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
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xvii, 228 leaves : ill. ; 29 cm.
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English
Creator:
Carroll, Joan F
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Subjects / Keywords:
Hypotension, Orthostatic -- Effect of exercise on   ( lcsh )
Cardiovascular system -- Effect of exercise on   ( lcsh )
Exercise for the aged   ( lcsh )
Treadmill exercise tests   ( lcsh )
Exercise and Sport Sciences thesis Ph.D
Dissertations, Academic -- Exercise and Sport Sciences -- UF
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bibliography   ( marcgt )
non-fiction   ( marcgt )

Notes

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

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University of Florida
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Full Text










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).