Schwellnus M P, Derman E W, Noakes T D
MRC/UCT Bioenergetics of Exercise Research Unit, University of Cape Town Medical School, Newlands, South Africa.
J Sports Sci. 1997 Jun;15(3):277-85. doi: 10.1080/026404197367281.
The aetiology of exercise-associated muscle cramps (EAMC), defined as 'painful, spasmodic, involuntary contractions of skeletal muscle during or immediately after physical exercise', has not been well investigated and is therefore not well understood. This review focuses on the physiological basis for skeletal muscle relaxation, a historical perspective and analysis of the commonly postulated causes of EAMC, and known facts about EAMC from recent clinical studies. Historically, the causes of EAMC have been proposed as (1) inherited abnormalities of substrate metabolism ('metabolic theory') (2) abnormalities of fluid balance ('dehydration theory'), (3) abnormalities of serum electrolyte concentrations ('electrolyte theory') and (4) extreme environmental conditions of heat or cold ('environmental theory'). Detailed analyses of the available scientific literature including data from recent studies do not support these hypothesis for the causes of EAMC. In a recent study, electromyographic (EMG) data obtained from runners during EAMC revealed that baseline activity is increased (between spasms of cramping) and that a reduction in the baseline EMG activity correlates well with clinical recovery. Furthermore, during acute EAMC the EMG activity is high, and passive stretching is effective in reducing EMG activity. This relieves the cramp probably by invoking the inverse stretch reflex. In two animal studies, abnormal reflex activity of the muscle spindle (increased activity) and the Golgi tendon organ (decreased activity) has been observed in fatigued muscle. We hypothesize that EAMC is caused by sustained abnormal spinal reflex activity which appears to be secondary to muscle fatigue. Local muscle fatigue is therefore responsible for increased muscle spindle afferent and decreased Golgi tendon organ afferent activity. Muscles which cross two joints can more easily be placed in shortened positions during exercise and would therefore decrease the Golgi tendon organ afferent activity. In addition, sustained abnormal reflex activity would explain increased baseline EMG activity between acute bouts of cramping. Finally, passive stretching invokes afferent activity from the Golgi tendon organ, thereby relieving the cramp and decreasing EMG activity.
运动相关性肌肉痉挛(EAMC)的定义为“体育锻炼期间或之后骨骼肌出现的疼痛性、痉挛性、非自主性收缩”,其病因尚未得到充分研究,因此目前还未被完全理解。本综述聚焦于骨骼肌放松的生理基础、EAMC常见假设病因的历史观点与分析,以及近期临床研究中关于EAMC的已知事实。从历史角度来看,EAMC的病因曾被认为是:(1)底物代谢的遗传性异常(“代谢理论”);(2)体液平衡异常(“脱水理论”);(3)血清电解质浓度异常(“电解质理论”);(4)极端的热或冷环境条件(“环境理论”)。对现有科学文献(包括近期研究数据)的详细分析并不支持这些关于EAMC病因的假设。在最近一项研究中,从跑步者在EAMC期间获取的肌电图(EMG)数据显示,基线活动增加(在痉挛发作之间),并且基线EMG活动的降低与临床恢复密切相关。此外,在急性EAMC期间,EMG活动较高,被动拉伸可有效降低EMG活动。这可能通过引发反向牵张反射来缓解痉挛。在两项动物研究中,在疲劳肌肉中观察到肌梭的异常反射活动(活动增加)和高尔基腱器官的异常反射活动(活动减少)。我们假设EAMC是由持续的异常脊髓反射活动引起的,这种活动似乎继发于肌肉疲劳。因此,局部肌肉疲劳导致肌梭传入活动增加和高尔基腱器官传入活动减少。在运动过程中,跨越两个关节的肌肉更容易处于缩短位置,从而会降低高尔基腱器官的传入活动。此外,持续的异常反射活动可以解释急性痉挛发作之间基线EMG活动的增加。最后,被动拉伸会引发来自高尔基腱器官的传入活动,从而缓解痉挛并降低EMG活动。