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1 Department of Integrative
Biology,
We evaluated the
hypotheses that alterations in glucose disposal rate
(Rd) 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
(
O2 peak)] and
after training [65% pretraining
O2 peak, same
absolute workload (ABT), and 65% posttraining
O2 peak, 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%
O2 peak. The power
output that elicited 66.0 ± 1.1% of
O2 peak before
training elicited 54.0 ± 1.7% after training. Whole body glucose
Rd 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%
O2 peak) 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%
O2 peak) promotes a
glucose shunt from inactive tissues to active muscle.
exertion; glycogen; lactate; stable isotopes; crossover concept
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