Modulation of autophagy signaling with resistance exercise and protein ingestion following short-term energy deficit
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ARC Linkage Project grant # LP100100010
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 (∼23%, P < 0.001) and remained below EB from 1 to 4 h postexercise in PLA (∼17%) and at 1 h in PRO (∼18%, P < 0.05). In addition, conjugated Atg5 (cAtg12) decreased below EB in PLA at 4 h (∼20, P < 0.05); however, its values were increased above this time point in PRO at 4 h alongside increases in FOXO1 above EB (∼22–26%, P < 0.05). Notably, these changes were subsequent to increases in unc-51-like kinase 1Ser757 phosphorylation (∼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 (∼417–864%) and PRO (∼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.
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