Exercise and energy availability independently impact rates of skeletal muscle protein synthesis. To date, no investigations have explored the concurrent effect of endurance exercise and energy deprivation on mixed skeletal muscle protein synthesis (MPS) or associated intracellular signaling proteins (ISPs) in humans.

Purpose. To characterize the effects of an acute, moderate energy restriction (ED) and an endurance exercise bout on MPS and associated ISPs in healthy adults.

Methods. Physically active volunteers (n=8, 21 yrs, 71 kg, 172 cm, 20% body fat, 53 mL·kg^-1·min ^-1 VO_2peak) participated in two, nine-day diet interventions [energy adeqaute (EA) and energy deficient (ED), ∼80% of energy needs] which provided 1.5 g protein.kg^-1·day^-1 and 30% total energy as fat. Muscle biopsies were obtained from participants at rest (REST; day 9) and following a 45 min run @ 65%VO_2peak (POST; day 7) for determination of MPS and phosphorylation of associated ISPs. MPS was determined using a primed, constant infusion of [²H ₅]-phenylalanine. Phosphorylation of ISPs was determined via Western blotting. Nitrogen balance (NBAL) was estimated from 24 hr protein intake and associated urinary nitrogen excretion.

Results. Subjects lost ∼1 kg body weight during ED (P < 0.0001) and NBAL was unaffected. POST MPS values did not differ between EA and ED. However, when compared to REST MPS values (EA: 0.069 ± 0.01; ED: 0.057 ± 0.01), POST MPS tended to increase 30% during ED (0.074 ± 0.02 %/h) but decrease 8% (0.064 ± 0.01 %/h) during EA (P=0.08). AMPKα phosphorylation tended to increase from 120 to 300 min POST during EA (P= 0.06). AKT phosphorylation, independent of energy state, was greater immediately compared to 3 h post-exercise (P=0.05) and remained elevated at 300 min POST during ED (P=0.05). The change in mTOR phosphorylation was greater 30 min POST during EA compared to ED (P<0.05).

Conclusion. These findings suggest that energy intake impacts post-exercise MPS and associated ISPs. Further research is needed to evaluate effects of long term energy deficits on exercise-associated responses in protein utilization.