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Acute neuroendocrine, pulmonary and cardiovascular responses to exercise in heart transplant recipients

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Title:
Acute neuroendocrine, pulmonary and cardiovascular responses to exercise in heart transplant recipients
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Braith, Randy, 1950-
Publication Date:
Language:
English
Physical Description:
v, 171 leaves : ill. ; 29 cm.

Subjects

Subjects / Keywords:
Blood ( jstor )
Cardiac output determination ( jstor )
Control groups ( jstor )
Cyclosporins ( jstor )
Exercise ( jstor )
Heart ( jstor )
Heart rate ( jstor )
Heart transplantation ( jstor )
Norepinephrine ( jstor )
Plasmas ( jstor )
Dissertations, Academic -- Health and Human Performance -- UF
Health and Human Performance thesis Ph. D
Heart -- Transplantation -- Patients -- Effect of exercise on ( lcsh )

Notes

Thesis:
Thesis (Ph. D.)--University of Florida, 1991.
Bibliography:
Includes bibliographical references (leaves 152-170).
General Note:
Typescript.
General Note:
Vita.
Statement of Responsibility:
by Randy Braith.

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University of Florida
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Copyright [name of dissertation author]. Permission granted to the University of Florida to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
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ACUTE NEUROENDOCRINE, PULMONARY AND CARDIOVASCULAR
RESPONSES TO EXERCISE IN HEART TRANSPLANT RECIPIENTS










By


RANDY BRAITH


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



UNIVERSITY OF FLORIDA

QQ1001














TABLE OF CONTENTS


page


CHABS T RA CT....................................................S.......................... .iv
CHAPTERS


Justification for Further Research...................
Purpose of the Study..........................................
H ypotheses............... .... ........................... ....... ...
Delim itations.......................................... ........ ....,


Limitations...


tJeuroendocrine ................ ....... ...................


Pulmonary Function..........
Skeletal Muscle Strength...


Subjects..... ..... ............


Day 1:


Experimental Protocol.


Day 2: Experimental Protocol.
Blood Sample Collection.........
Blood Sample Analysis.............
Statistical Analysis.....................


* ** .......... .58
* ~ 55~ SOS...... .60


5***** ~O0 *S*S***i*S4SSSS*t**.4*SS.*S. ~******* 550*60*4*~* ******** 55590&*S*~*~ 66


D nnnan ~~~ fl. -~ na ii, a vfl'% ni-a.., T rn









5 DISCU SSION ............................................................................... 111

N euroendocrine Responses to Exercise................................. 111
H em odynam ic Responses to Exercise.................................... 131
Pulmontary Functiron............................................................................134
Skeletal M uscle Strength...........................................................141
Sum m ary and Conclusions...................................................... 144

APPEN DIX......................................................................................................146

REFEREN CES............................................................................................... 152

BIOGRAPH ICAL SKETCH ..........................................................................171













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


ACUTE NEUROENDOCRINE


PULMONARY


AND CARDIOVASCULAR


RESPONSES TO EXERCISE IN HEART TRANSPLANT RECIPIENTS

By

Randy Braith


August, 1991


Chairman:


Michael L. Pollock


Major Department:


Health and Human Performance


Orthotopic heart transplantation (Tx) results in cardiac denervation.


consequences


denervation


are attenuated


chronotropic


inotropic


reserve and the absence of an immediate tachycardic response during exercise.


Recent evidence suggests


that physiologic mechanisms


other than


cardiac


denervation may be responsible for the exercise intolerance observed in heart


transplant recipients


(HTR).


However,


available


data


regarding


these


mechanisms


are sparse.


present study was designed


to answer three


related questions:


1) Does


alter the neuroendocrine response to exercise?


Does


function


immunosuppression


and,


What


therapy


skeletal


adversly


muscle


affect


strength


pulmonary
previously









weight.


Peak


VO2


in HTR


was 57


of CTR


(p<0.05)


consistent with


previous research.


Neuroendocrine activity


arterial blood gasses (ABG) and


cardiac hemodynamics were measured during two 10 minute periods of cycle


exercise at 40 and 70


of peak power output (PPO).


Relative change in cardiac


output (CO) was similar (p>0.05) in HTR and CTR, but CO was augmented


through increased stroke volume, not exercise tachycardia, in HTR.


Plasma


renin


activity,


norepinephrine,


atrial


natriuretic


peptide


vasopressmin


responses
intensity


were
>40%


greater


PPO


(p0.05)
was re


in HTR


quired


than


CTR.


to evoke


However,

heightened


an exercise
i response.


Pulmonary


function


(DLCO,


FVC


, FEVi)


improved


(p<0.05)


from


pre-


postT
ABG


pulmonary measures


were


submaximal


normal


exercise


CTR


at 70


of PPO


in HTR


HTR


(15-38


were


became


mmHg


(p<0.05)


than


hypoxemic


below


resting


cm.


during
values).


Although


lean


body


mass


was


similar


both


groups,


knee-extension


(quadriceps)


strength


HTR


was


CTR


(p<0.05).


These


data


demonstrate that reduced exercise capacity in HTR is the product of factors


other


than


function


intrinsic


and


muscle


cardiac


strength


performance.


may


Abnormalities


persistence


pulmonary
pre-existing


conditions characteristic of congestive heart failure.


It is probable that the


exercise


induced


neuroendocrine


overactivity


was


due


cardiac


deafferentation,


further


experiments


are necessary


to confirm


hypothesis.














CHAPTER 1
INTRODUCTION


Heart


transplantation


(Tx)


is now


an accepted


treatment


projected


15,000 end-stage cardiac disease patients who qualify annually


(Schroeder


and Hunt, 1987)


. At one


year postsurgery, orthotopic heart


transplant


recipients


(HTR)


are reported


to have fewer


problems


with


fatigue and lack of energy than coronary artery bypass graft patients one


year postbypass (Meister et al.,


1986).


Nonetheless


, 70% of coronary bypass


patients (typically older) are working within one year but only


HTR ever return to full time employment (Meister et al.,


30-35


1986).


past, HTR


have


been


considered


serious candidates


career rehabilitation because of concerns regarding 1) infection and donor


organ rejection, and 2)


decreased functional status.


Recent advances in


immunosuppres


sant


drugs,


(e.g.


cyclosporine,


azathioprine,


OKT3


prednisone)


greatly


reduced


periodic


transvenous


incidence


organ


endomyocardial


rejection


biopsies
infection


have


with


survival rates now exceeding 90


for the first


2 years and greater than 80


for the first 5 years after surgery (Heck et al.,


1989).


Exercise capacity,


major component of functional


status


improved


after


but despite


normal resting hemodynamics, many


HTR have some degree of exercise


intolerance.


The explanation for the decreased exercise capacity


however,










Stevenson et al.


(1990) recently reported that exercise capacity is low


in HTR (New


York Heart Association functional class 3 or 4).


Numerous


other


studies


have


reported


that


HTR


have


peak


systemic


oxygen


consumption


(VO2max) that are approximately one-half to two-thirds of


normal predicted values (Pope et al.,


1980


Savin et al


., 1980; Sietsema et


1987


Banner et al.


, 1988; Kavanagh et al.,


1988; Meyer et al.,


1989


Quigg


et al.


, 1989).


On the other hand, comparably good exercise capacity has


been observed in some HTR.


et al.


McLaughlin and associates (1980) and Yusuf


(1985) showed similar exercise capacity in normal individuals and


HTR.


Additionally, Kavanagh and coworkers (1988)


have demonstrated


that chronic exercise training can increase maximal exercise capacity, with
the most compliant HTR approaching normal values for VO2max after 16


months


endurance exercise


training.


Finally


individual


HTR have


competed


triathlon


events


, the


Boston


Marathon


performed


successfully as collegiate and professional athletes (Kavanagh et al., 1986;


Golding and Mangus,


1989


Thompson,


1990).


Thus


it cannot be stated


with


certainty


at present


whether


a limitation


exercise


capacity


inherent with Tx per


se, or if other factors are responsible.


Efferent cardiac denervation


, a necessary consequence of T


alters the


heart rate response to dynamic exercise.


Numerous animal and human


studies have shown that the denervated heart is characterized by a high

resting rate, a diminished chronotropic reserve during exercise and a slow
linear decline in heart rate following exercise (Schroeder, 1979; Savin et al.,










exercise


transition


(Banner


et al.,


1988).


Because


cardiac


denervation


eliminates efferent control of heart rate indefinitely (i.e. reinnervation in


humans


is unsubstantiated)


(Rowan


Billingham,


1988


Regitz et al.,


1990),


long-term


decrements


in exercise


capacity


have


typically


been


attributed to reduced


chronotropic reserve (Schroeder,


1979; Savin et al.,


1980; Pope et al.,


1980; Pflugfelder et al.,


1987


Nixon et al


., 1989; Colucci et


., 1989; Quigg et al.,


1989).


Although


efferent


denervation


diminishes


chronotropic


reserve,


dynamic exercise generates a variety of neural and humoral compensatory

responses to maintain systemic blood pressure and cardiac output in the


presence of cardiac denervation.


The sympathetic nervous system directly


maintains cardiac output through peripheral arteriolar vasoconstriction in


nonworking muscles,


the splanchnic and renal circulations as well as via


the venoconstriction of the capacitance vessels (Sagawa,


1983


Rowell and


O'Leary


1990).


Indirectly


the sympathetic nervous system augments the


heart


rate


response


through


effects


circulating


catecholamines


(Rowell,1986).


In HTR,


additional humoral


compensation


in heart rate


reserve


occurs


through


hypersensitivity


to circulating


catecholamines


(Bexton et al.,


1983; Lurie et al.,


1983; Vatner et al.,


1985;


Yusuf et al


1987


Gilbert et al.


, 1989; Port et al.,


1990; Bristow, 1990; Regitz et al.,


1990).


Also,


parameters


diastolic


function


contractile


reserve


are normal


some HTR which suggests that circulating catecholamines may also have a

very important inotropic influence during dynamic exercise (McLaughlin,










normal


efferent


autonomic


control


heart.


The denervated


heart


appears to function adequately during exercise with the possible exception

of exercise situations that require an immediate tachycardic response.


Justification for Further Research


Recent clinical and experimental evidence suggests that physiological


mechanisms other


than


efferent


denervation


may


underlie


exercise


intolerance


HTR.


Neuroendocrine


abnormalities


resulting


from


cardiac deafferentation (Zambraski et al.,


1984; Mohanty et al.,


1987


Myers


et al.


, 1988),


cyclosporine induced pulmonary gas exchange abnormalities


(Casan et al.,


1987) and skeletal muscle weakness (Kavanagh et al.,


1988)


are recent


postulates


unexplained


exercise


intolerance.


The


available


data


regarding


these


mechanism


however


, is sparse


conflicting and the physiologic nature of diminished exercise


HTR remains unclear.


capacity in


Therefore, further studies of medically stable HTR


involving


measurements


of muscular


strength


cardia


c, pulmonary


and neuroendocrine responses


to exercise are necessary


to elucidate the


mechanisms most responsible for diminished exercise capacity.

Cardiac Deafferentation and the Neuroendocrine Response to Exercise


Exercise capacity may be altered by the systemic effects of the cardiac


deafferentation associated with


(Thames et al.,


1971; Zambraski et al.,


1984;


Mohanty


et al.,


1987


Myers


et al.


, 1988).


When


heart


trz~ncn1nnt~d


tlho ff0ronnt ncrvac naccina tin thp dlnnr hart a wPIll as thp








5

the sensory receptors send afferent signals to the vasomotor control center


in the medulla (brain stem) via the vagal nerve.


Sensory input from the


cardiac


baroreceptor reflexes


plays


an important regulatory role


neural


and


hormonal


control


circulation.


Under


normal


circumstances


/ sensory receptors in


the atria and


ventricles exert a tonic


inhibitory
peripheral


influence


circulation


on sympathetic


as well


nervous


activity


to the


heart


and


as exerting a restraining influence on


circulating

epinephrine


level

(E),


pressor


arginine


hormones


vasopressm


such


(AVP)


as norepinephrine


(NE),


the renin-angiotensin-


aldosterone system


(RAAS)


(Paintal,


1953


Johnson et al.


1969


Ledsome


and Mason, 19


Mancia and Donald


, 1975; Quillen and Cowley


1983).


In congestive heart failure (CHF) patients awaiting


Tx, the function of


cardiac baroreflexes is profoundly impaired (Chidsey et al.,


1962;


Thomas


and Marks


1978


Dzau et al


1981


Goldsmith et al


., 1983a)


. Overt CHF is


characterized by stimulation of several neuroendocrine systems involved


in electrolyte balance and blood pressure homeostasis.


peptide (ANP), N
(Goldsmith et al.,

1990; Swedberg et


Atrial natriuretic


, E, AVP and RAAS in particular, are elevated in CHF


1983a; Raine et al.,


1990).


1986; Colucci et al., 1989; Francis et al.,


Tx restores cardiac function and reverses CHF


is uncertain


how


affects


neurohumoral


excitatory


state


associated with CHF


. Tx in humans has been reported to increase (Banner


et al.


,1989; Scherrer et al., 1990) and decrease (Thames et al.,


1971


Mohanty


et al.


1987


Banner et al.


, 1990) reflex elevations of plasma NE.


At this










hormones during exercise.


Exercise alters the release of AVP, ANP


and RAAS but the neuroendocrine response to exercise in HTR has not


been investigated.


The denervated heart is more reliant upon


the Frank


Starling mechanism to augment cardiac output and consequently


th


an increased dependence upon cardiac preload reserve (Pope et al.,


ere is

1980;


Pflugfelder et al.,


1987


Younis et al.,


1990).


It is


unknown, however, if


compensatory


mechanisms


responsible


for maintaining


blood


pressure


and


cardiac


output


during


exercise


are stimulated


HTR.


Thus,


determination


neuroendocrine


responses


during


various


levels


exercise


critical


resolution


issue.


more


precise


description of the temporal pattern of plasma AVP


RAAS and ANP


in HTR during steady-state and non-steady state exercise will offer a more


complete


understanding


compensatory


mechanisms


regulating


cardiac output following Tx.

Immunosuppression, Denervation and the Pulmonary Response to
Exercise


Tolerance for aerobic exercise in HTR may be limited by inadequate


pulmonary


exchange,


specifically


exchange


during


exercise


transition.


(DLCO)(Casan et al.,
0


ventilation


1987


Abnormal


Banner et


pulmonary

al., 1988) ar


diffusion


id sluggish


(VE) at the onset of exercise (Marconi et al.,


1987


capacity

pulmonary


Meyer et al.,


1989) have been reported following Tx.


The


nature


DLCO


impairment


HTR


unknown.










Bussieres et al., 1990).


However, because DLCO is markedly impaired in


CHF patients awaiting T


(McNeil et al.,


1958; Morley et al.,


1989


Wright et


1990;


Bussieres et al.


1990),


it is difficult to conclude that abnormal


DLCO postTx is due to immunosuppressive agents, the surgical procedure


or simply the persistence of pre-existing abnormalities (eg.


CHF, chronic


obstructive


pulmonary


disease


etc.).


Unfortunately,


studies


that


have


measured pulmonary function in the same patient sample before and after

Tx and accounted for differences in age, smoking history, disease severity

and months postTx are noticably absent from the literature.

Casan et al. (1987) compared pre- and postTx pulmonary function in


HTR (n


=10) and found improved lung volumes and flow rates but a 14


deterioration of DLCO.


The authors summarized their finding of reduced


DLCO


stating


that


a good


correlation


0.87)


existed


between


cyclosporine level in whole blood and the degree of reduction in DLCO.
They suggested that cyclosporine may induce interstitial infiltration and


vascular endothelial


proliferation similar to what is observed in


kidneys


renal


transplant


patients


receiving


high


doses


drug


(Myers et al.,


1984;


Taube et al.,


1985)


. These results, however, have not


been


replicated,


little evidence exists


to suggest


that


induction


immunosuppression


with


cyclosporine


may


complicated


lung


dysfunction.


Furthermore, most of the existing pulmonary function data


involving HTR has been collected during resting conditions.


It remains to


be determined


whether


HTR


who exhibit reduced


pulmonary


diffusion








8

pulmonary function and its influence on arterial blood gasses in patients


before and after


during both rest and exercise conditions.


Another explanation for inadequate pulmonary


gas exchange at the


onset of exercise in HTR has been proposed by Wasserman and coworkers


(Wasserman


et al.


, 1974;


Uchida


1976


Jones et al.,


1982).


They


found


highly


correlated


linear


relationships


(r=0.94)


between


expired


minute


ventilation


(VE)


changing


right


ventricular


load


in experimental


animals.


Because


the same relationship


existed


when


right ventricular


load was increased independent of cardiac output (by balloon obstruction),


authors


ventricular


concluded


stretch


that


receptors


a neural


may


pathway


stimulate


originating


ventilation


from


at the


right


onset


exercise


"cardiodynamic


hyperpnea").


The


neural


pathway


afferent limb of this reflex has not been identified in animals, and we are


unaware


other


data


to support


contention


that


cardiac


stretch


receptor


signals


may


timulus


exercise


hyperpnea


in man.


Denervated


HTR


provide


unique


opportunity


study


"cardiodynamic


hyperpnea"


hypothesis.


Serial


arterial


blood


measurements


(PaO2


PaCO2;


pH)


during


transition from


steady-state


exercise


would


determine


ability


HTR


to achieve


necessary ventilation and provide adequate gas exchange during the onset


exercise


well


as ascertain


whether


ventilatory


response


dependent upon the cardiac output response.

Disuse Atrophy, Steroid Therapy and Muscular Strength










treatment (eg.


prednisone)


for immunosuppression appears to adversely


affect strength and lead


Kavanagh et al.,


to skeletal muscle atrophy (Horber et al.,


1988; Squires, 1990).


1985;


Corticosteroids have been shown to


cause pronounced atrophy of skeletal muscle ("steroid myopathy") when


administered


Goodman,


1969


high


doses


DuJovne


prolonged


Azarnoff,


1975;


periods
Kinney


(Goldberg


Felig,


and


1979


Almon and Dubois, 1990).


body weight of HTR


Kavanagh et al.


was lower than


(1988) recently found that the


those of age matched controls and


that the difference in body weight was largely attributable to decreased lean


mass.


The authors speculate that increases in peak heart rate and exercise


capacity in HTR participating in endurance exercise training could largely


be due


to a strengthening


leg muscles.


Weight


gain frequently


follows


(Keteyian,


1989)


a better


understanding


the changes


which


occur


in specific


body


compartments


lean


body mass


vs fat


tissue) postoperatively would


assist with long-term


weight management.


Additionally,


there is evidence that muscle atrophy from prednisone can


be prevented or


attenuated


exercise


training


(Seene


Viru,


1982;


Horber et al


., 1985; Hickson et al.,


1986; Czerwinski et al.


1987; Horber et al.,


1987).


To date, however, no data are available concerning the influence of


exercise


training


muscular


strength


development


HTR.


Furthermore, the muscular strength of HTR has not been quantified with
a standardized criterion strength test and compared with normal control

values.









Purpose of the Study


Thus


there


are three


critical


questions


which


will


addressed


regarding

most HTR:


the etiology


1) Does


the diminished


exercise capacity


observed


Tx alter the neuroendocrine response during exercise?


2) Does


Tx and subsequent immunosuppression


therapy


adversely affect


minute


ventilation


DLCO


arterial


oxygenation


What


role


does muscle disuse atrophy and possible steroid myopathy play in limiting

exercise capacity?


present


study is


designed


to investigate these


three questions


which relate to mechanisms that may independently or collectively act to


diminish exercise capacity in HTR.


Specifically


the purposes of this study


to determine


temporal


pattern


of neuroendocrine responses


(AVP


RAAS


ANP)


cardiac


hemodynamics


(heart


rate,


stroke


volume, cardiac output) during the transition from rest to steady-state and


non-steady state exercise; 2)


to determine the temporal


pattern of blood


gasses (PaO2, PaCO2,


pH) during the transition from rest to steady-state


non-steady


state


exercise


compare


resting


pulmonary


mechanics and DLCO before and after


Tx; and 3) to quantify bilateral knee


extension (quadriceps) strength.


Hypotheses


When


examining


results


HTR


control


subjects


- U *










there will be no significant difference in arterial blood gas


responses during submaximal cycle exercise;


there will be no significant difference in cardiodynamic responses


during submaximal cycle exercise;


there will be no significant difference in resting pulmonary


function; and


there will be no significant difference in knee extension leg


strength.


When examining the test results of orthotopic heart transplant patients
before and after transplantation:
1) there will be no significant difference in resting pulmonary


function.


there will be no significant difference in arterial blood gasses.


Delimitations


This study was delimited to the following:


1) eleven volunteer HTR without clinical or endomyocardial biopsy
evidence of significant rejection, infection or other contraindications

for exercise;


eleven healthy


non-athletic and non-medicated control


subjects that matched the HTR with respect to gender,


age and body


size;










5) transplant patients receiving immunosuppressive therapy
with cyclosporine, azathioprine and prednisone;
6) persons not receiving cardiac beta-receptor blocking drugs; and

7) persons consenting not to change diet, prescription medications or


physical activity habits during the course of the study.


Limitations


This study was limited by the following:


1. The HTR were receiving antihypertensive medication that may
influence the cardiovascular and neuroendocrine responses to

exercise.


The HTR were not all receiving the same antihypertensive


medications.


3. Pre- and posttransplantation pulmonary function tests in the
HTR were not performed in the same laboratory.

4. Cardiac output was estimated by Electrical Bioimpedance


Cardiography.


Hemoglobin and hematocrit were obtained with a Centrifugal


Hematology System.


Only knee extension (quadriceps) strength was evaluated.














CHAPTER 2
REVIEW OF THE LITERATURE


Due to the nature of this investigation, the review of literature will


be divided


into


three major sections.


The first


section


will


review


research


that


deals


exercise in HTR and


with


neuroendocrine


responses


during volume reduction and


at rest


expansion


during

cardiac


denervated


animals.


The


second


portion


review


will


evaluate


current research


of pulmonary function following


The


third


section


review


available


research


that


describes


keletal


muscular


strength of HTR postoperatively.


Neuroendocrine


Hormones


Norepinephrine


Norepinephrine


(NE)


neurotransmitter


relea


postganglionic


synapses


sympathetic


nervous


system


(SNS).


addition, the adrenal medulla secretes epinephrine (E) and NE in a ratio of


approximately 4:1


(Guyton,


1986).


The adrenal medulla


however


, may be


considered a


"special


case"


within


the SNS.


Instead of directly secreting


neurotransmitter onto end


organs,


the adrenal medulla secretes


into


bloodstream and thus has profound actions at a distance.


Nonetheless


main source of plasma NE is spillover of the hormone released from the


- .,nn ftnn, ~ n a) c at rt ,n n i-I, ni-4 ,- nfl.. .nn r (t2r'.l A~. i-n4 lOQi a


*










sympathetic nerve fibers


causes


total


cardiac denervation,


the local


delivery of NE to the heart by sympathetic nerves is either greatly reduced


or entirely


absent


(Rowan


Billingham,


1988


Regitz


et al.


, 1990).


Therefore, beta-adrenergic receptor stimulation of the heart is solely due to


circulating plasma NE and E.


Although a number of other substances are


coreleased


with


E and NE


dopamine,


levels are generally regarded as


activity in response to exercise (Goldstein,


chromogranin A),


best humoral marker of


1981).


plasma NE

global SNS


Evidence to support the


use


plasma


as an index


SNS


activity


comes


from


recent


microelectrode studies which have demonstrated high correlations (r=0


to 0.81)


between antecubital


venous NE levels and


the number of action


potentials


recorded


during


direct


monitoring


peripheral


sympathetic


nerves (Leimbach et al.


1986


Victor et al.


1987


Seals et al.


,1988).


Norepinephrine Release During Exercise in HTR.


The purpose of this


portion


literature


review


is to


examine


available


evidence


regarding


SNS activity


plasma NE


response during


exercise in


HTR.


Resting SNS activity is increased in patients with CHF (Goldsmith et


., 1983a; Raine et al.,


1986


Colucci et al.


,1989; Francis et al.,


1990; Swedberg


et al


., 1990).


Tx restores cardiac function but it is uncertain


whether Tx


eliminates


sympathetic


overactivity


. Specifically


little


information


available regarding the SNS activity during exercise in HTR.


One of the earliest reported studies of


the exercise


response of the


denervated human heart included measurements of plasma NE (Pope et










increased to 1,970 pg/ml at 90 watts (6 fold increase from rest).


Increases in


contractility

shortening)


(defined


heart


authors


rate


were


as velocity


highly


correlated


circumferential


with


fiber


increasing


concentrations (r=0.92 and r=0.79


, respectively).


Unfortunately


however,


this study did not include a control group, so it is difficult to infer whether


levels


elicited


these


work


intensities


represent


sympathetic


overactivity


or an appropriate


response.


Moreover,


comparisons


with


more recent HTR studies that utilize upright exercise are difficult because
of the fact that lower NE levels are present during supine exercise than in


the upright position (Dimsdale and Ziegler,


1991).


Nonetheles


these data


are useful


that


they


were


first


to demonstrate


relationship


between


humoral


transplanted


human


adrenergic


heart


mechanisms


vigorous


and


exercise.


te adaptation

Confirmation


relationship was shown


others


who found


that beta


blockade greatly


attenuated


heart


rate


response


exercise


HTR,


indicating


that


humoral


catecholamines


contribute


to the


response


denervated


heart (Bexton et al.


/ 1983).


Moreover, the issue of inotropic support from


circulating catecholamines has recently been clarified by Port et al.


(1990),


who found


that the transplanted


human heart contains an


unexpectedly


high


percentage and density of beta adrenergic receptors which suggests


that circulating NE should provide inotropic stimulation.


More recently, Degre et al.


(1987) recorded plasma NE levels in 15 HTR


at rest and during a SL-GXT on an upright cycle.


Plasma NE was 158 pg/ml










are difficult to make.


Furthermore, HTR in this study were only 3810 days


postT


which


may


have


been


early


detect


effects


deafferentation


on cardiac


neuroendocrine


reflexes


that


maintain


blood


pressure


homeostasis.


been


shown


that


plasma


response to exercise is significantly greater than control in HTR studied


months after T


but NE levels were not different from control in patients


studied


< 3 months after


Tx (Quigg et al.,


1989).


Quigg et al.


(1989) measured levels of plasma NE at rest and at peak


exercise on an upright cycle ergometer in 23 HTR an average of 71 months


after


and in 23 control subjects matched for age.


HTR were grouped into


those studied


within 3 months of T


("early recipients"


n=11)


those


studied more than 3 months after


Tx ("late recipients"


n=12).


Plasma NE


at rest (324


vs 255 pg/ml)


peak exercise (1,972 v


1,653 pg/ml) was


similar (p>0.05) for early


HTR and control subjects, respectively


HTR, however, plasma NE at rest (452 vs


5 pg/ml),


. In late


peak exercise (2,886 vs


1,653 pg/ml) and the increment from rest to peak exercise (2,434 vs


1.398


pg/ml) was significantly (p<0.05) increased compared with control subjects.


These


data


suggest


that


sympathetic


response


to peak


exercise


increased in late HTR but the explanation for this trend is not clear.


Banner


coworkers


(1989)


also measured


plasma NE


levels


HTR during a SL-GXT on an upright cycle ergometer.


Compared to age and


sex matched control subjects, HTR had higher NE levels at rest (3.9 vs 2.9


nmol/L)


greater


(p

relative


increments


each








17
during submaximal exercise may be due to surgical deafferentation as well


as reduced


hypotheses


peripheral


offer


vascular responsiveness.


a viable


explanation


Although

observed


each


of these


sympathetic


overactivity


an alternative interpretation of their data may be indicated.


Considering the fact that VO2max and peak power output achieved by HTR


were only 60% of that achieved


by the control group, each submaximal


exercise stage would have required a higher relative percentage of maximal


effort in HTR.


Therefore,


the observed


increased


sympathetic response


during


linear


exercise may

relationship


responsiveness


(Chid


only


be indicative of


between

sey et al


relative

., 1962;


the well


exercise


Howley


documented


intensity


1976


positive


and


Goldstein,


SNS

1981;


Christensen and Galbo


, 1983; Rowell and O'Leary


1990).


To date, however,


no studies have been performed which compared plasma neuroendocrine
responses in HTR and matched control subjects during exercise at the same

relative levels of exercise intensity.


Younis et al.


(1990)


tudied hemodynamic responses in 10 HTR during


upright cycle exercise at three levels of relative intensity (50,


peak power output).


70 and 90


Plasma NE was measured at baseline and after each 5


minute submaximal exercise test.


Plasma NE levels averaged 456 pg/ml at


rest and rose to 1312


pg/ml at the second level of exercise and to


2157 pg/ml


at the


third


level


exercise.


Unfortunately


difficult


to draw


conclusions


from


these


data


regarding


relative


level


SNS


activity


because control NE data were not reported.








18

interesting feature of their data was that cyclosporine immunosuppression


appeared to be associated


with increased SNS activity


and hypertension.


HTR receiving cyclosporine (n=10) had higher (p<0.05) mean arterial blood
pressure than HTR not receiving cyclosporine (n=5) (112 vs 96 mmHg) and


7-fold higher rate of sympathetic nerve firing (80 vs


Plasma NE levels were higher in HTR


28 bursts/min).


who received cyclosporine than in


those who did not take cyclosporine or in normal control subjects (262, 174


pg/ml,


respectively).


Although


these


data


demonstrate


possible sympathoexcitatory effect of cyclosporine, cardiac deafferentation


may have enhanced the observed effect.


The investigators compared


effects


cyclosporine


HTR


with


normally


innervated


myasthenia


gravis
Similar


patients receiving immunosuppressive therapy with


doses of


cyclosporine were associated


cyclosporine.


with significantly (p0.05)


larger


increases


SNS


activity in


HTR


than


myasthenia


graves


patients (46 vs 25 bursts/min).


In addition to exercise


, head-up tilt has been used to test the integrity


cardiovascular


reduces stroke


This


activates


control


volume


cardiac


mechanisms


reducing
I arterial


HTR.


cardiac preload


baroreceptor


Passive


head-up


stroke


reflexes,


volume.


resulting


increased heart rate and contractility with peripheral


vasoconstriction and


associated neuroendocrine activity as compensatory measures to maintain


blood pressure and cardiac output.


Banner and coworkers (1990) reported


normal baseline NE levels but increased NE responses to head-up tilt in 8










necessary


to maintain


blood


pressure


cardiac output


HTR.


The


authors speculate that increased SNS activity may be due to an increased
activation of arterial baroreceptor reflexes related to the greater decrease in


cardiac output or due to the loss of tonic inhibition of the SNS


following


cardiac deafferentation.
Not all studies have reported normal and/or elevated SNS activity in


HTR.


Mohanty


coworkers


(1987)


studied


cardiovascular


control


mechanisms


HTR


measuring


plasma


NE,


blood


pressure


forearm


vascular resistance during lower-body negative pressure (LBNP).


This technique (at mild suction) unloads cardiac rather than arterial stretch


receptors,


which


typically


results


peripheral


vasoconstriction


increased levels of


circulating NE.


They reported


that heart rate,


mean


arterial


pressure


forearm


vasoconstriction


respond


during


application of LBNP (at -10,


-20 and -40 mmHg) and the NE response was


attenuated in HTR compared to the control group.


The authors concluded


that


likely


mechanisms


impairment


in reflex


control


circulation was cardiac deafferentation.


These results are not in opposition


to the findings in denervated subjects during exercise because LBNP is a
volume reduction intervention whereas exercise increases atrial stretch. It


is curious


, however, that significantly lower resting plasma NE levels were


unique to this group of HTR.


summary


circulating


been


shown


to have


important


chronotropic and inotropic effects upon the chronically denervated human










ascertained from


available data


because


control


HTR


were not


studied at similar relative exercise intensities.


Arginine


Vasopressin


Arginine vasopressin (AVP) is a nine amino acid polypeptide released


from


the nerve endings of


the posterior pituitary


gland


(Guyton,


1986).


The


primary


physiological


functions


AVP


antidiuresis


and


peripheral


vasoconstriction


(Johnson


et al


1969


Ledsome


and


Mason,


1972; Cowley et al.,


1974; Cowley et al.,


1984).


Extremely minute quantities


of AVP can cause antidiuresis.


In the presence of AVP


the permeability of


renal


collecting


ducts


tubules


to water increases greatly


and allows


most of the water to be reabsorbed


, thereby conserving water in the body


(Guyton,


1986).


Vasopressmin


at higher


plasma


concentrations


is also


potent vasoconstrictor


man.


When


AVP


is present in


moderate and


high


concentrations


vasoconstriction


those


AVP


receptors


vessels


thereby play


arterioles mediate
an important role in


regulating blood pressure and cardiac filling pressure (Cowley et al.,


1974;


Quillen and Cowley, 1983;
Early research genera


Manning and Sawer,

lly concluded that t


1984).


he normal plasma levels of


AVP (1


-2 pg/ml)


were too small


to exert a significant pressor effect and


participate in


the normal


daily


blood


pressure regulation


(Sawer,


1961).


Several noteworthy design flaws, however, may have masked the pressor


effect


AVP


Arterial


baroreflex


compensation,


sodium


pentobarbital


anesthetic and stress


induced


saturation of the system


with endogenous










undisturbed animals have demonstrated that between


5 and 10 mm Hg of


normal


arterial


pressure


is maintained


basal


level


AVP


Furthermore, it has been shown that when arterial


pressure fall,


pressure or left atrial


the reflex secretion of AVP is enough to bring mean arterial


blood pressure three forths of the way back to normal (Cowley et al.,


1974).


Vasopressmin


released


into


the circulation


through


activation


hypothalamic


"osmoreceptors"


The osmoreceptors,


in turn,


stimulate


adjacent


neurons


in the


upraoptic


paraventricular


nuclei


hypothalamus


which


have been shown


to be involved in AVP synthesis


(Ledsome and Mason,


1972; Quillen and Cowley,


1983)


In addition to osmoregulation, there is a large body of evidence which

argues that AVP release is mediated by low-pressure stretch receptors in the


left atrium which send their afferent signal via the vagal nerve.


the most powerful stimuli


for increasing the secretion


AVP i


Perhaps

Loss of


blood volume or decreased left atrial filling pressure (Quillen and Cowley,


1983).


The increased secretion of AVP is believed to result mainly from the


atrial


pressure


in the


heart


caused


blood


volume


and


resultant decrease in cardiac preload.


The unloading of the atrial stretch


receptors


removes


tonic


inhibition


ANP


evokes


reflexive


increase in AVP secretion (Johnson et al.,


1969


Ledsome and Mason


, 1972;


Mancia and Donald


1975


Quillen and Cowley, 1983).


However


the carotid


aortic


baroreceptors


also


participate


modulation


AVP


secretion (Cowley et al.,


1974; Cowley et al.,1984).










Furthermore,


response


was


eliminated


when


cervical


vagus


nerves were cooled


to block neural


transmission.


Henry


coworkers


(1956)


hypothesized


that


stretch


receptors


atrium


reflexly


inhibited the release of AVP and thereby increased diuresis.


The diuretic


response


to balloon


distension


atrium


was


used


several


investigators


to support


hypothesis


that


cardiac


receptors


play


important role in


the control


AVP secretion


(Gauer and Henry


1963;


Ledsome and Mason


1972).


However, these findings were confounded by


the discovery that left atrial receptors also modify sympathetic outflow to


kidney


independent

Subsequently


could


AVP


was


change


release


confirmed


urine


volume


(Karim


that


atrial


through


1972


stretch


mechanism


DiBona,


increased


1978).


atrial


volume receptor firing (type B receptors) and inhibited AVP release in dogs


(Johnson et al.,


1969; Ledsome and Mason,


1972).


Numerous studies using


balloon inflation or fluid infusion


decreased


to distend


the left atria have reported


plasma AVP in response to either stimulus.


contrast, right


atrial distension did not decrease plasma AVP levels.


More recently


Wang


et al.


(1988) demonstrated that ventricular receptors may also be involved


mediating


AVP


release.


Conversely


reduction


atrial


stretch


through hemorrhage or other means of volume contraction was associated

with an increase in plasma AVP.


These


anesthetized


responses,


subhuman


however,


primates


have


under


always


similar


been


demonstrated


circumstances.


Gilmore










thereby


help


maintain


blood


pressure


homeostasis


in a primate


that


frequently changes between the upright and the supine position.


AVP


Release


During


Exercise.


Atrial


pressure


increases


during


exercise but, despite this inhibitory influence, plasma AVP is increased in a


dose-response


relationship


with


increasing


exercise


intensity.


Exercise


alters a


variety of factors that are known


Plasma osmolality, angiotensin


to affect the secretion of AVP


II and cortisol are elevated


with exercise


while


plasma


volume decreases due


to the outward


movement of


fluid


from the vascular space to the interstitial space.


The outward movement


of fluid from the vascular space to the interstitial space during exercise is


dependent upon the intensity of the exercise (Wilkerson et al.,


1977).


resulting decrease in plasma volume has been associated with proportional


increases in electrolyte and protein concentrations.


All of the above factors


have


been


reported


to stimulate


AVP


release


from


pituitary


gland


(Wilkerson et al.


1977


Convertino et al.


1981


Wade and Claybaugh, 1980;


Geyssant et al.,


1981).


Available evidence indicates that an acute bout of exercise does result


an increase


plasma


AVP


(Convertino


, 1981


Wade


Claybaugh,


1980; Geyssant et al.,


1981).


The magnitude of


AVP release


appears to be related to the relative work intensity as measured in terms of


maximum oxygen consumption


(Wade and


Claybaugh,


1980


Convertino


et al.


1981


El-Sayed,


1990).


Convertino et al. (1981) reported nonsignificant


changes in plasma AVP at 40


of VO2 max but a
of V02 max but a


5 fold increase in AVP at










work intensity above 40


of VO2 max may be required to increase plasma


AVP concentrations during exercise but sufficient data is lacking to confirm

this relationship.


Factors


mediating


release of


AVP


during exercise


are not fully


understood.


The


acute


reduction


plasma


volume


that


accompanies


even short term exercise has been suggested as one mechanism responsible


for elevated AVP (Geyssant et al.,


1981).


Convertino and associates (1981)


suggested


that


hyp


rosmolality


evoked


transient


hemoconcentration


rather


reduction


plasma


volume,


results


AVP


release during


exercise.


Landgraf


et al.


(1982)


also


reported


that


plasma


osmolality


changes


were


significantly


correlated


with


AVP


responses during exercise.


Others have presented conflicting data which


indicates that AVP may not be mediated primarily by osmolality changes.


Beardwell and


coworkers


(1975)


Beaumont et al.


(1973)


have shown


that the


AVP


response


after


exercise


was


greater


than


that


found


after


dehydration


despite


that


osmolality


changes


were


similar


response to both conditions.


AVP Release In Cardiac Denervated Animals.


The reflex inhibition of


AVP release during distension of the left atria is absent in animals with


chronic cardiac denervation (Fater et al.,


1982).


Therefore it is conceivable


that


mechanisms


which


elevate


AVP


during


exercise


are unapposed


HTR and the result is a disproportionate elevation in AVP when compared

to innervated controls.








25

cardiac denervated humans also elicits a blunted AVP response (Banner et


,1990; Drieu et al.,


1986).


Wang et al. (1983) measured plasma AVP and PRA during continuous


hemorrhage


cardiac


denervated


sham-operated


conscious


dogs.


Baseline


AVP


control


concentrations


pg/ml)


were


cardiac


different


denervated


(p>0.05)


dogs


between


pg/ml).


Mild


hemorrhage (10 ml blood/kg body weight) caused a significant increase in


plasma


AVP


control


dogs


not in


cardiac


denervated


dogs.


increase in AVP


during hemorrhage of 20 and 30 ml


of blood/kg


body


weight was attenuated in the cardiac denervated animals when compared


to the response of the control dogs.


The mean concentration of AVP in the


cardiac denervated dogs was only


10-1


as elevated


as in the control dogs


vs 300 pg/ml).


AVP Release In HTR.


Several studies have measured resting plasma


AVP


HTR


relationship


between


exercise


intensity


AVP


response has not been reported in HTR.


Mertes et al.


(1991) followed 10 HTR for a period of 10 days following


surgery.
pg/ml).


Mean


preoperative


AVP


levels


were


found


to be


The postoperative changes in AVP were marked by


elevated


a secretary


peak occurring


on the first day


of recovery


pg/ml).


These elevated


levels decreased but remained slightly above normal through the 10th day
of recovery (4.9 pg/ml). The authors attributed the secretary peak, in part,

to the surgical stress of Tx. Similar findings have been reported by other










Oppermann


et al.,


1987).


Viinamaki


et al.


(1986)


reported


that


AVP


increased nearly 6-fold in human cardiac surgery patients (n=32) after 5 to


minutes


cardiopulmonary


bypass


and


remained


significantly


increased during the first postoperative day but returned to preoperative


levels by the 4th postoperative day.


Mean arterial blood pressure had also


decreased


to its


nadir


10 minutes


after induction


cardiopulmonary


bypass,


therefore the


authors


concluded


that


mechanism


leading to


AVP release was likely via baroreceptor activation.


Banner et al.


(1990) studied neuroendocrine responses to one hour of


head-up


8 recipients


combined


heart-lung


transplantation.


Baseline


AVP


concentrations


were similar in


the transplant


control


groups (2.6 vs 2.5 pmol/1),


and the authors report that AVP levels did not


increase significantly


during head-up


tilt in


either


group.


Inspection of


their


AVP


data


however


reveals that there was a


trend toward elevated


AVP in HTR


with AVP reaching plasma


concentrations at 60 minutes of


tilt that were approximately 1.6 times greater than baseline wheras AVP did


not change in the control group.


Because heart rate, systolic and diastolic


responses to tilt were the same in both groups, the authors concluded that


afferent


information


from


cardiac


stretch


receptors


efferent


cardiac


innervation were not essential


orthostatic stress.


to maintain systemic blood pressure under


However, the trend toward elevated AVP suggests that


blood


pressure homeostasis in HTR involved


higher


AVP secretary rates


perhaps made possible by the deafferentation of inhibitory


cardiac atrial










water load in 13 HTR.

minutes of supine rest.


A baseline AVP and PRA sample was drawn after 30
Lasix (40 mg) was then injected intravenously and


the subjects


walked


casually


for 60 minutes


after which


AVP


and PRA


samples were again drawn.


Basal plasma AVP was significantly elevated in


HTR compared to


10 healthy


control subjects (4.5


vs 3.1


pg/ml).


During


lasix


induced


volume


depletion,


however,


AVP


concentrations


respond in HTR (4.5 and 4.7


pg/ml before and after lasix) but increased 45%


from baseline in the control group.


Resting PRA


was not different between


groups (1


vs 1.2 ng/ml/hr for the control and HTR, respectively) and the


response


consistent


to volume


with


depletion


findings


was


after


similar


volume


(p>0.05).
depletion


These


results


hemorrhage


cardiac denervated dogs (Wang et al.,


1983).


It remains to be determined,


however,


what the AVP response will


be in HTR during increased atrial


pressure while exercising.


Higher plasma AVP is typically observed under


basal conditions in HTR and this may be attributed to the absence of tonic
inhibition of AVP release by the cardiac stretch receptors.


In summary


plasma AVP is released in a dose-response relationship


with increasing exercise intensity


. Factors mediating the release of AVP


during


exercise


are


acute


plasma


volume


reduction,


transient


hemoconcentration and SNS stimulation.


However


no data are available


on the possible modification of the AVP response during exercise in HTR.
Atrial Natriuretic Peptide


The discovery of secretary granules in rat atrial myocytes by de Bold et










vasorelaxant properties (deBold et al.,


1981).


These findings indicate that


the heart may have an endocrine function in electrolyte balance and blood

pressure homeostasis that is usually associated with the RAAS and SNS.

Although hundreds of studies on ANP have been performed since its


discovery


10 years ago, the role of ANP in the physiologic regulation of the


cardiovascular


system


remains


controversial.


Isolated


aorta


renal


vessel


partially


constricted


with


a variety


pressor


agents


have


been


shown


to relax in


the presence of


ANP


(Goetz,


1988).


Conflicting


data,


however


have


been


obtained for


other


arteries and


veins


(Goetz


, 1988).


Moreover, vasodilation does not always occur when ANP is given to intact


animals.


Studies on conscious animals have demonstrated that peripheral


resistance may remain constant


or even increase


when ANP is infused


(Goetz,


1988)


. The explanation for this response


to ANP


during in


vivo


experiments,


however


, may be that arterial


baroreceptors respond


to the


hypotensive


effects


ANP


elicit


reflex


increases


in sympathetic


vasoconstriction


, thereby offsetting any vasodilation induced directly by the


ANP.


Human


given


ANP


subjects

infusions.


respond


ANP


somewhat


causes


differently


cutaneous


than


animals


vasodilation


when


human


subjects


occasionally


develop


facial


flushing


hypotension


with


decrease in blood pressure being severe in some


cases.


It is apparent that


ANP


can


be a


potent vasodilator in normal human subjects.


Nearly


reports


indicate


that


a decrease


blood


pressure


elicited


ANP








29

ANP is also capable of decreasing plasma volume (Weidmann et al.,


1986).


Although


reduction


plasma


volume


obviously


would


expected (over time) in response to the diuretic and natriuretic properties


ANP


, plasma


volumes


are also


reported


to diminish


in anephric


animals that are given ANP


. Comparable results have been obtained after


removal of both kidneys and spleen (Goetz,


1988).


Goetz (1988) suggests


that the ability


ANP


cause


a net transfer


of fluid


from


plasma


interstitial space raises


the possibility that edema formation in CHF


other conditions associated with abnormally high plasma ANP levels (i
Tx) may be attributable in part to the effects of ANP.


Infusions of ANP that raised the plasma concentration of ANP


7 and


12 fold in


conscious dogs caused


atrial pressures (Goetz,


1988).


progressive decreases in right and left


Further work is needed to establish that the


effects


ANP


on arterial


pressures


are of


physiologic


importance.


However,


because


an increase in atrial


pressure


increases


the release of


ANP


which


in turn


may


decrease


cardiac


filling


pressure,


atrial


peptides may serve as part of a negative feedback
heart to influence its own filling pressures (Goetz,


temrn that enables the


1988).


The decrease in


cardiac filling pressure or preload appears to be primarily responsible for


the decrease in cardiac output that may be induced by ANP (Goetz,


1988).


In isolated tissue preparations, ANP blocks the vasoconstrictor effects


of NE and ANG II.


In normal healthy humans, elevated ANP appears to


exert


an inhibitory


effect


upon


RAAS


(Shenker


et al.


, 1985).


This








30

Notwithstanding these exceptions, ANP is thought by some investigators


to be an important counter-regulatory hormone to the RAAS.


Thus, it has


been hypothesized that ANP may be a potentially important hormone in


blood


pressure


homeostasis.


Specifically


elevated


ANP


may


physiologic


response


to protect


system


reducing


afterload


hypertension or afterload and preload in heart failure.
There is evidence to suggest that high plasma levels of ANP may also


influence


SNS.


High


infusion


rates


ANP


have


been


shown


increase the release rate of catecholamines (Goetz,


1988).


These data imply


that the more prominent hypotensive effects of high doses of ANP elicit a


more


powerful reflex


stimulation


the sympathetic nervous


arterial


baroreceptors.


The


baroreceptor


reflexes


(probably)


responsible for the increases in circulating NE that have been detected after
intravenous infusion of ANP in human subjects, and for the tachycardia


that commonly occurs in human subjects in response to ANP (Goetz,


1988).


Another


possible


stimulus


ANP


release


during


following


exercise


may


be elevated


circulating pressor


hormones


as NE


ANG II.


Uehlinger et al.


(1986)


studied


the release of endogenous


ANP


during infusions of NE


ANG


II in


normal


subjects.


Individual


doses


ANG


were


titrated


so that


mean


blood


pressure


increased 20 mmHg.


Plasma ANP increased significantly after 20 minutes


either


ANG


infusion,


ANP


was


more


pronounced during NE (from 25 to 80 pg/ml) than during ANG II infusion










injected min increasing


doses of


micrograms


progressively


decreased


blood


pressure


from


147/91


to 136/74


and


136/70


mmHg,


respectively, during maintenance of NE infusion at the highest level.


ANP Release In HTR.


It is now widely recognized that the release of


ANP


atrial


stretch


represents


a physiologic


mechanism


involved


maintenance of homeostasis


inm response


to volume expansion.


Cardiac


innervation


necessary


ANP


release


which


been


found


occur in


vitro from atrial fragments and in


vivo


dogs with surgically


denervated


hearts.


More


importantly


because


increased


plasma


ANP


levels have been reported in HTR, the question may be asked whether


increases


ANP


secretion.


However


, factors


other


than


interruption


cardiac nervous pathways may be implicated in increased plasma levels of


ANP in HTR, such as


the increased atrial dimensions and myocardial


mass due to the persistence of a cardiac remnant containing a rim of the


native atria,


the renal insufficiency related


to cyclosporine treatment,


3) possible changes in atrial function.


The human HTR presents interesting ANP characteristics.


Before


several of the neuroendocrine systems involved in electrolyte balance and


blood pressure regulation, RAAS and ANP in particular,


are stimulated in


the patient with severe CHF (Goldsmith


et al


., 1983a;


Raine et al


., 1986;


Colucci et al.


, 1989; Francis et al., 1990


Swedberg et al.,


1990).


Long term


follow-up


HTR


revealed


persistent


high


levels


ANP


release


despite resumption


of satisfactory


hemodynamic


tatus (Magovern et al.,










The


mechanism


underlying


raised


ANP


values


in HTR is


clear.


It has been suggested that elevated atrial pressure, ie. atrial stretch,


due to central hypervolemia and/or hypertension may be the stimulus for


higher


ANP release


Bold


et al.


1981


Raine


et al.


, 1986).


There


evidence to indicate, however,


that other factors may be responsible for the


abnormally


high


ANP levels


in HTR.


Magovern


et al.


(1987)


measured


ANP in


HTR


year


after


during routine endomyocardial


biopsy.


Plasma ANP levels in HTR were elevated 10 fold compared to normal (217


vs 20


pg/ml).


Furthermore,


ANP


concentrations


HTR


were


3 fold


greater than a group of 20 coronary artery disease patients studied in the


same laboratory during cardiac catheterization (217


vs 71


pg/ml).


Despite


significantly


higher


ANP


levels


HTR,


there


were


no s


significant


differences between the groups in right atrial pressure, pulmonary artery


pressure, pulmonary wedge pressure or cardiac index.


measured


Studies that have


plasma ANP in normal subjects during exercise have reported


that


high


ANP


levels


persist


to 30


minutes


during


recovery


from


exercise despite the fact that atrial pressure drops rapidly (Donckier et al.,


1988).


The elimination half-life of ANP


, ranging from


to 3 minutes


too short to explain the sustained elevation of ANP.

Deray and coworkers (1988) measured plasma ANP in 3 HTR 1,


days after


3 and 5


In all HTR, ANP had increased 20 to 74% from preTx levels


despite
between


reductions


plasma


right


ANP


atrial


pressure.


concentrations


correlation


right


atrial


was


pressure.


found


The










One possible explanation for the elevated ANP


observed


in HTR is


systemic


hypertension.


Hypertension


been


associated


with


modest


elevations in ANP, but it has not been associated with the large magnitude


of ANP increase that was found in HTR (Arendt et al.


, 1986).


Others have


speculated


that the


increased ANP


levels


HTR are a response


to the


lower hemoglobin concentration (Magovern et al.,


1987)


owing to the fact


that one of the primary actions of ANP is to cause hemoconcentration by


shifting


fluid


vascular


pace


(Weidmann


1986).


Experimental evidence, however


is lacking to confirm this hypothesis.


Sympathetic innervation


the heart appears


to be


unnecessary for


ANP


to be released from atrial myocytes.


Elevated basal levels of ANP


have been reported in HTR early and late after


Tx (Magovern et al.,


1987


Deray et al.,


1988; Mertes et al.


1991).


Mertes and coworkers (1991) studied


short-term


effects


on the


release of


ANP


during


days


recovery after


Tx in a series of 10 HTR.


PreTx ANP levels were elevated


(42.4 pg/ml) but ANP dropped during day


1 of recovery (25.1 pg/ml).


day 10 of recovery, plasma ANP returned to elevated level

that were comparable with those found before Tx.


Singer and coworkers (1990) measured ANP in


(38.4 pg/ml)


7 male HTR (47 yrs of


age;


wks postTx) at rest and during


a SL-GXT


on an


upright cycle


ergometer.


Resting ANP was significantly higher in HTR compared


toa


control


group


matched


gender


(31.3


vs 8.0


pg/ml).


ANP


increased at a lower level of exercise in HTR but the maximal percentage










ANP


Release


During


Exercise.


Plasma


ANP


been


shown


increase during exercise in normal subjects and the degree of increase is


proportional to the relative intensity of the exercise (Donckier et al.,


1988).


Donckier et al.


(1988) simultaneously measured plasma ANP


ventricular


volumes and ejection fraction in


13 normal subjects (7


males


6 females)


during 5 minute bouts of recumbant cycle ergometry at 20,


40 and 60


peak


power


output.


Although


baseline


exercise


ANP


levels


were


greater in


women,


the sex


by time interaction


was not significant.


Both


groups significantly increased plasma ANP (2 to 4 fold) at 40 and 60% of


peak


power


output


during


exercise at


The


highest


ANP


concentrations


were


found


at the


same


levels


as the


lowest


ventricular


volumes.


The degree of atrial stretch associated with decreased ventricular


volume was not measured during exercise.

Renin-Angiotensin-Aldosterone-System


RAAS


an important endocrine system in


electrolyte


balance


cardiovascular


hemodynamics.


system,


enzyme


renm


secreted


kidney


into


circulation


acts


state


angiotensinogen secreted from


the liver to


produce


angiotensin


This


decapeptide is then converted by angiotensin-converting enzyme (ACE),


dipeptidyl


peptidase


found


large


concentrations


lungs,


to the


peptide


hormone


angiotensin


(ANG


ANG


multiple target


organs


(such


as blood


vessel,


kidney


, adrenal


, heart,


brain,


pituitary,


reproductive


organs


etc.)


from


which


can


elicit


specific


responses








35

synthesis and release of aldosterone by the adrenal cortex in chronic blood

pressure homeostasis.


Previous


vitro


experiments


have


shown


that


stimulated renin production in rat kidney cortex slices by 43


1985).


cyclosporine

(Bellet et al.,


Cyclosporine doses of 20 to 25 mg/kg daily have also been shown to


stimulate plasma renin activity


(PRA)


levels in


vivo


with


dogs and rats


after


several


days.


These


results


therefore suggested


that


cyclosporine


affects


RAAS and


consequently


raises


blood


pressure.


Bellet


et al.


(1985),


however, reported that cyclosporine did not stimulate the RAAS in


a group of 15 hypertensive HTR.


Reported levels of plasma aldosterone,


angiotensinogen and ACE activity were all normal.


Furthermore, plasma


renin


activity


aldosterone


were


within


normal


limits


after


acute


treatment with captopril (1


mg/kg body weight).


However, they did find


that plasma volume was increased by


as measured by the radioiodine-


labeled serum albumin method (Bellet et al.


,1985).


The authors conclude


that


although


adaptation


stimulation


RAAS


of the RAAS to fluid retention


improbable


increase)


HTR


may


, poor
partly


responsible for the increase in blood pressure.

Thames et al. (1971) also found that dogs with autotransplanted hearts


abnormally


expanded


blood


volumes


subnormal


increases


plasma


renin


response


to hemorrhage.


authors


conclude


that


most likely explanation for the abnormal blood volumes and the abnormal


renin responses


to hemorrhage was


that


interrupts


reflexes


from








36

pressure and in mean right atrial pressure in the dogs were comparable to

the normally innervated control dogs.
It is likely that the expanded blood volumes and the subnormal renin


responses to bleeding in


Thames'


dogs after


Tx are related in a cause and


effect relationship.

might result from


There are two


possibilities:


blood


volume expansion


Tx in a manner which does not involve the mediation


RAAS.


denervation


The


associated


alternative


with


possibility


causes


that


an increase


cardiac


PRA


afferent


reflex


mechanism and that this in turn results in expansion of blood volume.


RAAS


HTR.


Held


et al.


(1989)


studied


PRA


response


sympathetic stimulation produced by infusion of isoprenaline and during


change in


posture in HTR (n=9) undergoing long-term treatment (6 to


months


postTx)


with


infusion is associated


cyclosporine.


In normal


subjects,


with a decrease in diastolic blood


an isoprenaline

pressure and an


increase in PRA.


Despite similar decreases in diastolic blood pressure in


both HTR and control groups (-17 vs -15 mmHg),


PRA


was reported to be


significantly lower among HTR


when compared with controls at baseline


vs 1.4 ng/kg/min) and did not increase during isoprenaline infusion


(0.5 vs


5 ng/kg/ml) or after change of posture.


The authors interpret their


findings as an indication of a defect in the ability of the kidneys to release


or produce renin in response to sympathetic (beta-receptor)


stimulation.


They


conclude


that


most


probable


explanation


a cyclosporine


mediated toxic effect on the kidney.










that leads


to plasma


volume expansion, atrial


distension and


release of


ANP


acute


increase


plasma


volume


leads


to immediate


renal


vasodilation, diuresis and natriuresis.


The renal response is mediated in


part by


the release of hormones


that act to directly relax renal


vascular


smooth muscle and inhibit tubular transport of sodium and water, and in

part by the simultaneous inhibition of hormones and renal SNS traffic that


causes vasoconstriction, antidiuresis and sodium retention.


Nerve fibers


in the walls of the atria that behave as mechanoreceptors play an important


role


inhibition


vasculature.


sensing


hormones


an increase


and


outflow


either


mechanical


renal


stretch


transmural pressure, they evoke signals that travel via the vagas nerve to


integrative


centers


in the


hypothalamus


medulla


oblongata.


These


centers


, in turn, exert a tonic inhibitory effect on renal


to promote natriuresis and


diuresi


vascular resistance


by reducing SNS outflow to the


renal


vasculature.


The


authors


noted


that


most


striking


difference


between control and HTR during and after water immersion was elevated


vascular


resistance


PRA


HTR.


They


conclude


that


likely


explanation


elevated


renal


vascular


resistance


and


PRA


unopposed and/or enhanced SNS traffic to the renal vasculature.


Pulmonary


Function


Normal


ventilation


(Sietsema


et al


1987


Banner


et al


., 1988)


decreased


ventilation


(Marconi et al.


1987


Meyer et al.,


1989)


have been


m m


.


.










than by


cardiac output abnormalities.


Oxygen


uptake (T 1/2


VO2-on)


during the rest to exercise transition was measured in 6 male HTR (1-8 mo


post-op).


T 1/2


VO2-on during


cycle exercise at 85


of peak


VO2


was


slower for HTR compared to age-matched,


untrained control subjects (65 vs


43 seconds).


Meyer


et al.


(1989)


studied


the kinetics of respiratory


cardiac


function in 21 HTR and


10 healthy controls.


Breath-by-breath analysis of


respiration and


impedance cardiography were used


during 5


minutes of


upright constant load cycle exercise at 50 watts.


The half-time of the on-


response


pulmonary


ventilation


was


significantly


slower


vs 42


seconds) in HTR but the kinetics of cardiac output (52 vs 40 seconds) were


only moderately impaired.


From


these data


the authors concluded


that


respiratory


exchange


rather


than


cardiac


function


was


limiting


factor during exercise of moderate intensity.

Contrastingly, Sietsema and coworkers (1987) reported that ventilation
a


VO2


increased


promptly in 4 HTR during progressive and constant


load cycle exercise.


The kinetics of the increase in


VO2 to its steady state


were reported to be "within the range found in normals during moderate
exercise" (4212 seconds).

Cardiac Denervation and DLCO


Diminished DLCO


been reported in


HTR


(Casan


et al


1987


Banner et al


., 1988).


Immunosuppression


therapy with


cyclosporine,


surgical


procedure and reduced hemoglobin have been cited


as possible










because the available data


does not include pre- and


postTx pulmonary


measures.


Considering


that


DLCO


markedly


diminished


many CHF patients awaiting


(McNeil et al.,


1958


Morley et al.,


1989;


Wright et al.,


1990


Bussieres et al.


, 1990),


possible that the abnormal


postoperative


DLCO observed


in some


HTR may not


be a


result of


surgical procedure or immunosuppression therapy but rather a persistence

of preexisting conditions.


The data of Casan et al.


DLCO in 10 HTR 6 to


(1987)


months after


howed a mean reduction of 14


Tx despite significant improvements


in FVC and FEV1


. The authors concluded that the reduction in DLCO was


an early manifestation of cyclosporine induced lung toxicity similar to that


which has been

(Myers et al., 198


documented in


4; Taube et al.,


the kidneys of


1985; Humes et al.,


renal


transplant patients


1985; Racusen et al.,


1986;


Macris et al.


,1989).


As indirect evidence for their conclusion, they reported


a high correlation (r=0.87) between the reduction in DLCO and the level of
cyclosporine in whole blood at the time of the pulmonary function tests.


Cyclosporine immunosuppression


therapy is frequently


complicated


development


hypertension


early


nephrotoxicity


hepatotoxicity (Myers et al.,


1984;


Taube et al


., 1985; Humes et al.,


1985;


Racusen et al.


1986


Macris et al


., 1989).


Additionally


neurologic toxicity


been


observed


liver


transplant


patients


and


HTR


receiving


cyclosporine (Berden et al.,


1985


Adams et al


1987


DeGroen et al.


1987


Vazquez de Prada et al.,


1990).


Several other side effects of cyclosporine










not been presented in the related literature.


Bennet and Norman (1986) in


an earlier review make no reference to the adverse effects of cyclosporine


on the lung.


Copeland et al. (1986) describe only infrequent pleural edema


secondary to cyclosporine therapy and these symptoms are transient.


In a


detailed review of drugs potentially toxic to the lung, Cooper et al. (1986) do


not include cyclosporine.


Macris et al.


(1989) in a recent review of clinical


contraindications for cyclosporine immunosuppression make no mention
of pulmonary dysfunction.

Cardiac Denervation and Exercise Hyperpnea


Numerous


hypotheses


neural-humoral mechanisms


involving
have been


neural


, humoral


and


postulated for control


combined


of exercise


hyperpnea and support for each has been found (Powers and Beadle, 1985).


Most investigators agree that the


initial fast phase (phase


1) of


exercise


hyperpnea


is neurally


mediated.


However,


origin


and


magnitude of
demonstrated


contribution remain


to be


mediated


contentious.


indirectly


through


The fast phase has


feedback


been


afferent


stimuli originating from skeletal muscle in the working limbs (Kao,


1963;


Tibes,


1977) or


directly via feedforward


efferent signals


from higher


centers of the brain (Eldridge et al.,


1981).


Another neurogenic hypothesis


to explain


the immediate hyperpnea


observed at the onset of exercise contends that the ventilatory response is


dependent on


the cardiac output response.


ventricular stretch receptors


have been shove


Afferent signals from cardiac

in to stimulate ventilation in










Cardiac denervation, a necessary consequence of T


would be expected


to ablate reflex


stimuli


originating from


the heart


thereby reducing


ability to appropriately control pulmonary ventilation.


Denervation of all


cardiac afferents would be expected to result in hypoventilation during the


onset


exercise


characterized


transient


hypercapnia


hypoxemia.


Banner


et al.


(1988)


investigated


hypothesis


examining


ventilatory and circulatory responses at the onset of exercise in 6 HTR, 5


subjects with combined heart-lung transplants and


subjects sat in a chair and pedalled a lever-arm system.


7 normal controls.


Exercise consisted


a one


minute


push-relax


rhythm


produced


either


voluntarily


subjects or involuntarily by


electrical stimulation of peripheral nerves of


the quadriceps and hamstring muscle groups.


Ventilatory variables and


cardiac output were measured


as average


values over


4 consecutive 30


second periods starting 1 minute before the onset of exercise.


There were


no significant differences between voluntary and involuntary initiation of


exercise for


respiratory


or cardiovascular variables.


Oxygen


consumption,


carbon


dioxide


production


ventilatory


and


respiratory rate responses were not significantly different between HTR and


control subjects.


Percentage changes in


ventilation


were plotted against


percentage


changes


in cardiac


output


revealing


that


normal


or even


exaggerated ventilatory responses at the onset of exercise can occur without


proportional


underlying


cardiac


output


heart-lung








42
Skeletal Muscle Strength


It has been suggested that skeletal muscle weakness may be a primary

mechanism responsible for exercise intolerance in otherwise healthy HTR


(Kavanagh


et al


., 1988).


date,


however,


no data


exists


comparing


peripheral muscle strength in HTR


with normative values.


Furthermore,


those studies that have conducted body composition analyses (ie.,


free tissue) in HTR are sparse.


Preoperative physical activity is typically restricted in


candidates


due to severely


limited cardiac output.


An extended waiting period for a


donor organ to become available may result in considerable deconditioning


and atrophy resulting from inactivity.


Following Tx, chronic corticosteroid


prednisone)


therapy


immunosuppression


is recommended


most HTR.


Corticosteroids cause pronounced atrophy of skeletal muscle


(steroid myopathy) when administered at high doses for prolonged periods


time


(Goldberg


and


Goodman


1969


Dujovne


and


Azarnoff,


1975;


Kinney and Felig,


1979).


Steroid induced myopathy leads to reduction in


muscle


mass,


depletion


muscle


protein


and


loss


strength.


important aspect of steroid myopathy is that the skeletal muscle fiber-type


response


within


musculature


variable.


Fast-twitch


white


glycolytic fibers (Type H b) are significantly atrophied in response to chronic


levels of


corticosteroids


while slow-twitch


oxidative fibers (Type I)


relatively resistant to atrophy (Goldberg and


Goodman,


1969


Kelly


and


(Znldmnink


1950


gpp~ga


Viri


19519


Almnn


and


Di ,bnis<


1991W


a a a aL a -F '~[ L a V 1 A V ass- a a a -r -


fat vs fat-










Horber et al.,


1987) but no data are available concerning strength training


results in HTR.


Weight gain after Tx is typical for most HTR (Keteyian et al.,


1989) but


little information is available to indicate whether the gain is fat or fat-free


tissue.


Keteyian et al.


(1989) observed an average


kg increase in total


bodyweight


immunosuppression


months

therapy


after

with


HTR


cyclosporine,


receiving

azathioprine


triple
and


prednisone.


A significant increase in bodyweight was found in all patients,


independent of preTx weight and participation in a


postT


to 12-week


exercise training program.


The conclusions that can be drawn from these


data, however, are limited by the fact that body composition analysis was

not performed before or after the rehabilitation programs.

Kavanagh and coworkers (1988) report a 5.0 and 1.3 Kg increase in total


bodyweight


moderately


high


compliant


HTR,


respectively,


participating in a 16 month walk/jog exercise program.


Body composition


analysis


with


skinfold


measurements


revealed


that


body


had


increased significantly but lean mass increased an average of


patients.
induced


2 Kg for all


The changes in body composition were accompanied by training


increases


in VO2max


(mean


ml/kg/min),


peak


heart


rate


(mean


there


13 beats/min) and peak power output (mean 49 watts).


are several


possible explanations


these


respon


Although
e authors


speculate that the increase in


performance could largely be attributed


strengthening


muscles.


The


authors


conclude


that


because










physiologic


functional


potential."


Unfortunately,


strength


measurements


were


included


their


otherwise


excellent


exercise


training study.


Horber


associates


(1985,


1987)


have investigated


the impact of


regular


physical


training


on prednisone-induced


myopathy


clinical


populations.


Compared


with normal matched control subjects,


kidney


transplant patients had a 20% lower mid-thigh muscle area, a 36% increase
in mid-thigh fat-to-muscle ratio and a 20% lower peak torque output of the


thigh


musculature during


isokinetic strength


testing.


After


days of


isokinetic strength training, muscle area of the thigh increased,


the fat-to-


muscle ratio of the thigh decreased and mean peak torque reached normal


values.


These results have not been replicated in HTR.













CHAPTER 3
METHODS

Subjects


Eleven patients (n=10 males


n=l female)


who underwent Tx surgery


at Shands Hospital, Gainesville, Florida,


study.


volunteered to participate in the


Tx had been performed according to the techniques described by


Baumgartner et al.

cardiomyopathy (
while one patient


(1990).


The original indications for Tx were idiopathic


patients)


ischemic


was a retransplant.


cardiomyopathy


patients


patients)


averaged 50.1+13


(meanSD) years of age (range=21-63 years) and they were studied 18.7+11.7
(meanSD) months after cardiac Tx (range=7-41 months).


Preliminary


creening


HTR


was


performed


clinical


onnel


from


Shands


Hospital


Heart


Transplant


Team.


Contraindications


coronary
evidence


artery


to participate


disease


donor


since


organ


Study

biopsy


rejection


requiring


included


or physical


therapy


a history


examination


since


supplemental oxygen therapy; 4) evidence of significant renal dysfunction;
and, 5) significant cardiac, pulmonary or orthopedic complications during


graded exercise testing.


Those HTR that appeared suitable for the


study


were invited to the Center For Exercise Science for further screening. All
I- lV lT/'DK ..nr rnr-l sr"ll'., rvi-.4kln ^- iy^1, .rl na ^^/1'v<^ firv anrn'ttrnrmw~rrf~c^a ~l ^1 dnnMo"tr










cyclosporine,


prednisone and azathioprine while two


HTR


were treated


with cyclosporine and prednisone.


Four of the HTR were receiving non-


thiazide


"loop"


diuretics


furosemidee)


fluid


retention


were


receiving


antihypertensive


drugs


mild-to-moderate


hypertension.


Antihypertensives included clonidine (3 pts),


nifedipine (6 pts),


captopril


(3 pts)


and enalapril (8 pts).


No beta-blockers or other cardiac medications


were


used


HTR at the time of the study.


It was deemed


unsafe to


withhold antihypertensive medications in certain HTR, therefore, all HTR


were instructed to comply with


their usual protocol of daily medications


during the study and on the days of experiments.
The control group consisted of 11 subjects that were selected to match


the HTR,


as closely


as possible,


with respect


age,


gender


and


body


composition.


They


were


normally


active


athletic


and


evidence


cardiac


or pulmonary


disease


as determined


clinical


examination, pulmonary screening and graded exercise testing.


None of


control


subjects


were


receiving


medication


at the


time


study.
All subjects were required to report to the Center For Exercise Science

for experimental testing on two days separated by a minimum of 72 hours.


The series of tests on


the first day habituated subjects to the laboratory


procedures, measured


body


composition,


pulmonary function and


peak


heart rate,


power output, systemic oxygen


consumption, neuroendocrine


activity


provided


exercise


intensity


criteria


to be


used


during










thirds of the previously determined peak power output.


All subjects were


asked


restrict


strenuous


physical


activity


hours


before


experiments and report to the laboratory 2-3 hours postprandial.


Day 1v


Experimental Protocol


Orientation


Upon arriving at the Center For


Exercise Science, the entire research


protocol and the inherent risks were outlined to the subject.


The protocol


was


approved


Institutional Review


Board


protection


human


subjects


at the


University


of Florida


College of Medicine.


subjects provided their written informed consent (Appendix) to participate


in the study.


The subjects then completed questionnaires that dealt with


demographic information, cardiovascular


health,


physical activity status


and smoking history.
Body Composition Analysis


Body


composition


was


then assessed anthropometrically from the


sum of seven skinfold


sites (chest,


axilla,


triceps,


subscapula,


abdomen,


suprailium and thigh) measured on the right side of the body with a Lange


skinfold caliper (Cambridge Scientific Industries,


Cambridge,


Md.).


methods


used


taking


kinfolds


have


been


outlined


Pollock


Wilmore (1990).


Subcutaneous fat was measured by grasping a skinfold of


firmly


thumb


and


index


finger.


The


caliper


was


held


perpendicular


to the


fold


at approximately


cm from


thumb


nra~fi ne-rawo


Thei maimer' arnr TA72aC fho-n rcolcacrI- cn\ +-h2- fba~ ^ili fonmcinn 1A72C








48

0.00043499 (sum of 7)+0.00000055(sum of 7)2-0.00028826(age)(Jackson and


Pollock


1978);


and


females:


.0970


-0.00046971(


sum


7)+0.00000056(sum


of 7)2-0.00012828(age)(Jackson et al.,


1980).


The Siri


equation


(Siri,


1961)


was


then


used


to estimate


percent


where


fat=((4.950/Db)-4.50)


x 100.


Height was measured to the nearest 0.1 cm on


wall-mounted


Harpenden


stadiometer


(Psister


Import,


#98-602,


Carlstadt, NJ) and weight to the nearest 0.1 Kg on an Acme Medical Chair

Scale (model 4000-0030, San Leandro, Ca.).


Pulmonary Function


Tests


Pulmonary function tests were performed before and after


Before


the pulmonary tests


were


performed in


Lung Station at Shands


Hospital


part


routine


preT


evaluation


using


Collins


Pulmonary Module (model Apex DS/620,


Braintree, Ma).


All pulmonary


function


tests


completed


after


were


performed


Center


Exercise Science using a Medical Graphics Corporation pulmonary testing


unit


(model


1070,


Paul,


Mn.).


The


unit


consisted


pneumotachometer,


analyzers, computers and


software necessary in


measurement


pulmonary


spirometry,


lung


volumes


diffusion


capacity.


Pulmonary measurements were compared with reference values


derived from prediction equations based on individuals randomly selected


from


the general population


(Crapo et al.,


1981


Miller et al.


, 1983).


pulmonary function test values before and after


Tx were calculated using


the same gender specific prediction equations with appropriate corrections










the neck extended.


The investigator demonstrated


the proper technique


before all maneuvers and the subject performed a practice test.


Repeated


trials of all tests were performed until two trials were in close agreement.


The


means


these


two


trials


served


as the


criterion


value.


Verbal


encouragement was


given


to help


the subjects


perform


procedures


properly.


Pulmonary


generate
volume


values


in one


spirometrv


forced


second


vital


(FEV1).


flow-volume


capacity


The


(FVC)


loop
and


flow-volume


was


forced


loop


used


expiratory
t involved


having the subject inspire maximally and then exhale forceably to residual


volume

volume


followed


a maximal


measured


inspiration.


on complete


The


expiration


FVC


after


largest
deepest


inspiration.


The reference FVC


values for males and females respectively


were calculated with the following equations (Crapo et al.,


1981):


males:


'NC


= (0.06000


x height)


- (0.0214


x age)


- 4.650; and females: FVC


= (0.0491


height)


- (0.0216


x age)


- 3.590.


The FEV1 is the volume of gas expired over


a one second interval during the performance of a FVC.


FEV1i


The reference


values for males and females respectively were calculated with the


following equations (Crapo et al.,


1981):


males: FEV1i


= (0.0414


x height)


(0.0244


x age)


- 2.190; and females: FEV1i


= (0.0342


x height)


- (0.0255


x age)


1.578.


Pulmonary


diffusion


capacity.


The single-breath technique was the


method


choice


used


measure


pulmonary


diffusion


capacity










measured


with appropriate correction for the subject'


hemoglobin level


on the day of the pulmonary function tests (Cotes and Hall,


1970).


After exhaling maximally the subject rapidly filled their lungs with a


4-gas diffusion mixture containing 0.5


neon (Ne)


carbon monoxide


(CO)


oxygen (02) and


78.2%


nitrogen (N2).


The subjects held their


breath for 9-10 seconds and


then exhaled


completely


. A minimum of 7


minutes was allowed between DLCO trials to insure adequate washout of


the diffusion gas mixture.


The DLCO was recorded in milliliters of CO


diffused


minute


millimeter


mercury.


The


milliliters


transferred is the difference in concentrations of CO in alveolar gas at the


beginning and end of the


10-second breath holding interval.


DLCO was


calculated according to


the procedure described by


Ruppel


(1975).


reference DLCOsb values for nonsmoking males and females respectively


were calculated


with the following equations (Miller et al.,


1983):


males:


DLCOsb


= 12.9113


- (0.229


x age) + (0.418


x height);


and females: DLCOsb


2.2382


- (0.1111


x age) + (0.4068


x height).


Alveolar


volume (VA) was also estimated during the diffusion test


by using inert and insoluble Ne


the diffusion mix.


values


were


considered


estimates


total


lung


capacity


(TLC


and


they


were


subsequently used in all calculations requiring total lung capacity values.


The


reference


TLCsb


values


males


females


respectively


were


calculated with the following equations (Miller et al., 1983):


males:


TLCsb


(0.1930


x height)


- (6.6896); and females: TLCsb


= (0.


1641


x height)


- (5.4404).










respectively were calculated


with


the following equations


(Miller


et al.,


1983):


males: DLCOsb/TLCsb


= (10.0882


- (0.0570


x height)


- (0.0309


x age);


and females: DLCOsb/TLCsb


= (8.3297


- (0.0460


x height)


- (0.01


x age).


Symptom Limited-


Graded Exercise Test


Before


symptom


limited-graded


exercise


(SL-GXT),


each


subject


underwent


physical


and


cardiovascular


examination


administered by


a physician.


Those subjects deemed suitable were then


prepared


undergo


SL-GXT


Combi


stem


5HR


electromagnetically braked cycle ergometer (Combi/Mitsui Co.,


Cleveland,


OH).


SL-GXT'


were


supervised


a physician


trained in


graded


exercise testing.


A crash cart with all necessary emergency medications,


supplemental oxygen and a defibrillator was immediately adjacent to the
cycle ergometer during every SL-GXT.


A short 20 or


gauge polyethylene cannula was inserted into an


antecubital


vein


under


aseptic conditions and


kept open


filling the


catheter with dilute heparinized saline.


milliliters of venous blood


After a 30 minute seated rest,


was drawn into a single plastic syringe and


immediately separated into individual aliquots for norepinephrine (NE),
arginine vasopressin (AVP), plasma renin activity (PRA), atrial natriuretic


peptide (ANP),
section entitled


angiotensin II (ANG II) and aldosterone (ALDO) assays (see
, "Blood Sample Collection").


Subjects then rested supine while blood pressure was measured by


auscultation


using a standard mercury sphygmomanometer.


Heart rate










lead placements were then moved


to abbreviated


positions on


the torso


and subjects returned to a seated position where blood pressure and a 1


lead


ECG


were


again


recorded


before


and


after


seconds


hyperventilation.


Measurements of heart rate and


blood


pressure with


the subject seated prior to mounting the cycle ergometer were considered


criterion baseline values.


Subjects were then seated on the cycle and the


seat height was adjusted so that the legs were in a position of slight flexion


at the nadir of the downstroke.


After a 5 minute rest, blood pressure and a


12-lead ECG were again recorded.


If blood


pressure exceeded


180/100


mmHg or if any significant ECG


abnormalities were evident during the


series of measurements made at rest such as life-threatening arrhythmias,


ST segment depression that was


1mm horizontal or downsloping, or 2mm


upsloping 0.08


other


ECG


seconds


patterns


from


associated


J-point, ST


with


significant


segment elevation,


cardiovascular


or any
disease,


subjects


were excluded


from


the study


(see


Appendix


"Criteria for


Exclusion of Subjects").


The SL-GXT


was a continuous, multistage protocol with an increase


in resistance every minute


until


the subject reached


voluntary maximal


exertion or became symptomatic with


positive hemodynamic or medical


indices. The test began with 5 minutes of quiet rest while the subject sat
on the cycle. The transition from rest to the predetermined initial exercise

stage was slow, with intensity increasing in a ramp-like manner during a
period of 1 minute. The initial exercise power output was 20 watts for the








53

every minute by 10 watts for the HTR and 20 watts for the control subjects


in an attempt to bring about exhaustion within an 8-12


minute period.


12-lead ECG and rating of perceived exertion (Borg, 1962) was recorded at


each


one-minute


interval.


Blood


pressure


was


measured


during the last 20 seconds

supported at chest level.


at 2 minute intervals


with


the subjects


arm


One


minute


collections


expired


air were


taken


in neoprene


meteorological balloons during the final 3-4 minutes of exercise for the
measurement of peak systemic oxygen consumption (VO2), expired carbon


dioxide (VCO2) and expired pulmonary ventilation (VE).


Samples of the


expired gasses were analyzed by a mass spectrometer (Perkin-Elmer, MGA


model


1100)


for fractional concentrations of oxygen and


carbon dioxide.


The mass spectrometer was calibrated


with


samples


of known


concentrations.


Expired volume was measured with a 120 L


compensated spirometer (Collins)


corrected


Tissot chain-


to STPD conditions for


VO2 calculations as described previously by Consolazio et al. (1963).


Subjects


were


verbally


encouraged


to continue exercise


as long


possible.


The test was continued until a pedal frequency of 60 rpm could


not be maintained.


Immediately upon completion of the test another


milliliter venous blood sample was drawn from the indwelling catheter.
During the first two minutes of recovery, subjects continued to pedal at a


rate


40-50


rpm


with


zero


resistance.


After


two


minutes


active


recovery on the cycle, the subjects were seated in a chair and heart rate and










Experimental Protocol


Subjects reported


to the Center


Exercise Science for the second


series of experiments a minimum of three days after Day 1.


Day 2 exercise


tests were performed at approximately the same time of day (12:00-3:00


pm) as


the SL-GXT


on Day


in order to control for a possible effect of


circadian rhythms.


Environmental conditions within the laboratory were


maintained relatively


constant at 22-23C


56-62%


relative humidity and


760-765 mmHg barometric pressure during the course of all experiments.
To determine the temporal pattern of cardiac hemodynamics, ABGs

and neuroendocrine activity during exercise, each subject was studied at


levels of exercise intensity


on the same electronically


braked


cycle


ergometer (Combi 5RH) used during the SL-GXT


. Cardiac output, ABG


and neuroendocrine measurements were made at rest and during two


minute


periods


constant


load


cycle exercise.


The


submaximal


exercise tests were separated by 20 minutes of seated rest.


The relative


exercise intensities selected for the study were


1) 40


and 2) 70


of the


peak power output (Watts) achieved during the SL-GXT


on Day


. These


power


outputs


were


chosen


because


they


represent


light


vigorous


exercise intensities, respectively.


It was felt that 40% of peak power output


would increase neuroendocrine activity moderately and 70


was expected


to increase neuroendocrine activity to a significantly higher level.


Using


heart rate to establish exercise intensity was considered inappropriate in


HTR.


The linear relationship between heart rate and VO2 cannot be used








55

experiments (Barr et al., 1964) have shown that subject apprehension often

alters the normal breathing pattern and thus may influence the behavior


ABG.


It was felt that the novelty


of using the


breathing valve


attached headgear as well as the elevated resistance to airflow introduced


by the rebreathing


valve


might


alter


respiratory


rhythm


and ABG


measurements.
Subiect Preparation


Each


subject


was


prepared


with


a radial


artery


catheter


nondominant


arm


physician


trained


technique.


The


dependent limb was examined by the Allen Test prior to catheter insertion


to insure adequate collateral


(ulnar


artery)


circulation


to the


hand


fingers.


After


aseptic preparation


with


Betadine


swabs


injection of 1


Xylocaine was administered for local anesthesia and a 20-


gauge arterial cannula was placed percutaneously in the radial artery. A
three-way stopcock and 3 inch t-connector were fastened to the catheter


kept


patent


with


dilute


heparinized


saline.


This


instrumentation


permitted


frequent


arterial


blood


sampling


to determine


temporal


pattern of ABGs and plasma levels of NE,


AVP


PRA


ANP


ANG II and


ALDO during exercise.


physician


was always present to direct their


attention


exclusively


to the


blood


sampling


condition


subject.


After placement of the arterial catheter,


subjects remained seated for


20 minutes while four Mylar strip electrodes (3M Co.,


St. Paul


, Mn.) were










lower.


Cardiac output data


were obtained from


the electrodes using a


Minnesota


Impedance


Cardiograph


and


Surcom


Cardiographic


microcomputer (model 7000,

(1966).

Submaximal Cycle Test


MPLS, Mn,) as first described by Kubicek et al.


Each submaximal exercise test was preceded by


10 minutes of quiet


with


subject


seated


on the


cycle.


After


period


Impedance Cardiography measurements


were made and


blood samples


were drawn


baseline


ABG,


hematocrit


(Hct),


hemoglobin


(Hb)


neuroendocrine hormone analysis.


Thus, there was a total of 30 minutes


between


catheter


insertion


withdrawal


first


blood


samples.


After


collection


final


resting


blood


sample,


subject


began


pedalling


at 60


revolutions


minute


with


desired


resistance


preselected,


peak


power


output


(Watts).


Impedance


Cardiography measurements (in


triplicate)


and blood samples for


ABG


analysis (1.5 ml) were taken every 30 seconds during the first 5 minutes of


constant load


exercise


at minute 6


8 and


during


second 5


minutes of the exercise bout.


Blood samples for neuroendocrine hormone


analysis (8 ml) were drawn at minutes


4, 6,


10 during exercise.


The blood sampling periods were chosen to allow detection of any possible


ABG


or plasma


neuroendocrine


hormone


alterations


that


might


occur


during the transition from rest to exercise and during sustained constant


load exercise.


A small portion of blood (< Iml) was also drawn before and








57

second cycle test at 70% of peak power output also began with the subject


seated quietly for


10 minutes on the cycle, thereby providing a total of 20


minutes


seated


recovery


between


tests.


The


same


pattern


data


collection as described above was repeated during the second


ride at 70


10 minute


of peak power output.


Cardiac output.


Cardiac output was non-invasively estimated at rest


and during submaximal exercise with the Impedance Cardiograph.


This


tonometric


technique evaluates changes in


the electrical


conductivity


thorax


that


result from


pulsatile changes


in thoracic


blood


volume


caused by velocity and volumetric variations in aortic blood flow during


the cardiac cycle.


Measured changes in impedance (Ohms) during systole


used


to estimate


stroke


volume


calculate


cardiac


output


(Kubicek,1966).


imperceptible


constant


sinusoidal


current


milliamperes with a frequency of 100 kilohertz is introduced through the


outer


electrodes.


inner


electrodes


detect


impedance


voltage


changes


during


cardiac


cycle.


The


impedance


signal


modified by variations in the velocity and volume of aortic blood during


the cardiac cycle.


The average of 4-6 cardiac cycles was used to estimate


cardiac output at rest and 2-3 cardiac cycles were averaged for each cardiac
output estimate during exercise.


Maximal Strength


Testing


After the submaximal cycle ergometer experiments were completed,


arterial


catheter was


removed


the subject rested in


chair for








58

was defined as the maximum weight that could be lifted for one repetition


of the movement (1-RM).


Subjects


were positioned in


tensiometer


chair and the back rest was adjusted so that the axis of rotation about the


knee extended approximately


5 cm beyond the edge of the chair.


The angle


of the back rest was fixed at 110 with respect to the seat.
secured in place with a seat belt placed around the pelvis.


Subjects were
During each


contraction, subjects were required to maintain contact with the back rest
and to hold onto hand grips located on each side of the seat.

Each testing session began with the subject performing a warm-up set


of 6-8 repetitions with a light weight.


Two minutes of rest were given


between the warm-up and the start of the 1-RM test.


The initial 1-RM was


standardized among subjects and represented approximately one-third of


their body weight.


When the weight was successfully lifted through a 120


range of motion (ROM=60


to 180


next trial was incremented by


of knee extension) the weight for the


3 to 9 kg.


1-RM trial was considered


successful if the weight was lifted within 10


of full extension to allow for


compression


pads


tissue.


The


increments


weight


were


dependent upon the effort required for the lift and became progressively


smaller


as the subject approached


1-RM.


Two


minutes of recovery


time were allowed between 1-RM attempts.


The last weight successfully


lifted


through


ROM


was


considered


1-RM.


Most subjects


reached their


1-RM in 3 to


5 trials.


Blood Sample Collection








59

venous blood was obtained in a SL-GXT and 75-80 ml of arterial blood was


drawn in a typical submaximal


10 minute cycle test and recovery period


for a total of 150-160 ml of arterial blood on Day


Blood samples were


drawn after aspirating and discarding the contents of the catheter and T-


connector dead space (~


ml).


Each ABG sample was uniformly drawn


under


anaerobic


conditions


using


a small


heparinized


plastic


syringe.


After the ABG sample was drawn, the syringe was immediately


capped and stored on ice until analysis.


Immediately before and after each


exercise


test a small


portion


blood


sample


was


placed


75mm


coated glass capillary tubes (duplicates) and centrifuged for measurement


of Hct and Hb.


Blood samples for neuroendocrine hormone analysis were


withdrawn into a plastic syringe containing no additives and immediately


separated into individual aliquots.


Blood for NE assay (2


ml) was added to


chilled


heparinized


vacutainers


containing


40 microliters


antioxidant


consisting of ethylene glycol-tetraacetic acid (EGTA,


90mg/ml) and reduced


glutathione (75mg/ml)(Sigma


Chemical).


Blood for


AVP


PRA


ANG II


ANP


assay


was


added


a chilled


vacutainer


containing


ethylene diamine-tetraacetic acid


(EDTA).


Blood for


ALDO assay (4 ml)


was


added


a vacutainer


containing


no additives


room


temperature for 20 minutes.


The blood samples were immediately mixed


and plasma or serum was separated by centrifugation at 2,200


x g at 4C for


20 minutes.


The plasma or serum


was


then


pipetted


to polypropylene


tubes which were frozen at either -40C


(AVP, PRA, ANP) or -80


(NE,









Blood Sample Analysis


Blood gas analysis.


ABG and pH analysis were performed on a Nova


5 ABG and acid-base analyzer (Nova


Biomedical,


Waltham, Mass.).


The instrument autocalibrated


using precision


gasses


buffers


after


each sample was analyzed.


ABG samples were kept on ice until analysis


determinations


were


performed


within


minutes


after


sample


collection.


Vasopressin


radioimmunoa


ssav


. Plasma AVP


was


measured


radioimmunoassay


using


a rabbit


anti-AVP


antibody.


The


anti-AVP


serum


was


generated in


the laboratory


of Dr.


Wood


, Department of


Physiology, University of Florida,


using AVP (Sigma Chemical) covalently


linked to bovine thyroglobulin with carbodiimide.


The crossreactivity of


antiserum


with


lysine


vasopressin


was


0.7%


Crossreactivity


with


oxytocin,


vasotocin, AVP (fragment 4-9),


CRF


ACTH


, angiotensin I,


angiotensin


was each


<0.001


AVP was


extracted


from


plasma


adsorption


to bentonite.


Plasma


was


extracted


and


then


reconstituted to 0.


ml with assay buffer (0.05 M phosphate buffer,


pH=7.4


containing
Wilmington,


EDTA


and


0.2%


DE.) was used as tracer.


from 0.05 to 10 pg/tube.


BSA).


125I-AVP


(Dupont


The range of the standard curve was


In previous studies using this assay


the intraassay


coefficient of variation (CV) for a low pool (0.40 pg/tube) was 4


and for a


high pool (4.0 pg/tube) was 14


Interassay CV was


(0.35 pg/tube).


Plasma renin activity radioimmunoassav


. PRA was measured using


--S. -










phosphate buffer (1:1.1


dilution of the sample) and protease activity was


inhibited


addition


of phenylmethylsulfonyl flouride


ethanol,


1:1.01 dilution; Sigma Chemical).


ANG I was generated for


.5 hours.


generation was linear over the total time of the incubation.


ANG


I was


measured by radioimmunoassay using rabbit anti-ANG I generated in the


laboratory


Phillips,


Department


Physiology,


University


Florida.


The range of the standard curve was from 0.078 to


5 ng/ml.


PRA


was


expressed


as the


rate of


generation


ANG


at 37


minus


generation of ANG I at 0 C.


In previous studies from this laboratory the


interassay CV


was 24.4


and the intraassay CV


was


The relation


between the PRA results using the present assay and PRA results using a


kit from


Clinical


Assays


(Baxter


Healthcare,


Cambridge,


Mass.)


are as


follows: Clinical Assays kit


= (present assay)


x (0.700.06); r2


= 0.93.


Atrial


natriuretic


peptide


radioimmunoassav.


ANP was extracted


from thawed plasma samples using SepPak Cg18 (octadecyl silica) cartridges


(Waters


Associates)


which


been


wetted


prewashed


with


5 ml


methanol


, 5 ml 1% triflouroacetic acid (TFA),


methanol/H20/TFA


(80:19:1) and 5 ml


1 ml 1


TFA.


polypep solution, 5
The samples were


acidified with an equal volume of 1


TFA and applied to the cartridges.


The cartridges were then


washed with


5 ml


TFA/I


NaCL and


ANP was eluted with 3 ml methanol/H20/TFA (80:19:1).


The eluate was


dried down under air at


The radioimmunoassay procedure was begun by reconstituting the










(rat)


(New


England Nuclear


Research


Products).


The


rabbit anti-ANP


serum


was generated in the laboratory of Dr. I. Phillips,


Department of


Physiology, University of Florida.


Antibody was added to the standard or


samples and incubated for 24 hours at +4 C. Iodinated ANP was then
added and incubated an additional 24 hours at +4 C. Bound ANP was


precipitated


with


goat-anti-rabbit


antiserum


and


normal


rabbit


serum


(both from Biotek Research) by a


2 hour incubation at room temperature.


The samples


were


centrifuged


at 2,000


30 minutes


at +4


, the


supernatant was discarded and


the precipitate was counted in a gamma


counter


(model


5500


, Beckman).


Counts


per minute


from


gamma


counter were fed directly into a DP5500 Beckman data reduction system


program


logit-log


method


analysis


developed


Rodbard


and


Leward (1970).


This program calculates the best fit straight line by use of


the linear regression


statistical method.


The


recovery


ANP


above extraction procedure was found to be 876


and the data presented


in this study have not been corrected for the recoveries.


Aldosterone


radioimmunoassav.


Plasma ALDO concentration


was


measured


RIA


in unextracted


serum


using


a kit


from


Diagnostics


Products Corp.,

polypropylene


Los Angeles, CA.


tubes


coated


Serum samples (0.200 ml) were added to


with antibodies


to ALDO.


1251


aldosterone tracer was added to the tubes and after a 3 hour incubation at


the supernatant was decanted and


the tubes counted on a gamma


counter.


ALDO concentration


was determined from


a standard


curve.










Aneiotensin II radioimmunoassav.


Plasma ANG II was measured by


RIA after extraction


on bentonite.


This assay


been


described more


fully elsewhere (Ben et al.,


1984


Raff et al.


, 1985).


The antiserum used has


than


1.0%


cross-reactivity


with


ANG


was


generated


laboratory


Wood


, Department


Physiology,


University


Florida.


Norevinephrine.


Plasma


concentrations of NE


were measured


high


performance


liquid


chromotography


(HPLC)


(ESA


Coulochem,


Bedford


/, MA).


was


extracted


adsorbing


plasma


samples


onto


alumina.


After washing the adsorbed alumina


was eluted from


the alumina


with


by treating it with an


buffer solution

acid solution.


3. 4-


Dihydroxybenzylamine


(DHBA)


was


used


as an internal


standard


extraction


efficiency


of NE


DHBA


was


based


on the extraction


known standards.


All NE samples were corrected for percent recovery


After extraction,


the NE samples were assayed


by injecting the samples


onto a reverse-phase C18 column.


An ESA 16-channel Coulochem multi-


electrode array detector was used to determine the concentration of NE in


the samples.


The within-assay CV was 1


Cvclosporine


radioimmunoassav


and the between assay CV was


Cyclosporine concentrations were


measured in whole blood specimens by Flourescent Polarization using an


Abbott


TDX


Flourometer


(Abbott


Laboratories,


Abbott


Park


cyclosporine was labelled with fluorescein to obtain fluorescent properties


Il).










recovery from samples was 95


and the samples were not corrected for


recovery.


Hematocrit and Hemoglobin.


Hct and Hb determinations were made


with a QBC II Centrifugal Hematology system (Becton Dickinson, Flanklin


Lakes, NJ.).


The QBC II method used flourescence measurements of blood


cells treated with fluorochrome acridine orange and the density gradient
layering of blood cells to measure the volumes of red cells, white cells and


platelets.


Layer


measurements


were


used


compute


Hct.


concentration


was derived


from


Hct and


measurements of red


density


as previously


described


Wardlaw


Levine


(1983).


percent change in plasma volume during each exercise test was calculated


from


preexercise and


postexercise Hct values (Van


Beaumont et al.


1973).


Statistical Analysis


Descriptive


characteristics


knee


extension


strength,


pulmonary


function


SL-GXT


measures


were


compared


between


groups


using


analysis of variance (ANOVA).


ANOVA


was also used to compare pre-


and postTx pulmonary function measures in the HTR.


Pearson


product-moment correlation coefficients


were calculated


determine the relationships among


cyclosporine


level


/, smoking history


pulmonary


diffusion


capacity,


changes


arterial


partial


TTnrcc1r1> fnTr nwv7oun diirina' 0oVoC1








65

measures was used to analyze the temporal pattern of all cardiodynamic


variables


ABGs and neuroendocrine hormones.


Initial baseline criterion


measures were used as the covariates.


When a statistically significant time


effect and/or group by time interaction effect was observed,


within group


comparisons


between


discrete


time


points


and/or


between


groups


comparisons at each time point were done using ANCOVA


with contrast


analysis for obtaining appropriate post hoc custom hypotheses tests.


statistical


analyses


were


completed


using


SAS


statistical


program.


An alpha level of p<0.05 was required for statistical significance.














CHAPTER 4
RESULTS

Descriptive Characteristics


The physical characteristics of HTR and control groups are presented


in table 1.


The two groups did not differ (p>0.05) with respect to age (50.4


vs 50.1


yrs),


height (178


vs 176 cm) and weight (85


.5 vs 85 kg).


Though the


groups did not differ significantly in body


composition, HTR had more


body fat (27
subjects (61.5


vs 24


.7%


) and less lean body mass (LBM) than the control


vs 63.7 kg).


Leg Strength


One repetition maximum (1-RM)


leg strength


values are also shown


table


1-RM


bilateral


knee-extension


strength


was


significantly


(p0.05) greater in the control group (95.0


vs 66.1 kgs).


When 1-RM was


calculated in relative terms ie.


, weight lifted per unit of LBM, the control


group was also significantly (p<0.05) stronger than HTR (3.28


vs 2.


39kg


lifted/kg LBM).

Responses During the Symptom Limited-Graded Exercise Test


Hemodynamic Changes
Baseline and peak exercise values for heart rate and blood pressure


n I a n


S -~* CT flfl, j.11 a










exercise heart rate in HTR was
a significantly higher (p<0.05)


57%
149S


higher than at baseline compared with
Increase from baseline in the control


group.


Mean chronotropic reserve for HTR was 53 beats/min compared to


100 beats/min for the control group(p<0.05).
Resting systolic blood pressure did not differ (p>0.05) between the two


groups (126


vs 126 mmHg).


Peak systolic blood pressure was


higher


(p<0.05) in the control group than in HTR (218


vs 190 mmHg).


Diastolic blood pressure at rest (90


vs77


mmHg) and at peak exercise


vs 76 mmHg) was significantly higher (p0.05) in HTR.


The change in


mean diastolic blood pressure from rest to peak exercise was -0


mmHg


control


HTR,


respectively,


change


during


exercise was not significant between groups (p0.05).


The rate-pressure product (peak HR


x peak SBP


x 10-2) at peak exercise


was 31


greater (po<0.05) in


the control group compared to HTR (369 vs


280).
Cardiorespiratorv Resoonses


Peak


cardiorespiratory


responses


during


SL-GXT


are further


summarized in table


The peak


VO2 achieved by HTR was


57%


of the


peak


attained


control


group


(18.3


vs 32.


ml-kg-1.min-


1)(p<0.05).


The dissimilarity in peak VO2 was further reflected in the peak


power output (Watts) at termination of the SL-GXT


with HTR achieving a


peak


power


output value that was


that


attained


by the control


group (109


vs 198 watts)(p<0.05).










(1.17 vs


1.15 for the control and HTR, respectively).


Peak expired carbon


dioxide (VCO2) (3.10 vs 1.73 1-min-1) and peak pulmonary ventilation (VE)


vs 69


1-min-


1)were also significantly higher (p<0.05) in the control


group with HTR achieving mean


VE values that were 71


of the control


group


value.


Peak


ventilatory


equivalent


VO2


(VE/V02)


was


significantly greater (p<0.05) in HTR (45


vs37


1-min


-1) indicating that


HTR


ventilated


more


a given level


oxygen


uptake


than


controls.


Neuroendocrine


Responses


Measurements


serum


aldo


sterone


(ALDO)


and


plasma


renin


activity


(PRA),


vasopressmn


(AVP),


atrial


natriuretic


peptide


(ANP),


norepinephrine (NE) and angiotensin II


(ANG II) were made at rest and


immediately


after the SL-GXT


. Baseline and


neuroendocrine hormones during the SL-GXT


peak concentrations of the
are presented in table 4.


The changes in ALDO and ANG II concentrations from rest to peak


exercise are shown in figure 1.


Baseline serum ALDO was not significantly


different (p>0.05) between the two groups (164.9


vs 119.9 pg/ml for HTR


and control


, respectively).


Serum ALDO values at peak exercise (300.1 and


241.4 pg/ml for HTR and control groups respectively) were significantly


greater


(p<0.05)


than


baseline


both


groups


group


time


interaction was not significant (p>0.05).


Baseline


between


plasma


ANG


the two groups


was


(4.1 vs 2.


significantly


7 pg/ml)


different


but HTR exhibited


(p>0.05)
a trend










greater (p>0.05) than in


the control group.


Peak exercise ANG II


values


reached 12.


1 and 12.5 pg/ml for HTR and control groups, respectively.


Baseline concentrations of plasma AVP were elevated in HTR (4.2 vs
2.8 pg/ml) compared to the control group but the difference did not reach


statistical


(p<0.05)


significance


both


(p=0.06).


groups


Plasma


during


AVP


increased


SL-GXT


significantly


increase


was


significantly greater (p<0.05) for HTR (


.3 and 16


.7 pg/ml at peak exercise


for HTR and control groups,


respectively).


Baseline PRA (8.3


(42.9


vs 1.5 ng/ml/hr) and plasma ANP


vs 18.1 pg/ml) were significantly higher (p<0.05)


the control group.


concentrations


in HTR compared to


Both groups significantly increased (p<0.05)


PRA and


ANP concentrations at peak exercise but the magnitude of increase in PRA


(200


vs 87 %) and ANP (221


vs 163 %) was greater (p<0.05) for HTR.


Plasma NE


at rest was


not significantly


different


between


groups


(0.478


vs 0.394


ng/ml)


HTR


demonstrated


a trend


toward


higher NE at rest (p=0.08).


NE at peak exercise was significantly higher


(p<0.05) than baseline for both groups but the increase in NE was greater


(p0.05) in HTR (7


vs 5 fold increase).


Pulmonary


Function


Tests


Pre- versus PostTransplant Pulmonary Function


The results of the


resting pulmonary function tests performed before


and after


Tx are presented in table 5.


One patient did not complete a ureT


n^










improvements


pulmonary


mechanics


were


observed


with


mean


increases of 14.4% in forced vital capacity (FVC) and 9.


in forced expired


volume in one


second (FEV1).


Total lung capacity (TLC) did not change


(p>0.05) in relation to


TLC values before


Tx (90.3 vs


of predicted


before and after Tx, respectively).


Pulmonary


diffusion


capacity


(DLCO)


also


improved


significantly


following


Tx (p0.05) with mean increases of 6.1


in whole lung DLCO


7.8% in DLCO per unit of total lung volume (DLCO/TLC).


Resting


PaO


(92.4 before vs


.2 mmHg after) and PaCO2 (35


.2 before vs 37.1


mmHg after) showed a trend toward improving after


were not significant (p>0.05)


Tx but the changes


. Given the increases observed in PaO2 and


PaCO2,


however,


alveolar


to arterial


gradient


oxygen


partial


pressure improved from 12.6 before to 3.3 mmHg after Tx.


The mean whole blood cyclosporine


concentration in HTR was 570


ng/ml


during the month


which


postT


pulmonary


function


was administered.


The correlation coefficient for the relationship between


the change in diffusing capacity from pre- to postT


and blood levels of


cyclosporine
relationship


was


between


significant


cyclosporine


(p=0.822)


(r=0.18)


immunosuppression


indicating


therapy


and


DLCO.


Furthermore,


significantly


correlated


the change in DLCO from


with


pre- to postT


*1


either patient age (p=0.335)(r=-0.34)


vas not
or the


number


months


postT


(p=0.792)(r=-0.10).


Additional


correlational


analysis did, however, demonstrate a high inverse relationship between










Although


general


pulmonary


function


was


improved


HTR


following


/, pulmonary function measures for


HTR


were significantly


(p<0.05) lower when compared to the control group.


Absolute and relative


of predicted) measures of diffusion capacity (DLCO, DLCO/TLC) and


pulmonary


mechanics


(FVC,FEV1)


were higher (p0.05)


the control


group compared to HTR, but total lung capacity (TLC) was not different


(p>0.05)


between


groups.


Pulmonary


function


values


PITh


following surgery and the control group are presented in table 6.


Responses During Submaximal Exercise


Relative Exercise Intensity


The means SEM of physiological parameters that were considered


valid indicators of


differences in relative exercise intensity between


two


groups


are shown


table


There


were


nonsignificant


(p>0.05)


differences between HTR and control groups for heart rate (% of heart rate


reserve),


rating of perceived exertion (RPE) and losses of plasma volume


A from rest) at the conclusion of each of the exercise conditions.


These


data indicate that the relative exercise stimulus during the submaximal
exercise tests was comparable between groups.


Arterial Blood Gas:


Transplant vs Control Groups


ABG data for one HTR and one control subject had to be rejected due


to technical difficulty with the ABG analysis machine.


Therefore, group


ARC


r1rmn1rincn 1c inrliiriA.


10 T-TTP ^,


1 A mn I-W -mi e, w'il-.nI/--cAb ,r










temporal


patterns


arterial


PO2,


PCO2


during


minutes of constant load cycle exercise at 40% of peak power output are


also illustrated in figure


Baseline PaO2


was not significantly


different


(p>0.05) between HTR and control groups.


During 10 minutes of constant


load cycle exercise at 40% of peak power output, arterial PO2


decreased


significantly


(p<0.05)


below


resting


values


within


minute


after


commencement of exercise in both groups.


PaO2 returned to values that


were not significantly


different


from


rest at


minutes


the control


group


PaO2


continued


to decrease linearly over time in HTR.


group by time interaction, however


was not significant (p>0.05).


Baseline


arterial


PCO2


levels


were


significantly


(p<0.05)


lower


HTR


and


continued to decrease during exercise with the temporal pattern of PaCO2

becoming significantly different (p<0.05) from baseline by 4 minutes after


onset


exercise


while


control


group


remained


isocapnic.


Nonetheless, the group by time interaction for PaCO2 was not significant


(p>0.05).


Arterial pH was similar (p0.05) at rest in both groups.


The pH


response during exercise was also similar (p0.05) with values decreasing

significantly (p<0.05) below resting values by the third minute of exercise
in both groups.
The temporal patterns of PaO2, PaCO2 and pH during 10 minutes of


constant load


figure 3.


cycle exercise at 70% of peak power output are shown in


Arterial PO2 decreased significantly (p<0.05) below resting values


within


minute


after


commencement


work


both


groups.


After










group


temporal


time


interaction


pattern


was


PaO2


significant


with


PaO2


(p<0.05)
values


with respect


HTR


to the


becoming


significantly


different


(p<0.05)


from


control


group


after


third


minute of exercise.


The group


by time interaction


was also significant


(p<0.05) with respect to the temporal pattern of PaCO2.


The magnitude of


decrease in PaCO2 values in HTR became significantly different (p0.05)
from the control group by 2 minutes of exercise and continued to decline

throughout the exercise bout. Arterial pH decreased linearly over time in


both groups and


was significantly


different (p0.05)


from resting values


after 2 minutes of exercise.


The group by time interaction for arterial pH


during cycle exercise at 70% of peak power was not significant (p>0.05).
Arterial Blood Gas Profile of the Transplant Group


Considerable variability was present in mean arterial P02, PCO2 and


values


during


both


submaximal


exercise


conditions


HTR.


further examine possible sources of variablility, HTR were separated into
groups; those with normal (NL-DLCO; n=5) and those with below normal


pulmonary diffusion capacity (LO-DLCO; n=5).


American Thoracic Society


guidelines


for pulmonary


function


testing were used


as the criteria for


group assignments (NL-DLCO70


of predicted reference values)(Miller


et al.


, 1983).


Individual HTR data for arterial PO2, PCO2 and pH during


exercise at 70


respectively.


Baseline


of peak power output are plotted in


These HTR


arterial


PO2,


data


were then


PCO


subjected


were


figures 4,
to further


significantly


5 and 6,


analysis.
different










group


time


interactions


arterial


PO2,


PCO2


were each


significant.


Arterial


PO2


LO-DLCO group


became significantly


(pS0.05) lower than the NL-DLCO group by 1.5 minutes after the onset of
exercise and continued to decrease over time, with PaO2 dropping below


70 mmHg in two HTR.


Arterial PCO2 in the LO-DLCO group decreased


significantly (p<0.05) more than


exercise and arterial


the NL-DLCO group by


pH dropped more rapidly in


3.5 minutes of


LO-DLCO group,


becoming significantly different from the NL-DLCO group by 4.5 minutes


after


commencement of


exercise.


Additional


correlational


analysis


revealed highly


significant inverse


relationships


between resting DLCO


transient


hypoxia


experienced


during


cycle


exercise


at 40


(p=0.014)(r=-0.94) and 70% (p=0.001)(r=-0.97) of peak power output in HTR.
Exercise Hyperpnea After Cardiac Transplantation


Additional


analyses of


ABG


alterations


during


transition from


rest to steady state exercise were performed on the NL-DLCO group and a


matched control group (n=5) to determine the effect of T


on pulmonary


ventilation in HTR with DLCO.


Figure


7 shows the ABG data for the NL


DLCO group and control group during cycle exercise at 40% of peak power.
The resting values for PaO2, PaCO2 and pH were not significantly different

(p>0.05) between groups. The absolute ABG changes during exercise did
not vary significantly (p>0.05) between the control and transplant groups.


Furthermore,


PaCO2 did


significantly


vary


(p>0.05)


from


baseline


values during exercise.


These data indicate that cardiac afferent reflexes










Cardiac Output


Cardiac output


data


one


transplant patient


to be


rejected


because the Impedance Cardiograph signal was not of sufficient quality to


enable any analysis to be performed.


Therefore, data from


the matched


control subject were also excluded from the analysis.


Because the control


and HTR


were closely matched


with respect to age, height and


weight,


cardiac output and stroke volume values are reported without correction


body


surface


area,


ie. cardiac


stroke


volume


index.


Absolute


values for cardiac output, stroke volume and heart rate during the two


submaximal testing conditions are shown in tables 10 and 11.


The relative


changes (%A from


baseline)


in cardiac output, stroke volume and heart


rate during exercise at 40% of peak power output are illustrated in figure 8.


Baseline


cardiac


significantly
control and


HTR,


output
(p<0.05)


was


than


respectively).


within


normal


the control group


Both groups


range


(4.94 and


increased


HTR


4.58 for the


cardiac


output


significantly (
commencement


)S0.05)


above


exercise


resting


reached


values w

?d values


within


seconds


10th


after


minute of


exercise that were


109 and 94


greater than baseline for the control and


HTR,


respectively.


Consistent with


results


from


SL-GXT


baseline


heart rate was significantly higher (p<0.05) in the HTR (105 vs 74 bpm).
Both groups increased heart rate significantly (p0.05) above baseline at all

measurement periods but the magnitude of increase was greater (p<0.05)


in the control group.


The peak increase in heart rate during cycle exercise








76

significantly (p<0.05) above baseline after 30 seconds of exercise in HTR but

stroke volume in the control group did not become significantly greater


(p<0.05)
exercise.


than


baseline


until


minutes


after


Stroke volume during exercise at 40%


commencement


of peak


power


output


increased 38 and 61% above baseline in the control and HTR, respectively.


Relative


increases


(%A


from


baseline)


cardiac


output,


stroke


volume and heart rate during 10 minutes of constant load cycle exercise at


70% of peak
significantly


power output are shown in figure 9.


increased


(p<0.05)


above


baseline


Cardiac output was


both


groups


at each


measurement period.


increase in


cardiac output was significantly


greater (p0.05) in the control group compared to HTR by 5 minutes after


the onset of exercise.


Peak cardiac output at 10 minutes of exercise was 158


and 132% greater than baseline for control and HTR, respectively.


Stroke


volume


increased


rapidly


at the


onset


exercise


HTR


and


was


significantly


greater (p<0.05)


than


baseline at each measurement period


during
(p<0.05)


exercise.


than


Stroke


baseline


volume


control


become


group


until


significantly


greater


2.5 minutes after


onset of exercise.


The relative increase in stroke volume was significantly


greater


(p<0.05)


HTR


at all


measurement


periods


compared


to the


control group.


Peak stroke volume was 33 and 69% greater than baseline


in the control and HTR, respectively.


Exercise heart rate for both groups


was significantly greater (p<0.05) than baseline at all measurement periods.


During the first minute of exercise at 70


of peak power, heart rate min










higher than at baseline.


Heart rate in the control group increased 98% by


10 minutes after the onset of exercise.


Neuroendocrine


Hormones


Absolute values for plasma AVP


, ANP and PRA during the two


submaximal exercise conditions are presented in


tables


Data


from


subjects


(n=11


HTR;


n=ll


control)


were


included


neuroendocrine


hormone


analysis


with


exception


Blood


samples were assayed for plasma NE in 6 control subjects and all 11 HTR.

Vasopressin


The changes


in AVP


during


cycle exercise


at 40


peak


power output and the SL-GXT are illustrated in figures 10 and 11.


Baseline


AVP was not significantly different (p>0.05) between the two groups (3.11


vs 3.55


pg/ml for


control and HTR respectively).


During


10 minutes of


constant load cycle exercise at 40


of peak power, AVP increased to levels


significantly


greater


(p<0.0


than


baseline


minutes


after


commencement


exercise


both


groups


group


time


interaction was not significant (p>0.05).


The resting


concentration


AVP prior


to the


second


submaximal


bout


vary


significantly


(p>0.05)


from


initial


baseline


values.


During


cycle


exercise


at 70%


peak


power


output,


AVP


increased


significantly


(p_0.05)


above


baseline


values


within


2 minutes after


onset of work in both groups.


AVP


continued to increase linearly


over










Plasma Renin Activity


Changes


in PRA


during


submaximal


exercise


the SL-GXT


illustrated in figures


12 and


Baseline PRA


values were significantly


greater


(p<0.05)


HTR


(8.98


1.10


ng/ml/hr for


HTR and


control


groups, respectively).
became significantly


During cycle exercise at 40% of peak power, PRA


greater than


baseline 6


minutes after


the onset of


exercise and continued to increase over time but the changes were similar
(p0.05) for both groups.


Resting


PRA


not vary


significantly


(p>0.05)


between


exercise tests for either group.


During cycle exercise at 70% of peak power


output,


PRA


values


were


significantly


greater


(p<0.05)


than


at all


measurement periods in both groups.


The group by time interaction was


significant and post hoc contrast analysis showed


that the magnitude of


increase by 4 minutes after the onset of exercise was significantly greater
(p<0.05) in HTR.
Atrial Natriuretic Hormone


Changes


in ANP


during submaximal


exercise


the SL-GXT


depicted
(p0.05)


figures


HTR


respectively).


ANP


(41.45


at rest


20.19 pg/ml


was


significantly


HTR and


control


ANP increased at the onset of cycle exercise at 40


elevated


groups,
of peak


power and was significantly (p


<0.05) greater than baseline by 8 minutes


after the onset of exercise in both groups and the group by time interaction
was not significant (p>0.05).








79

baseline at all measurement periods in both groups but the magnitude of
increase was significantly greater (p<0.05) in HTR compared to the control
group by 8 minutes after the onset of exercise.
Norepinephrine


Changes in NE during exercise at 40 and 70


of peak power output


are shown in figures 16 and 17. Basal NE values did not differ significantly
(p>0.05) between groups (0.396 vs 0.468 ng/ml for the control and HTR,


respectively).


elevated


Plasma


above resting


levels


concentrations


were


both groups


significantly
four minutes


(p<0.05)


after


onset of cycle exercise at 40% of peak power output.
interaction, however, was not significant (p>0.05).


The group by time


The


resting


concentrations


prior


second


bout


submaximal cycle exercise did not vary significantly (p>0.05) from initial
resting values. Both groups increased (p<0.05) plasma NE concentrations
above baseline within 2 minutes after the onset of cycle exercise at 70% of

peak power ouput. The group by time interaction was significant (p<0.05)


and post hoc analysis revealed


that the magnitude of NE elevation


greater (p0.05) in HTR at each measurement period


(minute


was


4, 6 and












Table 1.


Physical characteristics of the Control and Transplant groups.


VARIABLE


CONTROL


TRANSPLANT


MALES

FEMALES


AGE (yrs)


50.413.9


50.113.7


HEIGHT (cm)


178.26.


176.29.


WEIGHT (kg)


515.2


BODY FAT (


013.8

55.6


24.76.0


LEAN BODY MASS (kg)


1-RM LEG STRENGTHS (kg)


63.78.9


61.59.7


95.019.4


66.19.6*


values are mean standard deviation
a knee-extension (quadriceps) strength


*p50.05 Transplant


vs Control











Table


Heart rate and blood pressure values for both groups at rest and peak


exercise during the symptom limited-graded exercise test.


VARIABLE


CONTROL


TRANSPLANT


REST HEART RATEa (beats/min)

PEAK HEART RATE (beats/min)


687

16815


9410*

14712*


A BETWEEN REST


AND PEAK


10013


5312$


14925


5717$


REST SYSTOLIC PRESSUREa (mmHg)


12612


1269


PEAK SYSTOLIC PRESSURE


(mmHg)


21824


19019*


A BETWEEN REST AND PEAK


9324


6421$


7624


5119$


REST DIASTOLIC PRESSUREa (mmHg)


775


906*


PEAK DIASTOLIC PRESSURE


A BETWEEN REST


(mmHg)


AND PEAK


767


-0.28


9212*

2.08


0.112


2.29


PEAK RATE-PRESSURE PRODUCTb


36943


28043*


values are mean standard deviation
a measurement taken Drior to SL-GXT


with subject seated












Table 3.


Peak cardiorespiratory responses of the Control and Transplant


groups during the symptom limited-graded exercise test.


VARIABLE


CONTROL


TRANSPLANT


Vo2a (ml-kg-1.min


32.08.7

2.690.74


V02 (L'min-1)


18.33.3*

1.520.24*


VCO


b (L*min-1)


3.100.81


1.73+0.28*


(L-min-


97.6719.80


69.5016.80*


VE/V02

RESPIRATORY EXCHANGE RATIO

PEAK POWER (Watts)


'.558.97


1.170.06


19847


45.74+9.43*


1.150.05*


10920*


RATING OF PERCEIVED EXERTIONd


19.50.8


19.40.8


values are mean standard deviation
a peak systemic oxygen consumption
b peak expired carbon dioxide
c peak expired pulmonary ventilation (STPD)
d Borg (1962) Scale
* p<0.05 transplant vs control












Table 4. Aldosterone (ALDO), angiotensin II (ANGII),


plasma renin activity (PRA),


vasopressin (AVP),


atrial natriuretic peptide (ANP) and


norepinephrine (NE) at rest and immediately after the SL-GXT.


VARIABLE


ALDO
(pg/ml)


ANGII
(pg/ml)


GROUP


CONTROL


TRANSPLANT


CONTROL
TRANSPLANT


REST


119.868.7
164.965.8


71.5


4.12.0


PEAK-EXERCISE


241.4135.9*
300.1148.2*


.57.1*
.16.1*


AVP


CONTROL


(pg/ml)


PRA


TRANSPLANT


CONTROL


(ng/ml/hr)


ANP


(pg/ml)


TRANSPLANT


CONTROL


TRANSPLANT


80.9


4.21.9


1.50.8
8.36.0+


18.14.
42.99.


16.73.2*


27.37


2.82.1*
24.812.0*$


47.617.0*
137.560.0*$


CONTROL


(pg/ml)


TRANSPLANT


39429
47826


2,706639*
3,869470*$


values are mean standard deviation
+ p<0.05 transplant vs control at baseline
* p<0.05 vs rest
$ p<0.05 the change from rest different from control




















r-4r~C'1
to ~to N


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to a' to


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L0
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- -














Table 6.


Pulmonary function values of the control group and the transplant


group after cardiac transplantation.


VARIABLE


CONTROL


TRANSPLANT


DLCOsb (ml-min-1mmHg)
% predicted


29.204.39
106.210.4


20.744.21*
76.318.0*


DLCO/TLCsb


4.5110.75
99.512.3


predicted


3.751.13*
84.720.5*


FVC (L)


predicted


4.750.87
97.19.3


4.130.66*
89.47.5*


FEV1 (L)


3.740.71
104.612.3


predicted


TLCsb (L)


6.500.64
94.19.4


predicted


3.030.88*
89.420.7*


5.741.08
88.011.3


values are mean standard deviation
a absolute values are liters BTPS


DLCOsb


(single breath lung diffusion capacity)


DLCO/TLCsb


(diffusion capacity per unit total lung volume)


FVC (forced vital capacity)
FEV1 (volume expired in first second of FVC))
TLCsb (total lung capacity single breath technique)


* pO<0.05 transplant vs control
















Table


. Heart rate, rating of perceived exersion and plasma volume changes


during submaximal and maximal exercise tests.


PEAK POWER


VARIABLE


GROUP


40%


70%


HEART RATE (


HRR)


CONTR
TRANS


46.48.6
51.916.3


81.26.4
81.67.9


PERCEIVED EXERTIONc


CONTR
TRANS


12.21


.11.1


16.61


19.50.8
19.40.8


A PLASMA


VOLUME


CONTR
TRANS


-4.63.4


74.3


-10.82.4
-10.13.8


-12.95.6
-14.1+5.5


values are mean


+ standard


deviation


a heart rate expressed as


percentage of heart rate reserve


b percentage loss in plasma volume (rest-exercise)


Borg (1962) Scale











Table 8.


Changes in arterial PO2, PCO2 and pH during 10 minutes of


constant load cycle exercise at 40% of peak power output.


PaO2 (mmHg)


PaCO2 (mmHg)


CTRa


TIME
(min)


TXb


Cm


cm


REST


101.8
2.3
102.1
3.3
98.9*
2.7
99.1*
1.9
99.7*
1.8
100.4
1.6
102.0
1.6
101.8
1.0
101.8
0.9
101.8
1.9
100.9
1.3
100.9
1.4
101.3
1.6


1.9


101.1
4.1
99.9
4.3
97.4*
3.9
96.0*
5.9
95.1*
6.5
94.9*
7.2
94.7*
7.6
94.4*
7.3
94.9*
8.7
93.5*
8.4
93.4*
8.8
92.9*
8.9
92.8*
9.9
92.6*
10.4


+1.6
38.4
+1.1


+1.5
39.3
1.6
38.8
1.2
39.0
1.5
38.7
1.5
38.8
1.5
38.8
1.4
38.9
1.4
38.7
1.5
38.7
2.3
38.0
0.8
38.0
1.1


37.2+
1.4
37.2
1.7


37.3
1.9


1.9
36.9
2.0
36.6
2.1
36.6
2.1
36.5
2.1
36.1*
2.2
36.0*
2.1
35.8*
2.4
35.9*
2.4
35.4*
2.3
35.2*
2.5


7.42


0.01
7.41
0.01


0.01


0.02
7.40
0.02
7.40
0.01
7.39*
0.02
7.39*
0.02
7.39*
0.02
7.39*
0.02
7.38*
0.01
7.39*
0.02
7.39*
0.02
7.39*
0.02


0.02
7.42
0.02


0.02
7.41
0.02
7.40
0.02
7.39
0.03
7.39*
0.03
7.39*
0.02
7.38*
0.02
7.38*
0.02
7.38*
0.02
7.38*
0.03
7.38*
0.03
7.37*
0.03









Table 9.


Changes in arterial PO2, PCO2 and pH during 10 minutes of


constant load cycle exercise at 70% of peak power output.


PaO2 (mmHg)


PaCO2 (mmHg)


TIME
(min)


CTRa


CTR


CTR


REST


101.5


99.7
2.7
98.1*
+2.7
97.9*
+1.4
98.7*
+1.5
99.4
+1.7
100.5
2.1
100.6
2.2
101.0
2.0
101.6
+2.5
100.7
2.6
100.1
+2.1
100.2


2.6
100.0
+2.5


101.6
4.3


98.9
4.3
97.6*
5.3
94.8*
6.0
94.0*
6.6
93.5*
7.4
93.4*
7.9
91.8*$
6.8
92.1*$
8.3
90.8*$
8.9
90.2*$
9.8
89.3*$
+10.4
88.7*$


+11.9


87.5*$
13.1


37.9
1.5
37.4
1.4
38.1
1.3
38.3
1.3
38.4
1.5
38.4
1.4
38.5
2.0
38.4
2.3
37.9
2.0
37.8
1.8
37.8
1.8
37.5
2.1
36.9*


36.9*
1.7


36.8+


+1.1


36.5
+1.1
36.6
1.5
36.5
+1.8
36.2$
2.0
36.2$
+2.0
35.7*$
2.2
35.2*$
+2.4
34.9*$
2.1
34.6*$
2.2
34.6*$
2.4
34.2*$
2.4
33.7*$


2.6


33.3*$
2.5


+0.02
7.41
0.02
7.40
0.01
7.40
0.03
7.39
0.03
7.38*
0.02
7.38*
0.02
7.37*
0.02
7.37*
0.02
7.37*
0.02
7.36*
0.02
7.37*
0.03
7.36*
0.03
7.36*
0.03


7.42


+0.03
7.42
0.02
7.41
0.02
7.40
0.02
7.39
0.03
7.39*
0.02
7.38*
0.02
7.37*
0.03
7.37*
0.03
7.36*
0.03
7.36*
0.03
7.35*
+0.03
7.34*
0.03
7.33*
+0.03


values are mean + standard deviation








90
Table 10. Changes in cardiac output (Q), stroke volume (SV) and heart rate
(HR) during 10 minutes of constant load cycle exercise at 40% of peak
power output.


CARDIAC


STROKE


HEART


OUTPUT (L/min)


VOLUME (ml)


RATE


TIME CTRa TXb CTR TX CTR TX
(min)


REST


4.94


4.58+


105+


0.40


+0.27


5.94*


5.34*


108*$


1.00


+0.56


6.96*


6.00*


103*


110*$


1.00


0.71


7.47*


6.38*


106*


111*$


1.17


0.76


7.93*


6.80*


108*


113*$


1.21


1.04


8.22*


7.14*


108*


113*$


1.30


1.01


8.62*


7.58*


110*


115*$


1.36


8.89*


1.01


7.75*


110*


117*$


+1.42


1.05


9.16*


7.72*


110*


118*$


1.45


1.2


9.18*


7.91*


111*


119*$


1.32


1.19


9.56*
1.54
10.01*
1.37
10.15*
1.28
10.34*
1.27


8.31*


110*


120*$


1.28


8.50*


1.30
8.75*
1.24


8.75*


111*


112*


112*


121*$
10
122*$


123*$


1.27


values are mean standard deviation








91
Table 11. Changes in cardiac output (Q), stroke volume (SV) and heart rate
(HR) during 10 minutes of constant load cycle exercise at 70% of peak
power output.


CARDIAC


OUTPUT (L/min)


STROKE
VOLUME (ml)


TIME CTRa TXb CTR TX CTR TX
(min)


HEART


REST


5.16


0.44


4.59+


106+


+0.24


6.90*


1.12
7.76*
1.20
8.54*
1.33
9.40*
1.45
10.16*
1.55
10.57*
1.57
11.04*
1.61
11.51*
1.53
11.70*


5.87*


108*


+0.59
6.76*
0.70
7.42*
+0.99
7.90*
+1.20


121*


130*


132*


136*


8.46*


137*


111*$


114*$
11
117*$
11
121*$
14
125*$


1.11


8.64*


1.37


139*


8.91*


1.32


9.29*


+1.47


9.54*


143*


128*$


130*$


132*$


133*$


1.41


1.38


12.33*
1.51
12.83*
1.48
12.99*
1.40
13.31*
1.64


9.75*$
1.36
10.02*$
1.40
10.32*$
1.41
10.53*$
1.60


144*


146*


148*


150*


135*$
12
137*$
12
138*$
12
140*$
12


values are mean + standard deviation
a" _-~











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380

350

320

290

260

230

200

170

140

110

80


TRANSPLANT (n=11)


" CONTROL (n=11)


REST


PEAK EXERCISE


CONTROL (n=11)
TRANSPLANT (n=11)


p


I















-I.




*CONTROL
A TRANSPLANT


REST


.5 1 L5 2 2.5 3 3.5 4 4.5 5 6 8


CONTROL
TRANSPLANT


REST


.5 1 L5 2 2.5 3 3.5 4 4.5 5 6 8


7.44

7.42

7.40

7.38

736

7.34


V -- I -


CONTROL
TRANSPLANT




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AGREEMENT_INFO ACCOUNT UF PROJECT UFDC
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