Millet Guillaume Y, Lepers Romuald
Research Group Physiology and Physiopathology of Exercise and Handicap, University of Saint-Etienne, Saint-Etienne, France.
Sports Med. 2004;34(2):105-16. doi: 10.2165/00007256-200434020-00004.
It is well known that impairment of performance resulting from muscle fatigue differs according to the types of contraction involved, the muscular groups tested and the exercise duration/intensity. Depending on these variables, strength loss with fatigue can originate from several sites from the motor cortex through to contractile elements. This has been termed 'task dependency of muscle fatigue'. Only recently have studies focused on the origin of muscle fatigue after prolonged exercise lasting 30 minutes to several hours. Central fatigue has been shown to contribute to muscle fatigue during long-distance running by using different methods such as the twitch interpolation technique, the ratio of the electromyogram (EMG) signal during maximal voluntary contraction normalised to the M-wave amplitude or the comparison of the forces achieved with voluntary- and electrically-evoked contractions. Some central activation deficit has also been observed for knee extensor muscles in cycling but central fatigue after activities inducing low muscular damage was attenuated compared with running. While supraspinal fatigue cannot be ruled out, it can be suggested that spinal adaptation, such as inhibition from type III and IV group afferents or disfacilitation from muscle spindles, contributes to the reduced neural drive after prolonged exercise. It has been shown that after a 30 km run, individuals with the greatest knee extensor muscle strength loss experienced a significant activation deficit. However, central fatigue alone cannot explain the entire strength loss after prolonged exercise. Alterations of neuromuscular propagation, excitation-contraction coupling failure and modifications of the intrinsic capability of force production may also be involved. Electrically-evoked contractions and associated EMG can help to characterise peripheral fatigue. The purpose of this review is to further examine the central and peripheral mechanisms contributing to strength loss after prolonged running, cycling and skiing exercises.
众所周知，肌肉疲劳导致的运动能力受损会因所涉及的收缩类型、测试的肌肉群以及运动持续时间/强度的不同而有所差异。根据这些变量，疲劳导致的力量损失可能源于从运动皮层到收缩元件的多个部位。这被称为“肌肉疲劳的任务依赖性”。直到最近，研究才聚焦于持续30分钟至数小时的长时间运动后肌肉疲劳的起源。通过使用不同的方法，如抽搐插值技术、最大自主收缩期间肌电图（EMG）信号与M波振幅的归一化比值，或自愿收缩和电诱发收缩所达到力量的比较，中枢疲劳已被证明在长跑过程中会导致肌肉疲劳。在骑自行车时，也观察到了股四头肌的一些中枢激活不足，但与跑步相比，在引起低肌肉损伤的活动后中枢疲劳有所减轻。虽然不能排除脊髓上的疲劳，但可以认为脊髓适应性变化，如来自III型和IV型传入神经的抑制或肌梭的去易化，会导致长时间运动后神经驱动的降低。研究表明，在进行30公里跑步后，股四头肌力量损失最大的个体经历了显著的激活不足。然而，仅中枢疲劳并不能解释长时间运动后的全部力量损失。神经肌肉传导的改变、兴奋 - 收缩偶联失败以及力量产生内在能力的改变也可能参与其中。电诱发收缩及相关的肌电图有助于表征外周疲劳。本综述的目的是进一步研究长时间跑步、骑自行车和滑雪运动后导致力量损失的中枢和外周机制。
