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The contribution of heredity to the interindividual variability of maximum oxygen uptake and of cardiac size and function of healthy male twins, age 18 to 31 years, was studied to evaluate the role of the heart in the inheritance of aerobic power. Twelve pairs of monozygotic and 12 pairs of dizygotic twins were examined. Weight (p less than 0.05), relative weight (Quetelet index) (p less than 0.01) and skinfold thickness (p less than 0.01) were found to be genetically determined, as well as heart rate at rest (p less than 0.05) and systolic blood pressure (p less than 0.05). Genetic variation was significant (p less than 0.05) both for absolute and for weight-adjusted oxygen uptake, measured at peak exercise on the bicycle ergometer. However, the influence of inheritance on aerobic power was not associated with a significant genetic effect on the end-diastolic left ventricular internal diameter or on its fractional shortening as assessed by echocardiography. Genetic variation had a significant (p less than 0.05) effect on left ventricular mass, but this could be attributed to the inheritance of body size. These data indicate that cardiac factors are not significantly involved in the inheritance of aerobic power and suggest that cardiac hypertrophy in athletes is secondary to training.

Sixteen male bicyclists and 16 control subjects were studied to assess whether the left ventricular hypertrophy of athletes is associated with changes in diastolic left ventricular function. The cyclists had a larger left ventricular internal diameter on echocardiography (55.2 versus 47.9 mm; p less than 0.001) and a disproportionate increase in wall thickness relative to the internal diameter (0.48 versus 0.41; p less than 0.01), indicating a mixed eccentric-concentric type of hypertrophy. Left ventricular inflow Doppler velocimetry showed similar results in athletes and control subjects for peak flow velocities in the atrial contraction phase (30 versus 32 cm/s; p = NS) and in the early diastolic rapid filling phase (71 versus 67 cm/s; p = NS). The similar ratio of both velocities, that is, 0.43 in the cyclists and 0.49 in the control subjects, suggests that left ventricular distensibility is unaltered in cyclists. It is concluded that the left ventricular hypertrophy observed in cyclists is not associated with changes in ventricular stiffness, as estimated from left ventricular inflow Doppler velocimetry.

Ten male athletes engaged in throwing events and ten control subjects, matched for age, height, and weight, were investigated with echocardiography and Doppler velocimetry to assess cardiac structure and systolic and diastolic left ventricular function at rest. Left ventricular (LV) internal diameter, wall thickness, LV mass, and systolic LV function were not different between athletes and nonathletes. The possibility that strength training could alter LV diastolic function was further investigated. Both early diastolic function, estimated from the velocity of LV relaxation and the LV inflow pattern, and late diastolic function, assessed by Doppler velocimetry, were similar in throwers and controls. The unchanged ratio of the peak velocities of LV filing during atrial contraction and early filling suggests that LV distensibility is unaltered in these athletes. In conclusion, the amount and type of training performed by these throwers was not associated with changes in LV structure and function.

To assess left ventricular structure and function at rest and during exercise in endurance athletes, 10 elite marathon runners, aged 28 to 37 years, and 10 matched nonathletes were studied by echocardiography and supine bicycle ergometry. Each athlete's best marathon time was less than 2 h 16 min. Echocardiography was performed at rest, at a 60 W work load and at an individually adjusted work load, at which heart rate was 110 beats/min (physical working capacity 110 [PWC110]). Oxygen uptake at PWC110 averaged (+/- SD) 1.14 +/- 0.2 liters/min in the nonathletes and 2.0 +/- 0.2 liters/min in the runners (p less than 0.001). The left ventricular internal diameter at end-diastole was similar at the three activity levels in the control subjects but increased significantly from rest to exercise in the runners (p less than 0.001). Left ventricular systolic meridional wall stress remained unchanged during exercise in the nonathletes but was significantly higher at PWC110 in the athletes (p less than 0.05). Both the systolic peak velocity of posterior wall endocardial displacement and fractional shortening of the left ventricular internal diameter increased with exercise; at PWC110 the endocardial peak velocity was higher in the runners than in the control subjects (p less than 0.01). The endocardial peak velocity during relaxation was comparable in athletes and control subjects at rest, increased similarly at a 60 W work load, but was higher in the runners at PWC110 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)