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A central feature of sarcopenic remodeling is the preferential loss of fast\u2010twitch (Type II) fibers and alterations in contractile protein composition, leading to reduced force generation and impaired muscle quality. Maintenance of skeletal muscle function depends on the integrity of the contractile apparatus, including myosin heavy chain isoforms, titin, actin, troponin, and associated structural proteins, which undergo quantitative and qualitative changes with aging. Multiple aging\u2010related mechanisms including telomere attrition, epigenetic remodeling, mitochondrial dysfunction, ionic dyshomeostasis, hormonal alterations, and chronic low\u2010grade inflammation converge on fiber\u2010type regulation and sarcomeric stability. These upstream processes impair satellite cell renewal, disrupt excitation\u2013contraction coupling, accelerate proteolysis of contractile proteins, and promote maladaptive fiber\u2010type transitions. 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