Sesboüé B, Guincestre J-Y
Institut Régional de Médecine du Sport, MCU-PH, CHU Côte-de-Nacre, 14033 Caen cedex, France.
Ann Readapt Med Phys. 2006 Jul;49(6):257-64, 348-54. doi: 10.1016/j.annrmp.2006.04.021. Epub 2006 Apr 27.
Although everyone knows fatigue personally, it is a difficult concept to define. For muscular fatigue, one must know the aspect of performance affected. The most obvious demonstrations are decreased maximal force and slowed muscular answer. Fatigue can have a central origin, by reducing cognitive performance or lowering excitation of motoneurons. Various mediators are in question (serotonin, moduline, dopamine). The fatiguing muscular contractions are accompanied by reduced discharges of motoneurons. The neuromuscular junction does not seem to be in question. Cold reduces muscular power, whereas a hot environment limits exercise by a central mechanism, which starts the normal behavioural response to stop the exercise. Fatigue can also be the consequence of overtraining. In the periphery, the electric activity of the membrane's surface is the first possible sign of failure, which explains high-frequency fatigue: the accumulation of potassium outside the cell blocks the sodic channels to block the potentials of action or slow down their propagation. With fatigue, less calcium is released and limits the number of attached actin-myosin bridges connections of actin-myosin. The slowing down of the muscular answer represents a deterioration of the function of actin-myosin bridges. On the metabolic level, the most-often evoked changes are reduced pH and increased intracellular lactate level. However, these variations cannot all describe fatigue, since patients with Mc Ardle disease do not exhibit these variations but very quickly experience tiredness. In fact, an association of small metabolic intracellular variations could explain tiredness. The fast fibres are larger than slow fibres; their metabolic needs are higher and they are thus more sensitive to tiredness. The half time of recovery is within approximately 1 min: normal values of force and power are recovered after 5 to 10 min. During endurance activities, the limiting factors are glycogen reserves and levels of oxidative enzymes. On the whole, mechanisms of fatigue must be explored to completely understand the governing phenomena.
虽然每个人都亲身经历过疲劳,但它却是一个难以定义的概念。对于肌肉疲劳而言,必须了解其影响的表现方面。最明显的表现是最大力量下降和肌肉反应减慢。疲劳可能源于中枢,通过降低认知能力或降低运动神经元的兴奋性。多种介质都可能与此有关(血清素、调钙素、多巴胺)。引起疲劳的肌肉收缩会伴随着运动神经元放电减少。神经肌肉接头似乎没有问题。寒冷会降低肌肉力量,而炎热环境则通过一种中枢机制限制运动,这种中枢机制会引发正常的行为反应以停止运动。疲劳也可能是过度训练的结果。在周围组织中,细胞膜表面的电活动是功能衰竭的首个可能迹象,这解释了高频疲劳:细胞外钾离子的积累会阻断钠通道,从而阻止动作电位或减缓其传播。随着疲劳的出现,释放的钙减少,限制了肌动蛋白 - 肌球蛋白桥的连接数量。肌肉反应的减慢代表着肌动蛋白 - 肌球蛋白桥功能的恶化。在代谢层面,最常被提及的变化是pH值降低和细胞内乳酸水平升高。然而,这些变化并不能完全描述疲劳,因为患有麦克尔迪氏病的患者并不表现出这些变化,但却很快就会感到疲倦。实际上,细胞内微小代谢变化的综合作用可能解释疲劳现象。快肌纤维比慢肌纤维大;它们的代谢需求更高,因此对疲劳更敏感。恢复的半衰期约为1分钟:5到10分钟后力量和功率恢复到正常值。在耐力活动中,限制因素是糖原储备和氧化酶水平。总体而言,必须探索疲劳机制才能完全理解相关的控制现象。