Influence of Age-Related Changes in Tendon on Motor Performance

 描述（由申请人提供）：在行走的蹬离阶段期间跖屈肌力量的降低导致随着年龄的增长优选的行走速度减慢，这反过来对老年人的健康和独立性产生负面影响。虽然通常牵连，肌肉减少症和肌肉无力单独不能完全解释减少跖屈肌的权力或伴随的变化协调。我们假设，这种脱节产生于跟腱行为的年龄相关变化，改变了运动过程中的肌肉肌腱动力学。这项研究紧密结合了新的体内成像，计算建模和运动分析，以调查肌腱变形与生理负荷和运动的细节前所未有的水平。我们的总体假设是，肌腱弹性和肌束间粘连的年龄相关变化对肌肉在运动过程中产生足够的跖屈肌力量的能力有重大影响。这项研究有三个目标。第一个目的是确定年龄的增长如何影响在规定的踝关节屈曲运动生理负荷下的跖屈肌和跟腱的体内行为。我们将结合联合收割机高分辨率静态MRI、动态MRI和剪切波弹性成像来检验这一假设，即随着年龄的增长，跟腱组织弹性的空间模式会发生改变，从而预测测量的肌肉组织变形模式。第二个目的是预测跟腱组织力学的年龄相关变化对运动过程中跖屈肌性能的功能影响。我们将把人体运动的测量与一个独特的计算框架联系起来，该框架包括跖屈肌肌腱的3D形态及其动态相互作用的详细结构表示。我们将检验主要假设，即模拟跟腱弹性和肌束间粘连的年龄相关变化将减少功率产生并增加局部组织应变。第三个目的是研究行走过程中跟腱行为的年龄相关变化及其与功能运动性能和步态干预反应的相关性。我们将测量在体内跟腱变形，跖屈肌束的行为，和跖屈肌的权力在行走。我们将这些测量与生物反馈相结合，旨在引起跖屈肌功率输出的规定增加。我们将使用这些数据来检验以下假设：1）随着年龄的增长，行走过程中肌腱变形更加均匀，这反映了肌腱束之间滑动的减少，将预测踝关节动力学降低和跖屈肌束运动学改变，以及2）随着年龄的增长，将使用不同的协调策略来增加跖屈肌力量，适应性将与目标2模型预测一致。结合起来，这些目标将揭示跟腱力学中与年龄相关的变化对运动过程中跖屈肌肌肉行为的影响，这些见解对于制定明智的干预措施以维持或恢复活动性，同时降低肌肉肌腱组织损伤的风险至关重要。

 DESCRIPTION (provided by applicant): A reduction in plantarflexor power during the push-off phase of walking leads to the slowing of preferred walking speed with age, which in turn negatively affects old adults' health and independence. Although commonly implicated, sarcopenia and muscle weakness alone cannot fully explain the reduction in plantarflexor power or accompanying changes in coordination. We postulate that this disconnect arises from age-related changes in Achilles tendon behavior that alter muscle-tendon dynamics during movement. This study tightly integrates novel in vivo imaging, computational modeling, and motion analysis to investigate tendon deformations associated with physiological loading and movement to an unprecedented level of detail. Our overarching hypothesis is that age-related changes in tendon elasticity and inter-fascicle adhesions have a substantial effect on the ability for muscles to generate sufficient plantarflexor power during movement. This study has three aims. The first aim is to determine how advancing age affects the in vivo behavior of the plantarflexor muscles and Achilles tendon during prescribed ankle flexion movements under physiological loading. We will combine high-resolution static MRI, dynamic MRI, and shear wave elastography to test the hypothesis that advancing age brings altered spatial patterns of Achilles tendon tissue elasticity that predict measured muscle tissue deformation patterns. The second aim is to predict the functional implications of age- related changes in Achilles tendon tissue mechanics on plantarflexor performance during movement. We will link measurements of human movement with a unique computational framework that includes detailed structural representations of the 3D morphology of the plantarflexor muscle-tendons and their dynamic interactions. We will test the primary hypothesis that simulating age-related changes in Achilles tendon elasticity and inter-fascicle adhesions will diminish power production and increase localized tissue strains. The third aim is to investigate age-related changes in Achilles tendon behavior during walking and its relevance to functional motor performance and response to gait interventions. We will measure in vivo Achilles tendon deformations, plantarflexor fascicle behavior, and plantarflexor power during walking. We will couple these measurements with biofeedback designed to elicit prescribed increases in plantarflexor power output. We will use these data to test the hypotheses that: 1) more uniform tendon deformations during walking with aging, which would reflect a reduction in sliding between tendon fascicles, will predict reduced ankle joint kinetics and altered plantarflexor muscle fascicle kinematics, and 2) with aging, different coordination strategies will be used to increase plantarflexor power, adaptations that will be consistent with Aim 2 model predictions. Combined, these aims will reveal the influence of age-related changes in Achilles tendon mechanics on plantarflexor muscle behavior during movement, insights critical for developing informed interventions to maintain or restore mobility while mitigating risk for muscle-tendon tissue damage.