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为探讨长时间有氧运动至力竭时引起的自由基积累对线粒体正常生理功能的影响，本实验让大白鼠进行游泳运动至力竭，取心肌作为实验材料，研究力竭运动对自由基生成、线粒体膜通透性、线粒体内游离Ｃａ２＋浓度等一系列因素的影响。结果显示，大白鼠游泳至力竭时，心肌线粒体丙二醛（ＭＤＡ）含量显著升高（Ｐ＜０．０１），还原型谷胱甘肽（ＧＳＨ）含量下降（Ｐ＜０．０５内自由基生成和清除失衡，自由基在体内积累，即运动性内源自由基增生。同时观察到琉基含量下降（Ｐ＜０．０１），ＮＡＤＨ荧光值降低（Ｐ＜０．０５）利用Ｆｕｒａ－２ＡＭ做为荧光探针还测到游离Ｃａ２＋浓度下降（Ｐ＜０．０５），提示自由基攻击膜上巯基，膜的完整性受到一定程度损伤，导致Ｃａ２＋外流。Ｃａ２＋浓度下降，削弱了Ｃａ２＋对线粒体内Ｃａ２＋──敏感脱氢酶的激活作用，抑制了线粒体氧化代谢，使还原当量（ＮＡＤＨ）水平降低。而还原当量减少使膜上巯基更易受到自由基攻击，导致Ｃａ２＋进一步外流，形成恶性循环，结果是导致线粒体功能下降，机体产生疲劳。
In order to explore the long-time aerobic exercise caused by exhaustion of free radicals accumulation on the normal mitochondrial physiological function, the experiment for rats to swim to exhaustion, the myocardial as a test material to study exhaustive exercise on free radical generation , Mitochondrial membrane permeability, mitochondrial free Ca2 + concentration and a series of factors. The results showed that when swimming to exhaustion, the content of malondialdehyde (MDA) in myocardial mitochondria increased significantly (P <0.01) and the content of reduced glutathione (GSH) decreased (P <0.05) Free radicals were accumulated in the body, that is, exercise-induced endogenous free radical proliferation.At the same time, the content of thiourea was decreased (P <0.01) and the fluorescence value of NADH was decreased (P <0.05) 2AM as a fluorescent probe also detected a decrease in free Ca2 + concentration (P <0.05), suggesting that free radicals attack membrane thiol, the membrane integrity of a certain degree of damage, leading to Ca2 + outflow .Ca2 + concentration decreased, weakened the Ca2 + Mitochondrial Ca2 + -sensitive dehydrogenase activation, inhibition of mitochondrial oxidative metabolism, so reducing equivalent (NADH) level decreased, while reducing equivalent reduction of the membrane more vulnerable to free radical attack of sulfhydryl, leading to Ca2 + further outflow, the formation of a vicious cycle , The result is to lead to decreased mitochondrial function, body fatigue .