McManus Lara, Hu Xiaogang, Rymer William Z, Lowery Madeleine M, Suresh Nina L
University College Dublin, Belfield, Dublin, Ireland;
Rehabilitation Institute of Chicago, Chicago, Illinois; and.
J Neurophysiol. 2015 May 1;113(9):3186-96. doi: 10.1152/jn.00146.2015. Epub 2015 Mar 11.
The neuromuscular strategies employed to compensate for fatigue-induced muscle force deficits are not clearly understood. This study utilizes surface electromyography (sEMG) together with recordings of a population of individual motor unit action potentials (MUAPs) to investigate potential compensatory alterations in motor unit (MU) behavior immediately following a sustained fatiguing contraction and after a recovery period. EMG activity was recorded during abduction of the first dorsal interosseous in 12 subjects at 20% maximum voluntary contraction (MVC), before and directly after a 30% MVC fatiguing contraction to task failure, with additional 20% MVC contractions following a 10-min rest. The amplitude, duration and mean firing rate (MFR) of MUAPs extracted with a sEMG decomposition system were analyzed, together with sEMG root-mean-square (RMS) amplitude and median frequency (MPF). MUAP duration and amplitude increased immediately postfatigue and were correlated with changes to sEMG MPF and RMS, respectively. After 10 min, MUAP duration and sEMG MPF recovered to prefatigue values but MUAP amplitude and sEMG RMS remained elevated. MU MFR and recruitment thresholds decreased postfatigue and recovered following rest. The increase in MUAP and sEMG amplitude likely reflects recruitment of larger MUs, while recruitment compression is an additional compensatory strategy directly postfatigue. Recovery of MU MFR in parallel with MUAP duration suggests a possible role for metabolically sensitive afferents in MFR depression postfatigue. This study provides insight into fatigue-induced neuromuscular changes by examining the properties of a large population of concurrently recorded single MUs and outlines possible compensatory strategies involving alterations in MU recruitment and MFR.
目前尚不清楚用于补偿疲劳引起的肌肉力量不足的神经肌肉策略。本研究利用表面肌电图(sEMG)以及个体运动单位动作电位(MUAPs)群体的记录,来研究在持续疲劳收缩后以及恢复期后运动单位(MU)行为的潜在代偿性改变。在12名受试者的第一背侧骨间肌外展过程中,以20%最大自主收缩(MVC)记录肌电图活动,在进行30%MVC疲劳收缩直至任务失败之前和之后直接记录,在休息10分钟后再进行额外的20%MVC收缩。分析了用sEMG分解系统提取的MUAPs的幅度、持续时间和平均放电率(MFR),以及sEMG均方根(RMS)幅度和中位数频率(MPF)。疲劳后立即观察到MUAP持续时间和幅度增加,且分别与sEMG MPF和RMS的变化相关。10分钟后,MUAP持续时间和sEMG MPF恢复到疲劳前的值,但MUAP幅度和sEMG RMS仍保持升高。MU MFR和募集阈值在疲劳后降低,并在休息后恢复。MUAP和sEMG幅度的增加可能反映了较大运动单位的募集,而募集压缩是疲劳后直接采用的一种额外代偿策略。MU MFR与MUAP持续时间平行恢复,表明代谢敏感传入神经在疲劳后MFR降低中可能发挥作用。本研究通过检查大量同时记录的单个运动单位的特性,深入了解了疲劳引起的神经肌肉变化,并概述了涉及运动单位募集和MFR改变的可能代偿策略。