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

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ARC Linkage Project grant # LP100100010

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Smiles, W. J., Areta, J. L., Coffey, V. G., Phillips, S. M., Moore, D. R., Stellingwerff, T., Burke, L. M., Hawley, J. A., & Camera, D. M. (2015). Modulation of autophagy signaling with resistance exercise and protein ingestionfollowing short-term energy deficit. American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, 309(5), R603-R612.

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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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