摘要
80年代中期，许多研究证明，运动中乳酸的产生与体内是否缺氧无关，并指出“氧债”、“氧亏”、和“无氧阈”是3个错误概念，提出了“运动后过量氧耗”的概念。近年来提出的疲劳控制链或运动性疲劳突变理论，都力图从多方面说明疲劳的发生原因。运动可使骨骼肌纤维胞浆钙离子浓度升高；大负荷运动后骨骼肌延迟性结构变化，与胞浆Ca2＋浓度的延迟性升高在时间上具有一致性；运动可使自由基生成增加，自由基可造成组织损伤。研究表明，运动员肌纤维的机能对运动成绩的影响大于心肺功能，在这方面的研究已深到细胞、分子水平。
By the mid 1980 s, researches had proved that the production of lactate during exercise had noth ing to do with the deficit of oxygen of the body. ' Oxygen debt, ' 'oxygen deficit' and ' anaerobic threshold' had been proved to be three wrong concepts and instead, a concept of 'postexercise oxygen con sumption (EPOC)' had been proposed. In recent years with an attempt to explain the causes of fatigue from multiple aspects, a theory about control chain and mutation of exercise fatigue was advanced. Exercise can cause the increase of Ca2+ concentration of myoplasma; delayed structure alteration of skeletal muscles after exercise with large load is consistent to the time of delayed increase of Ca2+ concentration of myoplasma; exer cise can cause the increase of production of free base, which may cause the injuries of tissue. Researches.have indicated that the influence of muscle fiber function to the performance is greater than cardiorespiratory func tion. Researches on skeletal muscles have gone deep into the molecular and cellular level.
出处
《北京体育大学学报》
CSSCI
1994年第4期50-57,共8页
Journal of Beijing Sport University
关键词
运动生理学
研究
现状
exercise physiology, the present condition of research, macro-research, micro-research
