Human muscle fatigue: responsiveness of motoneurons and central contributions to the loss of muscle power

我的研究项目使用创新技术来促进我们对人类神经肌肉生理学的理解，重点是疲劳和衰老。由活动产生的疲劳是健康人的常见经历，并且在许多情况下被放大，使得即使是日常任务的执行也可能受到限制，特别是在老年人中。 实验的一个主题是研究由疲劳引起的脊髓运动神经元兴奋性降低的机制，这在最近的一系列论文中有所描述（McNeil等人，2009，2011 a，B，d）。通过结合多种刺激技术（经颅磁刺激，皮质脊髓束刺激，外周神经刺激），我将调查运动神经元兴奋性的措施，努力定位的机制（S）。肌肉的收缩是由运动神经元的输出控制的，因此对运动神经元特性的深入了解对于提高我们对运动系统的认识至关重要。 实验的第二个主题是致力于研究肌肉力量所产生的缩短收缩与固定负载。肌肉疲劳的研究很少使用这种功能最相关的收缩类型。我早期的工作（McNeil & Rice 2007）表明，老年男性的肌肉在这种情况下更容易疲劳，这与许多使用肌肉长度固定的静态任务的研究结果相反。这项研究还间接表明，疲劳几乎完全发生在外周（肌肉本身）。多年来，人们对静态任务持有类似的观点，但在过去的15年里，已经表明25-66%的力量损失可能是由于中枢神经系统的故障。使用新的技术和模型，如老化和性别，我打算探索中央和外周的贡献疲劳缩短收缩与固定负荷。对肌肉力量极限的更好理解对整个活动范围都有影响，从简单的日常任务到自愿锻炼或训练。

My research program uses innovative techniques to advance our understanding of human neuromuscular physiology, with emphasis on fatigue and aging. Fatigue produced by activity is a common experience for healthy people and is magnified in many conditions such that the performance of even day-to-day tasks can be limited, particularly in the elderly. One theme of experiments is to investigate the mechanism(s) of the reduction in spinal motoneuron excitability caused by fatigue which is described in a recent series of papers (McNeil et al. 2009, 2011a,b,d). By combining multiple stimulation techniques (transcranial magnetic stimulation, corticospinal tract stimulation, peripheral nerve stimulation), I will investigate measures of motoneuron excitability in an effort to localize the mechanism(s). Muscle contraction is controlled by motoneuron output so an improved understanding of motoneuron properties is critical to advance our knowledge of the motor system. The second theme of experiments is dedicated to the investigation of muscle power generated by shortening contractions with a fixed-load. Muscle fatigue has been studied sparingly using this most functionally-relevant contraction type. My earlier work (McNeil & Rice 2007) showed that muscles of elderly men are more fatigable in this situation, which is the opposite finding to numerous studies that used static tasks where muscle length was fixed. The work also suggested indirectly that fatigue occurs almost exclusively within the periphery (the muscle itself). A similar view was held about static tasks for many years but, in the last 15 years, it has been shown that 25-66% of force loss can be due to failure within the central nervous system. Using novel techniques and models such as aging and sex, I intend to explore central and peripheral contributions to fatigue developed by shortening contractions with a fixed-load. An improved understanding of limits to muscle power has implications across the full spectrum of activity, from simple daily tasks to voluntary exercise or training.