Disuse-induced skeletal muscle atrophy in disease and nondisease states in humans: mechanisms, prevention, and recovery strategies

Decreased skeletal muscle contractile activity (disuse) or unloading leads to muscle mass loss, also known as muscle atrophy. The balance between muscle protein synthesis (MPS) and muscle protein breakdown (MPB) is the primary determinant of skeletal muscle mass. A reduced mechanical load on skeleta...

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Bibliographic Details
Published in:American Journal of Physiology: Cell Physiology 2022-06, Vol.322 (6), p.C1068-C1084
Main Authors: Nunes, Everson A, Stokes, Tanner, McKendry, James, Currier, Brad S, Phillips, Stuart M
Format: Article
Language:English
Subjects:
Aging
Atrophy
Inflammation
Mechanical properties
Mechanical unloading
Molecular modelling
Muscle contraction
Musculoskeletal system
Physical activity
Protein biosynthesis
Proteins
Skeletal muscle
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Summary:Decreased skeletal muscle contractile activity (disuse) or unloading leads to muscle mass loss, also known as muscle atrophy. The balance between muscle protein synthesis (MPS) and muscle protein breakdown (MPB) is the primary determinant of skeletal muscle mass. A reduced mechanical load on skeletal muscle is one of the main external factors leading to muscle atrophy. However, endocrine and inflammatory factors can act synergistically in catabolic states, amplifying the atrophy process and accelerating its progression. In addition, older individuals display aging-induced anabolic resistance, which can predispose this population to more pronounced effects when exposed to periods of reduced physical activity or mechanical unloading. Different cellular mechanisms contribute to the regulation of muscle protein balance during skeletal muscle atrophy. This review summarizes the effects of muscle disuse on muscle protein balance and the molecular mechanisms involved in muscle atrophy in the absence or presence of disease. Finally, a discussion of the current literature describing efficient strategies to prevent or improve the recovery from muscle atrophy is also presented.
ISSN:0363-6143
1522-1563
DOI:10.1152/ajpcell.00425.2021