Skeletal muscle dysfunction with advancing age.

IF 6.7 2区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL Clinical science Pub Date : 2024-07-17 DOI:10.1042/CS20231197
Pardeep Pabla, Eleanor J Jones, Mathew Piasecki, Bethan E Phillips
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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.

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随着年龄的增长,骨骼肌功能出现障碍。
上个世纪,由于医学治疗和相关政策的进步,全球人口的预期寿命大幅提高,并仍在继续增长。然而,寿命与 "健康寿命"(处于健康、无疾病状态的时间长度)之间的脱节也在加剧,而骨骼肌是造成这种脱节的主要原因。生物衰老伴随着骨骼肌质量和功能的下降,即所谓的 "肌肉疏松症"。造成肌肉疏松症的机制是多因素的,已知包括肌肉蛋白质周转的明显改变和对肌肉神经输入的适应。然而,迄今为止,各因素的相对作用在很大程度上仍未得到探讨。具体来说,随着年龄的增长,肌肉蛋白质合成对关键合成代谢刺激的反应会减弱,而从运动皮质和运动神经元兴奋性到神经肌肉接头的神经成分的改变,可能是功能损失比质量损失更大的原因。这些损失的后果可能对个人、其支持网络和医疗保健服务造成破坏性影响;对临床(如死亡率、虚弱和治疗后并发症)和社会(如保持独立性)结果都有明显的不利影响。肌肉数量和质量的下降是否是老龄化不可避免的组成部分,这一点仍有待全面了解。然而,缓解肌肉数量和质量下降的策略对于改善老年人的健康状况至关重要。本综述旨在概述随着年龄的增长骨骼肌质量和功能的下降,描述这些下降的广泛影响,最后提出缓解这些下降的策略,包括新兴药物的优点。
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来源期刊
Clinical science
Clinical science 医学-医学:研究与实验
CiteScore
11.40
自引率
0.00%
发文量
189
审稿时长
4-8 weeks
期刊介绍: Translating molecular bioscience and experimental research into medical insights, Clinical Science offers multi-disciplinary coverage and clinical perspectives to advance human health. Its international Editorial Board is charged with selecting peer-reviewed original papers of the highest scientific merit covering the broad spectrum of biomedical specialities including, although not exclusively: Cardiovascular system Cerebrovascular system Gastrointestinal tract and liver Genomic medicine Infection and immunity Inflammation Oncology Metabolism Endocrinology and nutrition Nephrology Circulation Respiratory system Vascular biology Molecular pathology.
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