Resistance Exercise-Induced Hormone Change Promotes Autophagy Response In Untrained Women

Abstract

Introduction: Autophagy is a catabolic process for maintaining skeletal muscle homeostasis by recycling malfunctioning protein aggregates. Evidence suggests that hormones (e.g., cortisol) promote autophagic activity in muscle cells; however, no prior study has examined the effect of resistance exercise (RE)-induced hormonal response on the autophagic response. PURPOSE: To determine the effect of an acute RE-induced hormonal response on the autophagic response after muscle damage in untrained young women. METHODS: Untrained women (n=8, 20 ± 1y; height: 164.1± 9.2 cm; weight 60.7 ± 7.8 kg) completed 2 sessions of 80 unilateral maximal eccentric knee extensions followed by either an upper body RE protocol (EX; aimed to induce an increase in cortisol) or a 20-min rest (CON). Muscle samples were collected and analyzed for markers of autophagic initiation signaling (FOXO3A, AKT, MTOR), phagophore initiation (ATG5, ULK1, BECN1), elongation (ATG7, LC3A, LC3B), and autolysosomal degradation (SQSTM1/p62) by real-time PCR at before exercise (PRE), 12 hours (+12h) and 24 hours (+24h) after exercise. RESULTS: A significant (p<0.05) time x condition effect was found for ULK1. At +24h (0.81 ± 0.26-fold), ULK1 gene expression was greater in EX than CON. A significant time effect was found for FOXO3A. FOXO3A expression decreased at +12h (0.33 ± 0.07-fold) and +24h (0.25 ± 0.07-fold) from PRE. A trend was found for BECN1 (p=0.055) towards an increased in expression from PRE to +12h (1.94 ± 0.65-fold). A significant time effect was found for the AUC of cortisol with a greater AUC of cortisol for EX than CON. CONCLUSION: These results suggest that the RE-induced hormone response can be important to the initiation of the phagophore after muscle damage in untrained young women.