力竭运动导致运动性疲劳产生机制的研究

大鼠进行一次性力竭运动后,大鼠股四头肌红肌肌肉匀浆过氧化物丙二醛(MDA)的含量显著升高,红肌匀浆中碱性磷酸酶活性(AKP)及血清磷酸肌酸激酶(CK)活性也显著升高。MDA含量显著升高与这两种酶活性显著升高之间具有显著相关性。说明一次性力竭运动使大鼠股四头肌红肌自由基水平升高,从而导致股四头肌红肌生物膜的完整性丧失及损害,使肌肉工作能力下降而产生疲劳。

A Research on the Mechanism for the Fatigue in Rats Resulted from Exhausted Exercise

The purpose of the present study was designed to test the hypothsis that the extensive damage and injury to the normal structure and function of biomembrane resulted from the increase in free radical(FR)activity in exercise was the major cause of the decrease in exercise capacity and fatigue.Malondialdehyde (MDA) and alkaline phosphatase (AKP) activity in red muscle homogenate and creatine kinase (CK) activity in serum increased significantly after exhausted exercise. The rising level of MDA in red muscle homogenate was significantly correlated with the rising level of AKP; activity in red muscle homogenate (r=0.87, p<0.05) and with the rising level of CK activity in serum(r = 0.88,p<0.05). It indicated that exhausted exercise caused the significant increase in FR activity, which resulted from the damage to the normal structure and extensive injury to the normal function of biomembrane. As a result it caused the decrease in exercise capacity and led to fatigue.