Muscle Fatigue's Impact on Gait Mechanics and Neuromuscular Control in Knee Osteoarthritis

项目摘要 疲劳，缺乏体力和/或精神能量，是骨关节炎(OA)的常见症状， 可能会限制体能，并导致残疾。在健康的老年人中，肌肉疲劳一直是 被认为是疲劳症状的关键因素。膝关节伸肌功能障碍，包括下部 等长和等速扭矩和肌肉激活模式的改变在膝骨性关节炎中很常见。 (KOA)。这些神经肌肉功能的改变可能会增加膝关节骨性关节炎患者的运动肌疲劳。 与年龄匹配的对照组相比，每天必须使用更大比例的肌肉容量 像散步这样的活动。到目前为止，解释肌肉疲劳是否以及如何改变控制力和 KOA的行动协调是有限的。我们的工作假设是膝关节骨性关节炎相关的神经肌肉 变化可能加剧运动性肌肉疲劳(目标1)，并改变肌肉的神经机械反应 步态疲劳(目标2)，从而导致行动能力下降。在健康成年人中，中枢和外周 这两种机制都会导致肌肉疲劳。然而，无论疲劳的根源是不是个体 膝骨性关节炎是中枢还是外周尚不清楚，这可能是由于 可口可乐。评估和比较膝关节骨性关节炎患者长时间步行导致力量丧失的机制。 我们将使用经颅磁刺激来测量运动皮质的兴奋性和抑制性(目标3)。至 检验这些假设，将收集两组数据，每组10名男性和10名女性：KOA(65-80岁)和 老年健康对照组(70-80岁)。这两组人都将相对久坐不动，这将得到核实 使用加速度计进行定量测量。在这项横断面研究设计中，我们将实施我们的新 生理和临床相关的30分钟跑步机步行诱导膝关节伸肌疲劳和 然后通过步态力学、肌电图、体能表现和 运动皮质兴奋性。需要解决的问题是，膝关节骨性关节炎中的肌肉疲劳及其对活动能力的影响 这一点很重要，而且目前阻碍了许多老年人实现最佳健康寿命。理解 生理功能改变的潜在机制，如膝关节骨性关节炎患者的肌肉疲劳，将 允许更好地了解如何在这一人群中优化干预措施。该计划的完成 项目和拟议的培训计划活动，包括新的实验和 先进的计算方法以及专业发展活动将产生重大的、 对作为独立研究人员的国际和平研究所的发展产生积极影响，为实现既定目标作出贡献 美国国立卫生研究院加强对多样化劳动力的培训。

Project Summary Fatigue, lack of physical and/or mental energy, is a common reported symptom with osteoarthritis (OA) that may limit physical capacity and contribute to disability. In healthy older adults, muscle fatigue has been proposed as a key contributor to symptoms of fatigue. Knee extensor muscle dysfunction, including lower isometric and isokinetic torques and altered muscle activation patterns, are common with knee osteoarthritis (KOA). Together these changes in neuromuscular function may increase locomotor muscle fatigue in KOA compared to age-matched controls, as a greater percentage of the muscle’s capacity must be used for daily activities such as walking. To date, evidence to explain whether and how muscle fatigue may alter control and coordination of movement in KOA is limited. Our working hypothesis is that KOA-related neuromuscular changes may exacerbate locomotor muscle fatigue (Aim 1) and alter the neuro-mechanical response to muscle fatigue during gait (Aim 2), thereby contributing to mobility declines. In healthy adults, central and peripheral mechanisms can both contribute to muscle fatigue. However, whether the source of fatigue in individuals with KOA is central or peripheral is unclear which may be due to maladaptive neuroplastic changes that occur with KOA. To assess and compare the mechanisms for loss of force with a prolonged walk in individuals with KOA we will use transcranial magnetic stimulation to measure motor cortex excitability and inhibition (Aim 3). To test these hypotheses, data will be gathered on 2 groups of 10 men and 10 women: KOA (65-80 years) and older healthy controls (70-80 years). Both groups will be relatively sedentary, which will be verified quantitatively using accelerometry. In this cross-sectional study design, we will implement our new physiologically and clinically relevant 30-minute treadmill walk to induce knee extensor muscle fatigue and then quantify the response with measures of gait mechanics, electromyography, physical performance, and motor cortex excitability. The problem to be addressed, muscle fatigue in KOA, and its impact on mobility is significant and currently prevents many older adults from achieving an optimal health span. Understanding the mechanisms underlying changes in physical function, such as muscle fatigue in individuals with KOA will allow for a better understanding of how to optimize interventions in this population. The completion of the project and the proposed training plan activities including skill development in new experimental and advanced computational approaches as well as professional development activities will have a significant, positive impact on the development of the PI as an independent researcher, contributing to the stated goals of the NIH to enhance training of a diverse work force.