Concepedia

TLDR

Maintenance of muscle mass and strength supports mobility and quality of life, yet muscle atrophy, declining strength, and frailty are accepted aging consequences whose causes remain unknown. The study aims to clarify the mechanisms underlying age‑related muscle decline to assess their preventability and treatability. Age‑related muscle atrophy and strength loss are largely driven by motor unit remodeling through selective denervation and axonal sprouting, a process exacerbated by heightened contraction‑induced injury susceptibility and impaired regeneration. Across species, aging reduces muscle function by roughly 35 % in maximum force, 30 % in maximum power, and 20 % in normalized force and power, and aged mice show greater injury susceptibility and impaired recovery.

Abstract

Maintenance of muscle mass and strength contributes to mobility which impacts on quality of life. Although muscle atrophy, declining strength, and physical frailty are generally accepted as inevitable concomitants of aging, the causes are unknown. Clarification of the mechanisms responsible for these changes would enhance our understanding of the degree to which they are preventable or treatable. The decline in muscle function between maturity and old age is similar for muscles of many different animals including human beings, and is typified by the decreases of ∼35% in maximum force, ∼30% in maximum power, and 20% in normalized force (kN·m−2) and power (W·kg−1) of extensor digitorum longus (EDL) muscles in old compared with adult mice. Much of the age-associated muscle atrophy and declining strength may be explained by motor unit remodeling which appears to occur by selective denervation of muscle fibers with reinnervation by axonal sprouting from an adjacent innervated unit. Muscles in old mice appear more susceptible to injury than muscles in young or adult mice and have a decreased capacity for recovery. The process of age related denervation may be aggravated by an increased susceptibility of muscles in old animals to contraction-induced injury coupled with impaired capacity for regeneration.