Neuromuscular fatigue in healthy muscle: Underlying factors and adaptation mechanisms
Neuromuscular fatigue in healthy muscle: Underlying factors and adaptation mechanisms
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DOI：
10.1016/j.rehab.2011.01.001
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发表时间：
2011-03-01
影响因子：
4.6
通讯作者：
Guevel, A.
中科院分区：
文献类型：
--
作者：
Boyas, S.;Guevel, A.
目标。-本综述旨在定义神经肌肉疲劳的概念，并介绍造成这一现象的中枢和外周因素的最新知识。本综述还讨论了有关神经肌肉疲劳适应机制的文献。-参考PubMed(1954-2010)收录的182篇文献。-神经肌肉疲劳有中枢性和外周性起源。中枢性疲劳在长时间、低强度的运动中占主导地位，可能涉及大脑神经递质和肌肉传入纤维的活动引起的中枢指挥(运动、皮质、运动神经元)的下降。外周疲劳与从兴奋到肌肉收缩的机制受损有关，可能是由于钙离子运动的扰动、磷酸盐的积累和/或三磷酸腺苷储存的减少而引起的。为了补偿随之而来的力量生产的下降，生物体发展了几种明显涉及运动单位的适应机制。-疲劳的出现与力量产生所涉及的机制的改变有关。然后，中央和外围机制之间的相互作用导致一系列事件，最终导致观察到的部队生产减少。(C)2011年爱思唯尔·马森公司。版权所有。
Objectives. - 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.Method. - One hundred and eighty-two articles indexed in PubMed (1954-2010) have been considered.Results. - 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.Conclusion. - 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. (C) 2011 Elsevier Masson SAS. All rights reserved.