• Energy metabolism and mitochondrial function emerge as a central axis of aging muscle, where mitochondrial dysfunction and oxidative stress limit ATP production and contractile economy, contributing to VO2max decline in rodent models and broader energy deficits [1], [4], [8].

• Structural and neuromuscular remodeling underlies age-related weakness, with reduced in vivo cross-sectional area, lower specific force, and altered contractile muscle volume and coactivation patterns across age groups and muscles [3], [5], [13], [10].

• Cellular and molecular control of muscle mass shifts with age, encompassing satellite cell regulation, myostatin signaling, and gene-expression changes that influence hypertrophic capacity and tissue maintenance [11], [12], [7], [16].

• Exercise and nutrition shape aging muscle plasticity, showing delayed Muscle Protein Synthesis (MPS) responses to resistance exercise and essential amino acids, along with training-induced shifts in myosin heavy chain expression and mechanics, indicating adaptive but age-limited plasticity [20], [15], [2], [10].