Skeletal muscle disorders including
sarcopenia are prevalent during the complex biological process of aging. Loss of muscle mass and strength commonly seen in
sarcopenia is induced by impaired neuromuscular innervation, transition of skeletal muscle fiber type, and reduced muscle regenerative capacity, all attributable to chronic
inflammation, oxidative stress, and
mitochondrial dysfunction. Current literature suggests that
vitamin E molecules (α-, β-, γ-, δ-
tocopherols and the corresponding
tocotrienols) with their
antioxidant and anti-inflammatory capabilities may mitigate age-associated skeletal dysfunction and enhance muscle regeneration, thus attenuating
sarcopenia. Preclinical and human experimental studies show that
vitamin E benefits myoblast proliferation, differentiation, survival, membrane repair, mitochondrial efficiency, muscle mass, muscle contractile properties, and exercise capacity. Limited number of human cross-sectional observational studies reveal positive associations between serum
tocopherol level and muscle strength. Several factors, including difficulties in validating
vitamin E intake and deficiency, variations in muscle-protective activity and metabolism of diverse forms of
vitamin E, and lack of understanding of the mechanisms of action, preclude randomized clinical trials of
vitamin E in people with
sarcopenia. Future research should consider long-term clinical trials of with adequate sample size, advanced imaging technology and omics approaches to investigate underlying mechanisms and assess clinically meaningful parameters such as muscle strength, physical performance, and muscle mass in
sarcopenia prevention and/or treatment.