, Volume 11, Issue 5, pp 300-331
Date: 07 Oct 2012

The ‘Athletic Heart Syndrome’

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Cardiological findings in athletes are often similar to those observed in clinical cases. Electrocardiographic and cardiac imaging abnormalities as well as physical findings may be the same in both of these groups. Bradycardia and rhythm disturbances are the most common abnormalities in athletes. Most athletes with abnormal electrocardiograms are asymptomatic and numerous investigators have failed to detect heart disease in association with such electrocardiograms. In contrast to cardiac dysfunction observed in clinical cases, enhanced or normal ventricular systolic and diastolic function have been reported in athletes. In endurance athletes, this is associated with very high values for maximal aerobic power (V̇O2max).

Absolute and body size-normalised cardiac dimensions in most athletes do not approach values from chronic disease states, and may not exceed echocardiographic normal limits. In addition, pathological and physiological enlargement appear to be biochemically and functionally different. Myosin ATPase enzyme expression and calcium metabolism are different in rats with pathologically or physiologically induced enlargement. The reported biochemical differences underlie systolic and diastolic dysfunction in pathological enlargement. Conversely, trained rodents and humans have demonstrated enhanced systolic and diastolic function. It is important to note that cardiac enlargement observed in athletes is the result of normal adaptation to physical conditioning and/or hereditary influences. Conversely, pathological changes result from disease processes which can lead in turn to reduced function, morbidity and mortality.

Since the mid 1970s echocardiography has been used to compare cardiac dimensions in male endurance- and resistance-trained athletes. A sport-specific profile of eccentric and concentric enlargement has been documented in endurance and resistance athletes, respectively. Subsequent studies of athletes have examined factors such as age, sex and degree of competitive success to determine their contribution to these sport-specific cardiac profiles. Unique athletic subgroups have also been analysed and have included ballet dancers, rowers, basketball players and triathletes. However, there is a paucity of data on cardiac dimensions in female athletes. Finally, physical conditioning studies have also examined echocardiographic dimensions before and after endurance and resistance training. Significant enlargement of internal dimensions, wall thickness or left ventricular mass have been reported but such increases are relatively small and by no means universal.

Several conflicting explanations for enlarged cardiac dimensions appear in the literature. Chronic volume and pressure haemodynamic overloading during physical conditioning has been proposed to explain eccentric and concentric cardiac enlargement in endurance- and resistance-trained athletes respectively. However, twin studies suggest that hereditary factors may be important determinants of cardiac dimensions and/or the degree of cardiac adaptability to physical conditioning.

Another body of research has suggested the possibility that endocrine effects related to normal growth and/or physical conditioning may stimulate cardiac enlargement. Thyroid hormone, catecholamines, growth hormone and testosterone can alter cardiac dimensions and their blood levels are elevated with exercise. However, their influence on myocardial structure in athletes has not yet been clarified. In this regard, blood testosterone levels increase transiently following acute exercise bouts in young men and may contribute to the process of skeletal muscle hypertrophy. Significant statistical associations have been reported between skeletal and cardiac muscularity. Therefore, a common influence of testosterone or other hormones on skeletal and cardiac muscle hypertrophy has been hypothesised and may account for hereditary and/or conditioning induced cardiac enlargement in athletes. Future investigations should reassess the role of haemodynamic stress and clarify the quantitative role of heredity and endocrine factors in determining cardiac dimensions. In this way a clearer indication may be deduced as to the mechanism(s) involved in the apparent moderate cardiac enlargement reported in athletes. Research should first describe the cardiac profile of a wide range of female athletes and then determine the cause of any potential gender-based differences in cardiac size and adaptation to exercise.