摘要：运动性骨骼肌微损伤(exercise-induced muscle damage，EIMD)会引起肌肉功能的暂时性下降，如果处理不当，还可能造成更严重的损伤或者过度训练，甚至导致运动员运动寿命的结束。但是，已有研究表明恰当的离心运动训练在导致EIMD的同时比向心运动训练更能促进肌纤维肥大和相应的肌力增长，并且还有典型的“重复训练效应”，即EIMD恢复后一段时期内，肌肉重复同样的运动所引起的损伤或延迟性肌肉酸痛(DOMS)明显减轻。因此对其进行深入的研究不但有利于指导运动员避免或者减轻EIMD所带来的负面影响，同时有助于进一步阐明机体对运动训练产生适应的过程或机制。EIMD的诱发机制目前还不清楚，各种假说从本质上可以归纳为机械损伤学说和代谢紊乱学说。但不管是哪种机制诱发了EIMD，众多的实验结果已经证明机体在EIMD过程中发生了深刻的代谢变化，因此从代谢的角度对EIMD进行系统研究将成为此领域研究的重要方向。
关键词：运动人体科学；运动性骨骼肌微损伤；代谢机制；代谢反应；综述
中图分类号：G804.53文献标识码：A文章编号：1006-7116(2010)12-0112-06
Review of the metabolic mechanism and metabolic reaction of
slight kinetic skeletal muscle damage
LI Jiang-hua1，MAO Hai-feng2
（1.School of Physical Education，Jiangxi Normal University，Nanchang 330027，China；
2.School of Physical Education，Yichun College，Yichun 336000，China）
Abstract: Slight kinetic skeletal muscle damage (SKSMD) can cause the temporary deterioration of muscle functions, may also cause more serious damage or over training or even the end of athlete sports life if not treated properly. However, existing researches indicated that appropriate centrifugal exercise training can boot muscle fiber hypertrophy and corresponding muscle strength growth better than centripetal exercise training, and has a typical “repeated training effect”, i.e. within a certain period after recovery from SKSMD, the damage or delayed muscle ache caused by muscle repeating the same exercise is significantly reduced or alleviated. Therefore, in-depth study of it is conducive not only to guiding athletes to prevent SKSMD or negative effects brought by SKSMD, but also to further describing the process or mechanism for the body to adapt to exercise training. At present, the inducement mechanism of SKSMD is not clear; essentially various hypotheses can be reduced into the theory of mechanical damage and the theory of metabolic disorder. However, no matter which mechanism induced SKSMD, a lot of experimental results have proved that profound metabolic changes occurred in the process of SKSMD. Therefore, systematic study of SKSMD from the perspective of metabolism will become an important direction in the study in this area.
Key words: sports science of human body；slight kinetic muscle damage；metabolic mechanism；metabolic reaction；overview
现代竞技体育竞争的残酷性常常迫使运动员进行极限强度的训练。事实上，不断地进行超负荷训练，从而使身体产生适应，也是运动员竞技水平逐渐提高的必然过程。然而研究表明，大运动量训练(特别是离心运动或离心工作为主的运动)会导致骨骼肌延迟性肌肉损伤[1-3]。这种损伤不同于一般运动创伤学意义的肌肉挫伤、拉伤等，它在时间上表现为进行性加重，伴随延迟性肌肉酸痛(delayed onset muscle soreness，DOMS)[2，4-5]，并且会引起白细胞介素-6(IL-6)、肌酸激酶(CK)、和Ca2+的变化[6-7]，被称为运动性骨骼肌微损伤(exercise-induced muscle damage，EIMD)。一般来说，EIMD能够自愈，EIMD痊愈的时间因人而异，最短的33 d，最长的89 d[2]，并且连续运动后也没有观察到累加的迹象[1]。但是，EIMD无疑会引起肌肉功能的暂时性下降，以及动脉硬化等心血管问题[8]，影响运动员在此期间的比赛成绩[9-10]；同时，在肌肉功能没有得到充分恢复的情况下，继续进行大强度训练或比赛往往会造成更严重的损伤[11-12]或过度训练(overtraining)[13]，从而导致运动员运动寿命的结束。EIMD的诱发机制还不清楚，目前提出的各种假说从本质上可以归纳为机械损伤学说和代谢紊乱学说[14-15]。首先人们认为EIMD主要是由于运动引起的肌纤维的机械损伤所致，但是随着研究的深入，研究人员发现，EIMD的许多现象难以用机械损伤学说进行解释，于是又出现了代谢紊乱学说，最近Tee等人[15]甚至还提出，机械损伤和代谢紊乱都可能诱发EIMD。可是不管哪种机制诱发了EIMD，众多的实验结果已经证明机体在EIMD过程中发生了深刻的代谢变化。本文从代谢的角度综合阐述EIMD的发生机制及相应的代谢反应。