Rats on acute exhaustive swimming were used as experimental models. Sulfhydryl(-SH), Glutathione(GSH), phosphlipase A2(PLA2) and free Calcium(Ca2+) of myocardial mitochondrion after exhaustive exercise in rats were investigated. The results showed that -SH, GSH and Ca2+ content in myocardial mitochondrion after exhaustive exercise were significantly degraded than that of the resting group. According to the results, the relationship among the oxidant reduction reaction of exercise induced reactive oxygen species, the changes of myocardial mitochondria membrane structure and the fee calcium of matrix was discussed. It is suggested that increasing of PLA2 activity might be a key parameter of fatigue after prolonged exhaustive exercise. By means of further observation the molecules mechanism of prolonged exercise induced fatigue appearance could be further deeply understood.%本实验以力竭游泳(300±50 min)的大鼠为运动疲劳模型，观察了大鼠心肌线粒体的巯基(-SH)、还原型谷胱苷肽(GSH)、磷脂酶A2(PLA2)、游离钙(FCa2+)等指标，结果表明：长时间力竭游泳的大鼠心肌线粒体与对照组相比，-SH含量和GSH含量显著降低(p＜0.001)，PLA2的活性显著增加(p＜0.001)；FCa2+含量明显下降(p＜0.05)。本文根据以上结果探讨了运动时机体产生的活性氧的氧化过程与运动疲劳后心肌线粒体膜结构变化以及游离钙之间的关系，提出力竭运动后PLA2活性增加可能是其疲劳的关键指标，通过对这一指标的进一步观察能更好地了解长时间运动性疲劳发生的分子机制。
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