Short-term exercise training in humans reduces AMPK signalling during prolonged exercise independent of muscle glycogen

We examined the effect of short-termexercise training on skeletalmuscleAMP-activated protein kinase (AMPK) signalling and muscle metabolism during prolonged exercise in humans. Eight sedentary males completed 120 min of cycling at 66±1% ˙VO2peak, then exercise trained for 10 days, before repeating the exercise bout at the same absolute workload. Participants rested for 72 h before each trial while ingesting a high carbohydrate diet (HCHO). Exercise training significantly (P <0.05) attenuated exercise-induced increases in skeletalmuscle freeAMP : ATP ratio and glucose disposal and increased fat oxidation. Exercise training abolished the 9-fold increase in AMPK α2 activity observed during pretraining exercise. Since training increased muscle glycogen content by 93±12% (P <0.01), we conducted a second experiment in seven sedentary male participants where muscle glycogen content was essentially matched pre- and post-training by exercise and a low CHO diet (LCHO; post-training muscle glycogen 52±7% less than inHCHO,P <0.001). Despite the difference inmuscle glycogen levels in the two studies weobtained very similar results. Inboth studies the increase inACCβSer221 phosphorylation was reduced during exercise after training. In conclusion, there is little activation ofAMPKsignalling during prolonged exercise following short-term exercise training suggesting that other factors are important in the regulation of glucose disposal and fat oxidation under these circumstances. It appears thatmuscle glycogen is not an important regulator ofAMPKactivation during exercise in humans when exercise is begun with normal or high muscle glycogen levels.