Protein ingestion before sleep augments postexercise muscle protein synthesis during overnight recovery. It is unknown whether postexercise and presleep protein consumption modulates postprandial protein handling and myofibrillar protein synthetic responses the following morning. Sixteen healthy young (24 ± 1 yr) men performed unilateral resistance-type exercise (contralateral leg acting as a resting control) at 2000. Participants ingested 20 g of protein immediately after exercise plus 60 g of protein presleep (PRO group; n = 8) or equivalent boluses of carbohydrate (CON; n = 8). The subsequent morning participants received primed, continuous infusions of l-[ring- 2 H 5 ]phenylalanine and l-[1- 13 C]leucine combined with ingestion of 20 g intrinsically l-[1- 13 C]phenylalanine- and l-[1- 13 C]leucine-labeled protein to assess postprandial protein handling and myofibrillar protein synthesis in the rested and exercised leg in CON and PRO. Exercise increased postabsorptive myofibrillar protein synthesis rates the subsequent day (P < ), with no differences between CON and PRO. Protein ingested in the morning increased myofibrillar protein synthesis in both the exercised and rested leg (P < ), with no differences between treatments. Myofibrillar protein bound l-[1- 13 C]phenylalanine enrichments were greater in the exercised ( ± and ± MPE in CON and PRO, respectively) vs. rested ( ± and ± MPE in CON and PRO, respectively) leg (P < ), with no differences between treatments (P > ). The additive effects of resistance-type exercise and protein ingestion on myofibrillar protein synthesis persist for more than 12 h after exercise and are not modulated by protein consumption during acute postexercise recovery. This work provides evidence of an extended window of opportunity where presleep protein supplementation can be an effective nutrient timing strategy to optimize skeletal muscle reconditioning.
Two weeks prior to the study, each subject visited the laboratory to determine his workload maximum ( W max ) on a one-legged modified Krogh ergometer. After 5 min warming up without resistance, the subject began one-legged kicking (35 kicks per minute) for 3 min at kg resistance; this was increased by kg every 3 min until the subject could no longer maintain the cadence. The workload for each subject's subsequent 1 h exercise bout was defined as 67% of this W max ( Figs 1 and 2 ). The subjects were instructed to avoid physical activity and to maintain their habitual diet (as confirmed by 5-day diet diaries) for the 2 days before, and during, all testing days. On the test days the fasted subjects received a commercial clinical nutrient drink (Semper, Fredriksberg, DK: 15% protein, 64% carbohydrate and 21% fat) in doses every 30 min over the subsequent 4 h. The drink provided the equivalent of × basal metabolic rate (as estimated from the subject's fat-free mass determined by anthropometry ( Cunningham, 1982 ). The feeding was started with a double dose to bring the subjects rapidly into a fed state. No tracer was added to the oral feed. All subjects were ‘tracer virgins’ allowing assumption of basal enrichment of tissue proteins at natural abundance values.