Beyond Muscle Quantity: Rethinking Sarcopenia as a Disorder of Brain-Muscle Communication?

Sarcopenia is classically defined by age-related loss of muscle mass, strength, and function, yet strength and functional decline consistently outpace the loss of muscle tissue itself, a mismatch that a purely muscle-centered model cannot fully explain. Mounting evidence therefore hints towards neurogenic contributors to sarcopenia. In this concept study, we propose reframing sarcopenia as a disorder of brain-muscle communication, integrating a framework across three complementary levels of neuromuscular organization: i) corticospinal connectivity, ii) motor-unit behavior, and iii) muscle synergies, introducing the concept that each level is individually informative but insufficient alone to capture the neural contribution to sarcopenia-related muscle weakness. We further argue that conventional static and single-task assessments may underestimate this neural component, and that combining them with dynamic and ecologically valid dual-task paradigms could reveal compensatory motor control reorganization. Moreover, we propose a self-reinforcing loop in which selective fasttwitch fiber loss and impaired neural drive interact to amplify functional decline over time. If validated, multimodal neurophysiological profiling could help identify individual neural phenotypes and inform personalized resistance and motor-cognitive training. The evidence remains cross-sectional and hypothesis-generating: the key emerging tool is unvalidated in sarcopenia, and etiological heterogeneity across sarcopenia subtypes is unaddressed.