Korge P, Männik G
Department of Sport Physiology, Tartu University, Estonia, USSR.
Int J Sports Med. 1990 Oct;11(5):387-92. doi: 10.1055/s-2007-1024824.
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.
随着游泳运动时间的增加,心脏对缺血的敏感性降低,这是通过运动后立即出现的缺血性挛缩的发展速率来评估的。缺血性挛缩发展的延迟显然是由于在糖酵解产生ATP的能力下降的情况下,代谢变化旨在降低心脏能量消耗。1)与肌膜阴离子位点结合的快速可交换Ca2+量的减少以及2)肌原纤维Ca2+敏感性的降低似乎起着重要作用。以显著的心脏肥大和心脏糖原含量增加为特征的定期游泳运动,提高了能量动员过程对儿茶酚胺作用的敏感性。当心脏在儿茶酚胺刺激后缺血时,这些变化加速了ATP的消耗和不可逆损伤的发展。获得的结果以及文献数据强调了对接受高强度训练的年轻运动员进行包括超声心动图在内的心脏功能定期检测的重要性。