Abstract

With increasing duration of swimming exercise the heart becomes less sensitive to ischemia, as evaluated by the rate of development of ischemic contracture immediately after the exertion. This delay in the development of ischemic contracture was apparently due to metabolic changes directed to decrease the heart energy consumption in conditions where the capacity for glycolytic ATP production was decreased. A decrease in: 1) the amount of rapidly exchangeable Ca2+, which is bound to anionic sites on the sarcolemmal membrane and 2) the myofibrillar Ca2+ sensitivity seems to play an important role. Regular swimming exercise, which is characterized by a significant cardiac hypertrophy and enhanced heart glycogen content, increased the sensitivity of energy mobilizing processes to catecholamine action. These changes accelerated ATP depletion and the development of an irreversible injury when the heart was made ischemic after catecholamine stimulation. Obtained results together with data from literature underline the importance of regular testing of cardiac function, including echocardiography, in young sportsmen undergoing high-intensity training. Verf.-Referat