Supraspinal and segmental mechanisms of fatigue

神经肌肉疲劳被定义为一种逐渐的、由活动引起的产生肌肉力量的能力下降。尽管中枢神经系统有几种机制可以优化肌肉激活并抵消与疲劳相关的力量下降，但也有一些脊柱和棘上的“失败”机制导致疲劳。在大多数情况下，调节肌肉激活的脊髓和棘上输入被视为不同的输入并独立评估。然而，脊髓运动神经元的输入主要是通过整合感觉输入、来自大脑的兴奋驱动、来自大脑的调节驱动和脊髓运动神经元本身的内在特性的网络。在中心疲劳研究中，这些分段电路的适应性及其在力生产的维持或失效中的作用一直是一个被忽视的领域。本研究计划的目的是确定节段性神经元间通路中棘上输入和传入输入的整合如何有助于维持疲劳时对肌肉的自愿驱动。这项研究意义重大，因为在我们了解调节健康人肌肉输出的主要机制之前，我们无法完全了解损伤、衰老和疾病中运动功能受损的机制。

Neuromuscular fatigue is defined as a gradual, activity-induced reduction in the ability to generate muscle force. Athough the central nervous system has several mechanisms which function to optimize muscle activation and offset the fatigue-related decline in force, there are a number of spinal and supraspinal mechanisms of "failure" that contribute to fatigue. For the most part, spinal and supraspinal inputs that modulate muscle activation have been treated as distinct inputs and assessed independently. However, input to spinal motor neurons is largely via networks which integrate sensory input, excitatory drive from the brain, modulatory drive from brain, and the intrinsic properties that are built into the spinal motor neuron itself. The adaptability of these segmental circuits and their role in the maintenance or failure of force production has been a neglected area in the study of central fatigue. The purpose of this research program is to determine how the integration of supraspinal and afferent inputs in segmental interneuronal pathways contribute to the maintenance of voluntary drive to muscle during fatigue. This research is significant because until we understand the central mechanisms that modulate muscle output in healthy people, we cannot fully understand the mechanisms of impaired motor function in injury, ageing, and disease.