Abstract

Objective: Chronic dynamic exercise leads to regulative and structural adaptations of the heart (athlete’s heart). To what extent the enlargement and physiologic hypertrophy of the heart lead to changes in the function of the valves, particularly regurgitation, is not yet clear. The aim of this study was to examine the regurgitation levels of different states of “athlete’s heart.” Methods: Our study population consisted of 5124 healthy subjects (4046 male and 1078 female, 18–60 years), regularly exercising 1 to 20 h/wk. Subjects were divided into 3 groups depending on their relative heart volumes (RHVs): (1) very enlarged heart group (VEHG; male, n = 1251; female, n = 201), with RHVs of greater than 14 (male) and 13 (female) mL/kg; (2) mildly enlarged heart group (MEHG; male, n = 702; female, n = 224), with RHVs of 12 to 14 (male) and 11 to 13 (female) mL/kg; and (3) control subjects (CS; male, n = 2093; female, n = 653), with RHVs of less than 12 (male) and 11 (female) mL/kg. Results: According to US Food and Drug Administration criteria for valve regurgitation, it could be shown by Doppler sonography that as physiologic enlargement and hypertrophy increased significantly, the frequency and severity of aortic valve regurgitation (mean ± SD: VEHG, 0.04 ± 0.09; MEHG, 0.09 ± 0.10; CS, 0.10 ± 0.11; P < .05) and high mitral regurgitation (VEHG, 0.10 ± 0.17; MEHG, 0.20 ± 0.29; CS, 0.26 ± 0.32; P < .01) decreased. On the contrary, pulmonary regurgitation (VEHG, 0.79 ± 0.45; MEHG, 0.47 ± 0.33; CS, 0.35 ± 0.38; P < .01) and tricuspid valve regurgitation (VEHG, 0.42 ± 0.29; MEHG, 0.47 ± 0.33; CS, 0.35 ± 0.38; P < .01) increased highly significantly with heart size. Conclusions: These findings strongly support the view of athlete’s heart as a physiologic adaptation of the heart, at least on the left side, not causing increased valvular regurgitation. Verf.-Referat