Skeletal muscle AMPK is not activated during 2 h of moderate intensity exercise at ∼65%V?O2peakin endurance trained men

Key points AMP-activated protein kinase (AMPK) is considered a major regulator of skeletal muscle metabolism during exercise. However, we previously showed that, although AMPK activity increases by 8-10-fold during similar to 120 min of exercise at similar to 65%V?O2peakin untrained individuals, there is no increase in these individuals after only 10 days of exercise training (longitudinal study). In a cross-sectional study, we show that there is also a lack of activation of skeletal muscle AMPK during 120 min of cycling exercise at 65%V?O2peakin endurance-trained individuals. These findings indicate that AMPK is not an important regulator of exercise metabolism during 120 min of exercise at 65%V?O2peakin endurance trained men. It is important that more energy is directed towards examining other potential regulators of exercise metabolism. AMP-activated protein kinase (AMPK) is considered a major regulator of skeletal muscle metabolism during exercise. Indeed, AMPK is activated during exercise and activation of AMPK by 5-aminoimidazole-4-carboxyamide-ribonucleoside (AICAR) increases skeletal muscle glucose uptake and fat oxidation. However, we have previously shown that, although AMPK activity increases by 8-10-fold during similar to 120 min of exercise at similar to 65%V?O2peakin untrained individuals, there is no increase in these individuals after only 10 days of exercise training (longitudinal study). In a cross-sectional study, we examined whether there is also a lack of activation of skeletal muscle AMPK during 120 min of cycling exercise at 65%V?O2peakin endurance-trained individuals. Eleven untrained (UT;V?O2peak= 37.9 +/- 5.6 ml.kg(-1) min(-1)) and seven endurance trained (ET;V?O2peak= 61.8 +/- 2.2 ml.kg(-1) min(-1)) males completed 120 min of cycling exercise at 66 +/- 4%V?O2peak(UT: 100 +/- 21 W; ET: 190 +/- 15 W). Muscle biopsies were obtained at rest and following 30 and 120 min of exercise. Muscle glycogen was significantly (P < 0.05) higher before exercise in ET and decreased similarly during exercise in the ET and UT individuals. Exercise significantly increased calculated skeletal muscle free AMP content and more so in the UT individuals. Exercise significantly (P < 0.05) increased skeletal muscle AMPK alpha 2 activity (4-fold), AMPK alpha Thr(172)phosphorylation (2-fold) and ACC beta Ser(222)phosphorylation (2-fold) in the UT individuals but not in the ET individuals. These findings indicate that AMPK is not an important regulator of exercise metabolism during 120 min of exercise at 65%V?O2peakin endurance trained men.