Wikis
Muscle Atrophy
Muscle atrophy is a reduction in the size or mass of muscle tissue. In skeletal muscle, it commonly involves shrinkage of individual muscle fibers, seen as a decrease in their cross-sectional area and loss of contractile material. Atrophy can affect an individual muscle or occur more broadly across the body .1,2
Skeletal muscle size is maintained partly through the balance between the production and removal of cellular proteins. Atrophy often involves a sustained shift toward net protein loss. This can result from reduced muscle protein synthesis, increased protein degradation, or both. Cellular protein-removal systems, including the ubiquitin-proteasome and autophagy pathways, participate in the loss of muscle proteins and other cellular components during many forms of atrophy .1
Muscle atrophy can develop in different physiological and clinical settings, including prolonged inactivity or immobilization, loss of normal neural input, malnutrition, aging, and serious illness. The underlying mechanisms and the muscle fibers most affected can differ depending on the cause. For example, aging is often associated with preferential atrophy of Type II fibers .1,2
Atrophy of individual fibers should be distinguished from muscle-fiber loss. Both can reduce overall muscle mass, and both may occur together, particularly with aging. Muscle atrophy is also not synonymous with muscle weakness, because strength depends on neural activation and other characteristics of muscle as well as muscle size. Sarcopenia is a broader age-related condition involving loss of skeletal muscle mass and function .2
References
- Ebert SM, Al-Zougbi A, Bodine SC, Adams CM Skeletal Muscle Atrophy: Discovery of Mechanisms and Potential Therapies. Physiology. 2019;34(4):232-239. PMCID: PMC6863373. 2019. About this source DOI
- Wilkinson DJ, Piasecki M, Atherton PJ The age-related loss of skeletal muscle mass and function: Measurement and physiology of muscle fibre atrophy and muscle fibre loss in humans. Ageing Research Reviews. 2018;47:123-132. PMCID: PMC6202460. 2018. About this source DOI
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