- History of athletic training and performance.
- Enhanced exercise ability (V̇o2max > 40 mL/kg/min).
- Resting bradycardia.
- Increased left ventricular mass by echocardiography.
The concept of the athlete’s heart is one that has been postulated for almost 100 years, promulgating the idea that myocardial
hypertrophy could be a purely physiologic phenomenon. Media attention
to the sudden deaths of widely known athletes has helped focus attention
on the important distinction between pathologic cardiac hypertrophy
and physiologic hypertrophy and the upper limits of the latter.
The adaptations of the human body to physical training involve (but are not confined to) the cardiovascular system. The exercise-related
changes in other organ systems influence the cardiovascular response
to exercise. It is important for the physician to be familiar with
the physiologic responses to physical training in order to distinguish
them from similar changes that can occur with cardiovascular disease.
Different forms of exercise produce a number of physiologic responses. Also, cardiovascular responses to short-term training and prolonged
training differ. Exercise generally takes two basic physiologic
forms—dynamic and static, or isometric, exercise—although
most athletic activities are a variable combination of both forms
of exercise. Dynamic exercise constitutes an alteration in the length
of skeletal muscle with comparatively little change in muscle tension. Static
exercise is essentially the reverse—that is, a marked alteration
in skeletal muscle tension with little or no change in muscle length.
Distance running is a classic example of dynamic exercise; weight
lifting is a classic example of static exercise.
The morphologic and physiologic consequences of dynamic and isometric exercise are significant and may simulate changes associated with
cardiac disease. The normal limits of changes that are due to athletic
conditioning require careful identification. Awareness of these
limits improves the physician’s ability to determine the
end points at which normal anatomy and physiology become clinical disease.
Maron BJ et al. The heart of trained athletes:
cardiac remodeling and the risks of sports, including sudden death. Circulation. 2006 Oct 10;114(15):1633–44.
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.
Cardiovascular response to exercise. A: Response to dynamic exercise progressively increasing workload to maximal oxygen consumption. B: Response to static handgrip contraction at 30% maximal voluntary contraction. ABP, systolic, mean and diastolic arterial blood pressures; HR, heart rate; Q, cardiac output; SV, stroke volume; TPR, total peripheral resistance; V̇o2, oxygen consumption.
(Reprinted with permission from Mitchell JH, Raven PB. Cardiovascular adaption to physical activity. In: Bouchard C et al, editors. Physical Activity, Fitness and Health: International Proceedings and Consensus statement. Human Kinetics Publishers: Champain IL; 1994.)
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 ...