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采用递增负荷力竭性运动模型，观察了ＳＤ大鼠急性运动至力竭后心肌和骨骼肌线粒体内膜流动性和ＡＴＰ酶活性的变化。发现心肌和骨骼肌线粒体内膜荧光偏振值和微粘度均较安静时增高，示内膜流动性显著降低（均Ｐ＜０．０１）；心肌和骨骼肌线粒体内膜ＡＴＰ酶活性分别较安静时下降７４．３％和４５．７％（Ｐ＜０．０１和Ｐ＜０．０５）。研究提示，力竭性运动后大鼠心肌和骨骼肌线粒体呼吸链内膜分子动力学改变直接影响内膜磷酸化过程，可能是运动性疲劳的线粒体膜分子特征之一。
Incremental load exhaustive exercise model was used to observe the changes of mitochondrial inner membrane fluidity and ATPase activity in SD rats after acute exercise to exhaustion. It was found that the mitochondrial fluorescence polarization and microviscosity of myocardium and skeletal muscle were higher than that of resting myocardium and skeletal muscle, indicating that the endometrial fluidity was significantly decreased (all P <0.01). The mitochondrial intrinsic ATPase activity in myocardium and skeletal muscle were respectively quiescent Decreased by 74.3% and 45.7% respectively (P <0.01 and P <0.05). Studies have shown that exhaustive exercise in rat myocardium and skeletal muscle mitochondrial respiratory chain endomembrane molecular dynamics directly affect the process of endometrial phosphorylation may be one of the molecular features of exercise-induced fatigue mitochondrial membrane.