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Molecular and Cellular Mechanisms of Muscle Aging and Sarcopenia and Effects of Electrical Stimulation in Seniors

机译:老年人肌肉衰老和肌肉减少的分子和细胞机制以及电刺激的影响

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摘要

The prolongation of skeletal muscle strength in aging and neuromuscular disease has been the objective of numerous studies employing a variety of approaches. It is generally accepted that cumulative failure to repair damage related to an overall decrease in anabolic processes is a primary cause of functional impairment in muscle. The functional performance of skeletal muscle tissues declines during post- natal life and it is compromised in different diseases, due to an alteration in muscle fiber composition and an overall decrease in muscle integrity as fibrotic invasions replace functional contractile tissue. Characteristics of skeletal muscle aging and diseases include a conspicuous reduction in myofiber plasticity (due to the progressive loss of muscle mass and in particular of the most powerful fast fibers), alteration in muscle-specific transcriptional mechanisms, and muscle atrophy. An early decrease in protein synthetic rates is followed by a later increase in protein degradation, to affect biochemical, physiological, and morphological parameters of muscle fibers during the aging process. Alterations in regenerative pathways also compromise the functionality of muscle tissues. In this review we will give an overview of the work on molecular and cellular mechanisms of aging and sarcopenia and the effects of electrical stimulation in seniors..
机译:骨骼肌强度在衰老和神经肌肉疾病中的延长已成为采用各种方法的众多研究的目标。人们普遍认为,与合成代谢过程总体下降有关的修复损伤的累积失败是肌肉功能受损的主要原因。骨骼肌组织的功能性能在出生后会下降,并且在不同疾病中会受到损害,这是由于肌纤维成分的改变以及随着纤维化侵袭取代了功能性收缩组织而使肌肉完整性整体下降的缘故。骨骼肌衰老和疾病的特征包括肌纤维可塑性的显着降低(由于肌肉质量的逐渐丧失,尤其是最强大的快速纤维的丧失),肌肉特异性转录机制的改变和肌肉萎缩。蛋白质合成速率的早期降低之后是蛋白质降解的更高速率,从而影响衰老过程中肌肉纤维的生化,生理和形态参数。再生途径的改变也损害了肌肉组织的功能。在这篇综述中,我们将概述衰老和肌肉减少症的分子和细胞机制以及老年人电刺激的作用。

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