Fat oxidation and glucose uptake are increased following an acute bout of resistance exercise: Role of AMPK, ACC, Akt/PKB, and AS160

We hypothesized that an increase in muscle AMPK signaling to ACC2 and AS160 would enhance fat oxidation and glucose uptake during recovery after resistance exercise. We studied young subjects before, during and for 2 hr following a bout of leg resistance exercise. We used femoral catheterization, muscle biopsies, indirect calorimetry, and immunoblotting methods to measure fat oxidation, leg glucose uptake, and the phosphorylation status or activity of AMPKα2, ACC2, Akt/PKB, and AS160. RQ increased during exercise and significantly decreased during recovery (P<0.05). Whole body fat oxidation was significantly higher (relative to baseline) during post‐exercise recovery (P<0.05). Glucose uptake increased during exercise and remained elevated for the next 2 hr (P<0.05). AMPKα2 activity increased immediately after exercise and remained elevated for 1 hr (P<0.05). ACC2 phosphorylation also increased during post‐exercise recovery (P<0.05). Akt/PKB phosphorylation increased within 1 hr post (P<0.05). AS160 phosphorylation tended to increase during exercise and remained elevated during recovery (P<0.05). We conclude that the activation of AMPK and subsequent signaling to AS160 may be a key cellular mechanism enhancing fat oxidation (increased ATP) and glucose uptake (increased substrate) in order to replenish muscle glycogen during recovery after resistance exercise. Support: NIH R01AR049877 and NIH P30 AG17231