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作 者:李彤[1]
出 处:《北京体育大学学报》2009年第9期62-64,共3页Journal of Beijing Sport University
基 金:辽宁省教育厅科学技术研究项目(编号:2009A670)
摘 要: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 and chronic intermittent hypoxia training on myocardial uhrastructure of intercalated disc and mitochondrial ATPase. Methods: Myocardial uhrastructure of intercalated disc are observed by transmission electron microscope, meanwhile the activities of Na^+ K^+ ,Ca^2+ ,Mg^2+ and Ca^2+ Mg^2+ ATPase are tested. Results: acute hypoxic stress can induce myocardial ultrastructure damage and the activity of ATPase decreases. The damages to the rats exposed to hypoxia with 4-week training are alleviated and the activity of ATPase increased significantly. Intermittent hypoxic training acclimatization improves uhrastructure of intercalated disc. Conclusion: The severest damages in acute hypoxic exercise groups may be caused by exercise together with hypoxia. The results indicate that there is close relationship between the damages of myocardial ultrastructure and hypoxia, and the results suggest that training protects myocardial cells from injury induced by hypoxia and improve energy metabolism.
分 类 号:G804.7[文化科学—运动人体科学]
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