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CARDIOVASCULAR
ADAPTATIONS TO PHYSICAL
TRAINING
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C Gunnar Blomqvist
Bengt Saltin
Students
After After Olympic
Control bedrest training athletes
Maximaloxygenuptake, liters/rain 3.30 2.43 3.91 b5.38
Maximalvoluntary ventilation, liters/min 191 201 197 219
Transfer coefficient for 02, (ml/min)/(mmHg) 96 83 86 95
Annu. Rev. Physiol. 1983.45:169-189. Downloaded from arjournals.annualreviews.org
CARDIOVASCULAR
ADAPTATIONSTO TRAINING 171
172 BLOMQVIST
& SALTIN
MYOCARDIALADAPTATIONS
The increased stroke volumethat is a salient effect of training in normal
subjects can be achieved simply by increasing cardiac dimensions or by
improving the performance characteristics of the heart. Pumpperformance
maybe increased by (a) enhancingthe intrinsic contractile properties of the
myocardiumand the responses to inotropic stimulation and (b) extramyo-
eardial adaptations that have secondary effects on performance--e.g, by
increasing ventrieular filling or decreasing myocardialwork.
Comprehensiveanalysis of myocardial function includes simultaneous
consideration of force, velocity, and fiber length (64). The velocity axis can
often be disregarded without serious loss of information in the analysis of
the performanceof the intact heart. The ventricular pressure-volume rela-
tionship (34, 86, 106, 115) provides a useful frameworkfor analysis and
link between muscle mechanicsand ventricular function. It is also helpful
when considering peripheral or extracardiac factors. The pressure-volume
relation defines contractile state as the maximalpressure (or tension) that
can be developed at any given volume(or fiber length). Maximalventricular
pressure is normally a linear function of volume.Implicit in the concept is
that the amountof shortening or stroke volumethat can be achieved from
any given diastolic volumeor fiber length can be increased only by reducing
afterload or by enhancing contractile state. Similarly, an increase in the
amount of shortening at a given afterload requires either an increased
end-diastolic volumeor an increased contractile state. The linear relation-
ship betweenpeak systolic pressure and end-systolic volumeclosely approx-
imates the rdation between maximal tension and volume. End-systolic
volumeis independent of preload. This modelmakes it feasible to evaluate
intra- and intedndividual physiological differences in ventdeular contractile
performance even if the experimental conditions make it impossible to
control preload and afterload. However, the slope and intercept of the
systolic pressure-volumerelationship are affected both by the basal or in-
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Cardiac Dimensions
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176 BLOMQVIST
& SALTIN
Contractile Performance
Avariety of preparations have beenused to evaluate training effects on
myocardialfunction. Isolated papillary muscles and isolated perfused
hearts have been employedto analyze the effect on intrinsic myocardial
conttractile propertiesmi.e, the performanceof denervatedheart muscle
under rigidly controlled conditions. Nutter & Fuller (70) reviewedsix
studies of the effect of training on the mechanicalperformance of isolated
left ventricular papillary muscles.Passiveor diastolic myocardiallength-
tension relationships did not change.Isometricor isotonic contractile per-
formancewas increased in two series, decreased in two, and showedno
changein two.
Severalinvestigators haveexamined the effects of training on the perfor-
manceof the isolated perfusedheart. Scheuerandassociates (5, 7, 94, 95)
havemadea systematicstudy of the responseto different formsof training
--i.e. running and swimming in maleand femalerats. Theyconcluded(94)
that both activities produceskeletal .muscleadaptations (e.g. increased
cytochromeoxidaseactivity) in both maleand femalerats and an increased
heart-weight/body-weight ratio. Absoluteincreases in heart weightrelative
to weight-matched control rats occur only in femaleswimmers.Theyfound
evidence for improvedcontractile performance(measurementsnormalized
with respect to heart weightandobtainedat severallevels of left ventrieular
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filling pressure) in male and female swimmersand male runners but not in
female runners. These findings correlated closely with increased calcium
binding in isolated sarcoplasmie reticulum and increased aetomyosin
ATPase(95). However, Fuller & Nutter (29), who studied the effects
running in male rats and essentially replicated the methodsused by Scheuer
and collaborators, were for reasons that are not apparent unable to demon-
strate any training effects on contractile performance.Studies of the intact
in situ heart of anesthetized rats (19) and in the awakechronically instru-
menteddog (11) have also failed to demonstrate any significant changes
Annu. Rev. Physiol. 1983.45:169-189. Downloaded from arjournals.annualreviews.org
growth normally continues throughout adult life. Furthermore, the rat has
myocardialmembranecharacteristics that differ significantly from those of
other mammals(78). Other animal models also present problems in terms
of ~Lpplicability of findings to humans. The dog has a very high native
aerobic capacity, often well abovethe levels recorded in olympicathletes.
The heart-weight/body-weight ratio is also about twice as high as in hu-
marts--i.e. 8 g/kg body weight vs 4-5 in humans(96). The horse (101)
pig (93) mayprovide modelsin which baseline characteristics and responses
to training more closely resemble those in humans.
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EXTRAMYOCARDIAL ADAPTATIONS
Coronary Blood Flow
Dynamicexercise at graded work load levels causes a progressive increase
in myocardial work with increasing heart rate, wall tension, and velocity
of fiber shortening--i.e, the principal determinants of myocardial oxygen
demand--but there is no indication that exercise produces ischemia in
normal subjects. Myocardial isehemia causes left ventrieular dysfunction,
but performance is normally enhanced during exercise. Tension develop-
ment and ejection fraction increase progressively and maximalvalues are
reached during maximal exercise (76). Direct measurements of coronary
flow in normal humansubjects have also demonstrated that a linear rela-
tionship between myocardial work and coronary blood flow is maintained
during heavy exercise (38, 45). Furthermore, recent studies in the pig (117)
have shown that a coronary vasodilator reserve is present also during
m~rdmalexercise.
Longitudinal studies (104, 105) have demonstrated that changes in coro-
nary flow patterns occur very early after the onset of a training program,
which suggests significant regulatory adaptations. There is also experimen-
tal evidence for a training-induced increase in the size of the coronary
vascular bed (40, 67, 97, 122) with changes involving both capillaries and
larger vessels. The extent to which the increase in vascularity exceeds the
increase in muscle mass in the normal heart remains to be determined.
Schaible & Scheuer (95) have reported increases in coronary ttow propor-
tional to the degree of training-induced increase in heart weight. Others (53,
102, 107) have described an increase in the size of the coronary tree after
training even in the absence of changes in heart weight. Neogenesis of
coronary capillaries is suggested by studies based on light- and electronmi-
croscopy and autoradiographic techniques (53, 60, 62) as well as by data
on the rate of incorporation of 3H-thymidinein myocardial capillaries in
young rats exercised by swimming(60). Older animals maybe less respon-
sive (109). The larger heart size in wild animals than in domesticsedentary
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Peripheral VascularAdaptations
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tracardiae pressures were not measuredin their study but other investiga-
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tors have found progressively increasing left ventricular filling pressure with
increasing work loads (6, 24). Intrapleural pressures also becomeincreas-
ingly negative with increasing ventilation (63). This contributes to a further
increase in effective or transmural diastolic pressure whichnevertheless fails
to produce an increase in volume.
blockade
abolishedthctrainingeffectina scales
ofyoung healthy
subjects.
Liangctal (58)concludedthatthemajorcardiovascular
trainingeffects
can
be,elicitedsimplyby fl-adrenergic
cardiacstimulationbychronicdobuta-
mineinfusionin dogs.However, themethodusedby Sablect al (85)
determine
theintensity of training
(equalization
ofheartrates, expressed
as percentof maximal heartratemeasured duringt-blockadeandplacebo
trc~Ltmcnt)
islikely tohaveproduceda lower
relativeintensity
inthecxpcd-
mcntalgroupthanin thccontrol group.Theresults reportedby Lianget
al(158)includeda largedecrease
incardiac output
during submaximal
levels
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ofexercise.Thisfindingrepresents
a significant
deviation fromthehcmody-
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namiceffectsusuallyobservedaftertraininginnormal subjects.
CONCLUSIONS
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