Neural mechanisms of dynapenia

缺乏缺乏的神经机制

• 批准号: 8632154
• 负责人: Brian C Clark
• 金额: $ 34.88万
• 依托单位: OHIO UNIVERSITY ATHENS
• 依托单位国家: 美国
• 财政年份: 2014
• 资助国家: 美国
• 起止时间: 2014-09-01 至 2019-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8632154
• 关键词: Address; Age; Aging; Case-Control Studies; Coin; Comorbidity; Data; Development; Elderly; Exercise; Exhibits; Gender; Greek; Imagery; Impairment; Individual; Intervention; Knee; Knowledge; Life; Limb structure; Magnetic Resonance Imaging; Measures; Minor; Mission; Modeling; Motor; Muscle; Muscle Contraction; Muscle Fatigue; Muscle Weakness; Outcome; Participant; Performance; Physical Function; Physical activity; Physiologic pulse; Physiological; Play; Poverty; Public Health; Randomized; Research; Resistance; Risk; Risk Factors; Role; Skeletal Muscle; Techniques; Testing; Training; Transcranial magnetic stimulation; Translations; White Matter Hyperintensity; Work; base; disability; inflammatory marker; insight; mortality; muscle form; muscle strength; neuromechanism; neurophysiology; physical property; public health relevance; quadriceps muscle; sarcopenia; trait; white matter

PROJECT SUMMARY A loss of voluntary muscle strength predisposes elders to a 4-fold increase in functional limitations and a 2-fold increase in mortality. For decades, the loss of strength in aging has been largely attributed to the loss of muscle mass. However, recent findings clearly demonstrate that muscle size plays a relatively minor role, and our preliminary data suggests that weak elders activate a substantially smaller proportion of their total muscle during a maximal strength task in comparison to their stronger age-matched counterparts. Despite the significance of maintaining physical strength in aging, virtually all of the research on this topic has focused exclusively on maintaining muscle mass, and little is known regarding the neural mechanisms of weakness. We hypothesize that dynapenic elders have a decreased ability to voluntarily (neurologically) activate skeletal muscle maximally due to increased intracortical inhibition. To test our hypothesis we will conduct a case-control study on dynapenic (i.e., weak) and non-dynapenic elders (n=50/group; >65 yrs). Additionally, the dynapenic individuals will be randomly assigned to one of two interventions (motor imagery (MI) or unilateral resistance exercise (URE) training) to provide an experimental manipulation to increase strength and VA, which will permit us to better elucidate physiological mechanisms. This project will address three specific aims. The first is to determine whether dynapenic elders exhibit differences in knee extensor voluntary activation (VA) in comparison to non-dynapenic elders. The second is to determine whether dynapenic elders exhibit differences in intracortical excitability (assessed via paired-pulse transcranial magnetic stimulation) of the quadriceps femoris muscles in comparison to non-dynapenic elders, and to examine the association between measures of intracortical excitability and VA. The last is to determine the association between the changes in strength, VA, and intracortical excitability induced by motor imagery training and unilateral resistance exercise training in dynapenic individuals. MI of strong muscle contractions has been shown to enhance strength and VA. URE training has also been shown to enhance strength and VA in both the trained and untrained limbs. We will use these interventions as manipulations to enhance strength and VA. This will allow us to better elucidate the mechanistic role of intracortical excitability by examining the association/disassociation between the respective outcomes. While not part of the specific aims per se, we will obtain a number of additional outcomes to characterize the participants, serve as covariates, and use for secondary analyses (e.g., muscle size via MRI, muscle fatigue, white matter hyperintensity, physical activity, electrically-stimulated contractile properties, physical performance, trait and state measures related to exercise, etc.). The proposed work will provide evidence that weakness in the elderly is associated with impairments in VA and will provide insight on the neural mechanisms of this impairment. Collectively, this knowledge will guide the development of targeted strategies to ameliorate weakness and enhance physical function in seniors.

项目摘要 自愿性肌肉力量的丧失使长老的功能局限性增加了4倍，而2倍 死亡率增加。几十年来，衰老的力量损失主要归因于丧失 肌肉质量。但是，最近的发现清楚地表明，肌肉大小起着相对较小的作用，并且 我们的初步数据表明，弱长老会激活其总肌肉的比例较小 与年龄匹配的同行相比，在最大的力量任务中。尽管有 维持衰老的体力的重要性，几乎所有关于该主题的研究都集中在 仅在保持肌肉质量上，关于虚弱的神经机制知之甚少。 我们假设Dy​​napenic长老具有自愿（神经学）激活骨骼的能力降低 肌肉最大程度地是由于皮质内抑制的增加。为了检验我们的假设，我们将进行病例对照 对DYNAPENIC（即弱）和非脱氧核糖核酸长者（n = 50/组;> 65年）的研究。另外，Dynapenic 个人将被随机分配给两种干预措施之一（运动图像（MI）或单侧阻力 锻炼（URE）训练）提供实验操作以增加强度和VA，这将 允许我们更好地阐明生理机制。该项目将解决三个具体目标。第一个 是为了确定Dynapenic Elders是否在膝盖伸肌自愿激活（VA）中是否表现出差异 与非二氮长老的比较。第二个是确定Dynapenic长老是否表现出差异 股四头肌中的皮质内兴奋性（通过成对的脉冲经颅磁刺激评估） 与非二氧化碳长老相比，股肌肉，并检查 皮质内兴奋性和VA。最后一个是确定强度变化Va， 以及由运动图像训练和单方面阻力运动训练引起的皮质内兴奋性 Dynapenic个人。强烈的肌肉收缩的MI已被证明可以增强强度和VA。 ure 还显示训练可以增强训练有素和未经训练的四肢的力量和VA。我们将使用 这些干预措施作为操纵以增强力量和VA。这将使我们更好地阐明 通过检查相应的相关性/分离，对物质内兴奋性的机械作用 结果。虽然不是特定目标本身的一部分，但我们将获得许多其他结果 表征参与者，用作协变量，并用于辅助分析（例如，通过MRI肌肉大小， 肌肉疲劳，白质超强度，体育活动，电刺激的收缩特性， 身体绩效，特质和与运动有关的状态措施等）。拟议的工作将提供 证据表明，老年人的弱点与VA的损害有关，并将提供有关 这种障碍的神经机制。总的来说，这些知识将指导有针对性的发展 改善弱点并增强老年人身体机能的策略。