RESEARKA

The geroscience hypothesis posits that fundamental aging processes—cellular senescence, mitochondrial dysfunction, chronic inflammation, and proteostatic decline—drive multiple age-related diseases simultaneously, suggesting that targeting these hallmarks could compress morbidity and extend healthspan. This framework has motivated repurposing of existing drugs such as metformin and rapamycin, as well as development of novel senolytics and NAD+ precursors. Within this logic, muscle function occupies a privileged position: skeletal muscle is both a major insulin-sensitive tissue and a reservoir of amino acids critical for immune competence and wound healing. Grip strength longevity research thus emerges from two converging lines of evidence—the epidemiological observation that muscle weakness predicts mortality and the mechanistic insight that muscle-derived myokines modulate systemic inflammation and metabolic health. However, the geroscience hypothesis remains a framework, not a validated therapeutic doctrine, and its translation to clinical endpoints has been uneven. The question of whether improving grip strength longevity through exercise or pharmacology actually retards aging biology, rather than simply improving functional reserve, has been proposed but not definitively tested. This gap between mechanistic plausibility and causal proof defines the intellectual context for the present review.

Citation Support

• source_1 Jayanama 2022
• source_2 TurBoned 2026
• source_3 Karahan 2026
• source_4 Cui 2021
• source_5 Aksoy 2026