MULTITASK ASSESSMENT OF MOTOR UNIT FATIGUE

神经肌肉疲劳，定义为力量能力的急剧下降 肌肉活动所带来的神经肌肉系统的 普遍存在的现象。疲劳是在日常活动中和在 在工作场所，它是一些神经肌肉衰弱的因素 疾病包括肌营养不良症、重症肌无力和多发性 硬化症，已被认为是新生儿呼吸道疾病的一个因素 失败，它严重阻碍了瘫痪肌肉的恢复 功能性电刺激。尽管它被普遍接受 疲劳在一定程度上是由肌肉内过程的损伤引起的， 神经系统在疲劳中扮演的角色仍然存在争议。 据信，长时间活动期间神经行为的调整 通过优化肌肉的输入来减缓力量损失的速度 机械功能发生了变化。相反，有人建议， 神经系统未能充分发挥作用导致力量下降 在长时间的运动中刺激肌肉。可能存在的意见分歧 源于1)导致疲劳的范例不同和2) 把肌肉当作同质实体而不是系统来对待 由一群不同的机动部队组成。的总体目标是 拟议的研究是为了确定神经系统是否对 通过检测人体的适应性来研究受试者在疲劳过程中的力量损失 在单个电机单元的机械、电气和神经功能方面 不同类型的长时间活动。 一个特定的目标是量化收缩和肌电的变化 遵循自愿疲劳方案的不同发动机部件的特性。 这将通过记录力和肌电响应来实现 单运动轴突神经内刺激率的不同 手部固有肌肉在各种运动前和之后的神经支配 疲劳任务(持续/间歇、次长/最长)。第二个目标 是记录电机单元的放电行为的适应情况 在同一类型的疲劳协议中使用的第一个目标。 排泄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。一种新技术将是 利用刺激在不同的日子激活相同的运动单元 仅在模式(连续/间歇， 恒定/随机刺激间间隔)，而不是刺激数 送来了。第四个具体目标是比较 肌肉激活的刺激率模式，模拟减少 在自愿收缩期间运动单位放电到I 刺激利率保持不变。这些实验的结果 应该有助于阐明运动单位活动的适应性在 长时间的肌肉收缩可以防止或导致疲劳。

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.