The acute cardiovascular responses to exercise are specific and vary with different forms of exercise (Figure
34–1). There are also specific adaptive responses to exercise, particularly to dynamic exercise. In particular, the adaptive change in heart rate from an alteration in vagal parasympathetic
tone defines the normal physiologic range; as noted earlier, this may be initially misinterpreted as representative of cardiovascular disease.
Acute Responses to Exercise
Several acute cardiovascular responses to dynamic exercise are typical (Figure 34–1). As would be anticipated in meeting the demands of aerobic exercise, oxygen consumption increases because of an increase in both cardiac output and the arteriovenous oxygen difference. The increase in arteriovenous oxygen difference
results from an increase in the oxygen extraction, or demand, by the exercising
skeletal muscle and the increase in muscular capillary blood flow. Oxygen
consumption is linearly related to the workload achieved during dynamic exercise. Maximal oxygen consumption (V̇o2max) is a highly reproducible measure of total aerobic capacity and thus dynamic exercise performance. Aerobic capacity varies with training, lean body mass, age, and gender and is significantly influenced
by the individual’s genetic characteristics. In children,
gender differences are seen only after puberty, when the aerobic
capacity of girls and young women tends to be approximately 30% less
than that of boys and young men of the same age. Although incompletely explained,
these differences are believed to be multifactorial; females, for
example, have a lower lean body mass and a lower hemoglobin level.
Maximal oxygen consumption diminishes with increasing age, as a
result of such factors as the gradual detraining effect of age,
an alteration in cardiac stiffness, and a reduction in β-adrenergic
responsiveness that produces an attenuated heart rate response to
exercise. Although it may be improved by dynamic training in older
individuals, this improvement may well be due to an increased arteriovenous
oxygen difference as much as to an increase in cardiac output and
stroke volume. Furthermore, the improvement in V̇o2max is relative when the overall decline in fitness is taken into account.
Oxygen consumption is also linearly related to cardiac output during dynamic exercise. The increase in cardiac output results principally from an increase in heart rate. Some increase in stroke
volume takes place, resulting from the increase in venous return
produced by the increasing skeletal muscle activity. The increase
in left ventricular stroke volume during dynamic exercise is larger
in an upright than in a supine position, but the absolute stroke
volume at peak exercise is greatest in the supine position. Other
hemodynamic responses contribute to the increased stroke volume. Intrathoracic
pressure is reduced, left ventricular filling pressure rises, the mitral
valve orifice enlarges, and the left ventricular end-diastolic volume increases.
The net effect of these changes is activation of the Frank-Starling
mechanism during the early initial and lower levels of dynamic exercise. Subsequently,
at higher levels of exercise, sympathetic activation augments the
Frank-Starling response in increasing stroke volume by increasing
myocardial contractility and reducing end-systolic volume.
Resting heart rate is determined by vagal tone coupled with the level of sympathetic reflex activation. In the upright (versus supine)
position, for example, resting heart rate is higher because of a mildly
increased level of sympathetic activation. The initial increase
in heart rate during exercise is due to a reduction in vagal tone,
a central nervous system response mediated by stimulation of mechanoreceptors
in the activated skeletal muscles. The heart rate increase is subsequently
maintained by sympathetic activity and increased circulating catecholamines.
Systolic blood pressure increases during dynamic exercise, with a minimal increase in either diastolic or mean arterial pressure.
The magnitude of the response is determined by the size of the activated muscle mass. Thus, the response during large muscle or leg exercise is greater than during small muscle or arm exercise. There is a greater increase in pulmonary arterial pressure than in systemic pressure during exercise because the change in vascular resistance is less in the pulmonary vasculature. This relative increase in pulmonary pressures is believed to augment pulmonary oxygen transport during exercise.
In static exercise, intramuscular pressure increases dramatically, with a resultant reduction or obliteration of exercising skeletal
muscle blood flow (Figure 34–1).
Static exercise is sustained by anaerobic mechanisms, and the consequent increases
in oxygen consumption and cardiac output are much less than during dynamic exercise. Furthermore, oxygen consumption and cardiac output increase after
static exercise, presumably because of an immediate increase in blood
flow to the involved muscles to rectify the oxygen debt acquired
by anaerobic mechanisms during the static exercise.
The increase in cardiac output during static exercise is due mainly to the increase in heart rate; stroke volume remains almost
unchanged. Systolic blood pressure increases significantly during
static exercise. Because stroke volumes and systemic vascular resistance
change only minimally, this increased arterial pressure is due to
the effects of increased muscle contraction on arterial pressure
waves. Although arteriovenous oxygen difference remains unchanged during static exercise, an increase does take place immediately following
release as a result of increased blood flow to the muscle bed.
Effects of Systematic Exercise Training
As previously stated, V̇o2max is an accurate and reproducible measure of aerobic capacity and thus becomes an objective measure of dynamic fitness. In normal men, V̇o2max ranges from 25 mL/kg/min to 40 mL/kg/min, with the lower values occurring in the older individuals. More than 50 mL/kg/min is considered representative of an elite level of fitness (the level may go as high as 80 mL/kg/min), reflecting an increase in maximal cardiac output and arteriovenous oxygen difference.
Dynamic Exercise Training
This type of training decreases resting heart rate because of an adaptive increase in vagal tone; it also decreases the heart rate
response at any level of exercise. The heart rate response to maximal exercise, however, is identical in both the trained and untrained individual. Therefore, the increase in maximum cardiac output associated with dynamic training is due to increased stroke volume. It should also be noted that these physiologic adaptive changes to dynamic training occur in association with morphologic and physiologic changes in the heart.
This type of training does not produce the same degree of V̇o2max as does dynamic training. It is probable that the use of anaerobic rather than aerobic mechanisms to generate muscle energy requires a lower increase in cardiac output. Although morphologic changes do occur, the hemodynamic response to static exercise is similar in trained and untrained individuals.
Dynamic training improves the response to static exercise in that the increased stroke volume at a lower heart rate allows the subject to sustain a greater cardiac pressure load and thus improve isometric performance. Static exercise training does not improve dynamic performance, however, except in areas or activities where greater
strength or power is required (eg, pole vaulting).
The frequency, intensity, and duration of exercise all affect the cardiovascular response. To obtain a significant training effect requires 30 minutes of dynamic exercise at 60–80% of maximal V̇o2 three times per week. Little effect is seen unless rates of more than 130 bpm are achieved for prolonged periods. Although lower levels and less frequent episodes of training may create a training effect, cessation of exercise produces a rapid detraining effect—which
is complete within 3 weeks.
Measurement of the heart rate provides a good index of training. As discussed earlier, the alteration in resting heart rate is said to be due to an increase in vagal parasympathetic tone rather than a decrease in sympathetic tone or lower circulating catecholamine levels. In trained athletes, circulating levels of both epinephrine and norepinephrine are lower during dynamic and static exercise, with a lower heart rate response to the relative intensity of both
forms of exercise.
Systematic training has some effects on other organ systems. Total blood and plasma volumes increase with dynamic training; these
changes are thought to be related to increases in renin activity
and serum albumin levels. Higher hemoglobin levels lead to an increase in both maximal oxygen consumption and endurance. Well-trained athletes use oxygen more efficiently, and the vascular conductance of skeletal
muscle changes, resulting in a greater arteriovenous oxygen difference
during dynamic exercise. Dynamic exercise training also increases high-density
lipoprotein levels and decreases low-density lipoprotein and very-low-density
lipoprotein levels, as well as body weight.
Morphologic Responses to Training
Physiologic hypertrophy is a prominent feature of the athlete’s heart. The morphologic adaptations to the increased stroke volume
induced by exercise conform to the principles of Laplace law, which
relates the wall tension to intracavitary size and pressure. The
increase in wall thickness in the setting of volume and pressure
overload tends to normalize wall stress in both dynamic and isometric
exercise (Figure 34–2).
Distribution of cardiac dimensions in large populations of highly trained male and female athletes. Top: Left ventricular end-diastolic dimension. Middle: Transverse left atrial dimension. Bottom: Maximal left ventricular wall thickness.
(Reprinted with permission from Pelliccia A et al. Ann Intern Med. 1999;130:23 and Pelliccia A et al. J Am Coll Cardiol. 2005;46:690 and Pelliccia A et al. N Engl J Med. 1991;3324:295.)
The availability of two-dimensional and Doppler echocardiography and radionuclide ventriculography has allowed for the assessment
of the mechanics of systolic and diastolic function in the trained athlete.
The value of these technologies, although substantial, is limited
by the inability to directly measure changes in intracardiac pressures,
making absolute conclusions regarding detailed adaptive changes
more difficult. Nevertheless, when compared with matched controls (age,
gender, and body surface area), any relative changes in parameters
of systolic or diastolic function are valid. It is also evident
that the functional changes are consequences of the adaptive morphologic
changes of the dynamically and isometrically trained athlete. Noninvasive parameters
of systolic function in trained athletes usually fall within accepted
normal limits. The occasional abnormal findings may be satisfactorily
explained as secondary to the adaptive morphologic changes associated
with the different types of training. Similarly, noninvasive parameters
of diastolic function usually fall within a normal range of values
at rest, irrespective of the type of training.
Echocardiography allows cardiac anatomy to be detailed in a noninvasive serial manner; it is particularly useful in finding and documenting changes in cardiac morphology in athletes. Changes in cavity sizes, left ventricular wall thickness, and left ventricular mass have been documented in a number of studies of athletes undergoing both dynamic and static exercise training (Figure 34–2).
A consistent finding in dynamically trained athletes is an increased left ventricular end-diastolic dimension, which is present irrespective of
body surface area, height, or gender. Compared with sedentary control
subjects, the left ventricular end-diastolic dimension is increased
by approximately 10% in the trained athlete, which represents
an increase in end-diastolic volume of approximately 33%.
Most dynamically trained athletes have an end-diastolic dimension
of 60 mm or less. In contrast, left ventricular end-diastolic dimension
is not altered with static exercise training, whether expressed
in absolute values, or normalized by body surface area, weight,
or lean body mass. This difference is believed to reflect the pressure,
rather than volume load, on the left ventricle that is created by isometric training. The end-systolic dimension and volume remain within normal limits in the endurance athlete, producing the increase in stroke dimension and volume associated with dynamic exercise training.
Left Ventricular Wall Thickness
Concomitant with the increase in left ventricular cavity size in the dynamically trained athlete, left ventricular posterior wall
and interventricular septal thickness increase. The increase (compared
with sedentary controls) in left ventricular posterior wall thickness
is as high as 19%; in the same study, 98% had
a left ventricular posterior wall thickness of 12 mm or less. Isometric
exercise produces septal wall thicknesses of up to 16 mm. These increased
values fall within an acceptable range when normalized for body surface
area, weight, or lean body mass.
Although septal hypertrophy is a characteristic of hypertrophic cardiomyopathy, the increase in septal thickness in athletes is rarely above 16 mm and the septal-posterior wall thickness ratio does not increase above 1.2:1. Furthermore, there is no evidence in the literature that primary hypertrophic cardiomyopathy
may develop with training.
Estimates of left ventricular mass incorporate measurements of intraventricular septum and posterior wall thickness, both of which increase significantly in trained athletes. It is therefore reasonable to expect a significant increase in left ventricular mass in both dynamically and isometrically trained athletes. An increase of as much as 45% is found, even after normalization for body surface area.
Increases of up to 24% in right ventricular cavity dimensions may be seen in trained athletes.
Increases in left atrial cavity size are also found in trained athletes and appear to be related to both the intensity and duration of the exercise.
Any type of athletic training in any form can alter the electrocardiogram (ECG) (Table 34–1). In a recent survey of 1005 trained athletes, 40% of ECGs were abnormal.
It is important to know the effects of normal training on the ECG
as well as the ECG abnormalities that warrant further investigation.
Alterations on the ECG also depend on the nature, intensity, and
level of training. The ECG reflects the morphologic adaptive changes
of the heart—sinus bradycardia and voltage criteria for left
ventricular hypertrophy (LVH)—that are due to the nature
of the training. In the dynamically trained athlete in particular,
the sinus bradycardia, which can be profound, reflects the adaptive
increase in left ventricular cavity size that delivers large stroke
volumes at rest and during exercise. Sinus bradycardia is usually due
to high vagal tone, which may also be associated with sinus arrhythmia, sinoatrial
block, multifocal atrial rhythms, junction rhythms, first-degree
atrioventricular block, and Mobitz I second-degree atrioventricular
block. All these abnormalities disappear during exercise. The P
wave of the ECG may be notched and increased in amplitude. Interventricular
conduction abnormalities are common in athletes. The ST segment
may be elevated and the T wave increased in amplitude. Occasionally
in trained athletes, the ST segment may be depressed and the T wave
biphasic or inverted, all of which correct during exercise. These latter
findings at rest are characteristic of ischemic heart disease, however,
and their existence in the athlete warrants further investigation.
Table 34–1. Effects of Dynamic and Isometric Exercise and Training on the Electrocardiogram.
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Table 34–1. Effects of Dynamic and Isometric Exercise and Training on the Electrocardiogram.
|Notched P waves|
|Voltage criteria for LVH|
|Interventricular conduction abnormalities|
|Symmetric peaked T waves|
|Multifocal atrial rhythm|
|First-degree AV block|
|Mobitz I second-degree AV block|
Distinguishing between physiologic and pathologic LVH by ECG may not be possible, particularly in a young athlete. The adaptive
development of LVH and sinus bradycardia is characteristic of the trained
athlete, as is the loss of these adaptive characteristics as a detraining effect.
In the older athlete, where the prevalence of ischemic heart disease
is much higher, voltage criteria for LVH, ST- and T-wave abnormalities,
and repolarization abnormalities of the QRS complex are more common.
The threshold for pursuing further investigation of abnormal ECG
findings should be much lower in these older athletes.
Racial Differences in Response to Training
No detailed studies addressing the adaptive responses to training in the black athlete have yet been completed. Circumstantial evidence,
however, would suggest that these responses may differ in black
athletes. It is known that LVH is more prevalent in a black hypertensive population
than in a white population, given similar levels of blood pressure elevation.
Because a racial difference appears to exist in the blood pressure response
to both dynamic and isometric exercise, the potential for an increased prevalence
and greater degree of LVH appears to exist among black athletes.
A study of black collegiate athletes showed that more than 30% had
an interventricular septal thickness of more than 13 mm; a separate
study of white athletes found only 3% with similar increases
in thickness. These factors, coupled with the occurrence of sudden
death in athletes—including black athletes—clearly
indicate the need for studies of trained black athletes as well
as comparative studies of black and white athletes.
The adaptive responses to both dynamic and isometric exercise training persist only if the training continues with sufficient
duration and intensity. Cessation of the training activity results
in a temporal regression of these adaptive changes: the detraining
effect. Although this effect is consistent despite age, gender,
or the overall duration or type of training, the time course appears
to be influenced by these factors. Following cessation of training,
a regression of physiologic hypertrophy of up to 60% takes
place within 7 days, so-called left ventricular remodeling. Both
posterior left ventricular wall thickness and interventricular septal thickness
regress equally, and the septal-posterior wall thickness ratio remains unchanged.
The left ventricular end-diastolic dimension decreases within 7
days, with little change thereafter. The detraining effect is also
associated with a reduction in V̇o2max.
After 12 weeks of inactivity (cessation of training), V̇o2max decreases up to 16%, with half of this loss occurring in the first
3 weeks. Maximal cardiac output during exercise is also reduced
by up to 8% in the first 3 weeks of detraining.
Germann CA et al. Sudden cardiac death in athletes: a guide for emergency physicians. Am J Emerg Med. 2005 Jul;23(4):504–9.
Pellicia A et al. Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation. 2000 Jul 18;102(3):278–84.
Pelliccia A et al. Remodeling of left ventricular hypertrophy
in elite athletes after long-term deconditioning. Circulation. 2002
Sharma S et al. Physiologic limits of left ventricular hypertrophy in elite junior athletes: relevant to differential diagnosis of athlete’s
heart and hypertrophic cardiomyopathy. J Am Coll Cardiol. 2002 Oct 16;40(8):1431–6.