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在人体次最大力量疲劳收缩过程中神经肌肉传递的损害。

Impairment of neuromuscular propagation during human fatiguing contractions at submaximal forces.

作者信息

Fuglevand A J, Zackowski K M, Huey K A, Enoka R M

机构信息

Department of Exercise and Sport Sciences, University of Arizona, Tucson 85721.

出版信息

J Physiol. 1993 Jan;460:549-72. doi: 10.1113/jphysiol.1993.sp019486.

Abstract
  1. The purpose of the study was to examine the dependence of neuromuscular propagation impairment on the level of isometric force sustained to the endurance limit. The task involved human volunteers sustaining a submaximal abduction force with the index finger by activating the first dorsal interosseous muscle as long as possible. 2. The submaximal force was sustained at one of three levels (20, 35 or 65% of maximum) by increasing motor unit activity, as indicated by the electromyogram (EMG), during the fatiguing contraction. Although the EMG increased during the fatiguing contraction, the EMG was significantly less than maximum at the endurance limit for all subjects (deficit of 19-55% of maximum). This deficit was inversely related to the level of the sustained submaximal force. 3. The maximum voluntary contraction and twitch forces were significantly reduced following the fatiguing contraction. As with the EMG, the degree of force reduction was greatest for the subjects who sustained the low target forces. 4. The fatiguing contraction caused a 12-23% decline in M wave amplitude, a 33-51% increase in M wave duration, and no change in M wave area. The decline in M wave amplitude, which is an index of neuromuscular propagation impairment, was greatest among the subjects who sustained the low target forces. 5. The mean power frequency of the EMG decreased by a similar amount (50-57%) during the fatiguing contraction for all three groups of subjects. 6. A model representing the interaction of processes that enhance and impair force was developed to explain the recovery of twitch force following the sustained contractions at different target forces. 7. We conclude that the fatigue experienced by a subject when force is sustained at a submaximal value does involve an impairment of neuromuscular propagation. This impairment is one factor that limits muscle excitation during a submaximal, fatiguing contraction and contributes to the diminished force capability by the end of the fatigue task.
摘要
  1. 本研究的目的是检验神经肌肉传导损伤与维持到耐力极限的等长力水平之间的相关性。该任务要求人类志愿者通过激活第一背侧骨间肌,尽可能长时间地维持食指的次最大外展力。2. 在疲劳收缩过程中,通过增加运动单位活动(如肌电图(EMG)所示),将次最大力维持在三个水平之一(最大力的20%、35%或65%)。尽管在疲劳收缩过程中EMG增加,但所有受试者在耐力极限时的EMG均显著低于最大值(比最大值低19 - 55%)。这种差异与维持的次最大力水平呈负相关。3. 疲劳收缩后,最大自主收缩和单收缩力显著降低。与EMG一样,维持低目标力的受试者力降低的程度最大。4. 疲劳收缩导致M波振幅下降12 - 23%,M波持续时间增加33 - 51%,M波面积无变化。M波振幅下降是神经肌肉传导损伤的指标,在维持低目标力的受试者中下降最为明显。5. 三组受试者在疲劳收缩过程中,EMG的平均功率频率均下降了相似的幅度(50 - 57%)。6. 建立了一个代表增强和削弱力量过程相互作用的模型,以解释在不同目标力下持续收缩后单收缩力的恢复情况。7. 我们得出结论,当力维持在次最大水平时,受试者所经历的疲劳确实涉及神经肌肉传导的损伤。这种损伤是限制次最大疲劳收缩期间肌肉兴奋的一个因素,并导致在疲劳任务结束时力量能力下降。

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