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目的:研究急性低氧运动和慢性间歇低氧训练对大鼠心肌心室闰盘和心肌线粒体ATP酶的影响,旨在探讨心肌低氧适应的机制,为高原训练方案的制定提供理论依据。方法:采用透射电镜技术观察大鼠心肌心室闰盘超微结构在低氧适应过程中的变化,同时用分光光度法测定心肌线粒体Na~+K~+、Ca~(2+)、Mg~(2+)和Ca~(2+)Mg~(2+)四种ATP酶的活性。结果:急性低氧运动可造成心肌超微结构的损伤,Na~+K~+-ATPase和Ca~(2+)-ATPase明显下降;经过4周的运动训练后再进行低氧应激,心肌的损伤减轻,线粒体ATP酶的活性都显著升高。结论:急性运动后进入急性低氧应激,导致心肌损伤加重,是由于运动缺氧损伤和低氧损伤双重作用的结果,而长期间歇低氧训练可减轻低氧环境心肌的损伤,能量代谢得到改善。
Objective: To study the effects of acute hypoxic exercise and chronic intermittent hypoxia training on myocardial ventricular intercaentricular platelet and myocardial mitochondrial ATPase in order to explore the mechanism of myocardial hypoxia adaptation, and to provide a theoretical basis for the establishment of plateau training program. Methods: Transmission electron microscopy was used to observe the change of ultrastructure of rat ventricular intercalary disc during hypoxia adaptation. At the same time, the myocardial mitochondrial Na ~ + K ~ +, Ca ~ (2 +), Mg ~ (- 2+) and Ca ~ (2+) Mg ~ (2+) four ATPase activity. Results: Acute hypoxia induced myocardial ultrastructure damage, Na ~ + K ~ + -ATPase and Ca ~ (2 +) - ATPase decreased significantly. After 4 weeks of exercise training, hypoxia stress and myocardium Lessened the injury, mitochondrial ATPase activity were significantly increased. Conclusion: Acute hypoxia stress after acute exercise, leading to increased myocardial injury, is due to the dual role of exercise hypoxia and hypoxia injury results, and long-term intermittent hypoxic training can reduce myocardial hypoxia injury, energy metabolism improve.