EA 4334, UFR STAPS de Nantes, laboratoire « Motricité, Interactions, Performance », université de Nantes, 25 bis, boulevard Guy-Mollet, 44322 Nantes cedex 3, France.
Ann Phys Rehabil Med. 2011 Mar;54(2):88-108. doi: 10.1016/j.rehab.2011.01.001. Epub 2011 Feb 18.
This review aims to define the concept of neuromuscular fatigue and to present the current knowledge of the central and peripheral factors at the origin of this phenomenon. This review also addresses the literature that focuses on the mechanisms responsible for the adaption to neuromuscular fatigue.
One hundred and eighty-two articles indexed in PubMed (1954-2010) have been considered.
Neuromuscular fatigue has central and peripheral origins. Central fatigue, preponderant during long-duration, low-intensity exercises, may involve a drop in the central command (motor, cortex, motoneurons) elicited by the activity of cerebral neurotransmitters and muscular afferent fibers. Peripheral fatigue, associated with an impairment of the mechanisms from excitation to muscle contraction, may be induced by a perturbation of the calcium ion movements, an accumulation of phosphate, and/or a decrease of the adenosine triphosphate stores. To compensate for the consequent drop in force production, the organism develops several adaptation mechanisms notably implicating motor units.
Fatigue onset is associated with an alteration of the mechanisms involved in force production. Then, the interaction between central and peripheral mechanisms leads to a series of events that ultimately contribute to the observed decrease in force production.
本文旨在定义神经肌肉疲劳的概念，并介绍导致这种现象的中枢和外周因素的最新知识。本文还讨论了侧重于导致神经肌肉疲劳适应的机制的文献。
共查阅了 1954 年至 2010 年间在 PubMed 上索引的 182 篇文章。
神经肌肉疲劳有中枢和外周起源。中枢疲劳在长时间、低强度运动中占主导地位，可能涉及到大脑神经递质和肌肉传入纤维活动引起的中枢指令（运动、皮层、运动神经元）下降。外周疲劳与兴奋到肌肉收缩机制的损伤有关，可能是由钙离子运动的干扰、磷酸盐的积累和/或三磷酸腺苷储存的减少引起的。为了弥补力量产生的相应下降，机体发展了几种适应机制，特别是涉及运动单位。
疲劳的发生与参与力量产生的机制的改变有关。然后，中枢和外周机制的相互作用导致一系列最终导致观察到的力量产生下降的事件。
