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采用递增负荷力竭性运动模型，观察了Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠急性运动至力竭后心肌线粒体内膜流动性、ＮＡＤＨ－ＣｏＱ还原酶及ＡＴＰ酶活性的变化。结果表明，大鼠心肌线粒体内膜荧光偏振值较安静时显著增高（Ｐ＜０．０１），示膜流功性降低。线粒体内膜ＮＡＤＨ－ＣｏＱ还原酶和ＡＴＰ酶活性分别较安静时下降６１．６％和７４．３％（Ｐ＜０．０５，Ｐ＜０．０１）。提示，力竭性运动后大鼠心肌线粒体内膜功能改变，其膜流动性和呼吸链酶活性变化，可能是运动性疲劳的重要膜分子机制之一。
Incremental load exhaustive exercise model was used to observe changes of myocardial mitochondrial inner membrane fluidity, NADH-CoQ reductase and ATPase activity after acute exercise to exhaustive Sprague-Dawley rats. The results showed that the mitochondrial fluorescence in rat myocardial mitochondrial polarization was significantly higher (P <0.01), decreased membrane fluidity. The mitochondrial NADH-CoQ reductase and ATPase activities were decreased by 61.6% and 74.3% (P <0.05, P <0.01), respectively. It is suggested that changes of mitochondrial inner membrane function, membrane fluidity and respiratory chain enzyme activity in rat myocardial after exhaustive exercise may be one of the important membrane molecular mechanisms of exercise-induced fatigue.