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Pathophysiology of sarcopenia 

Pathophysiology of sarcopenia
Chapter:
Pathophysiology of sarcopenia
Author(s):

Townsend Benard

and Roger A. Fielding

DOI:
10.1093/med/9780198701590.003.0055
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date: 24 August 2019

A number of mechanisms have been proposed to contribute to the accelerated loss of muscle mass and/or function in sarcopenia. Ageing induces a loss of the anabolic nature of food and muscle contraction, failing to adequately stimulate muscle protein synthesis. Reductions in protein intake and/or blunting of vasodilation in muscle may contribute to this impairment, though conclusive evidence is still lacking. Increasing adiposity, particularly within muscle, has been associated with physical and functional declines in ageing. Short-term disuse, such as hospitalization or injury, appears to disproportionately accelerate muscle mass loss in older people. Age-induced, low-level, chronic elevations in NF-kβ‎-mediated pro-inflammatory cytokines (TNF-α‎, IL-6 & IL-1) have shown robust relationships with sarcopenia. Accelerated reactive oxygen species generation brought on by mitochondrial dysfunction may stimulate myocyte apoptosis, though this mechanism is still debated. Age-induced neuromuscular adaptations appear to contribute to sarcopenia, particularly for changes in muscular function.

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