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1 Rigshospitalet
2 University of Copenhagen
3 Copenhagen Muscle Research Centre
4 University of Copenhagen,
* To whom correspondence should be addressed. E-mail: thorbjorn_akerstrom{at}inflammation-metabolism.dk.
Glucose ingestion during exercise attenuates activation of metabolic enzymes and expression of important transport proteins. In light of this, we hypothesized that glucose ingestion during training would result in an attenuation fo the increase in 1) FA uptake and oxidation during exercise, 2) lower citrate synthase (CS) and
-hydroxyacyl-CoA dehydrogenase (
-HAD) activity, and glycogen content in skeletal muscle, and 3) attenuated endurance performance enhancement in the trained state. To investigate this we studied 9 male subjects who performed 10 weeks of one-legged knee-extensor training. They trained one leg while ingesting a 6% glucose solution (Glc) and ingested a sweetened placebo while training the other leg (Plc). The subjects trained their respective legs 2 hours at a time on alternate days 5 days a week. Endurance training increased peak power (Pmax) and time-to-fatigue at 70% of Pmax ~14% and ~30%, respectively. CS and
-HAD activity increased and glycogen content was greater after training, but there where no differences between Glc and Plc. After training the rate of oxidation of palmitate (ROx) and the % of rate of disappearance that was oxidized (%Rdox) changed. The %Rdox was on average 16.4% greater during exercise after training whereas, after exercise %Rdox was 30.4% lower. ROx followed the same pattern. However, none of these parameters were different between the Glc and Plc. We conclude that glucose ingestion during training does not alter training adaptation related to substrate metabolism, mitochondrial enzyme activity, glycogen content or performance. .
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