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

<h2>Abstract</h2> 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 ∼20–30 % loss in skeletal muscle strength and size, 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 different recovery periods. To evaluate acute and chronic recovery physiology, recovery periods included both shorter term (5 days and 15 days refeeding) and longer term recovery (30 days refeeding). Muscle mass, strength, and protein synthesis/degradation pathways were assessed. AN led to substantial reductions in muscle mass and strength (∼21 % lower maximal plantar flexion and ∼20 % lower maximal grip strength) which remained depressed in shorter term recovery rats. While muscle mass recovered within 30 days, muscle strength remained depressed in rats with a prior history of AN (∼6 % lower maximal plantar flexion and ∼14 % lower maximal grip strength). Moreover, moderators of protein synthesis (<i>Igf1, Redd1, Deptor</i>) remained altered following 30 days of AN and subsequent recovery. There were no differences in 24-h protein synthesis rates during AN or following any recovery periods. These findings suggest muscle impairments in AN may persist beyond weight restoration in a rodent model of AN.