["Geriatrics &Gerontology International, Volume 26, Issue 6, June 2026. ", "\nAdrenomedullin optimizes muscle quality in youth by reducing energy‐expensive fibers via p70S6K suppression. Conversely, in old age, it rescues muscle function by stabilizing the vascular niche and preserving satellite cells through AMPK activation. This highlights adrenomedullin's dual, context‐dependent role in maintaining skeletal muscle homeostasis across the lifespan.\n\nABSTRACT\n\nIntroduction\nSarcopenia has recently become a major public health issue. Adrenomedullin (AM) exerts diverse physiological effects, including angiogenesis, but its role in skeletal muscle is unclear. This study investigates whether AM can attenuate sarcopenic changes in aged mice compared to young adults.\n\n\nMethods\nYoung and old male C57BL/6J mice were randomly divided into two groups: the AM‐treated group, which received subcutaneous administration of AM (50 nmol/kg body weight) 6 days a week, and the sham‐treated group, which was injected with vehicle. After 3 months of treatment, we performed multi‐muscle analyses (EDL, SOL, and PLA) using western blotting and immunohistochemistry.\n\n\nResults\nAM treatment significantly increased AM levels in plasma and muscle tissue. In young mice, AM was associated with changes in muscle fiber‐type composition, including a reduction in Type IIx fibers, suggesting muscle‐specific functional adaptation. In aged mice, AM increased CD31‐positive capillary density and Pax7‐positive muscle satellite cells (MuSCs), indicating improved vascular and stem cell niches. These changes occurred without alterations in muscle mass but were accompanied by improved motor function in aged mice.\n\n\nConclusions\nAM exerts age‐dependent effects on skeletal muscle, with distinct responses observed in young and aged mice. These findings suggest that AM may contribute to muscle adaptation through context‐dependent mechanisms involving vascular remodeling and fiber‐type modulation.\n\n"]