Voluntary vs Electrically Stimulated Activation in Age-Related Muscle Weakness

Abstract

The scientific and medical communities have long recognized that muscle weakness is a major risk factor for physical limitations, outright physical disability, and early death in older adults.1 It was long assumed that age-related loss of lean mass (ie, sarcopenia) was the primary contributor to weakness. This led to a number of pharmaceutical companies pursuing compounds that mechanistically act on muscle (eg, hypertrophy-inducing myostatin inhibitors) with the goal being to enhance muscle and physical function.2 Most of these have failed to enhance muscle strength and physical function, in part because of the multiple factors associated with muscle strength and physical function that extend well beyond muscle mass. For instance, longitudinal data clearly demonstrate that loss of strength is only modestly associated with loss of mass in older adults.3 Given that muscle force production is driven both by skeletal muscle size and quality as well as the nervous system,4 this cross-sectional study specifically examined the role of the nervous system in clinically meaningful, age-related weakness. Specifically, we sought to determine whether older adults with clinically meaningful weakness exhibit impairments in their nervous systems’ (peripheral and central) ability to activate their lower extremity muscles compared with their stronger counterparts. Here, we calculated the degree of voluntary inactivation (VIA) by comparing voluntary and electrically stimulated muscle forces.5 While this does not give insight about where in the nervous system impairment may occur, it does provide insight into whether the nervous system may have a global involvement in weakness.