Jakubowski Kristen L, Martino Giovanni, Beck Owen N, Sawicki Gregory S, Ting Lena H
bioRxiv. 2024 Aug 19:2024.08.14.607976. doi: 10.1101/2024.08.14.607976.
Successful reactive balance control requires coordinated modulation of hip, knee, and ankle torques. Stabilizing joint torques arise from feedforward neural signals that modulate the musculoskeletal system's intrinsic mechanical properties, namely muscle short-range stiffness, and neural feedback pathways that activate muscles in response to sensory input. Although feedforward and feedback pathways are known to modulate the torque at each joint, the role of each pathway to the balance-correcting response across joints is poorly understood. Since the feedforward and feedback torque responses act at different delays following perturbations to balance, we modified the sensorimotor response model (SRM), previously used to analyze the muscle activation response to perturbations, to consist of parallel feedback loops with different delays. Each loop within the model is driven by the same information, center of mass (CoM) kinematics, but each loop has an independent delay. We evaluated if a parallel loop SRM could decompose the reactive torques into the feedforward and feedback contributions during balance-correcting responses to backward support surface translations at four magnitudes. The SRM accurately reconstructed reactive joint torques at the hip, knee, and ankle, across all perturbation magnitudes (R >0.84 & VAF>0.83). Moreover, the hip and knee exhibited feedforward and feedback components, while the ankle only exhibited feedback components. The lack of a feedforward component at the ankle may occur because the compliance of the Achilles tendon attenuates muscle short-range stiffness. Our model may provide a framework for evaluating changes in the feedforward and feedback contributions to balance that occur due to aging, injury, or disease.
Reactive balance control requires coordination of neurally-mediated feedforward and feedback pathways to generate stabilizing joint torques at the hip, knee, and ankle. Using a sensorimotor response model, we decomposed reactive joint torques into feedforward and feedback contributions based on delays relative to center of mass kinematics. Responses across joints were driven by the same signals, but contributions from feedforward versus feedback pathways differed, likely due to differences in musculotendon properties between proximal and distal muscles.
成功的反应性平衡控制需要对髋、膝和踝关节扭矩进行协调调节。稳定关节扭矩源于前馈神经信号,该信号调节肌肉骨骼系统的固有机械特性,即肌肉短程刚度,以及神经反馈通路,后者根据感觉输入激活肌肉。虽然已知前馈和反馈通路可调节每个关节的扭矩,但每条通路在跨关节平衡校正反应中的作用却知之甚少。由于前馈和反馈扭矩反应在平衡扰动后的不同延迟时间起作用,我们修改了先前用于分析对扰动的肌肉激活反应的感觉运动反应模型(SRM),使其由具有不同延迟的并行反馈回路组成。模型中的每个回路由相同的信息,即质心(CoM)运动学驱动,但每个回路都有独立的延迟。我们评估了并行回路SRM是否能够在对四种幅度的向后支撑面平移的平衡校正反应期间,将反应性扭矩分解为前馈和反馈成分。SRM在所有扰动幅度下都能准确重建髋、膝和踝关节的反应性关节扭矩(R>0.84且VAF>0.83)。此外,髋部和膝部表现出前馈和反馈成分,而踝部仅表现出反馈成分。踝部缺乏前馈成分可能是因为跟腱的顺应性会减弱肌肉短程刚度。我们的模型可为评估因衰老、损伤或疾病导致的平衡前馈和反馈成分的变化提供一个框架。
反应性平衡控制需要神经介导的前馈和反馈通路的协调,以在髋、膝和踝关节产生稳定关节扭矩。使用感觉运动反应模型,我们基于相对于质心运动学的延迟,将反应性关节扭矩分解为前馈和反馈成分。跨关节的反应由相同信号驱动,但前馈与反馈通路的贡献不同,这可能是由于近端和远端肌肉之间的肌腱特性差异所致。