Abstract

The effect of nutrient‐dense food ingestion immediately after resistance exercise as a nutritional strategy to promote muscle anabolism has not been clearly established. Given that a coordinated anabolic response is necessary for the regulation of muscle protein synthesis with exercise and protein ingestion, our aim was to determine whether egg whites or whole eggs ingestion influenced post‐exercise mechanistic target of rapamycin complex 1 (mTORC1) and mitogen‐activated protein kinase (MAPK) signaling phosphorylation in human skeletal muscle. In crossover trials, 10 healthy resistance‐trained men (21±1 y; 88±3 kg; bodyfat: 16±1%; means±SD) completed lower body resistance exercise (4 sets of 10 repetitions at 80% of 10‐RM for both leg press and leg extensions) before ingesting whole eggs (18 g protein, 17 g fat) or egg whites (18 g protein, 0 g fat) in scrambled form. Muscle biopsies were obtained before exercise and at 2 and 5H after protein ingestion to assess the phosphorylation of candidate anabolic signaling molecules by Western blotting. The phosphorylation of mTORser2448 increased ~34% above fasted at 5H following whole egg and egg white consumption (time effect; P<0.01) with no difference between conditions (P>0.66). Downstream of mTORC1, 4E‐BP1Thr37/46 was elevated above fasted at 2H (~22–44%; P<0.01) and was sustained above fasted at 5H (P<0.01) with no differences between conditions (P>0.14). There was no effect of food ingestion on S6K1Thr389 and eEF2Thr56. The phosphorylation of the MAPK ERK1/2Thr202/Tyr204 was similarly suppressed at 2 and 5H following feeding for the whole egg and egg white conditions (~430–780%; P<0.001). Ingestion of isonitrogenous amounts of whole egg and egg white similarly stimulates anabolic signaling in young trained males. These findings would suggest a similar increase in mRNA translation initiation during recovery from resistance exercise in healthy young men. Identification of the intracellular localization of mTORC1 and its colocalization with positive (e.g. Rheb) and negative (e.g. TSC2) regulators via immunofluorescence is ongoing.

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