Chronic Alcohol and Skeletal Muscle

Abstract

At-risk alcohol use is associated with tissue pathophysiology with significant adverse effects on multiple organ systems. Chronic alcoholic myopathy affects 40–60%, while alcohol-related liver injury affects only about 10–15% of people with at-risk alcohol use. Alcohol-induced mechanisms of dysfunctional muscle mass are multifactorial, complex, and interrelated. Alcohol decreases differentiation potential of muscle stem cells and dysregulates extracellular matrix remodeling decreasing muscle regenerative capacity in response to injury and atrophy. Alcohol-induced muscle loss is mediated by altering the balance of anabolic and catabolic pathways of muscle mass maintenance and mitochondrial dysfunction. Adaptations to exercise could directly reduce alcohol-associated myopathy; however, peri-exercise alcohol consumption may interfere with exercise performance and adaptive physiological processes. Emerging evidence indicates that epigenomic adaptations mediate this alcohol-induced myopathy. Muscle cross talk with multiple organs via myokines and extracellular vesicles is emerging as novel endocrine and paracrine mechanisms. How alcohol modulates this interorgan communication is under active investigation. In this chapter, we review the current understanding of pathophysiological mechanisms involved in alcohol-mediated myopathy together with emerging areas of research focus.