Whether prolonged and highly-intensive athletic conditioning may be responsible for irreversible cardiac changes and/or systolic dysfunction is unresolved. Methods: We assessed clinical profile and cardiac dimension and function in 114 Olympic athletes (89 male and 25 female; 22.1±3.8 years of age), free of cardiovascular disease, engaged in endurance sports, undergoing uninterrupted training over a period of = 2 consecutive Olympic Games (mean 8.6±3.7). Results: LV cavity dimension did not change (57.3±4.3 to 57.5±4.1 mm; ns), nor did wall thickness (10.5±1.2 to 10.6±1.2 mm; ns), mass index (123.80±20.2 to 125.08±22.3 g/m2; ns) and geometry index (0.36±0.04 to 0.36±0.03; ns). Left atrial dimensions signifi cantly increased (32.4±2.7 to 32.9±3.3 mm; p<0.007). Global LV systolic function was unchanged (62±5 % to 63±5; ns) and no wall motion abnormalities were observed. LV fi lling pattern remained within normal limits; however, atrial peak-fl ow velocity increased (32.3±10.0 to 42.3±9.4 cm/ sec, p<0.001), and the early-to-late diastolic ratio decreased (2.5±0.7 to 1.8±0.4, p<0.001). No cardiac events occurred during follow-up; one athlete incurred myocarditis, four showed worsening of ventricular tachyarrhythmia (requiring ablation in one), and two abnormal ECG response to exercise. Conclusion: Long term, intensive training is not responsible of progressive LV dilatation or dysfunction in healthy athletes. Left atrial enlargement may occur, likely representing a physiologic mechanism to enhance systolic cardiac function. However, prolonged athletic conditioning may not be completely benign in all individuals and may trigger clinical occurrence of ventricular arrhythmia or otherwise silent cardiac abnormalities.
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