Muscle net glucose uptake and glucose kinetics after endurance training in men

We evaluated the hypotheses that alterations in glucose disposal rate (R-d) due to endurance training are the result of changed net glucose uptake by active muscle and that blood glucose is shunted to working muscle during exercise requiring high relative power output. We studied leg net glucose uptake during 1 h of cycle ergometry at two intensities before training [45 and 65% of peak rate of oxygen consumption ((V) over dot o(2peak))] and after training [65% pretraining (V) over dot o(2peak), same absolute workload (ABT), and 65% posttraining (V) over dot o(2peak), same relative workload (RLT)]. Nine male subjects (178.1 +/- 2.5 cm, 81.8 +/- 3.3 kg, 27.4 +/- 2.0 yr) were tested before and after 9 wk of cycle ergometer training, five times a week at 75% (V) over dot o(2peak). The power output that elicited 66.0 +/- 1.1% of (V) over dot o(2peak) before training elicited 54.0 +/- 1.7% after training. Whole body glucose R-d decreased posttraining at ABT (5.45 +/- 0.31 mg . kg(-1) . min(-1) at 65% pretraining to 4.36 +/- 0.44 mg . kg(-1) . min(-1)) but not at RLT (5.94 +/- 0.47 mg . kg(-1) . min(-1)). Net glucose uptake was attenuated posttraining at ABT (1.87 +/- 0.42 mmol/min at 65% pretraining and 0.54 +/- 0.33 mmol/min) but not at RLT (2.25 +/- 0.81 mmol/min). The decrease in leg net glucose uptake at ABT was of similar magnitude as the drop in glucose Rd and thus could explain dampened glucose flux after training. Glycogen degradation also decreased posttraining at ABT but not RLT. Leg net glucose uptake accounted for 61% of blood glucose flux before training and 81% after training at the same relative (65% (V) over dot o(2peak)) workload and only 38% after training at ABT. We conclude that 1) alterations in active muscle glucose uptake with training determine changes in whole body glucose kinetics; 2) muscle glucose uptake decreases for a given, moderate intensity task after training; and 3) hard exercise (65% (V) over dot o(2peak)) promotes a glucose shunt from inactive tissues to active muscle.