MULTITASK ASSESSMENT OF MOTOR UNIT FATIGUE

神经肌肉疲劳，定义为力量能力的急剧下降 由肌肉活动引起的神经肌肉系统，是一种 普遍现象。 疲劳是在日常活动中遇到的， 工作场所，它是一个削弱因素，在一些神经肌肉 肌肉萎缩症、重症肌无力和多发性硬化症等疾病 硬化症，它已被牵连作为一个贡献者新生儿呼吸道 失败，它严重阻碍了瘫痪肌肉的恢复， 功能性电刺激 虽然它被普遍接受， 疲劳的部分原因是肌肉内的过程受损， 神经系统在疲劳中所起的作用仍然存在争议。 在长时间的活动中，神经行为的调整被认为是 通过优化肌肉的输入来减缓力量损失的速度， 机械功能改变。 相反，有人建议， 神经系统由于不能充分地 在长时间的活动中刺激肌肉。 观点的分歧很可能 源于1）用于诱导疲劳的范例的差异和2） 把肌肉当作一个同质实体而不是一个系统来处理 由不同的运动单位组成。 的广泛目标 拟议的研究是确定神经系统是否有助于 通过检查适应性， 单运动单位的机械、电和神经功能 不同类型的长期活动。 一个具体的目标是量化收缩和肌电的变化， 不同的运动单位自愿疲劳协议后的性能。 这将通过记录力和EMG响应来完成， 单个运动轴突的不同速率的神经内刺激 在各种运动之前和之后， 疲劳任务（持续/间歇，次最大/最大）。 第二个目的 是记录运动单位放电行为的适应性 在第一个目标中使用的相同类型的疲劳协议期间。 放电率和变异性的变化将从长期 肌内记录的运动单位动作电位序列 钨微电极 第三个目标是确定 神经活动影响运动单位疲劳。 一项新技术将 用于在不同的日子用刺激激活相同的运动单位 仅在模式（连续/间歇， 恒定/随机刺激间隔），但不是刺激数量 交付。 第四个具体目标是比较 肌肉激活的刺激率模式，模仿减少 运动单位放电过程中自愿收缩的i， 刺激速率保持恒定。 这些实验的结果 应该有助于阐明运动单位活动的适应是否在 长时间的肌肉收缩可防止疲劳或有助于疲劳。

Neuromuscular fatigue, defined as an acute decline in the force capacity of the neuromuscular system brought about by muscular activity, is a prevalent phenomenon. Fatigue is encountered in daily activities and in the workplace, it is a debilitating factor in a number of neuromuscular diseases including muscular dystrophy, myasthenia gravis, and multiple sclerosis, it has been implicated as a contributor to neonatal respiratory failure, and it seriously impedes the re-animation of paralyzed muscle by functional electrical stimulation. Although it is generally well-accepted that fatigue is caused, in part, by impairment of processes within muscle, the role played by the nervous system in fatigue remains controversial. Adjustments in neural behavior during prolonged activity are believed to slow the rate of force loss by optimizing the input to muscle as its mechanical function alters. Conversely, it has been suggested that the nervous system contributes to force decline by failing to adequately excite muscle during prolonged activity. The disparity of views likely stems from 1) differences in the paradigms used to induce fatigue and 2) the treatment of muscle as a homogenous entity rather than as a system comprised of a diverse population of motor units. The broad goal of the proposed research is to determine if the nervous system contributes to force-loss during fatigue in human subjects by examining the adaptations in mechanical, electrical and neural function of single motor units during different types of prolonged activity. One specific aim is to quantify the changes in contractile and myoelectric properties of different motor units following voluntary fatigue protocols. This will be accomplished by recording force and EMG responses to different rates of intraneural stimulation of single motor axons innervating intrinsic hand muscles before and immediately after various fatigue tasks (sustained/intermittent, submaximal/maximal). A second aim is to document the adaptations in the discharge behavior of motor units during the same type of fatigue protocols used in the first aim. Alterations in discharge rate and variability will be determined from long trains of motor unit action potentials recorded with intramuscular tungsten microelectrodes. A third aim is to determine how the pattern of neural activity influences motor unit fatigue. A new technique will be employed to activate the same motor unit on separate days with stimulus protocols that will vary only in the pattern (continuous/intermittent, constant/random interstimulus intervals) but not number of stimuli delivered. The fourth specific aim is to compare the force-decline in muscle activated with a stimulus-rate pattern that mimics the reduction in motor unit discharge during voluntary contraction to that i which the stimulus rate is maintained constant. The results of these experiments should help elucidate whether adaptation of motor unit activity during prolonged muscle contraction protects against or contributes to fatigue.