中文摘要：

目的：观察耐力运动训练对骨骼肌卫星细胞线粒体能量代谢的影响，并探讨其对成肌分化的调控机制。方法：C57BL／6小鼠随机分为安静对照组（N组）和运动训练组（T组）。12周训练后，两步酶消化法分离骨骼肌卫星细胞，免疫化学染色鉴定卫星细胞纯度。原代培养并体外诱导成肌分化，倒置显微镜观察卫星细胞成肌分化程度。分别在分化0h和24h测定线粒体呼吸功能、ATP合成活力、膜电位和MyHC、COXⅣ、AMPK、p-AMPK、p21蛋白表达量。结果：免疫化学染色显示desmin阳性细胞〉90％，表明获取的卫星细胞纯度高。HE染色结果显示T组腓肠肌肌纤维横截面积显著高于N组（P〈0．05）。分化0h时，T组态3呼吸速率（ST3）、呼吸控制比（RCR）、线粒体ATP合成活力、p21表达较N组显著升高（P〈0．05），P—AMPK表达显著降低（P〈0．05）。分化24h时，T组肌管形成数量及MyHC表达较N组显著升高（P〈0．05），ST3、RCR、ATP合成活力、膜电位、p21及COXIV表达显著增加（P〈0．05），P—AMPK表达显著降低（P〈0．05）。结论：耐力运动训练可提高未分化卫星细胞线粒体能量代谢水平．继而抑制AMPK活化而增加p21表达，从而促进成肌分化的启动和进程。

英文摘要：

Objective To observe the effect of endurance exercise on the mitochondrial bioenergetic metabolism in skeletal muscle satellite cells and its effect on the myogenesis. Methods C57BL/6 mice were randomly divided into two groups： normal control group （N） and exercise training group （T）. The animals in group T exercised on a treadmill for 12 weeks. Purified satellite cells were obtained and im- munohistochemical staining was employed to identify the satellite cells cultured in vitro. Differentiation was induced by changing the growth medium and observed by inverted microscopy. At 0 and 24 h of differentiation,mitochondrial respiration parameters,ATP synthetase activity,mitochondrial membrane potential （A~）,MyHC, COXIV ,AMPK, p-AMPK, and p21 protein expression were measured. Results Comparing with group N, at 0 h of differentiation, ST3, RCR, ATP synthesis activity, and p21 protein ex- pression dramatically increased（P 〈 0.05）, and p-AMPK protein expression significantly decreased（P 〈 0.05） in group T. At 24 h of differentiation, comparing with group N, the formation of myotubes and ex- pression of MyHC markedly increased in group T （P 〈 0.05）. In addition,ST3,RCR,and ATP synthesis activities, A~,p21 ,and COX IV protein expression showed significantly enhanced （P 〈 0.05）,and p- AMPK protein expression significantly diminished （P 〈 0.05）. Conclusion Endurance exercise markedly promotes the mitochondrial bioenergetic metabolism,which in turn enhances the myogenic differentiation through inactivation of AMPK and up-regulation of p21.