. These findings reflected the continued dominance of GRF as a revenue source in the State of Florida support for community colleges, and the relative insignificance of the lottery as a revenue source. The stepwise analysis supported the conclusion that supplantation of GRF resulted from the allocation of Florida Lottery dollars to the Florida community college system. Redistribution. The data supported the decis i on to reject the null hypothesis. There was evidence of redistribution in the sources of community college revenues,

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102 with the colleges becoming less reliant on GRF. The regression coefficient B 2 was -.232, the F was a large 2 151.38, and the R was a large .35. The effect of categorical versus noncategorical lottery allocation. The data supported the decision to reject the null hypothesis at the a= .05 level of significance. There was evidence that the percentage of the lottery allocation that was a categorical award was predictive of TOTSTATE. The sign of the regression coefficient B 2 (8203082) indicated that the relationship between CAT and TOTSTATE was positive. As CAT increased, so did TOTSTATE; similarly, as CAT declined, TOTSTATE declined. Therefore, a lottery allocation which was awarded as mostly categorical was associated with a larger state allocation, from all state sources. The F 1 f th d 1 th 2 d va ue or is mo e was 48.13; e R was .14, a me ium effect size. Conclusions The introduction of the Florida Lottery as a community college revenue source coincided with a downturn in the funds expended at the community colleges. Lottery funds supplanted general revenue dollars; however, lottery dollars comprised such a small percentage of the state allocation that their influence on community college funding was minimal. Over the 22 years of data in this study, the general revenue fund explained 98% of the variance in State

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103 of Florida support for the community colleges, while the lottery explained only 2%. There was evidence of redistribution in the funding sources of the Florida community colleges. There was an increasing gap between the per-FTE expenditures at the community colleges and the state allocation per FTE, despite the addition of a state-operated lottery as a revenue source. It was shown that the extent to which the lottery allocation was categorical correlated with the size of the state all-source allocation to the community colleges. The college finances fared somewhat better in years when the categorical percentage of the lottery allocations was greatest.

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CHAPTER 5 SUMMARY AND CONCLUSIONS The purpose of this dissertation was to determine whether a public institution benefitted from being a designated recipient of a portion of the profits from a state-operated lottery. A state system of public community colleges was used for the analysis. The method used to address this question was to determine whether there had been any change since the inception of the Florida Education Lotteries in the available resources and actual expenditures of the 28 state-supported community colleges in Florida. Did the Florida community colleges, in fact, benefit financially from being earmarked for a portion of the proceeds from the Florida Lottery? Impact. The first issue addressed in this study concerned the efficacy of a state lottery when used as a revenue source for a designated, state-supported beneficiary. Did lottery dollars have a measurable effect on the financial status of the beneficiary? Specifically, did the Florida community colleges incur greater expenditures after the Florida Lottery was added as a revenue source? Supplantation. The second issue addressed in this study was whether or not the lottery had an effect on the amount 104

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105 of state nonlottery funds that were allocated to the beneficiary. Were lottery dollars in addition to, or a substitute for, nonlottery state funds? In other words, did the addition of lottery funds result in the enhancement or supplantation of nonlottery funds? Specifically, did the 1987 introduction of lottery dollars as a revenue source for Florida community colleges affect the total amount of state funds that were allocated to the 28 community colleges in Florida? Redistribution. The third issue addressed in this study concerned the extent to which the annual, current expenditures by the beneficiary were derived from state funds. Did state all-source allocations decline or increase relative to the beneficiary's current expenditures that were funded through all sources? In this analysis, the annual expenditures per weighted full time equivalent student (FTE) at each of the Florida community colleges were examined as a function of State of Florida general revenue fund allocations to the community colleges. Categorical versus noncategorical allocations. The fourth and final issue addressed in this study was whether or not expenditure restrictions on lottery dollars affected the amount of nonlottery dollars allocated to the beneficiary. In Florida, lottery funds were initially allocated exclusively as categorical, restricted-expenditure awards. The extent to which the lottery allocation was

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106 categorically restricted decreased each year. The FY 1993 lottery allocation to Florida community colleges was completely noncategorical. Did the percentage of each college's annual lottery allocation that bore categorical spending restrictions correlate with the supplantation, enhancement, or redistribution of state nonlottery funds? In this analysis, total state expenditures from all sources, including lottery funds, were examined as a function of the percentage to which the lottery allocation was categorical. Fiscal and enrollment data for each of the 28 community colleges were obtained from the State of Florida Department of Education, Division of Community Colleges. Fiscal Years (FY) 1972 through 1993 were used for all models except those involving year-end Funds I and II expenditure data (TOTAL E&G and FTEX12), data subsets that were only available through FY 1991 at the time of this study. Data points were reported for each community college, rather than the system as a whole, in order to increase the power of the statistics. The success of this decision was reflected in the sizable F test values reported for each of the models, especially when student enrollment, or FTE, was used as a controlling variable. Controlling for FTE was important because of the wide variation among the 28 Florida community colleges in terms of enrollment and wealth.

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Summary of Results Impact The first question investigated whether or not the lottery allocations correlated with a change in the expenditure patterns of the beneficiary. Did the start of the Florida Lottery coincide with a change in the expenditure trends of the Florida community colleges? 107 The results of this study indicated that the addition of lottery funds as a community college revenue source correlated with a change in community college expenditures. The relationship between lottery dollars and total community college expenditures was inverse (B 2 = -2.08, F = 302.04, R 2 = .42). Thus, adding lottery funds to the state allocation was associated with lower community college expenditures. Supplantation The second question investigated whether Florida Lottery funds either supplanted or enhanced state general revenue funds that were expended in support of community college education. Evidence of supplantation was demonstrated in the relationship between genera l revenue fund and lottery allocations from FY 1972 through FY 1993 (Figure 5). After an annual increase from FY 1972 through FY 1989, the general revenue fund allocation was flat in FY 1989, dipped substantially in FY 1991, and by FY 1993 still

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108 had not regained the FY 1990 level. The data reflected current dollar calculations; the effect would have been more dramatic had the sums been converted to constant dollars. The supplantation effect exerted by the addition of lottery funds in FY 1987 was still more evident when the influence of FTE was controlled. The general revenue fund (GRF) allocation expressed per FTE declined in current dollars beginning in FY 1990 (Table 3). The FY 1993 GRF allocation was greater than that for FY 1992, yet was still below the FY 1983 per-FTE allocation. The addition of lottery dollars to GRF dollars beginning in FY 1987 resulted in a larger State of Florida allocation to the community colleges, yet lottery dollars were too few to fully compensate for the decline in GRF that began in FY 1989. Even when lottery dollars were counted, the state support to the Florida community colleges in FY 1993 was below the level of FY 1989. This study found no statistical evidence of either supplantation or enhancement of general revenue funds at the a= .05 level of significance selected for this study. When viewed within the context of 22 fiscal years, the lottery allocations were too small to have exerted a significant effect on the magnitude of the state total allocation to community colleges. However, supplantation of GRF was shown to have occurred.

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109 Stepwise regression was conducted using the all-source state allocation {TOTSTATE) as the dependent variable. The full model selected used the general revenue allocation {GRF, partial R 2 = .98), the lottery allocation {LOT, partial R 2 = .02), and the percentage of the lottery allocation which was a categorical award (CAT, partial R 2 = .00) as the explanatory variables for a model R 2 which rounded to 1.00. The partial R 2 of .98 for GRF indicated that 98% of the total variance was explained by GRF alone. The total effect of lottery dollars on Florida's community colleges was very small relative to the magnitude of the general revenue allocation. Redistribution The third question investigated whether the addition of the lottery as a revenue source resulted in a change, or redistribution, in the proportion of community college expenditures that were funded through state sources. The results of this study indicated that redistribution did occur. The community colleges were shown to have been increasingly dependent on nonstate sources of revenue, from the inception of the Florida Lottery in FY 1987 until FY 1991, the last year for which expenditure data were available at the time of this study. In other words, the funds that were expended at the community colleges were increasingly derived from nonstate sources.

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110 Stepwise regression showed the significance of both lottery and nonlottery state allocations to community colleges, when all variables were controlled for FTE. The dependent variable was community college Funds I and II expenditures per FTE {FTEX12), while the predictor variables were the general revenue allocation {GRFFTE, partial R 2 = .42), lottery allocation {LOTFTE, partial R 2 = .005), and State of Florida all-source allocation {STATFTE, partial R 2 2 = .08), controlled in each case for FTE. The model R was .50, and the F value was 6.6, which met the a= .05 test of significance. Based on these results, it appeared that general revenue dollars continued to exercise the greatest effect on community college expenditures, far beyond the influence of the lottery dollars. At the same time, community college expenditures were increasingly dependent on variables other than state support. Thus, it appeared that redistribution occurred in the funding sources of Florida community colleges. Categorical versus noncategorical lottery awards The fourth question investigated the effect of the proportion of the lottery allocation that was released to community colleges in the form of a categorical award, versus lottery dollars that flowed without spending restrictions into the Community College Program Fund {CCPF).

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111 The goal of this investigation was to determine whether the percentage of categorical restrictions correlated with the total amount of state funds allocated to the community colleges. The results of this study indicated that the percentage of the lottery allocation awarded with categorical spending restrictions correlated with the amount of the total all source state allocation. The relationship was positive (B 2 = 2 8203082, R = .14, F = 48.13); hence, the greater the extent to which the lottery allocation was a categorical award, the larger the state total allocation to the community colleges. Conclusions Based on the results of this study, it was apparent that the addition of a state lottery as a revenue source had a definite, adverse effect on the fiscal status of one beneficiary. It appeared that the Florida Lottery coincided with a downturn in community college finance, in three different ways. The first way involved supplantation of general revenue dollars. The second way involved redistribution of funding sources. The third way involved the extent to which categorical restrictions were placed on the lottery allocation. When the lottery allocation was made without categorical spending restrictions, the community colleges received a lower total allocation from all state revenue sources.

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112 Impact The Florida Lottery was added as a community college revenue source in FY 1987. The result was that the colleges actually incurred lower expenditures, once they began to receive lottery dollars. Therefore, the results of this study indicated that the addition of a state lottery as a revenue source had an adverse effect on the fiscal health of one designated beneficiary. Supplantation General revenue fund allocations to the beneficiary declined after the addition of the lottery allocation. The results of this study showed a decrease in the general revenue fund allocation to community colleges. State of Florida general revenue allocations to the Florida community colleges declined after the inception of the Florida Lottery. The regression model used in this study produced results that showed a supplantation effect; however, it was not statistically significant. This fact in itself demonstrated that, relative to the total college budget, lottery dollars were too few to exert a significant effect on the financial health of the Florida community colleges. It was concluded that the magnitude of the supplantation effect was the result of the relatively small amount of funds made available from lottery profits.

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113 The findings of this study supported the conclusions of other researchers that high-grossing state lotteries that were earmarked for public education were found in states with an otherwise eroding financial support for public education (Hines, 1992). This study also supported the findings of others, that being earmarked for lottery profits did not lead to better financial support for the beneficiary (Jones & Brinkman, 1990; Karl, 1991). The Florida Lottery was proposed as a way to generate new funds for public education without implementing a new tax, which was the rationale adopted in other states as well (Allen, 1991; Borg & Mason, 1990; Clotfelter & Cook, 1989; Mikesell & Zorn, 1987; Wyett, 1991). This study found an actual deterioration in the overall fiscal status of one lottery beneficiary after the lottery was added as a revenue source. This study did not support the findings of Stark (1991) and Stark, Honeyman, and Wood (1991), who found statistically significant evidence of supplantation of general revenue dollars when lottery funds became a revenue source for Florida's K-12 system. This study provided evidence that lottery dollars supplanted general revenue dollars awarded to community colleges, but the results were not statistically significant. This study further showed that lottery and general revenue allocations, combined, comprised a decreasing share of community college support.

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114 Because the lottery funds to community colleges were so small relative to general revenue funds and other funding sources, no statistically significant evidence of supplantation was found. In FY 1992, lottery funds comprised about 8% of the total state allocation to education in Florida. This study found that, over the 22 fiscal years of this study, lottery dollars explained only about 2% of the variation in the state allocation to community colleges. In the year-to-year view, however, lottery dollars comprised as much as 29% of the state allocation to community colleges (Table 3). Redistribution State funds from all sources have comprised a declining proportion of community college expenditures. This study found indications of a widening gap between all-source annual expenditures by the colleges and the total state allocation. Since the start of the Florida Lottery, all source current expenditures at the community colleges were increasingly funded through nonstate revenue sources. The results of this study indicated that supplantation effects were influenced by redistribution; that is, the percentage to which total Education and General Funds (TOTAL E&G, or Funds I and II) were comprised of State of Florida funds. When FTE was controlled, general revenue dollars explained only 42% of the variance in E&G expenditures by

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115 the community colleges (FTEX12). While the full model included both state all-source funds (STATFTE) and lottery funds (LOTFTE) controlled for FTE, the proportion of variance explained by lottery funds was only .005, which was not a statistically significant effect size. The Florida Lottery was found to be typical of other contemporary state lotteries in one additional way. The implementation of a state lottery had a markedly suppressing effect on State of Florida parimutuel revenues, a finding which supports the studies of other lottery states conducted by Vasche (1990) and Borg, Mason, and Shapiro (1993). The Effects of Categorical Awards The results of this study suggested a significant effect that resulted from the varying extent to which categorical spending restrictions were placed on the lottery allocation. There were indications of a lower state all source allocation that coincided with lifting the categorical spending restrictions on the Florida community college lottery allocation in FY 1990. Based on these findings, it appeared that the community colleges received greater all-source state allocations when there were categorical spending restrictions placed on a sizable percentage of the community college lottery allocation. Perhaps as a consequence of gaining the budgetary flexibility of a noncategorical lottery allocation, the

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116 community colleges received fewer state dollars after the lottery allocations became noncategorical. Since FY 1990, the community colleges increasingly received the lottery allocation in the form of an unrestricted, noncategorical award, while the K-12 and SUS system shares were categorical to a greater extent. For FY 1993, the community college lottery allocation was wholly noncategorical. Community college leaders should assess whether the gains in fiscal flexibility that accrued from lifting the categorical restrictions on lottery allocations justified the parallel loss of state dollars. Just as redistribution was shown above to be influenced by supplantation, so was the issue of categorical awards linked to redistribution and supplantation in a circular manner. The beneficiary was a state-supported institution. The state government experienced growing demands from the citizens for services of all kinds. Citizens' wages were flat or even eroding; therefore, more social services were needed at the same time that citizens resisted the imposition of higher taxes. Alternative, nontax revenue sources were sought Hence, the governments of 35 states and the District of Columbia implemented some form of lottery specifically to raise new, nontax monies. In Florida as well as the majority of other states, the lottery funds were earmarked for enhancement dollars for one or more publicly supported beneficiary. Because of the pressures on the state

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117 general revenue fund, the lottery dollars, in fact, were used to supplant general revenue dollars. At the same time, the pressure on the general revenue fund resulted in a decline in the proportion of state support for the beneficiary--in effect, in redistribution. Because of the growing needs of the citizenry, the government imposed more demands that specific services be provided by the beneficiary; yet, because of the pressure on the general revenue fund, categorical awards to pay for those specific services were no longer forthcoming. The result was a situation that is prevalent today at state-supported institutions across the United States: more governmental demands for accountability; more lump-sum budgeting and site-based management; fewer categorical awards; more alternative, nontax revenue sources; and an eroding share of state support. Implications and Suggestions for Future Research These findings raise the question of the differential effect of categorical allocation on the educational systems. It should be determined whether the budgetary enhancement effect of a categorical lottery allocation is found in all systems. Future studies should examine any effects that coincide with a change in the financial status of the lottery itself. The Florida Lottery reported in this study may experience a

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118 continued plateau or an actual decline in gross revenues for two separate reasons: first, as a result of market competition from the Georgia Lottery's implementation in FY 1993; second, because of the trend toward declining revenues that was shown in recent years by maturing lotteries across the country (Calkins, 1992; DeBoer, 1986, 1990; Mikesell, 1987; Mikesell & Zorn, 1987, 1988). The Florida Legislature used lottery revenues to shore up the state allocation of funds to community colleges, at a time when general revenue allocations were in decline. If lottery profits decline, then the burden to support education will shift to Florida's general revenue fund. A separate question for future studies concerns the related issues of supplantation and redistribution of state general revenue funds. The fates of other state-supported agencies are linked to that of the lottery beneficiary. When the lottery is a lucrative revenue source, funds are generated for the beneficiary that may mask a decline, or supplantation, of general revenue funds. The supplanted funds are readily redistributed to other state-supported agencies. When the lottery becomes less prosperous, the supplanted, redistributed funds are not so readi l y returned to the beneficiary (Borg & Mason, 1990; MacManus & Spindler, 1989; Wyett, 1991). Now that state lotteries are both maturing and widely prevalent, the redistributional effects

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119 should be examined as they are influenced by the changing fortunes of the state lotteries. To what extent have other state revenues been suppressed as a consequence of the state lottery? This question should be addressed for each state which operates a sizable state lottery. Borg, Mason, and Shapiro {1993) found that state own-source revenues were suppressed by lottery profits, at a rate of 15 to 23 for every dollar of state lottery revenue. Their investigation should be extended to other states. While not a primary focus of this study, the background research provided evidence to support the contention of other researchers that a dollar of lottery revenue is not a wholly-new state dollar (Borg, Mason, & Shapiro, 1993; Clotfelter & Cook, 1989). According to data provided by the State of Florida Governor's Office of Planning and Budgeting (1993), Florida's parimutuel tax revenues declined by 19%, or nearly $25 million, from the inception of the lottery through FY 1991 (Figure 4). The decline that began in FY 1987 followed 22 years of consecutive growth since parimutuel taxes were introduced as a State of Florida revenue source in 1965. The results of this study indicated that a beneficiary may not financially benefit by being earmarked to receive state lottery profits. It is possible that the legislature of the State of Florida may have benefitted by the adoption of a state lottery as a revenue source; however, results of

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120 this study indicated that at least one earmarked beneficiary, the community colleges, did not benefit. The lottery allocations correlated with a reduction in state all-source allocations to Florida community colleges. Despite the revenue-producing success of the Florida Education Lotteries, lottery revenues never comprised more than a minimal share of the total allocation to community colleges. It was a share which was shown to be too small to offset the erosion of the state share. Finally, the community colleges as a group are increasingly reliant on nonstate revenue sources. This fact raises the concern that some institutions are more successful than others at fund raising. All colleges pursue grant funding, some with the efforts of a full-fledged resource development department. Most of the colleges have a college foundation for private fund raising. Some college administrators have pursued referenda to levy local taxes. Grant-writing, college foundations and local tax referenda illuminate the concerns raised by this study about horizonal equity. One of the arguments commonly used in favor of state support for community colleges is that students everywhere in the state will have an equal opportunity for higher education. A state system of community colleges is designed for horizontal equity, so that citizens across the state may receive an equivalent education at any of the institutions. A question which needs to be addressed is whether the

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121 horizonal equity of the Florida community college system has been eroded as a result of the search for nonstate revenue sources. The question must address the consequence of the redistribution of the state's contribution relative to other funding sources.

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APPENDICES

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APPENDIX A THE FLORIDA COMMUNITY COLLEGES Community College 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. Brevard Community College Broward Community College Central Florida Community College Chipola Community College Daytona Beach Community College Edison Community College Florida Community College at Jacksonville Florida Keys Community College Gulf Coast Community College Hillsborough Community College Indian River Community College Lake City Community College Lake-Sumter Community College Manatee Community College Miami-Dade Community College North Florida Junior College Okaloosa-Walton Community College Palm Beach Community College Pasco-Hernando Community College Pensacola Junior College Polk Community College st. Johns River Community College St. Petersburg Junior College Santa Fe Community College Seminole Community College South Florida Community College Tallahassee Community College Valencia Community College Source : Florida Department of Education (199 2 b) p 3 123 Established 1960 1960 1958 1948 1958 1962 1966 1965 1957 1968 1960 1962 1962 1958 1960 1958 1964 1933 1972 1948 1964 1958 1947 1966 1966 1966 1966 1967

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APPENDIX B STATE-OPERATED LOTTERIES, CONSTITUTIONAL AND STATUTE CITATIONS, AND LOTTERY FUND BENEFICIARIES State Alabama Alaska Arizona Arkansas California Colorado Connecticut Delaware a Year Begun none none 1981 none 1985 1983 1972 1975 Citation Designated Beneficiaries AL Const. n/a Art. 4, AK St. n/a .15.187(f) AZ St. ,6 parks, 5.522 transport., AR Const. Art. 19, CA Const. Art. IV {d), CA Code T. 2 Chpt. 12.5 Art. 1 .1 CO Const. Art. 18 .7 CT Gen. st. T. 12 Chpt. 226 -568 DE Const. Art. 2 {a), DE St. T. 29 124 commerce & economic dev. n/a education, all levels parks, recreation, open spaces education

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State District of Columbia Florida Georgia Hawaii Idaho Illinois Indiana Iowa Kansasc Kentucky Louisiana Year Citation Begun 1982 DC Code 1981 -2501; 95 St. 1174; PL 97-91 1988 FL Const. Art. X ( c) ( 1) ; FL St. 24 (2)(a), (5) (a-b) pending GA Code 27apprvd 13(3)(b)(l), 19 9 2 ( c) ( 3) ; GA Const. Art. 1, 2, P VIII none 1989 1974 1989 1985 1987 1989 1992 1974 HI Organic Act ID Chpt. 20 /2 IL Chpt. 20 /2 IN Code 4-301-1 IA Code T. 5 Chpt. 99E; T. 12 Chpt. 262B KS Const. Art. 15 c; KS St. 874 KY Const. ; KY St. A.130. LA Const. Art. 12 ME St. T. 8 Designated Beneficiaries GRFb public schools, community colleges & universities educational purposes & projects n/a school buildings common sch~ol fund & GRF capital improvements education, agriculture, university research & econ. dev. GRFb Vietnam Veterans b bonus, GRF GRFb 125

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State Maryland Massachusetts Michigan Minnesota Mississippi Missouri Montana d Nebraska Nevada New Hampshire 8 New Jersey New Mexico Year Begun 1973 1972 1972 1990 none 1986 1987 none none 1964 1970 none Citation MD Const. Art. 3 ; MD st. Govt. -120 MA St. 10 MI Const. Art. 4 MN Const. Art. 11, MN St. A.10 Designated Beneficiaries Stadium facJlities, GRF arts education environment & natural resources MS Const. n/a Art. 4 MO St. GRFb 313.321 MT Code 20-9equalization 343, aid for school districts, ed. telecomm., juvenile detention NE St. 1,101; -507 NV Const. Art. 4 NH Const. Part 2 Art. 6-b NJ Const. Art. 4 7-2; St. 5: 9 NM St. 1978 -19-2 n/a n/a education state-funded institutions, education & senior citizens n/a 126

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State New York North Carolina North Dakota Ohio Oklahoma Oregon Pennsylvania Rhode Island South Carolina South Dakota Tennessee Texas Utah Vermont 8 Year Citation Begun 1967 NY Const. Art. 1 9-1; NY St. FL Chpt. 56 Art. 6 92-c2,3,4-b-1; NY TL Chpt. 60 Art. 34 none NC St. 290 none ND Const. Art. 11 1974 OH St. .01-.06 none OK St. T. 21 1985 OR St. .543(1) 1972 PA PL 351 no. 91 1974 RI Const. Art. 6, s 15; RI St. 61-15 none SC Const. Art. 17 1987 SD St. 42-7A24 none TN Const. Art. 11 pending TX Civ. St. apprvd 1992 none 1978 Art. 179g UT Const. Art. 6 VT St. T. 31 .11 (d), Designated Beneficiaries public and nonpublic elementary & secondary education; winter sports physical ed. n/a n/a education n/a higher ed sports programs senior citizens GRFb n/a corrections facility construction n/a n/a 127

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State Virginia Washington West Virginia Wisconsin Wyoming Year Begun 1988 1982 1986 1988 none Citation VA Code .2-334.3 WA St. 67.70.900, 67.70.240 WV St. 22-7 WI Cons. Art. 4(6);WI st. 79.10 WY St. -23106 Designated Beneficiaries GRFb education, senior citizens property tax relief n/a Source: annotated statutes for each of the SO states and the District of Columbia. Additional source for "Year Begun," Clotfelter & Cook, 1989 pp. 26-27, 146. Notes: aTri-State Lotto Contract approved 1985 among Maine New Hampshire & Vermont. Delaware added to the Tri-State Contract in 1987 bGRF--General Revenue Fund. cKansas approved a Multi-State Lottery in 1988 to permit a lottery to be cooperatively operated with any other state or the District of Columbia (KS St. .8731). dNebraska permits noncomputerized, "small lotteries with profits going into the GRF 128

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APPENDIX C RAW DATA SETS

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Data Set C-I The variables OBS, cc, YR, LT, CAT, GRF, TOTSTATE, FTE, and FTEX12 OBS CC YR LT CAT GRF TOTSTATE FTE FTEX12 1 1 72 0 0% 5560749 5560749 5960 1161 2 2 72 0 0% 6597758 6597758 7443 1168 3 3 72 0 0% 1827264 1827264 1974 1124 4 4 72 0 0% 1405885 1405885 1419 1227 5 5 72 0 0% 3679468 3679468 3994 1266 6 6 72 0 0% 1538002 1538002 1702 1221 7 7 72 0 0% 11053476 11053476 13238 966 8 8 72 0 0% 721141 721141 660 2050 9 9 72 0 0% 1843055 1843055 2075 1031 10 10 72 0 0% 4635417 4635417 5306 1145 11 11 72 0 0% 2283643 2283643 2474 1303 12 12 72 0 0% 1894951 1894951 1877 1366 13 13 72 0 0% 868469 868469 902 1269 14 14 72 0 0% 2346990 2346990 2625 1282 15 15 72 0 0% 24029602 24029602 26578 1311 16 16 72 0 0% 1215672 1215672 1055 1536 17 17 72 0 0% 2084359 2084359 2227 1232 18 18 72 0 0% 4313251 4313251 4953 1263 19 19 72 0 0% 395244 395244 391 1349 20 20 72 0 0% 5990544 5990544 6988 1187 21 21 72 0 0% 2578717 2578717 2871 1215 22 22 72 0 0% 4733211 4733211 953 1452 23 23 72 0 0% 2560333 2560333 8125 1372 24 24 72 0 0% 657032 657032 5597 1211 25 25 72 0 0% 1126540 1126540 2970 1138 26 26 72 0 0% 7588870 7588870 580 1309 27 27 72 0 0% 1767834 1767834 2022 1214 28 28 72 0 0% 3093768 3093768 3707 1093 29 1 73 0 0% 6230065 6230065 6605 1254 30 2 73 0 0% 7403004 7403004 8007 1299 31 3 73 0 0% 2259965 2259965 2446 1028 32 4 73 0 0% 1440781 1440781 1319 1364 33 5 73 0 0% 4208023 4208023 4806 1151 34 6 73 0 0% 1689728 1689728 1984 1287 35 7 73 0 0% 13766161 13766161 15626 1047 36 8 73 0 0% 805567 805567 767 1666 37 9 73 0 0% 2025913 2025913 2112 1478 38 10 73 0 0% 5154171 5154171 6099 1225 39 11 73 0 0% 2939649 2939649 3406 1143 40 12 73 0 0% 2208156 2208156 2308 1392 41 13 73 0 0% 966102 966102 839 1497 42 14 73 0 0% 2461046 2461046 2640 1375 43 15 73 0 0% 24402869 24402869 28993 1274 44 16 73 0 0% 1162224 1162224 867 1692 45 17 73 0 0% 2213912 2213912 2428 1147 130

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131 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 46 18 73 0 0% 4875402 4875402 4764 1434 47 19 73 0 0% 846489 846489 636 1738 48 20 73 0 0% 7406426 7406426 8595 1142 49 21 73 0 0% 2717386 2717386 2968 1258 50 22 73 0 0% 1057528 1057528 830 1612 51 23 73 0 0% 7886759 7886759 8485 1368 52 24 73 0 0% 5374870 5374870 6182 1337 53 25 73 0 0% 3292116 3292116 3781 1079 54 26 73 0 0% 678459 678459 636 1374 55 27 73 0 0% 1920253 1920253 2034 1240 56 28 73 0 0% 3836310 3836310 4231 1273 57 1 74 0 0% 6872189 6872189 7632 2249 58 2 74 0 0% 8325164 8325164 8798 2679 59 3 74 0 0% 2695417 2695417 2632 2193 60 4 74 0 0% 1626338 1626338 1542 2665 61 5 74 0 0% 5252457 5252457 5890 2271 62 6 74 0 0% 2045440 2045440 2359 2495 63 7 74 0 0% 16472233 16472233 18611 2076 64 8 74 0 0% 1025515 1025515 917 2665 65 9 74 0 0% 2090623 2090623 2424 2183 66 10 74 0 0% 6849449 6849449 8323 2107 67 11 74 0 0% 4223121 4223121 4433 2264 68 12 74 0 0% 2115213 2115213 2470 2264 69 13 74 0 0% 1039890 1039890 1030 2918 70 14 74 0 0% 2651438 2651438 3125 2463 71 15 74 0 0% 28112909 28112909 33230 2499 72 16 74 0 0% 1119876 1119876 969 2831 73 17 74 0 0% 2531516 2531516 3047 2089 74 18 74 0 0% 4960629 4960629 4970 2917 75 19 74 0 0% 1291139 1291139 1341 2548 76 20 74 0 0% 8907053 8907053 9692 2238 77 21 74 0 0% 3075182 3075182 3453 2342 78 22 74 0 0% 1052186 1052186 891 3352 79 23 74 0 0% 8576762 8576762 9300 2533 80 24 74 0 0% 6617403 6617403 7336 2491 81 25 74 0 0% 3830844 3830844 4685 2162 82 26 74 0 0% 911623 911623 745 2792 83 27 74 0 0% 2024037 2024037 2196 2425 84 28 74 0 0% 4722969 4722969 5536 2322 85 1 75 0 0% 7350934 7350934 8129 1324 86 2 75 0 0% 8731019 8731019 9916 1361 87 3 75 0 0% 2868115 2868115 2827 1170 88 4 75 0 0% 1636132 1636132 1612 1412 89 5 75 0 0% 5484654 5484654 5963 1379 90 6 75 0 0% 2073016 2073016 2448 1337 91 7 75 0 0% 16791979 16791979 18442 1204 92 8 75 0 0% 1367544 1367544 988 1668 93 9 75 0 0% 2263164 2263164 2444 1276 94 10 75 0 0% 7757747 7757747 8680 1233 95 11 75 0 0% 3921937 3921937 4256 1426

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132 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 96 12 75 0 0% 2899464 2899464 2971 1291 97 13 75 0 0% 1337970 1337970 1166 1374 98 14 75 0 0% 2986046 2986046 3196 1445 99 15 75 0 0% 31218838 31218838 33637 1441 100 16 75 0 0% 1260746 1260746 1030 1538 101 17 75 0 0% 2594048 2594048 2671 1314 102 18 75 0 0% 5161349 5161349 5558 1306 103 19 75 0 0% 1627555 1627555 1742 1389 104 20 75 0 0% 8833093 8833093 9769 1327 105 21 75 0 0% 3244504 3244504 3616 1369 106 22 75 0 0% 1265969 1265969 1049 1682 107 23 75 0 0% 8569002 8569002 10182 1291 108 24 75 0 0% 6652669 6652669 7042 1489 109 25 75 0 0% 3892149 3892149 4658 1420 110 26 75 0 0% 1052145 1052145 909 1492 111 27 75 0 0% 2065149 2065149 2237 1406 112 28 75 0 0% 4870032 4870032 5602 1474 113 1 76 0 0% 7885123 7885123 8194 1485 114 2 76 0 0% 9531132 9531132 10408 1414 115 3 76 0 0% 2975612 2975612 3143 1381 116 4 76 0 0% 1750128 1750128 1458 1615 117 5 76 0 0% 5915842 5915842 6947 1343 118 6 76 0 0% 2334392 2334392 2505 1529 119 7 76 0 0% 17888996 17888996 17914 1376 120 8 76 0 0% 1420722 1420722 1073 2101 121 9 76 0 0% 2413908 2413908 2465 1483 122 10 76 0 0% 8400940 8400940 8406 1456 123 11 76 0 0% 4021198 4021198 4504 1555 124 12 76 0 0% 3126260 3126260 3029 1586 125 13 76 0 0% 1444454 1444454 1206 1714 126 14 76 0 0% 3196076 3196076 3374 1532 127 15 76 0 0% 33455239 33455239 33378 1571 128 16 76 0 0% 1372842 1372842 1009 1861 129 17 76 0 0% 2752500 2752500 2595 1549 130 18 76 0 0% 5573842 5573842 5601 1456 131 19 76 0 0% 1881884 1881884 1789 1796 132 20 76 0 0% 9828403 9828403 10057 1531 133 21 76 0 0% 3544441 3544441 3489 1495 134 22 76 0 0% 1424409 1424409 1086 1759 135 23 76 0 0% 9328323 9328323 10272 1444 136 24 76 0 0% 7028524 7028524 6293 1794 137 25 76 0 0% 4279350 4279350 4896 1454 138 26 76 0 0% 1092657 1092657 987 1614 139 27 76 0 0% 2222625 2222625 2225 1431 140 28 76 0 0% 5529037 5529037 6514 1438 141 1 77 0 0% 8759273 8759273 8505 1613 142 2 77 0 0% 11296174 11296174 11001 1675 143 3 77 0 0% 3300085 3300085 3336 1468 144 4 77 0 0% 1849533 1849533 1410 1871 145 5 77 0 0% 7969764 7969764 7748 1437

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133 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 146 6 77 0 0% 2473256 2473256 2656 1526 147 7 77 0 0% 19803489 19803489 19679 1433 148 8 77 0 0% 1529443 1529443 1058 2166 149 9 77 0 0% 2545886 2545886 2697 1413 150 10 77 0 0% 9118078 9118078 8241 1549 151 11 77 0 0% 4881277 4881277 4951 1609 152 12 77 0 0% 3294844 3294844 2901 1577 153 13 77 0 0% 1521202 1521202 1267 1797 154 14 77 0 0% 3535329 3535329 3650 1509 155 15 77 0 0% 35087174 35087174 34901 1669 156 16 77 0 0% 1422662 1422662 1037 2099 157 17 77 0 0% 2863177 2863177 2759 1521 158 18 77 0 0% 5851841 5851841 5756 1529 159 19 77 0 0% 2069081 2069081 1858 1765 160 20 77 0 0% 11118155 11118155 10518 1624 161 21 77 0 0% 3702262 3702262 3543 1553 162 22 77 0 0% 1579838 1579838 1127 1924 163 23 77 0 0% 10569290 10569290 10522 1594 164 24 77 0 0% 7396614 7396614 6617 1784 165 25 77 0 0% 4255801 4255801 5429 1597 166 26 77 0 0% 1333251 1333251 1182 1527 167 27 77 0 0% 2330748 2330748 2311 1421 168 28 77 0 0% 6934304 6934304 6639 1702 169 1 78 0 0% 9586655 9586655 8580 2941 170 2 78 0 0% 12519919 12519919 11643 3305 171 3 78 0 0% 3541333 3541333 3578 2682 172 4 78 0 0% 1988248 1988248 1426 3686 173 5 78 0 0% 8490626 8490626 8160 2684 174 6 78 0 0% 2806032 2806032 2765 2973 175 7 78 0 0% 21487306 21487306 18950 2767 176 8 78 0 0% 1644151 1644151 1086 4062 177 9 78 0 0% 2787432 2787432 2702 3099 178 10 78 0 0% 8636237 8636237 8469 3008 179 11 78 0 0% 5644200 5644200 5156 2741 180 12 78 0 0% 3526402 3526402 2829 3203 181 13 78 0 0% 1656994 1656994 1311 3457 182 14 78 0 0% 3843864 3843864 3662 3136 183 15 78 0 0% 36748930 36748930 34633 3222 184 16 78 0 0% 1529362 1529362 1059 3728 185 17 78 0 0% 3023788 3023788 2768 3138 186 18 78 0 0% 6238445 6238445 5992 3130 187 19 78 0 0% 2224262 2224262 2017 3020 188 20 78 0 0% 12174908 12174908 11074 2913 189 21 78 0 0% 3811526 3811526 3538 3142 190 22 78 0 0% 1658070 1658070 1065 4130 191 23 78 0 0% 11425823 11425823 10736 3193 192 24 78 0 0% 7229807 7229807 7079 2960 193 25 78 0 0% 5664967 5664967 5519 2655 194 26 78 0 0% 1627084 1627084 1155 3057 195 27 78 0 0% 2531923 2531923 2404 2873

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134 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 196 28 78 0 0% 7455547 7455547 6831 3259 197 1 79 0 0% 10523149 10523149 8822 1931 198 2 79 0 0% 13946427 13946427 12182 1765 199 3 79 0 0% 4594613 4594613 3568 1783 200 4 79 0 0% 2127425 2127425 1406 2467 201 5 79 0 0% 10122590 10122590 8687 1889 202 6 79 0 0% 3461836 3461836 2959 1933 203 7 79 0 0% 23726629 23726629 19252 1664 204 8 79 0 0% 1816463 1816463 1071 2828 205 9 79 0 0% 3407759 3407759 2952 1769 206 10 79 0 0% 9986436 9986436 8553 1719 207 11 79 0 0% 6747071 6747071 5797 2040 208 12 79 0 0% 3883630 3883630 2899 1912 209 13 79 0 0% 1935035 1935035 1292 2114 210 14 79 0 0% 4314549 4314549 3957 1836 211 15 79 0 0% 42437624 42437624 35129 2010 212 16 79 0 0% 1658154 1658154 869 2820 213 17 79 0 0% 3488605 3488605 2879 1692 214 18 79 0 0% 7438018 7438018 6467 1654 215 19 79 0 0% 2570890 2570890 2193 1879 216 20 79 0 0% 13767534 13767534 11082 1478 217 21 79 0 0% 4349127 4349127 3457 1804 218 22 79 0 0% 1763023 1763023 1084 2233 219 23 79 0 0% 13036454 13036454 11155 1780 220 24 79 0 0% 8847483 8847483 7637 1855 221 25 79 0 0% 7076408 7076408 6073 1733 222 26 79 0 0% 1719944 1719944 1269 1779 223 27 79 0 0% 2952791 2952791 2673 1585 224 28 79 0 0% 8496951 8496951 7126 1885 225 1 80 0 0% 11555226 11555226 9515 1972 226 2 80 0 0% 15316654 15316654 12730 1911 227 3 80 0 0% 5041277 5041277 3686 2027 228 4 80 0 0% 2437201 2437201 1421 2246 229 5 80 0 0% 11564588 11564588 9363 1931 230 6 80 0 0% 3894699 3894699 3310 1971 231 7 80 0 0% 26043956 26043956 19860 1808 232 8 80 0 0% 1989322 1989322 1238 2733 233 9 80 0 0% 3866967 3866967 3004 2112 234 10 80 0 0% 11048133 11048133 8327 1930 235 11 80 0 0% 7891052 7891052 6047 2582 236 12 80 0 0% 4261398 4261398 3119 1932 237 13 80 0 0% 2170943 2170943 1309 2321 238 14 80 0 0% 4738137 4738137 4069 1850 239 15 80 0 0% 46681329 46681329 35828 2144 240 16 80 0 0% 1815251 1815251 876 2642 241 17 80 0 0% 3917700 3917700 3024 1862 242 18 80 0 0% 8509460 8509460 6950 1892 243 19 80 0 0% 2823976 2823976 2448 2106 244 20 80 0 0% 15113132 15113132 11169 1779 245 21 80 0 0% 4774107 4774107 3610 1965

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135 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 246 22 80 0 0% 2005885 2005885 1128 2491 247 23 80 0 0% 14317337 14317337 11829 1928 248 24 80 0 0% 10142550 10142550 7579 2074 249 25 80 0 0% 7770743 7770743 6860 1810 250 26 80 0 0% 2159984 2159984 1541 1682 251 27 80 0 0% 3406597 3406597 3602 1407 252 28 80 0 0% 9333444 9333444 8009 1941 253 1 81 0 0% 12981318 12981318 6390 3098 254 2 81 0 0% 17836504 17836504 9112 3176 255 3 81 0 0% 5563207 5563207 2046 3958 256 4 81 0 0% 2817150 2817150 962 3844 257 5 81 0 0% 12884577 12884577 6243 3149 258 6 81 0 0% 4493429 4493429 2461 3041 259 7 81 0 0% 28471406 28471406 15022 2627 260 8 81 0 0% 2309903 2309903 803 4523 261 9 81 0 0% 4227469 4227469 2017 3273 262 10 81 0 0% 12087777 12087777 5919 2829 263 11 81 0 0% 8625787 8625787 4825 3142 264 12 81 0 0% 4791685 4791685 1350 4807 265 13 81 0 0% 2508044 2508044 693 5030 266 14 81 0 0% 5632905 5632905 2811 2989 267 15 81 0 0% 50940269 50940269 25835 3326 268 16 81 0 0% 1983001 1983001 564 4884 269 17 81 0 0% 4315435 4315435 2152 2894 270 18 81 0 0% 10161208 10161208 5164 2857 271 19 81 0 0% 3378772 3378772 1599 3656 272 20 81 0 0% 16521827 16521827 8253 2689 273 21 81 0 0% 5218159 5218159 2578 2959 274 22 81 0 0% 2250185 2250185 706 4264 275 23 81 0 0% 16475851 16475851 8118 3064 276 24 81 0 0% 11442184 11442184 5105 3437 277 25 81 0 0% 9088985 9088985 5313 2481 278 26 81 0 0% 2686767 2686767 1076 3493 279 27 81 0 0% 3964531 3964531 2450 2608 280 28 81 0 0% 10886009 10886009 5882 3037 281 1 82 0 0% 14910125 14910125 7308 2949 282 2 82 0 0% 18220190 18220190 9792 3385 283 3 82 0 0% 5556647 5556647 2474 3408 284 4 82 0 0% 2841710 2841710 925 4301 285 5 82 0 0% 12982626 12982626 6305 3102 286 6 82 0 0% 4728287 4728287 2646 2921 287 7 82 0 0% 28812822 28812822 14373 2826 288 8 82 0 0% 2379558 2379558 780 4520 289 9 82 0 0% 4380723 4380723 2032 3462 290 10 82 0 0% 12223221 12223221 5941 3006 291 11 82 0 0% 8691224 8691224 4612 2794 292 12 82 0 0% 4824264 4824264 1547 4399 293 13 82 0 0% 2528259 2528259 833 4484 294 14 82 0 0% 5698449 5698449 3144 2936 295 15 82 0 0% 51480544 51480544 24746 3451

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136 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 296 16 82 0 0% 2000686 2000686 683 3912 297 17 82 0 0% 4567140 4567140 2181 2928 298 18 82 0 0% 10857472 10857472 5599 3217 299 19 82 0 0% 3417659 3417659 1750 2957 300 20 82 0 0% 16786575 16786575 8877 2705 301 21 82 0 0% 5280730 5280730 2733 3050 302 22 82 0 0% 2307528 2307528 798 3990 303 23 82 0 0% 16667061 16667061 8588 2969 304 24 82 0 0% 11534441 11534441 5244 3311 305 25 82 0 0% 9741818 9741818 5400 2605 306 26 82 0 0% 2709515 2709515 1166 2679 307 27 82 0 0% 4887365 4887365 2716 2509 308 28 82 0 0% 12014389 12014389 5842 3286 309 1 83 0 0% 16888548 16888548 7866 2976 310 2 83 0 0% 21085065 21085065 9963 3326 311 3 83 0 0% 6233431 6233431 2409 3773 312 4 83 0 0% 3159011 3159011 927 4512 313 5 83 0 0% 14555190 14555190 6711 3126 314 6 83 0 0% 5461484 5461484 2749 3295 315 7 83 0 0% 32120718 32120718 13557 3154 316 8 83 0 0% 2664607 2664607 756 5230 317 9 83 0 0% 5077950 5077950 2133 3678 318 10 83 0 0% 13829756 13829756 6101 3260 319 11 83 0 0% 10100781 10100781 4465 3194 320 12 83 0 0% 5338143 5338143 1381 5096 321 13 83 0 0% 2876399 2876399 819 4900 322 14 83 0 0% 6450395 6450395 3223 3359 323 15 83 0 0% 58482491 58482491 24180 3812 324 16 83 0 0% 2216068 2216068 676 3875 325 17 83 0 0% 5129575 5129575 2296 2994 326 18 83 0 0% 12370856 12370856 5487 3535 327 19 83 0 0% 3884339 3884339 1586 3420 328 20 83 0 0% 18740691 18740691 7777 3260 329 21 83 0 0% 6036263 6036263 2538 3467 330 22 83 0 0% 2574824 2574824 719 4686 331 23 83 0 0% 19020795 19020795 8600 3347 332 24 83 0 0% 13014798 13014798 5025 3820 333 25 83 0 0% 10886176 10886176 4830 3185 334 26 83 0 0% 2993707 2993707 1101 3570 335 27 83 0 0% 5641011 5641011 2599 3181 336 28 83 0 0% 13619659 13619659 6026 3447 337 1 84 0 0% 17687965 17687965 6996 3724 338 2 84 0 0% 22061740 22061740 9535 3671 339 3 84 0 0% 6462449 6462449 1979 4381 340 4 84 0 0% 3329586 3329586 964 4885 341 5 84 0 0% 15431276 15431276 6188 3580 342 6 84 0 0% 5950206 5950206 2679 3515 343 7 84 0 0% 33483370 33483370 11683 3954 344 8 84 0 0% 2794579 2794579 753 5323 345 9 84 0 0% 5286018 5286018 2091 4290

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137 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 346 10 84 0 0% 14722946 14722946 5696 3870 347 11 84 0 0% 10237617 10237617 4629 3313 348 12 84 0 0% 5313273 5313273 1579 5106 349 13 84 0 0% 2947870 2947870 747 5804 350 14 84 0 0% 7046365 7046365 3020 3830 351 15 84 0 0% 61145917 61145917 23682 3994 352 16 84 0 0% 2299346 2299346 642 4673 353 17 84 0 0% 5341882 5341882 2172 3299 354 18 84 0 0% 12977916 12977916 5532 3636 355 19 84 0 0% 3913508 3913508 1495 3735 356 20 84 0 0% 19469294 19469294 7049 3790 357 21 84 0 0% 6152359 6152359 2366 3578 358 22 84 0 0% 2611105 2611105 696 5093 359 23 84 0 0% 19849039 19849039 8428 3445 360 24 84 0 0% 13881173 13881173 4904 4059 361 25 84 0 0% 10810434 10810434 4917 3197 362 26 84 0 0% 3195063 3195063 1166 4019 363 27 84 0 0% 5856979 5856979 2560 3232 364 28 84 0 0% 14186402 14186402 5892 3830 365 1 85 0 0% 18428999 18428999 6691 3907 366 2 85 0 0% 23588913 23588913 9290 3828 367 3 85 0 0% 6631081 6631081 2097 4699 368 4 85 0 0% 3574428 3574428 1041 4722 369 5 85 0 0% 15743739 15743739 6688 3340 370 6 85 0 0% 6435088 6435088 2659 3744 371 7 85 0 0% 34535013 34535013 12134 3735 372 8 85 0 0% 2965367 2965367 693 6123 373 9 85 0 0% 5718296 5718296 2095 4383 374 10 85 0 0% 15627411 15627411 5764 3911 375 11 85 0 0% 10854982 10854982 4325 3894 376 12 85 0 0% 5628368 5628368 1549 5519 377 13 85 0 0% 3133784 3133784 811 5166 378 14 85 0 0% 7501678 7501678 3051 3789 379 15 85 0 0% 65954509 65954509 23995 4232 380 16 85 0 0% 2461695 2461695 703 5148 381 17 85 0 0% 5558391 5558391 2088 3886 382 18 85 0 0% 13741791 13741791 5694 3526 383 19 85 0 0% 4120346 4120346 1610 3826 384 20 85 0 0% 20204048 20204048 7087 4001 385 21 85 0 0% 6429769 6429769 2221 4216 386 22 85 0 0% 2820741 2820741 746 5013 387 23 85 0 0% 21094748 21094748 8189 3827 388 24 85 0 0% 14762605 14762605 5141 4115 389 25 85 0 0% 11531387 11531387 5220 2982 390 26 85 0 0% 3380768 3380768 1629 2952 391 27 85 0 0% 6202124 6202124 2755 3298 392 28 85 0 0% 15455828 15455828 6270 3856 393 1 86 0 0% 19753731 19753731 7270 3951 394 2 86 0 0% 25853057 25853057 9575 7200 395 3 86 0 0% 7062751 7062751 2251 4281

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138 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 396 4 86 0 0% 3882550 3882550 1068 5207 397 5 86 0 0% 17624145 17624145 6733 3599 398 6 86 0 0% 7217968 7217968 2894 3778 399 7 86 0 0% 36213777 36213777 12207 4111 400 8 86 0 0% 3182052 3182052 678 6763 401 9 86 0 0% 6291923 6291923 2270 4453 402 10 86 0 0% 17383842 17383842 6268 4005 403 11 86 0 0% 12260759 12260759 4661 3891 404 12 86 0 0% 6186303 6186303 1919 4581 405 13 86 0 0% 3499129 3499129 854 5648 406 14 86 0 0% 8615962 8615962 3216 4182 407 15 86 0 0% 73264240 73264240 25085 4321 408 16 86 0 0% 2692718 2692718 784 4758 409 17 86 0 0% 6073614 6073614 2078 4038 410 18 86 0 0% 15747968 15747968 6000 3923 411 19 86 0 0% 4517136 4517136 1650 3724 412 20 86 0 0% 20786235 20786235 7025 4094 413 21 86 0 0% 6906693 6906693 2283 4612 414 22 86 0 0% 3348164 3348164 945 4503 415 23 86 0 0% 23531294 23531294 8304 4182 416 24 86 0 0% 16214337 16214337 5417 4262 417 25 86 0 0% 13237322 13237322 5287 3180 418 26 86 0 0% 4188328 4188328 1647 3809 419 27 86 0 0% 7578708 7578708 3074 3792 420 28 86 0 0% 17129841 17129841 6631 4001 421 1 87 1 87% 20920147 21068649 7492 4260 422 2 87 1 84% 27794044 27996207 9701 4670 423 3 87 1 92% 7469077 7503448 2406 4654 434 4 87 1 89% 4317154 4333806 1136 5118 425 5 87 1 89% 19226300 19331816 6709 4127 426 6 87 1 82% 7869719 7936123 3104 4040 427 7 87 1 82% 38603966 38869968 12305 4301 428 8 87 1 26% 3277316 3480329 760 6413 429 9 87 1 93% 6681789 6717495 2424 4493 430 10 87 1 90% 18566697 18654839 6562 4282 431 11 87 1 85% 13201794 13280316 4959 4173 432 12 87 1 64% 6555500 6637572 1708 5660 433 13 87 1 94% 3709740 3722657 888 5532 434 14 87 1 84% 9364438 9430308 3632 3999 435 15 87 1 86% 78087015 78585138 26096 4651 436 16 87 1 79% 2916709 2952395 860 4692 437 17 87 1 90% 6510756 6544657 2246 4062 438 18 87 1 82% 16870578 17000102 6306 4284 439 19 87 1 94% 4776866 4802401 1833 3879 440 20 87 1 83% 22186116 22329852 7253 4400 441 21 87 1 86% 7522103 7558453 2442 4752 442 22 87 1 94% 3568352 3582823 1110 4348 443 23 87 1 88% 25108881 25239682 8544 4235 444 24 87 1 89% 17327851 17411191 5731 4609 445 25 87 1 87% 14162594 14266249 5871 3272

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139 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 446 26 87 1 93% 4695475 4720524 1926 3590 447 27 87 1 84% 8823775 8872759 3533 4682 448 28 87 1 90% 18907125 19032602 7293 4113 449 1 88 1 62% 23467838 24159066 7810 4335 450 2 88 1 28% 29915427 32802781 10330 4718 451 3 88 1 72% 8083389 8348955 2443 5194 452 4 88 1 55% 5119450 5266370 1349 5102 453 5 88 1 61% 21430384 22059382 6918 4540 454 6 88 1 62% 8955768 9256571 3251 4344 455 7 88 1 59% 41519719 42690922 14350 3953 456 8 88 1 62% 3489802 3597256 729 7410 457 9 88 1 67% 7579353 7825970 2617 4747 458 10 88 1 63% 19774404 20361624 78450 388 459 11 88 1 62% 14335826 14808874 5419 4319 460 12 88 1 65% 7629116 7840264 1830 5385 461 13 88 1 66% 4085410 4209647 918 6393 462 14 88 1 57% 10485636 10829082 3919 4171 463 15 88 1 61% 83606087 86032228 27496 4849 464 16 88 1 60% 3270087 3384976 870 5607 465 17 88 1 63% 7221694 7455002 2598 4180 466 18 88 1 62% 19205662 19780955 6653 4452 467 19 88 1 62% 5445545 5635779 2108 4043 468 20 88 1 58% 23617102 24302139 7670 4374 469 21 88 1 56% 8126009 8388820 2740 4671 470 22 88 1 57% 4203763 4341546 1336 4507 471 23 88 1 61% 27172909 28015472 9097 4378 472 24 88 1 55% 19006701 19582484 6323 4587 473 25 88 1 67% 16084582 16597516 6240 3790 474 26 88 1 65% 5815434 6007496 2274 3746 475 27 88 1 55% 10292009 10646893 4071 4510 476 28 88 1 67% 21470539 22109153 8031 4863 477 1 89 1 41% 24361041 26593012 8452 4599 478 2 89 1 29% 30325390 35273429 11341 4902 479 3 89 1 47% 8707692 9508829 2852 5403 480 4 89 1 38% 5157568 5604472 1424 5409 481 5 89 1 39% 21550539 23589782 7715 4593 482 6 89 1 42% 9460757 10406210 3746 4490 483 7 89 1 37% 41565298 45497955 16192 4191 484 8 89 1 31% 3502198 3811435 850 6628 485 9 89 1 49% 8155110 8931049 2668 5412 486 10 89 1 37% 21268564 23280457 8301 4447 487 11 89 1 41% 15914087 17390646 6062 4503 488 12 89 1 43% 7674048 8343134 2015 5312 489 13 89 1 36% 4056237 4425248 1018 6335 490 14 89 1 36% 11201760 12301466 4170 4475 491 15 89 1 37% 87941772 96116930 29504 52 1 2 492 16 89 1 27% 3394750 3712385 959 5001 493 17 89 1 45% 7570686 8295058 3103 4231 494 18 89 1 41% 20433851 22351517 7614 4722 495 19 89 1 44% 5747043 6319444 2458 4134

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140 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 496 20 89 1 34% 23771601 26014895 7137 5210 497 21 89 1 39% 8249577 9063676 2975 4818 498 22 89 1 29% 4695684 5120212 1615 4682 499 23 89 1 43% 27498884 30223861 9723 4769 500 24 89 1 33% 20034311 21926937 6739 4922 501 25 89 1 41% 17047287 18687400 6185 4515 502 26 89 1 34% 6219822 6807030 2320 4402 503 27 89 1 33% 11571877 12669974 4596 5000 504 28 89 1 42% 23062611 25242900 8761 5135 505 1 90 1 33% 24107872 27067232 8626 4671 506 2 90 1 20% 29969649 35919696 12295 4670 507 3 90 1 38% 8503711 9592028 3156 5441 508 4 90 1 27% 5200162 5836484 1531 5257 509 5 96 1 25% 20903085 23541875 8312 4449 510 6 90 1 22% 9491757 10813734 4223 4260 511 7 90 1 22% 43219800 48737643 16847 4107 512 8 90 1 17% 3661144 4084527 836 6966 513 9 90 1 38% 8291634 9323214 2894 5064 514 10 90 1 23% 22248099 25154780 9317 4062 515 11 90 1 27% 16033161 18022100 6628 4069 516 12 90 1 19% 7589588 8441188 2070 5223 517 13 90 1 38% 3999967 4512494 1053 6618 518 14 90 1 21% 11241996 12785854 4337 4261 519 15 90 1 24% 87912742 98794313 31845 5100 520 16 90 1 17% 3315849 3724728 971 5095 521 17 90 1 30% 8327969 9436279 3242 4137 522 18 90 1 27% 20569342 23220586 8366 4464 523 19 90 1 25% 6414112 7275867 2786 3771 524 20 90 1 21% 23050451 25722237 7393 5131 525 21 90 1 26% 8309678 9441854 3162 4641 526 22 90 1 18% 4868402 5538343 1749 4335 527 23 90 1 26% 26704489 30390721 10251 4647 528 24 90 1 23% 19859642 22437364 7004 4824 529 25 90 1 24% 16871522 19094375 6267 4504 530 26 90 1 23% 6418867 7167869 2684 3924 531 27 90 1 22% 12401882 14121572 5108 5681 532 28 90 1 35% 23139215 26260811 9833 4643 533 1 91 1 3% 21604039 27513681 9159 4592 534 2 91 1 6% 27522298 35835709 12217 4733 535 3 91 1 9% 8173361 10238578 3297 5120 536 4 91 1 10% 4793779 5809511 1475 5679 537 5 91 1 1% 18602048 24334074 8890 4021 538 6 91 1 2% 8547599 11429236 4451 4150 539 7 91 1 1% 40121228 51527108 17759 3940 540 8 91 1 4% 3454633 4069265 913 6234 541 9 91 1 13% 7304508 9299264 3156 4848 542 10 91 1 1% 20636714 27043702 10188 4112 543 11 91 1 2% 14290699 18874266 6963 4125 544 12 91 1 0% 6949979 8344996 2042 5593 545 13 91 1 5% 3846632 4566953 1121 5851

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141 OBS cc YR LT CAT GRF TOTSTATE FTE FTEX12 546 14 91 1 1% 9771987 12813799 4508 4372 547 15 91 1 3% 76745032 98410720 33629 4893 548 16 91 1 0% 3087578 3735119 836 6427 549 17 91 1 2% 8162533 10327959 3423 4246 550 18 91 1 1% 18090652 23794536 8549 4268 551 19 91 1 9% 6097418 8023103 3015 3871 552 20 91 1 3% 20315387 25350699 7886 4538 553 21 91 1 4% 7625474 9763097 3217 4492 554 22 91 1 0% 4659174 5848684 1826 4153 555 23 91 1 4% 23709764 30675309 10570 4782 556 24 91 1 1% 17040265 21772652 7131 4736 557 25 91 1 1% 14777618 18986431 6738 4024 558 26 91 1 2% 5837329 7633149 2492 4536 55 9 27 91 1 2% 10720932 14144481 5273 4944 560 28 91 1 2% 21196129 27883708 10971 4364 561 1 92 1 3% 21963612 27742948 9051 n/a 562 2 92 1 6% 28032683 36167275 12604 n/a 563 3 92 1 12% 8065797 10084683 3482 n/a 564 4 92 1 5% 4872820 5864018 1455 n/a 565 5 92 1 2% 19049686 24659841 9824 n/a 566 6 92 1 1% 8708236 11529900 4662 n/a 567 7 92 1 1% 40810016 51965671 18414 n/a 568 8 92 1 3% 3518882 4117316 824 n/a 56 9 9 92 1 1% 7439834 9390385 3326 n/a 570 10 92 1 1% 21022184 27292474 10844 n/a 571 11 92 1 3% 14564555 19051485 7553 n/a 572 12 92 1 4% 7080540 8440618 2186 n/a 573 13 92 1 2% 3905900 4607833 1161 n/a 574 14 92 1 2% 9956261 12933173 4229 n/a 575 15 92 1 2% 77789514 98979524 32957 n/a 576 16 92 1 1% 3145802 3777408 848 n/a 577 17 92 1 9% 8276152 10393893 3353 n/a 578 18 92 1 2% 18422981 24005935 8608 n/a 579 19 92 1 7% 6209760 8094628 3105 n/a 580 20 92 1 3% 20913126 25832626 8234 n/a 581 21 92 1 4% 7765486 9856025 3273 n/a 582 22 92 1 0% 4747034 5909403 1934 n/a 583 23 92 1 5% 24150645 30964967 11065 n/a 584 24 92 1 3% 17360705 21988287 7427 n/a 585 25 92 1 1% 14959126 19075849 6645 n/a 586 26 92 1 2% 5943422 7700908 2490 n/a 587 27 92 1 0% 10922703 14273802 5115 n/a 588 28 92 1 4% 21428168 27974455 11466 n/a 589 1 93 1 0% 22084384 26841460 7597 n/a 590 2 93 1 0% 30104938 38069628 13018 n/a 591 3 93 1 0% 8411206 10611543 3716 n/a 592 4 93 1 0% 4996472 5927919 1480 n/a 593 5 93 1 0% 21183379 27391338 10462 n/a 594 6 93 1 0 % 9827834 12773834 5059 n/a 595 7 93 1 0% 43059874 54696006 19189 n/a

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OBS CC 596 8 597 9 598 10 599 11 600 12 601 13 602 14 603 15 604 16 605 17 606 18 607 19 608 20 609 21 610 22 611 23 612 24 613 25 614 26 615 27 616 28 YR 93 93 93 93 93 93 93 93 93 93 93 93 93 93 93 93 93 93 93 93 93 LT CAT 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% 1 0% GRF 3696209 7863942 23470220 16454379 7482882 3995354 10720604 82287352 3404443 8422645 20090910 6938398 22069363 8227227 5025108 25825502 18511382 15726365 6416299 12307083 23686208 TOTSTATE 4273150 9965700 30322735 21227253 8864254 4729010 13569289 1.04E+08 3940309 10585067 25530457 8900502 27272573 10295493 6247237 32817671 23204634 19984226 7991038 15639185 30931776 FTE 849 3611 11937 7953 2205 1204 4424 35028 781 3522 9107 3417 8675 3366 2065 11595 7675 6909 2556 5460 12669 FTEX12 n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a rr/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a 142 Source: State of Florida Department of Education 1990a pp. 3 6 ; 1 990b, pp 3-4, 25; 1991 pp 3-4, 7; 1992 pp. 3-5 8 ; 1993 p. l ; S t at e o f Florida Department of Education Division of Communit y Colleges 1 974 p p. 48 70-74 ; 1975, pp 32, 61-65 ; 1976 pp. 30 56 58-61 ; 197 7, pp 34, 63 65-72; 1978, pp 34, 62, 64-71; 1979, pp 32, 60 62-69 ; 1 980, pp 33 63 65-74 ; 1981 pp. 11 42 44-53; 1982 pp. 11 42, 44-53 ; 1983 pp 44-53; 1984, pp. 11, 42 44-48; 1985, pp 11, 39 4 1-45 ; 1 986 pp 14, 52 54-58 ; 1987 pp. 13 73 75-79 ; 1988a 1988b pp 15 7 5 77-8 1 ; 1989, pp. 15 77, 79-83; 1990a, 1990b, pp. 13 79 81-85 ; 199 1 a 1 991 b 1991c; 1992a pp 28-29, 76-77; 1992b; 1993a 1993b)

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Data Set C-II Th e v a ria b les OBS, LOT, LOTFTE, GRFFTE, STATFTE, and TOTAL E&G OB S L OT L O TFTE GRFFTE STATFTE TOTAL E&G 1 0 0 933 933 6918751 2 0 0 886 886 8692915 3 0 0 926 926 2219371 4 0 0 991 991 1741497 5 0 0 921 921 5057168 6 0 0 904 904 2077506 7 0 0 835 835 12788319 8 0 0 1093 1093 1352909 9 0 0 888 888 2138664 10 0 0 874 874 6072968 11 0 0 923 923 3223592 12 0 0 1010 1010 2563657 13 0 0 963 963 1145016 14 0 0 894 894 3364367 15 0 0 904 904 34847752 1 6 0 0 1152 1152 1620642 17 0 0 936 936 2743775 18 0 0 871 871 6255216 19 0 0 1011 1011 527304 20 0 0 857 857 8292973 21 0 0 898 898 3488006 22 0 0 1182 1182 1384190 23 0 0 934 934 11148737 24 0 0 846 846 6776436 25 0 0 862 862 3379237 26 0 0 1133 1133 759107 27 0 0 874 874 2453851 28 0 0 835 835 4050971 29 0 0 943 943 8285451 30 0 0 925 925 10401041 31 0 0 924 924 2515661 32 0 0 1093 1093 1798659 33 0 0 876 876 5532810 34 0 0 852 852 2553162 35 0 0 881 881 16362653 36 0 0 1050 1050 1277931 37 0 0 959 959 3122270 38 0 0 845 845 7468256 39 0 0 863 863 3894100 40 0 0 957 957 3213610 41 0 0 1151 1151 1256090 42 0 0 932 932 3630767 43 0 0 842 842 36948271 44 0 0 1340 1340 1467349 45 0 0 912 912 2783898 143

PAGE 405

144 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 46 0 0 1023 1023 6830643 47 0 0 1332 1332 1104474 48 0 0 862 862 9814900 49 0 0 916 916 3732906 50 0 0 1274 1274 1337961 51 0 0 929 929 11606506 52 0 0 869 869 8264027 53 0 0 871 871 4080665 54 0 0 1067 1067 873052 55 0 0 944 944 2522496 56 0 0 907 907 5386676 57 0 0 900 900 17165726 58 0 0 946 946 23569328 59 0 0 1024 1024 5772298 60 0 0 1054 1054 4109656 61 0 0 892 892 13377762 62 0 0 867 867 5884738 63 0 0 885 885 38642392 64 0 0 1119 1119 2442716 65 0 0 862 862 5292854 66 0 0 823 823 17539148 67 0 0 953 953 10034606 68 0 0 856 856 5591986 69 0 0 1010 1010 3004368 70 0 0 848 848 7697124 71 0 0 846 846 83035148 72 0 0 1156 1156 2742500 73 0 0 831 831 6364840 74 0 0 998 998 14498366 75 0 0 963 963 3418124 76 0 0 919 919 21693894 77 0 0 891 891 8087576 78 0 0 1181 1181 2984880 79 0 0 922 922 23555386 80 0 0 902 902 18276712 81 0 0 818 818 10127036 82 0 0 1224 1224 2079980 83 0 0 922 922 5326330 84 0 0 853 853 12853964 85 0 0 904 904 10762483 86 0 0 880 880 13493896 87 0 0 1015 1015 3307225 88 0 0 1015 1015 2276593 89 0 0 920 920 8223617 90 0 0 847 847 3272375 91 0 0 911 911 22199655 92 0 0 1384 1384 1648754 93 0 0 926 926 3117941 94 0 0 894 894 10701940 95 0 0 922 922 6069326

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145 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 96 0 0 976 976 3837078 97 0 0 1147 1147 1602230 98 0 0 934 934 4617136 99 0 0 928 928 48483577 100 0 0 1224 1224 1585201 101 0 0 971 971 3510756 102 0 0 929 929 7260198 103 0 0 934 934 2419034 104 0 0 904 904 12964530 105 0 0 897 897 4951275 106 0 0 1207 1207 1764761 107 0 0 842 842 13140881 108 0 0 945 945 10483499 109 0 0 836 836 6613426 110 0 0 1158 1158 1355929 111 0 0 923 923 3145846 112 0 0 869 869 8254972 113 0 0 962 962 12165735 114 0 0 916 916 14711829 115 0 0 947 947 4339637 116 0 0 1201 1201 2353780 117 0 0 852 852 9332402 118 0 0 932 932 3830500 119 0 0 999 999 24655712 120 0 0 1324 1324 2254332 121 0 0 979 979 3656012 122 0 0 999 999 12242831 123 0 0 893 893 7004226 124 0 0 1032 1032 4802853 125 0 0 1198 1198 2066597 126 0 0 947 947 5169667 127 0 0 1002 1002 52420787 128 0 0 1361 1361 1877628 129 0 0 1061 1061 4019674 130 0 0 995 995 8155093 131 0 0 1052 1052 3212870 132 0 0 977 977 15394477 133 0 0 1016 1016 5216053 134 0 0 1312 1312 1910283 135 0 0 908 908 14830489 136 0 0 1117 1117 11291540 137 0 0 874 874 7119329 138 0 0 1107 1107 1592464 139 0 0 999 999 3183321 140 0 0 849 849 9367511 141 0 0 1030 1030 13716280 142 0 0 1027 1027 18431920 143 0 0 989 989 4897623 144 0 0 1312 1312 2637808 145 0 0 1029 1029 11131282

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146 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 146 0 0 931 931 4053396 147 0 0 1006 1006 28196669 148 0 0 1445 1445 2292014 149 0 0 944 944 3809527 150 0 0 1106 1106 12766775 151 0 0 986 986 7966297 152 0 0 1136 1136 4574243 153 0 0 1201 1201 2277117 154 0 0 969 969 5507893 155 0 0 1005 1005 58249953 156 0 0 1372 1372 2175554 157 0 0 1038 1038 4196473 158 0 0 1017 1017 8801983 159 0 0 1113 1113 3280985 160 0 0 1057 1057 17086082 161 0 0 1045 1045 5500662 162 0 0 1401 1401 2169596 163 0 0 1005 1005 16766406 164 0 0 1118 1118 11802178 165 0 0 784 784 8666859 166 0 0 1128 1128 1805227 167 0 0 1009 1009 3283579 168 0 0 1044 1044 11298733 169 0 0 1117 1117 25237106 170 0 0 1075 1075 38478518 171 0 0 990 990 9597858 172 0 0 1395 1395 5254478 173 0 0 1040 1040 21903186 174 0 0 1015 1015 8219362 175 0 b 1134 1134 52442444 176 0 0 1514 1514 4411352 177 0 0 1032 1032 8374144 178 0 0 1020 1020 25477580 179 0 0 1095 1095 14133348 180 0 0 1247 1247 9059812 181 0 0 1264 1264 4531728 182 0 0 1050 1050 11483014 183 0 0 1061 1061 111585854 184 0 0 1444 1444 3948350 185 0 0 1092 1092 8686532 186 0 0 1041 1041 18751354 187 0 0 1103 1103 6091320 188 0 0 1099 1099 32259282 189 0 0 1077 1077 11118306 190 0 0 1557 1557 4397684 191 0 0 1064 1064 34276676 192 0 0 1021 1021 20953954 193 0 0 1026 1026 14654620 194 0 0 1408 1408 3531536 195 0 0 1053 1053 6904242

PAGE 408

147 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 196 0 0 1091 1091 22264140 197 0 0 1193 1193 17038542 198 0 0 1145 1145 21497635 199 0 0 1288 1288 6361184 200 0 0 1513 1513 3468444 201 0 0 1165 1165 16405314 202 0 0 1170 1170 5721477 203 0 0 1232 1232 32032230 204 0 0 1696 1696 3029780 205 0 0 1154 1154 5222925 206 0 0 1168 1168 14702754 207 0 0 1164 1164 11825071 208 0 0 1340 1340 5541708 209 0 0 1498 1498 2730697 210 0 0 1090 1090 7263511 211 0 0 1208 1208 70594346 212 0 0 1908 1908 2450303 213 0 0 1212 1212 4871603 214 0 0 1150 1150 10697533 215 0 0 1172 1172 4121587 216 0 0 1242 1242 16375375 217 0 0 1258 1258 6236094 218 0 0 1626 1626 2420894 219 0 0 1169 1169 19856224 220 0 0 1158 1158 14170189 221 0 0 1165 1165 10523971 222 0 0 1356 1356 2257828 223 0 0 1105 1105 4236812 224 0 0 1192 1192 13429584 225 0 0 1214 1214 18768032 226 0 0 1203 1203 24321653 227 0 0 1368 1368 7471186 228 0 0 1715 1715 3191032 229 0 0 1235 1235 18084082 230 0 0 1177 1177 6522975 231 0 0 1311 1311 35916485 232 0 0 1607 1607 3383150 233 0 0 1287 1287 6342945 234 0 0 1327 1327 16069492 235 0 0 1305 1305 15613701 236 0 0 1366 1366 6026677 237 0 0 1658 1658 3038319 238 0 0 1165 1165 7526989 239 0 0 1303 1303 76797549 240 0 0 2073 2073 2313237 241 0 0 1296 1296 5631257 242 0 0 1224 1224 13150740 243 0 0 1153 1153 5155482 244 0 0 1353 1353 19869395 245 0 0 1323 1323 7091980

PAGE 409

148 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 246 0 0 1779 1779 2808825 247 0 0 1210 1210 22810659 248 0 0 1338 1338 15718028 249 0 0 1133 1133 12420362 250 0 0 1401 1401 2592606 251 0 0 946 946 5068163 252 0 0 1165 1165 15544849 253 0 0 2032 2032 19798314 254 0 0 1957 1957 28943367 255 0 0 2719 2719 8097818 256 0 0 2928 2928 3698305 257 0 0 2064 2064 19658102 258 0 0 1826 1826 7483971 259 0 0 1895 1895 39462680 260 0 0 2877 2877 3631989 261 0 0 2096 2096 6601922 262 0 0 2042 2042 16745785 263 0 0 1788 1788 15159245 264 0 0 3549 3549 6489488 265 0 0 3619 3619 3485898 266 0 0 2004 2004 8401049 267 0 0 1972 1972 85915913 268 0 0 3516 3516 2754349 269 0 0 2005 2005 6228108 270 0 0 1968 1968 14752728 271 0 0 2113 2113 5846389 272 0 0 2002 2002 22194772 273 0 0 2024 2024 7628576 274 0 0 3187 3187 3010049 275 0 0 2030 2030 24872497 276 0 0 2241 2241 17546814 277 0 0 1711 1711 13181015 278 0 0 2497 2497 3758898 279 0 0 1618 1618 6389139 280 0 0 1851 1851 17865829 281 0 0 2040 2040 21548869 282 0 0 1861 1861 33146059 283 0 0 2246 2246 8430578 284 0 0 3072 3072 3978414 285 0 0 2059 2059 19556836 286 0 0 1787 1787 7728204 287 0 0 .'2005 2005 40611638 288 0 0 3051 3051 3525771 289 0 0 2156 2156 7035106 290 0 0 2057 2057 17861315 291 0 0 1884 1884 12885908 292 0 0 3118 3118 6805448 293 0 0 3035 3035 3735456 294 0 0 1812 1812 9230750 295 0 0 2080 2080 85399453

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149 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 296 0 0 2929 2929 2671564 297 0 0 2094 2094 6386757 298 0 0 1939 1939 18014758 299 0 0 1953 1953 5174852 300 0 0 1891 1891 24012560 301 0 0 1932 1932 8336603 302 0 0 2892 2892 3183855 303 0 0 1941 1941 25501774 304 0 0 2200 2200 17361356 305 0 0 1804 1804 14067024 306 0 0 2324 2324 3123375 307 0 0 1799 1799 6815546 308 0 0 2057 2057 19197403 309 0 0 2147 2147 23412242 310 0 0 2116 2116 33138274 311 0 0 2588 2588 9089749 312 0 0 3408 3408 4182720 313 0 0 2169 2169 20981793 314 0 0 1987 1987 9057234 315 0 0 2369 2369 42763645 316 0 0 3525 3525 3954211 317 0 0 2381 2381 7845708 318 0 0 2267 2267 19888492 319 0 0 2262 2262 14260503 320 0 0 3865 3865 7037153 321 0 0 3512 3512 4013228 322 0 0 2001 2001 10824993 323 0 0 2419 2419 92172652 324 0 0 3278 3278 2619568 325 0 0 2234 2234 6874134 326 0 0 2255 2255 19398879 327 0 0 2449 2449 5424872 328 0 0 2410 2410 25353696 329 0 0 2378 2378 8798968 330 0 0 3581 3581 3369127 331 0 0 2212 2212 28783745 332 0 0 2590 2590 19196173 333 0 0 2254 2254 15382672 334 0 0 2719 2719 3930149 335 0 0 2170 2170 8268649 336 0 0 2260 2260 20769638 337 0 0 2528 2528 26051626 338 0 0 2314 2314 35003042 339 0 0 3266 3266 8669459 340 0 0 3454 3454 4709473 341 0 0 2494 2494 22154213 342 0 0 2221 2221 9415602 343 0 0 2866 2866 46199314 344 0 0 3711 3711 4007900 345 0 0 2528 2528 8970665

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150 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 346 0 0 2585 2585 22045496 347 0 0 2212 2212 15337159 348 0 0 3365 3365 8062359 349 0 0 3946 3946 4335897 350 0 0 2333 2333 11567347 351 0 0 2582 2582 94580438 352 0 0 3582 3582 2999771 353 0 0 2459 2459 7164496 354 0 0 2346 2346 20114996 355 0 0 2618 2618 5584044 356 0 0 2762 2762 26715721 357 0 0 2600 2600 8466487 358 0 0 3752 3752 3544921 359 0 0 2355 2355 29037581 360 0 0 2831 2831 19906467 361 0 0 2199 2199 15721270 362 0 0 2740 2740 4686162 363 0 0 2288 2288 8273307 364 0 0 2408 2408 22569148 365 0 0 2754 2754 26142346 366 0 0 2539 2539 35561527 367 0 0 3162 3162 9854665 368 0 0 3434 3434 4916093 369 0 0 2354 2354 22334577 370 0 0 2420 2420 9954010 371 0 0 2846 2846 45318276 372 0 0 4279 4279 4243537 373 0 0 2729 2729 9182869 374 0 0 2711 2711 22540568 375 0 0 2510 2510 16843691 376 0 0 3634 3634 8548776 377 0 0 3864 3864 4189768 378 0 0 2459 2459 11560966 379 0 0 2749 2749 101536716 380 0 0 3502 3502 3618742 381 0 0 2662 2662 8113427 382 0 0 2413 2413 20076906 383 0 0 2559 2559 6159146 384 0 0 2851 2851 28353905 385 0 0 2895 2895 9364579 386 0 0 3781 3781 3739705 387 0 0 2576 2576 31339444 388 0 0 2872 2872 21155552 389 0 0 2209 2209 15565528 390 0 0 2075 2075 4809565 391 0 0 2251 2251 9086699 392 0 0 2465 2465 24174432 393 0 0 2717 2717 28726582 394 0 0 2700 2700 68938254 395 0 0 3138 3138 9636714

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151 O BS L O T LOTFTE GRFFTE STATFTE TOTAL E&G 396 0 0 3635 3635 5560876 397 0 0 2618 2618 24231621 398 0 0 2494 2494 10934026 399 0 0 2967 2967 50184544 400 0 0 4693 4693 4585061 401 0 0 2772 2772 10108426 402 0 0 2773 2773 25102239 403 0 0 2630 2630 18134357 404 0 0 3224 3224 8790994 405 0 0 4097 4097 4823009 406 0 0 2679 2679 13447856 407 0 0 2921 2921 108386361 408 0 0 3435 3435 3730102 409 0 0 2923 2923 8391339 410 0 0 2625 2625 23540020 411 0 0 2738 2738 6144093 412 0 0 2959 2959 28757739 413 0 0 3025 3025 10529641 414 0 0 3543 3543 4254870 415 0 0 2834 2834 34729248 416 0 0 2993 2993 23089520 417 0 0 2504 2504 16815091 418 0 0 2543 2543 6273293 419 0 0 2465 2465 11656901 420 0 0 2583 2583 26527670 421 1173622 157 2792 2949 31914792 422 1235343 127 2865 2992 45303041 423 407350 169 3104 3274 11197366 434 156883 138 3800 3938 5813962 425 992266 148 2866 3014 27685256 426 361075 116 2535 2652 12540639 427 1448815 118 3137 3255 52920447 428 272597 359 4312 4671 4873538 429 478181 197 2757 2954 10891694 430 850849 130 2829 2959 28101391 431 528996 107 2662 2769 20694009 432 225989 132 3838 3970 9667579 433 233458 263 4178 4441 4912627 434 417070 115 2578 2693 14522754 435 3495902 134 2992 3126 121377802 436 172445 201 3392 3592 4035024 437 335596 149 2899 3048 9122892 438 706562 112 2675 2787 27015224 439 463901 253 2606 2859 7110030 440 835200 115 3059 3174 31916501 441 260311 107 3080 3187 11603228 442 248168 224 3215 3438 4826499 443 1078102 126 2939 3065 36183646 444 760101 133 3024 3156 26412826 445 802662 137 2412 2549 19212720

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152 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 446 342632 178 2438 2616 6913461 447 314406 89 2498 2587 16542810 448 1308485 179 2593 2772 29994491 449 1804371 231 3005 3236 33858938 450 4010751 388 2896 3284 48733861 451 942333 386 3309 3695 12688180 452 326322 242 3795 4037 6882844 453 1595918 231 3098 3328 31406092 454 796781 245 2755 3000 14123661 455 2879739 201 2893 3094 56718438 456 284328 390 4787 5177 5402239 457 756917 289 2896 3185 12423373 458 1605457 205 2521 2725 30445936 459 1244011 230 2645 2875 23404489 460 602076 329 4169 4498 9853962 461 363970 396 4450 4847 5868362 462 795662 203 2676 2879 16347273 463 6159525 224 3041 3265 133319634 464 288936 332 3759 4091 4878489 465 638614 246 2780 3026 10858809 466 1510630 227 2887 3114 29620197 467 504733 239 2583 2823 8522799 468 1641308 214 3079 3293 33547958 469 595369 217 2966 3183 12799701 470 318522 238 3147 3385 6021194 471 2155980 237 2987 3224 39829361 472 1283011 203 3006 3209 29001610 473 1571219 252 2578 2829 23650849 474 542589 239 2557 2796 8517705 475 787328 193 2528 2722 18359866 476 1945222 242 2673 2916 39052866 477 3788078 448 2882 3330 38869136 478 6972985 615 2674 3289 55595499 479 1523962 534 3053 3588 15410399 480 724718 509 3622 4131 7701805 481 3367032 436 2793 3230 35437846 482 1624852 434 2526 2959 16819651 483 6209599 383 2567 2951 67861917 484 451199 531 4120 4651 5633820 485 1532844 575 3057 3631 14439338 486 3191724 384 2562 2947 36914308 487 2512611 414 2625 3040 27297779 488 1173923 583 3808 4391 10702987 489 579411 569 3985 4554 6448568 490 1717932 412 2686 3098 18659094 491 13054068 442 2981 3423 153786433 492 432940 451 3540 3991 4795619 493 1308110 422 2440 2861 13129376 494 3223172 423 2684 3107 35955592 495 1022597 416 2338 2754 10161789

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153 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 496 3422628 480 3331 3810 37180529 497 1325598 446 2773 3219 14334549 498 599994 372 2908 3279 7561891 499 4739658 487 2828 3316 46371280 500 2825619 419 2973 3392 33170944 501 2801016 453 2756 3209 27922546 502 888104 383 2681 3064 10212278 503 1641943 357 2518 2875 22981701 504 3751533 428 2632 3061 44984063 505 4400169 510 2795 3305 40289391 506 7468281 607 2438 3045 57415497 507 1767011 560 2694 3254 17173117 508 867289 566 3397 3963 8049010 509 3517767 423 2515 2938 36977594 510 1705431 404 2248 2651 17990774 511 7095365 421 2565 2987 69187358 512 511278 612 4379 4991 5823565 513 1669410 577 2865 3442 14654618 514 3784616 406 2388 2794 37846116 515 2711037 409 2419 2828 26972453 516 1056513 510 3666 4177 10812590 517 828175 786 3799 4585 6968799 518 1955815 451 2592 3043 18480407 519 14378284 452 2761 3212 162395989 520 492731 507 3415 3922 4947234 521 1590694 491 2569 3059 13412852 522 3649440 436 2459 2895 37342381 523 1152393 414 2302 2716 10505286 524 3397198 460 3118 3577 37933958 525 1525969 483 2628 3111 14673562 526 821967 470 2784 3253 7581772 527 4980077 486 2605 3091 47634452 528 3327469 475 2835 3311 33785706 529 2913931 465 2692 3157 28225510 530 971011 362 2392 2753 10532702 531 2208309 432 2428 2860 29017353 532 4776366 486 2353 2839 45653922 533 6099242 666 2359 3025 42057596 534 8801111 720 2253 2973 57826965 535 2263017 686 2479 3165 16880469 536 1131732 767 3250 4017 8375856 537 5811226 654 2092 2746 35743024 538 2946637 662 1920 2582 18471212 539 11476947 646 2259 2905 69972724 540 637432 698 3784 4482 5691477 541 2283156 723 2314 3038 15299994 542 6473388 635 2026 2661 41892508 543 4667567 670 2052 2723 28723049 544 1397017 684 3404 4088 11420120 545 756721 675 3431 4106 6559259

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154 OBS LOT LOTFTE GRFFTE STATFTE TOTAL E&G 546 3088012 685 2168 2853 19710416 547 22241388 661 2282 2943 164546530 548 650741 778 3693 4472 5372995 549 2219826 649 2385 3033 14534700 550 5762884 674 2116 2790 36487389 551 2108485 699 2022 2722 11671912 552 5165178 655 2576 3231 35782936 553 2221223 690 2370 3061 14450377 554 1189510 651 2552 3203 7583214 555 7292345 690 2243 2933 50543671 556 4798654 673 2390 3063 33775180 557 4263413 633 2193 2826 27111563 558 1838820 738 2342 3080 11302814 559 3490349 662 2033 2695 26067920 560 6838979 623 1932 2555 47877697 561 5961736 659 2427 3085 n/a 562 8615492 684 2224 2908 n/a 563 2293286 659 2316 2975 n/a 564 1045198 718 3349 4067 n/a 565 5700155 580 1939 2519 n/a 566 2848464 611 1868 2479 n/a 567 11257155 611 2216 2828 n/a 568 618034 750 4270 5021 n/a 569 1969351 592 2237 2829 n/a 570 6334490 584 1939 2523 n/a 571 4636130 614 1928 2542 n/a 572 1412078 646 3239 3885 n/a 573 713933 615 3364 3979 n/a 574 3047579 721 2354 3075 n/a 575 21568357 654 2360 3015 n/a 576 638806 753 3710 4463 n/a 577 2318741 692 2468 3160 n/a 578 5682106 660 2140 2800 n/a 579 2016068 649 2000 2649 n/a 580 5094385 619 2540 3159 n/a 581 2175739 665 2373 3037 n/a 582 1162369 601 2455 3056 n/a 583 7170722 648 2183 2831 n/a 584 4778831 643 2338 2981 n/a 585 4169323 627 2251 2879 n/a 586 1801486 723 2387 3110 n/a 587 3367099 658 2135 2794 n/a 588 6802887 593 1869 2462 n/a 589 4757076 626 2907 3533 n/a 590 7964690 612 2313 2924 n/a 591 2200337 592 2264 2856 n/a 592 931447 629 3376 4005 n/a 593 6207959 593 2025 2618 n/a 594 2946000 582 1943 2525 n/a 595 11636132 606 2244 2850 n/a

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OBS LOT 596 576941 597 2101758 598 6852515 599 4772874 600 1381372 601 733656 602 2848685 603 21250759 604 535866 605 2162422 606 5439547 607 1962104 608 5203210 609 2068266 610 1222129 611 6992169 612 4693252 613 4257861 614 1574739 615 3332102 616 7245568 LOTFTE GRFFTE STATFTE 680 582 574 600 626 609 644 607 686 614 597 574 600 614 592 603 611 616 616 610 572 4354 2178 1966 2069 3394 3318 2423 2349 4359 2391 2206 2031 2544 2444 2433 2227 2412 2276 2510 2254 1870 5033 2760 2540 2669 4020 3928 3067 2956 5045 3005 2803 2605 3144 3059 3025 2830 3023 2892 3126 2864 2442 TOTAL E&G n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a 155 Source: State of Florida Department of Education 1990a, pp. 3, 6; 1990b, pp. 3-4, 25; 1991, pp 3-4, 7 ; 1992, pp. 3-5, 8; 1993, p. l; State of Florida Department of Education Division of Community Colleges 1974, pp 48, 70-74 ; 1975, pp. 32, 61-65; 1976, pp. 30, 56 58-61; 1977, pp 34, 63, 65-72; 1978, pp 34, 62 64-71; 1979, pp. 32, 60, 62-69; 1980, pp. 33, 63, 65-74; 1981, pp 11, 42, 44-53; 1982, pp 11, 42, 44-53; 1983 pp. 44-53; 1984, pp 11, 42, 44-48; 1985, pp 11, 39, 41-45; 1986, pp. 14, 52, 54-58; 1987, pp. 13, 73, 75-79; 1988a 1988b, pp. 15, 75, 77-81; 1989, pp. 15, 77, 79-83; 1990a, 1990b, pp. 13, 79, 81-85; 1991a, 1991b 1991c; 1992a, pp. 28-29, 76-77; 1992b; 1993a, 1993b

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163 State of Florida Department of Education Division of Community Colleges (1985). Report for Florida community colleges 1983-1984 (Part I). Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1986). Report for Florida community colleges 1984-85: The fact book. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1987). Report for Florida community colleges: The fact book June 1987. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1988a, Oct. 25). Annual financial report for 1987-88: Revenue detail for the general current fund, all Florida community colleges. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1988b). Report for Florida community colleges: The fact book June 1988. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1989). Report for Florida community colleges: The fact book June 1989. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1990a, July 25). Florida Public Education Educational Enhancement Trust Fund (lottery): Summary. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1990b). Report for Florida community colleges: The fact book 1989-1990. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1991a, April 25). Annual financial report for 1989-90: Revenue detail for the general current fund, all Florida community colleges. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1991b). Report for Florida community colleges: The fact book 1990-1991. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1991c). Schedule of revenue, expenditures, and fund balance by general ledger code for the fiscal year 1990-91. Tallahassee: Author.

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164 State of Florida Department of Education Division of Community Colleges (1992a). Report for Florida community colleges: The fact book 1991-1992. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1992b). Schedule of revenue, expenditures. and fund balance by general ledger code for the fiscal year 1991-92. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1993a, June 1). Aid to Colleges Allocations-1980-81 through 1993-94. Tallahassee: Author. State of Florida Department of Education Division of Community Colleges (1993b, June 1). Florida community colleges funding history-1981-82 through 1993-94. Tallahassee: Author. State of Florida Governor's Office of Planning and Budgeting, Revenue and Economic Analysis Policy Unit (1993, July 8). Tax revenues. Tallahassee: Author. Stover, M.E. (1987). Revenue potential of state lotteries. Public Finance Quarterly, 15(4), 428-440. Stover, M.E. (1990). Contiguous state lotteries: Substitutes or complements? Journal of Policy Analysis and Management, ~(4), 565-568. Swartz, s., & Baum, s. (1992). Education. In C.T. Clotfelter (ed.), Who benefits from the nonprofit sector? (pp. 5591). Chicago, IL: University of Chicago Press. Swartz, T.R., & Peck, J.E. (1990). The changing face of fiscal federalism. Challenge, 33(6), pp. 41-46. Sweeney, R.M. (1991). Report of the states (1991 annual budget and fiscal survey update of the American Association of State Colleges and Universities Council of State Representatives. Washington, DC: AASCU. Tatsuoka, M.M. (1975). The general linear model: A "new'' trend in analysis of variance. Selected topics in advanced statistics: An elementary approach (7). Champaign, IL: Institute for Personality and Ability Testing. Taylor, T. (1985). The state role in financing community colleges: A model for improvement. Community College Review, 13(2), 43-50.

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Thomas, S.B., & Webb, L.D. (1984). The use and abuse of lotteries as a revenue source. Journal of Education Finance, ~(3}, 289-311. Tullock, G. (1983}. Economics of income redistribution. Hingham, MA: Kluwer-Nijhoff Publishing. 165 Vasche, J.D. (1990). The net revenue effect of California's lottery. Journal of Policy Analysis and Management, 9(4), 561-564. Wattenbarger, J.L., & Mercer, S.L. (1985}. Financing community colleges: 1985. Gainesville: University of Florida, Institute of Higher Education. Wattenbarger, J.L., & Mercer, S.L. (1988} Financing community colleges: 1988. Washington DC: American Association of Community and Junior Colleges. Weinstein, D., & Deitch, L. (1974). The impact of legalized gambling: The socioeconomic consequences of lotteries and off-track betting. New York, NY: Praeger Publishers Wood, R.C., & Honeyman, D.S. (1992}. Rapid growth and unfulfilled expectations: Problems for school finance in Florida. In J.G. Ward & P. Anthony (Eds }, Who pays for student diversity?, 12th annual yearbook American Education Finance Association 1991, Newbury Park, CA: Corwin Press. Wyett, T.A. (1991, Spring). State lotteries: Regressive taxes in disguise Section of Taxation of the American Bar Association, 44 Tax Law 867 (WESTLAW document reproduction service).

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BIOGRAPHICAL SKETCH Susan Robinson Summers was born on April 7, 1952, in Waukegan Illinois. The fourth of six children born to John and Hazel Floyd Robinson, she moved with her family to Lake City, Florida, in 1959. She was educated in the Columbia County public schools from second through eleventh grade She departed Columbia High School before receiving her diploma in 1970. To pursue her interest in the French language and culture, she studied at the L'Universite de Dijon, France, in the summer 1969, and entered the Florida State University in the fall of 1969 as an early admission student. Ms. Summers was awarded the Bachelor of Science degree cum laude from Florida State in 1973. She majored in clinical psychology, with minor concentrations in humanities and communications. She was employed during her undergraduate years as a staff writer for the campus publications, and was a member of the first group of students in the Florida State University London Studies Program. On graduation, Ms. Summers entered the University o f Florida as a postbaccalaureate student in the premedical program. She had decided to carry her family's medica l 166

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167 heritage by becoming a psychiatrist. After reassessing her personal and career goals, she decided to meet the intellectual challenge by completing all prerequisites for medical sch~ol, but declined to pursue a career in medicine. She completed the coursework in 1974, and enrolled in the Rehabilitation Counseling program, College of Health-Related Professions at the University of Florida. She was awarded the Master of Rehabilitation Counseling degree in 1975. Ms. Summers' professional career began with nine years of employment at a community mental health center, where she founded and directed a community support program for the chronically mentally ill. She married Gordon Summers, a Lake City businessman, in 1976. During those years, she also consulted as a rehabilitation counselor, served as an adjunct instructor at Lake City Community College, and assumed a leadership role in her community. Through her work as a program director and a community fund raiser, she became interested in management and finance. She enrolled in accounting and other business courses at Lake City Community College. Her interest in finance led her to accept a position in 1984 as controller of Summers Chevrolet Company, which she owned and operated with her husband. Her children, Sam and Catherine, were born in 1985 and 1988, during her years as a businesswoman. In 1988 Ms. Summers accepted a position as Director of Continuing Education at Lake City Community College. She

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168 found that higher education fit well with her personal career goals as well as the needs of her young children. In 1989, she met Dr. James L. Wattenbarger, who recruited her for the University of Florida doctoral program in higher education administration, and later became her mentor. She enrolled in January of 1990, and maintained her position at Lake City Community College while attending classes. Ms. Summers became interested in education finance through a course with Dr. David Honeyman in 1991. Through the guidance of Drs. Wattenbarger and Honeyman, she concentrated the remainder of her studies on community college finance. She became a graduate research assistant in 1991 to Dr. Wattenbarger, who was director of the Institute of Higher Education. She was admitted to candidacy in January of 1992 and gave birth to her third child, Daniel, in July, 1992. The academic year of 1992-1993 was spent on professional leave from Lake City Community College, in order to work as research assistant to Dr. Honeyman, who became acting director of the Institute on the retirement of Dr. Wattenbarger. During this period she became intrigued with the role of the Florida Lottery in Florida community college finance, an interest which led to this study. At the time of publication of this d i ssertation, Ms. Summers was living with her family in Lake City, Florida, and working as Chairperson, Divison of Extended Studies at Lake City Community College.

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I certify that I have read this study and that i n my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree of Doctor of Philosophy. 2 ~9 es L. Wattenbarger, 171-stinguished Service Professor Emeritus of Educational Leadership I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree of Doctor of Philosophy. avid s. ssociate Professor of Educational Leadership I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree of Doctor of Philosophy. c. Arthur Sandeen Professor of Educational Leadership I certify that I have read this study and that in my opinion it conforms to acceptable standards of scholarly presentation and is fully adequate, in scope and quality, as a dissertation for the degree of Doctor of Philosophy s stant Professor of Counselor Education

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This dissertation was submitted to the Graduate Faculty of the College of Education and to the Graduate School and was accepted as partial fulfillment of the requirements for the degree of Doctor of Philosophy. December, 1993 Dean, College of Education Dean, Graduate School

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