关键词: activity aging neuromuscular physical function skeletal muscle

Mesh : Humans Muscle, Skeletal / physiopathology metabolism Sarcopenia / physiopathology metabolism therapy Aging / physiology Aged Muscle Proteins / metabolism

来  源:   DOI:10.1042/CS20231197   PDF(Pubmed)

Abstract:
As a result of advances in medical treatments and associated policy over the last century, life expectancy has risen substantially and continues to increase globally. However, the disconnect between lifespan and \'health span\' (the length of time spent in a healthy, disease-free state) has also increased, with skeletal muscle being a substantial contributor to this. Biological ageing is accompanied by declines in both skeletal muscle mass and function, termed sarcopenia. The mechanisms underpinning sarcopenia are multifactorial and are known to include marked alterations in muscle protein turnover and adaptations to the neural input to muscle. However, to date, the relative contribution of each factor remains largely unexplored. Specifically, muscle protein synthetic responses to key anabolic stimuli are blunted with advancing age, whilst alterations to neural components, spanning from the motor cortex and motoneuron excitability to the neuromuscular junction, may explain the greater magnitude of function losses when compared with mass. The consequences of these losses can be devastating for individuals, their support networks, and healthcare services; with clear detrimental impacts on both clinical (e.g., mortality, frailty, and post-treatment complications) and societal (e.g., independence maintenance) outcomes. Whether declines in muscle quantity and quality are an inevitable component of ageing remains to be completely understood. Nevertheless, strategies to mitigate these declines are of vital importance to improve the health span of older adults. This review aims to provide an overview of the declines in skeletal muscle mass and function with advancing age, describes the wide-ranging implications of these declines, and finally suggests strategies to mitigate them, including the merits of emerging pharmaceutical agents.
摘要:
由于上个世纪医疗和相关政策的进步,预期寿命大幅增加,并在全球范围内继续增加。然而,寿命和“健康跨度”之间的脱节(在健康状态下花费的时间长度,无病状态)也有所增加,骨骼肌是造成这种情况的重要因素。生物老化伴随着骨骼肌质量和功能的下降,称为肌少症。支撑肌肉减少症的机制是多因素的,并且已知包括肌肉蛋白质周转的显着改变和对肌肉神经输入的适应。然而,到目前为止,每个因素的相对贡献在很大程度上仍未被探索。具体来说,肌肉蛋白质对关键合成代谢刺激的合成反应随着年龄的增长而减弱,虽然改变了神经成分,从运动皮层和运动神经元兴奋性到神经肌肉接头,与质量相比,可以解释更大的功能损失。这些损失的后果对个人来说可能是毁灭性的,他们的支持网络,和医疗保健服务;对两种临床都有明显的不利影响(例如,死亡率,脆弱,和治疗后并发症)和社会(例如,独立性维护)结果。肌肉数量和质量的下降是否是衰老的必然因素仍有待完全了解。然而,减轻这些下降的策略对于改善老年人的健康状况至关重要。这篇综述旨在概述骨骼肌质量和功能随着年龄的增长而下降,描述了这些下降的广泛影响,最后提出了减轻它们的策略,包括新兴药物的优点。
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