Abstract

Resistance exercise is a potent stimulator of muscle protein synthesis. The increase in muscle protein synthesis following resistance exercise is usually detected within 3 hours and remains elevated for up to 48 hours. However, during and immediately after exercise muscle protein synthesis is inhibited. Skeletal muscle AMP-activated protein kinase (AMPK?2) and acidosis have recently been identified as inhibitors of muscle protein synthesis. PURPOSE: To determine if muscle AMPKα2 activity and/or acidosis would be elevated in conditions associated with reduced protein synthesis (i.e., during and immediately post resistance exercise). METHODS: We studied 8 young subjects before, during, and for 2 hours following a bout of resistance exercise (Leg Extensions: 10 sets X 10 repetitions, 70% 1RM). Muscle biopsies were collected from the vastus lateralis before, immediately post exercise, and at 1hr and 2 hr post exercise. We utilized immunoprecipitation methods to measure muscle AMPKα2 activity. Mixed muscle fractional protein synthetic rate (FSR) was measured using stable isotope techniques. RESULTS: Muscle AMPKα2 activity (pmol*g−1*min−1) at baseline was 243 ± 15, increased immediately post exercise (298 ± 23), and remained elevated at 1hr (317 ± 30) and 2hr (321 ± 32) hours post exercise (P <0.05). Preliminary data on muscle protein synthesis (n=3) indicate that muscle FSR was not significantly different from baseline following resistance exercise (P >0.05). Femoral vein lactate increased 14-fold (0.8 ± 0.1 to 11 ± 0.8 mM) during the resistance exercise bout. The average blood lactate during the first hour post exercise remained 3-fold higher (P <0.05) and then returned to baseline values during the second hour post exercise. Femoral vein pH decreased significantly during exercise (7.37 ± 0.01 to 7.17 ± 0.01, P <0.05) and returned to baseline values during the next two hours. CONCLUSIONS: The attenuation of muscle protein synthesis during and immediately after resistance exercise was associated with both increased AMPKα2 activity and acidosis. Further research is required to determine the specific roles of AMPK and acidosis in inhibiting muscle protein synthesis.

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