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以大鼠渐增负荷力竭性跑台跑为运动性疲劳模型，观察了运动后大鼠骨骼肌线粒体电子漏和质子漏的变化。测定线粒体超氧阴离子生成量和脂质过氧化水平。分别测定线粒体以苹果酸＋谷氨酸和以琥珀酸为底物的态4呼吸、态3呼吸、呼吸控制比及磷氧比。结果表明，运动性疲劳状态下大鼠骨骼肌线粒体超氧阴离子生成增加，脂质过氧化水平也显著增加；以苹果酸十谷氨酸或以琥珀酸为底物的态4呼吸速率明显加快，呼吸控制比、磷氧比显著下降。结果提示，力竭性运动后下大鼠骨骼肌线粒体电子漏导致线粒体质子漏增多，是运动性疲劳状态下线粒体氧化磷酸化偶联程度下降的重要因素。实验结果支持电子漏引起质子漏的假说。
The rats were subjected to exhaustive treadmill exercise with increasing load to exercise fatigue model. The change of mitochondrial electron leakage and proton leakage in skeletal muscle of rats were observed. The mitochondrial superoxide anion production and lipid peroxidation were measured. The mitochondria were tested for the state 4 respiration, state 3 respiration, respiration control ratio and the ratio of phosphorus to oxygen, respectively, using malic acid + glutamic acid and succinic acid as substrates. The results showed that the generation of mitochondrial superoxide anion and the level of lipid peroxidation in rat skeletal muscle increased significantly under exercise-induced fatigue. The respiration rate of state 4 in the presence of 10-glutamic acid or succinic acid was significantly increased, Respiratory control ratio, phosphorus-oxygen ratio decreased significantly. The results suggest that prolonged exercise after the mitochondrial electron leak in rat skeletal muscle lead to increased proton leak of mitochondria, is an important factor in mitochondrial oxidative phosphorylation coupling degree of exercise-induced fatigue. The experimental results support the hypothesis that electron leakage causes proton leakage.