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为探讨运动对线粒体模结构和功能的影响，本研究以力竭游泳大鼠为运动疲劳模型，观察了大鼠力竭运动后心肌线粒体脂质过氧化水平（MDA）和还原性谷胱甘肽（GSH）含量的变化．发现运行后即刻心肌线粒体脂质过氧化水平显著升高（P＜0．01），GSH含量显著下降（P＜0．01）．结果提示，力竭运动后心肌线粒体内源自由基生成增加而消除能力下降可能是线粒体膜损伤的原因之一．
In order to explore the effect of exercise on the structure and function of mitochondria, exhaustive swimming rats were used as sports fatigue model to observe the changes of myocardial mitochondrial lipid peroxidation (MDA) and reducing glutathione (GSH) content changes. It was found that myocardial mitochondrial lipid peroxidation increased significantly (P <0.01) and GSH content decreased significantly after operation (P <0.01). The results suggest that after exhaustive exercise, mitochondrial endogenous free radical production increased and decreased ability to eliminate may be one of the causes of mitochondrial membrane damage.