Sarcopenia, an age-related decline in muscle mass and function, is a primary contributor to frailty and disability in the elderly, significantly affecting quality of life. The development and progression of sarcopenia are influenced by pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6. Furthermore, one important element that leads to muscle aging is persistent inflammation. These cytokines induce muscle atrophy, interfere with satellite cell activity, and hinder the production of muscle proteins. It is proved that exercise, especially resistance and aerobic training, can improve muscle health in older people, lower systemic inflammation, and modify the inflammatory cytokine profile. The therapeutic effect of exercise in regulating inflammatory cytokines in muscle aging is examined in this review, with particular attention to the manner in which physical activity affects important inflammatory mediators and muscle regeneration pathways. We look at how exercise triggers anti-inflammatory processes such myokine regulation, NF-κB activation, and inflammation resolution while suppressing the release of pro-inflammatory cytokines. We also talk about how exercise affects protein turnover, satellite cell activation, and muscle tissue remodeling—all of which are critical for preventing the muscle loss linked to sarcopenia.
Li et al. (Tue,) studied this question.