Mechanical and neural factors underlying muscle performance during submaximal voluntary shortening contractions

许多日常运动需要肌肉改变长度，同时产生加速或减速身体的力量，但我们在这些条件下预测体内肌肉力量的能力很差。这可能是因为用于预测肌肉力量的传统肌肉模型通常忽略了肌肉长度变化的历史，这影响了肌肉的力量产生能力及其潜在的神经控制。具体来说，在主动肌肉缩短之后，与基于普遍接受的肌肉收缩理论的预期相比，力量输出会受到抑制。这种现象被称为残余力抑制（rFD），我们目前对rFD如何影响神经肌肉功能的理解是不完整的。这是因为我们通常在恒定肌肉肌腱单位（MTU）长度条件下评估肌肉的最大发力能力，而忽略了MTU顺应性允许在这些条件下肌肉缩短，从而导致rFD。因此，我们低估了人体运动肌肉的真实体内等距力能力，并且我们未能解释由于rFD可能发生的神经肌肉功能变化。目前缺乏对肌肉力量的理解导致了日常运动中肌肉力量预测的不准确，这严重限制了我们在整个生命周期中有效恢复、改善和补充人类运动的能力。因此，该项目旨在揭示rFD如何与(I)肌肉的发力能力，（II）运动皮层和脊髓的上游兴奋性，以及（III）肌肉的潜在神经驱动相互作用。这些目标将通过四项研究来解决，这些研究将系统地操纵人体胫骨前肌（对行走和姿势控制很重要的主要背屈肌）的体内肌肉长度、长度变化和肌肉活动水平，同时通过生物力学和神经生理学的前沿实验技术的独特组合来探索皮质脊髓系统的兴奋性和肌肉的运动单位行为(例如超声成像，无创脑和脊髓刺激，高密度表面肌电图)。初步结果表明，与肌长不变的收缩条件相比，在亚最大自愿固定端收缩期间肌肉缩短由于MTU的依从性而引起rFD，这可能随后增加皮质脊髓兴奋性并改变运动单位行为。rFD对神经肌肉功能的影响以前被忽视了，但对于开发更有效的策略来提高肌肉性能、降低损伤风险或预防与年龄和残疾相关的功能衰退是有用的信息。这项研究对于推进当前的神经肌肉骨骼模型也很重要，这些模型用于解释日常运动中的肌肉功能，评估临床状况的后果，以及为手术计划和机电设计提供信息。

Many everyday movements require that muscles change length while producing force to accelerate or decelerate the body, yet our ability to predict in vivo muscle force under these conditions is poor. This might be because the conventional muscle models used to predict muscle force typically neglect the muscle’s history of length change, which affects the muscle’s force-producing capacity and its underlying neural control. Specifically, following active muscle shortening, force output is depressed compared with what is expected based on generally-accepted theories of muscle contraction. This phenomenon is termed residual force depression (rFD) and our current understanding of how rFD affects neuromuscular performance is incomplete. This is because we typically assess a muscle’s maximum force-producing capacity under constant muscle-tendon unit (MTU) length conditions and we neglect that MTU compliance permits muscle shortening under these conditions, which induces rFD. Consequently, we underestimate the true in vivo isometric force capacity of human locomotor muscles and we fail to account for the changes in neuromuscular function that might occur due to rFD. This current lack of understanding contributes to inaccurate muscle force predictions during everyday movements, which severely limits our ability to effectively restore, improve and supplement human movement across the lifespan. This project therefore aims to uncover how rFD interacts with (I) the muscle’s force-producing capacity, (II) the upstream excitability of the motor cortex and spinal cord, and (III) the muscle’s underlying neural drive. These aims will be addressed across four studies that will systematically manipulate human tibialis anterior (a major dorsiflexor muscle important for walking and postural control) in vivo muscle lengths, length changes and muscle activity levels while the excitability of the corticospinal system and the muscle’s motor unit behaviour are probed with a unique combination of cutting-edge experimental techniques from biomechanics and neurophysiology (e.g. ultrasound imaging, non-invasive brain and spinal cord stimulation, high-density surface electromyography). Preliminary results indicate that muscle shortening during submaximal voluntary fixed-end contractions induces rFD due to MTU compliance, which might subsequently increase corticospinal excitability and change motor unit behaviour compared with constant muscle length contraction conditions. This effect of rFD on neuromuscular function has previously been neglected and is useful information for developing more effective strategies to enhance muscle performance, reduce injury risk or prevent age-and-disability-related functional decline. This research is also important for advancing current neuromusculoskeletal models, which are used to interpret muscle function during everyday movements and assess the consequences of clinical conditions, as well as inform surgical planning and mechatronic design.