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Articles in PresS, published online ahead of print July 17, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00266.2002
Submitted on June 17, 2002
Accepted on July 11, 2002
1 Department of Integrative Biology, University of California, Berkeley, CA, USA
* To whom correspondence should be addressed. E-mail: gbrooks{at}socrates.berkeley.edu.
To evaluate the hypothesis that precursor supply limits gluconeogenesis (GNG) during exercise we examined training induced changes in glucose kinetics (rates of appearance (Ra), and disappearance (Rd)), oxidation (Rox), and recycling (Rr) with an exogenous lactate infusion to 3.5-4.0 mM during rest and to pre-training 65% VO2peak levels during exercise. Control and clamped trials (LC) were performed at rest pre- (PRR, PRR-LC) and post-training (POR, POR-LC), and during exercise pre- (PREX) and post-training at absolute (POAB, POAB-LC) and relative (PORL, PORL-LC) intensities. Glucose Rr was not different in any rest or exercise condition. Glucose Ra did not differ as a result of LC. Glucose Rox was significantly decreased with LC at POR (0.38±0.03 vs. 0.56±0.04 mg/kg/min) and POAB (3.82±0.51 vs. 5.0±0.62 mg/kg/min). Percent of Glucose Rd oxidized decreased with all LC except PORL-LC (PRR, 32%; PRR-LC, 22%; POR, 27%; POR-LC, 20%; POAB, 95%; POAB-LC, 77%), which resulted in a significant increase in oxidation from alternative carbohydrate (CHO) sources at rest and POAB. We conclude that; 1) increased arterial [lactate] did not increase glucose Rr measured during rest or exercise after training, 2) glucose disposal or production did not change with increased precursor supply, and 3) infusion of exogenous CHO in the form of lactate resulted in the decrease of glucose Rox.
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