Modulation of autophagy signaling with resistance exercise and protein ingestion following short-term energy deficit

Autophagy contributes to remodeling of skeletal muscle and is sensitive to contractile activity and prevailing energy availability. We investigated changes in targeted genes and proteins with roles in autophagy following 5 days of energy balance (EB), energy deficit (ED), and resistance exercise (REX) after ED. Muscle biopsies from 15 subjects (8 males, 7 females) were taken at rest following 5 days of EB [45 kcal.kg fat free mass (FFM)(-1).day(-1)] and 5 days of ED (30 kcal.kg FFM-1.day(-1)). After ED, subjects completed a bout of REX and consumed either placebo (PLA) or 30 g whey protein (PRO) immediately postexercise. Muscle biopsies were obtained at 1 and 4 h into recovery in each trial. Resting protein levels of autophagy-related gene protein 5 (Atg5) decreased after ED compared with EB (similar to 23%, P < 0.001) and remained below EB from 1 to 4 h postexercise in PLA (similar to 17%) and at 1 h in PRO (similar to 18%, P < 0.05). In addition, conjugated Atg5 (cAtg12) decreased below EB in PLA at 4 h (similar to 20, P < 0.05); however, its values were increased above this time point in PRO at 4 h alongside increases in FOXO1 above EB (similar to 22-26%, P < 0.05). Notably, these changes were subsequent to increases in unc-51-like kinase 1(Ser757) phosphorylation (similar to 60%) 1 h postexercise in PRO. No significant changes in gene expression of selected autophagy markers were found, but EGR-1 increased above ED and EB in PLA (similar to 417-864%) and PRO (similar to 1,417-2,731%) trials 1 h postexercise (P < 0.001). Postexercise protein availability, compared with placebo, can selectively promote autophagic responses to REX in ED.