Protective effects of acute exercise preconditioning on disuse-induced muscular atrophy in aged muscle: a narrative lite
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he Journal of Physiological Sciences Open Access
MINI-REVIEW
Protective effects of acute exercise preconditioning on disuse‑induced muscular atrophy in aged muscle: a narrative literature review Toshinori Yoshihara* and Hisashi Naito
Abstract Aging is associated with a progressive loss of skeletal muscle mass and strength, resulting in frailty and lower quality of life in older individuals. At present, a standard of clinical or pharmacological care to prevent the adverse effects of aging does not exist. Determining the mechanism(s) responsible for muscular atrophy in disused aged muscle is a required key step for the development of effective countermeasures. Studies suggest an age-related differential response of genes and signalings to muscle disuse in both rodents and humans, implying the possibility that effective countermeasures to prevent disuse muscle atrophy may be age-specific. Notably, exercise preconditioning can attenuate disuse-induced muscular atrophy in rodent and human skeletal muscles; however, information on age-specific mechanisms of this exercise-induced protection remains limited. This mini-review aimed to summarize the protective effects of acute exercise preconditioning on muscular atrophy in aged muscle and provide potential mechanisms for its preventive effect on skeletal muscle wasting. Keywords: Growth arrest and DNA damage-inducible 45α, Histone deacetylase 4, Exercise intervention, Aged skeletal muscle, Sarcopenia Background Aging is associated with frailty, impaired health span, and lower quality of life [1]. Aging impacts muscle adaptations, such as muscle hypertrophy, increased antioxidant capacity, muscle regeneration, and muscle atrophy. Interestingly, several studies have demonstrated that there are age-specific gene and signaling responses to skeletal muscle disuse in both rodents and humans [2–6]. For instance, Leeuwenburgh et al. demonstrated that old rats (32 months old) have a greater apoptotic response to hindlimb unloading in rat soleus muscle than in young rats (6 months old), suggesting that apoptotic
*Correspondence: t‑[email protected] Graduate School of Health and Sports Science, Juntendo University, 1‑1 Hirakagakuendai, Inzai, Chiba 270‑1695, Japan
regulation during disuse is distinct in young and aged muscles [2]. In human skeletal muscle, one paper comparing age-related differential mechanisms in disuse muscle atrophy (21–27 years vs. 60–72 years) found an age-specific upregulation of Bax and p53 in aged muscle after 2 days of immobility with significant increases in TdT-mediated dUTP nick end labeling and DNA fragmentation in old muscle [6]. Moreover, recent evidence has revealed that growth arrest and DNA damageinducible 45α (Gadd45α) are required for skeletal muscle atrophy induced by different muscle stressors, such as fasting, denervation, and immobilization [7]. Gadd45α is a soluble, primarily myonuclear protein that causes muscle fiber atrophy by altering skeletal muscle gene expression, stimulating protein breakdown, reducing protein synthesis
