Resistance training for the prevention and management of sarcopenia in older adults: Mechanisms, efficacy, and future applications

Sarcopenia is a major health concern in aging populations. Resistance training (RT) is widely recommended to improve muscle mass, strength, and physical function in older adults. In recent years, research on both biological mechanisms and clinical effects of RT has increased. However, these two fields have largely progressed in parallel, with limited evidence linking biological mechanisms to clinical efficacy. This narrative review integrates preclinical and clinical mechanistic evidence on RT in sarcopenia. It evaluates consistency across key biological pathways, including protein metabolism, mitochondrial function, chronic inflammation, and satellite cell regulation. Furthermore, it summarizes clinical evidence on RT in older adults and analyzes potential broader benefits. Finally, the review discusses the translational relevance of RT-related mechanisms and offers practical recommendations for prescribing RT. Current evidence suggests that improvements in mitochondrial adaptations show relatively consistent findings across preclinical and human studies. However, translation remains limited for protein metabolism regulatory mechanisms and chronic inflammation. YAP/TAZ proteins in the Hippo pathway may link mechanical signaling induced by RT to satellite cell regulation. Overall, although the preclinical mechanisms of RT in sarcopenia are relatively clear, translating them into clinical practice should be approached with caution. This review provides a practical guide to optimizing RT strategies and to guide future translational research. • Preclinical studies provide mechanistic support for RT in sarcopenia, despite heterogeneity. • RT improves muscle mass, strength, and function, and may reduce fall risk and chronic disease burden. • Translational consistency is higher for mitochondrial adaptations than for protein metabolism and inflammation. • YAP/TAZ signaling may link RT mechanical signaling to satellite cell regulation. • Translation of preclinical mechanisms to clinical outcomes requires caution.