Changes in muscle strength and moderators of protein turnover in a rodent model of anorexia nervosa and recovery

Anorexia nervosa (AN) is a psychiatric disorder characterized by severe caloric restriction, leading to health complications. In addition to fat loss, AN also results in profound skeletal muscle loss, yet molecular pathways underlying these musculoskeletal complications or how long-lasting these musculoskeletal consequences may be are currently unknown. The purpose of this study was to investigate the effects of AN and subsequent weight recovery on muscle strength, size, and moderators of protein turnover in a rat model of AN. Female Sprague Dawley rats (n=11/group, 8 weeks of age) underwent 30 days of simulated AN (50-60% food restriction) followed by varying recovery periods. Muscle mass, strength, and protein synthesis/degradation pathways were assessed. AN led to substantial reductions in muscle mass and strength. While muscle mass recovered within 30 days, muscle strength remained depressed in rats with a prior history of AN, suggesting alterations to muscle quality. Moreover, moderators of protein synthesis (Igf1, Redd1, Deptor) remained altered following 30 days of AN and subsequent recovery. These findings suggest muscle impairments in AN may be longer-lasting than previously thought and may contribute to increased health complications and reduced quality of life in those with a history of AN.