Cardinal features of involuntary force variability can arise from the closed-loop control of viscoelastic afferented muscles.
Cardinal features of involuntary force variability can arise from the closed-loop control of viscoelastic afferented muscles.
复制标题
非自愿性变异性的主要特征可能是由于粘弹性传入肌肉的闭环控制而产生的。
DOI：
10.1371/journal.pcbi.1005884
复制
发表时间：
2018-01
影响因子：
4.3
通讯作者：
Valero-Cuevas FJ
中科院分区：
文献类型：
--
作者：
Nagamori A;Laine CM;Valero-Cuevas FJ
低于15 Hz的无意识力变异性由许多因素引起并受其影响，这些因素包括下行神经驱动、本体感受反馈以及肌肉和肌腱的机械特性。然而，他们的潜在的相互作用，引起结构良好的频谱的不自主力的变化没有得到很好的理解，由于缺乏实验技术。在这里，我们研究了产生，调制和不同来源的力的变化之间的相互作用，使用生理接地闭环模拟的传入肌肉模型。闭环仿真包括肌肉肌腱模型，肌梭，高尔基腱器官（GTO），和一个跟踪控制器，使目标引导的力跟踪。我们证明，闭环控制的传入肌肉肌腱足以复制和解释令人惊讶的许多主要功能的不随意力的变化。具体来说，我们提出1）与运动单位放电率的共同调节相关的低频力变异性的潜在起源（即，“共同驱动”），2）本体感受反馈通路如何足以产生5-12 Hz生理震颤的深入表征，和3）证明那些反馈通路的调节（即，Ia和Ib传入的突触前抑制，以及通过梭动驱动的纺锤体敏感性）影响力变异的全部谱。这些结果突出了以前低估的重要性，闭环神经机械的相互作用，在解释自愿“等距”力控制过程中的不自主力的变化。此外，这些结果提供了一个统一的理论，涉及脊髓回路的各种表现改变不随意力的变化，疲劳，衰老和神经系统疾病的基础。肌肉力量的无意识波动是人类运动控制的不可避免的后果，也是运动执行错误的基础。不随意力变异的放大和扭曲是在各种神经系统疾病和疲劳中发现的常见现象。然而，其潜在机制往往不清楚。我们研究了产生和调制的不自主力的变化所产生的不同来源，以及它们之间的相互作用。我们使用了一个闭环模拟，其中包括一个生理接地模型的传入肌肉肌腱和误差控制器。我们表明，神经噪音、肌肉肌腱力学、本体感受反馈和纠错之间的相互作用是力控制的关键组成部分，通过考虑到这些因素，我们的模型能够复制并解释之前报道的不自主力变异性的许多基本特征。实验。此外，我们的研究结果表明，以前未被认识到的途径，通过该途径，力的可变性可能会改变疲劳和某些神经系统疾病。最后，我们强调了从相对简单的非侵入性力测量中提取重要临床和科学信息的潜力。
Involuntary force variability below 15 Hz arises from, and is influenced by, many factors including descending neural drive, proprioceptive feedback, and mechanical properties of muscles and tendons. However, their potential interactions that give rise to the well-structured spectrum of involuntary force variability are not well understood due to a lack of experimental techniques. Here, we investigated the generation, modulation, and interactions among different sources of force variability using a physiologically-grounded closed-loop simulation of an afferented muscle model. The closed-loop simulation included a musculotendon model, muscle spindle, Golgi tendon organ (GTO), and a tracking controller which enabled target-guided force tracking. We demonstrate that closed-loop control of an afferented musculotendon suffices to replicate and explain surprisingly many cardinal features of involuntary force variability. Specifically, we present 1) a potential origin of low-frequency force variability associated with co-modulation of motor unit firing rates (i.e.,‘common drive’), 2) an in-depth characterization of how proprioceptive feedback pathways suffice to generate 5-12 Hz physiological tremor, and 3) evidence that modulation of those feedback pathways (i.e., presynaptic inhibition of Ia and Ib afferents, and spindle sensitivity via fusimotor drive) influence the full spectrum of force variability. These results highlight the previously underestimated importance of closed-loop neuromechanical interactions in explaining involuntary force variability during voluntary ‘isometric’ force control. Furthermore, these results provide the basis for a unifying theory that relates spinal circuitry to various manifestations of altered involuntary force variability in fatigue, aging and neurological disease. Involuntary fluctuations in muscle force are an unavoidable consequence of human motor control and underlie movement execution errors. Amplification and distortion of involuntary force variability are common phenomena found in various neurological conditions and in fatigue. However, the underlying mechanisms for this are often unclear. We investigated the generation and modulation of involuntary force variability arising from different sources, as well as their interactions. We used a closed-loop simulation which included a physiologically-grounded model of an afferented musculotendon and an error-controller. We show that interactions among neural noise, musculotendon mechanics, proprioceptive feedback, and error correction are critical components of force control, and by taking these into account, our model was able to both replicate and explain many cardinal features of involuntary force variability previously reported experimentally. Also, our results suggest previously unrecognized pathways through which force variability may be altered in fatigue and in certain neurological diseases. Finally, we emphasize the potential for important clinical and scientific information to be extracted from relatively simple, non-invasive measurements of force.
登录
查看更多内容
影响因子：
2.5
作者：
Baudry, Stephane;Maerz, Adam H.;Enoka, Roger M.
通讯作者：
Enoka, Roger M.
影响因子：
2
作者：
Cohen, R. G.;Sternad, D.
通讯作者：
Sternad, D.
影响因子：
64.8
作者：
通讯作者：
--
影响因子：
3.3
作者：
Contessa, Paola;Adam, Alexander;De Luca, Carlo J.
通讯作者：
De Luca, Carlo J.
影响因子：
5.5
作者：
Baldissera, F;Cavallari, P;Cerri, G
通讯作者：
Cerri, G