运动性骨骼肌疲劳亚细胞机制的探讨

本实验采用持续性下坡跑运动，观察大鼠骨骼肌运动后不同时相线粒体形态、代谢、机能等指标的变化，结果表明：大鼠运动后即刻线粒体钙含量、细胞膜丙二醛（ＭＤＡ）值明显增加，ＡＴＰ含量和细胞膜Ｎａ＋，Ｋ＋－ＡＴＰ酶活性下降；运动后２４ｈ线粒体钙含量、ＭＤＡ值增加最明显，ＡＴＰ含量仍未恢复，细胞膜Ｎａ＋，Ｋ＋－ＡＴＰ酶活性基本恢复，线粒体体密度、平均体积比运动前明显增加，比表面缩小；运动后４８ｈＡＴＰ含量完全恢复，线粒体钙含量、ＭＤＡ值开始恢复。本研究结果提示，急性运动引起的细胞膜脂质过氧化加强、线粒体形态、代谢机能异常抑制线粒体氧化磷酸化过程、减少ＡＴＰ生成可能是运动性骨骼肌疲劳的亚细胞机制之一。耐力训练可以通过改善线粒体形态、代谢、机能提高机体的运动能力。

STUDY ON SUBCELLULAR MECHANISM OF EXERCISE-INDUCED SKELETAL MUSCLE FATIGUE

The purpose of this paper was to study the subcellular mechanism of exercise-induced skeletal muscle fatigue by examining the changes of indexes such as mitochondrial morphology,metabolism and function after running in rats. It was found that mitochondrial calcium (Mit Ca)and malondialdehyde (MDA) values increased immediately after exercise, whereas ATP content,Na , K -ATPase activity decreased. Compared with the control group, the Mit ca, MDA and ATP values did not recover by 24 hours after running, while Na , K -ATPase activity recovered basically. A significant increase was observed in mitochondrial volume density (VQ) and mean volume (VQ), and a decrease was shown in mitochondrial specific surface (S / V). In comparison with the control group. there was a complete recovery of ATP content and a partial recovery of Mit Ca and MDA values by 48 hours. Therefore, it is suggested that increase in exercise-induced lipid peroxides, morphologic and metabolic abnormalities of mitochondria, which inhibit the oxidative phosphorylation and reduce the ATP production, may be the major causes of exercise induced fatigue. Moreover, endurance training could help to improve exercise capacity by maintaining metabolism and morphology of mitochondria at a normal level.