与年龄相关的肌肉性能和身体机能丧失的神经机制。
Neural Mechanisms of Age-Related Loss of Muscle Performance and Physical Function.
机构信息
Ohio Musculoskeletal and Neurological Institute (OMNI) and the Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA.
出版信息
J Gerontol A Biol Sci Med Sci. 2023 Jun 16;78(Suppl 1):8-13. doi: 10.1093/gerona/glad029.
BACKGROUND
This article discusses the putative neural mechanisms of age-related muscle weakness within the broader context of the development of function-promoting therapies for sarcopenia and age-related mobility limitations. We discuss here the evolving definition of sarcopenia and its primary defining characteristic, weakness.
METHODS
This review explores the premise that impairments in the nervous system's ability to generate maximal force or power contribute to sarcopenia.
RESULTS
Impairments in neural activation are responsible for a substantial amount of age-related weakness. The neurophysiological mechanisms of weakness are multifactorial. The roles of supraspinal descending command mechanisms, spinal motor neuron firing responsivity, and neuromuscular junction transmission failure in sarcopenia are discussed. Research/clinical gaps and recommendations for future work are highlighted.
CONCLUSION
Further research is needed to map putative neural mechanisms, determine the clinical relevance of age-related changes in neural activation to sarcopenia, and evaluate the effectiveness of various neurotherapeutic approaches to enhancing physical function.
背景
本文讨论了与年龄相关的肌肉无力的假定神经机制，其更广泛的背景是为肌肉减少症和与年龄相关的活动能力受限开发促进功能的治疗方法。在这里，我们讨论了正在发展的肌肉减少症的定义及其主要特征，即无力。
方法
本综述探讨了这样一个前提，即神经系统产生最大力量或功率的能力受损导致了肌肉减少症。
结果
神经激活的损伤导致了大量与年龄相关的无力。无力的神经生理学机制是多因素的。讨论了在肌肉减少症中，中枢下行指令机制、脊髓运动神经元放电反应性以及神经肌肉接头传递失败的作用。强调了研究/临床差距和对未来工作的建议。
结论
需要进一步研究以描绘假定的神经机制，确定神经激活与年龄相关的变化对肌肉减少症的临床相关性，并评估各种神经治疗方法对增强身体功能的有效性。
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