Post-exercise Skeletal Muscle Protein Synthesis And Intracellular Signals During Negative Energy Balance In Active Adults

Abstract

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 VO2peak) participated in two, nine-day diet interventions [weight maintenance (WM) 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%VO2peak (POST; day 7) for determination of MPS and phosphorylation of associated ISPs. MPS was determined using a primed, constant infusion of [2H5]-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 not affected. POST MPS values did not differ between WM and ED. However, when compared to REST MPS values (WM: 0.065 ± 0.01; ED: 0.043 ± 0.01), POST MPS tended to increase 75% during ED (0.076 ± 0.02%/h) but decrease 7% (0.060 ± 0.01%/h) during WM (P = 0.08). 4E-BP1 phosphorylation also tended to be greater POST during WM compared to ED (P = 0.08). AKT phosphorylation, independent of energy state, was greater immediately compared to 3 h post-exercise (P= 0.05). CONCLUSION: These finding 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.