Metabolic and cardiorespiratory responses to "the lactate clamp"

To evaluate the hypothesis that precursor supply limits gluconeogenesis (GNG) during exercise, we examined training-induced changes in glucose kinetics [rates of appearance (R-a) and disappearance (R-d)], oxidation (R-ox), and recycling (R-r) with an exogenous lactate infusion to 3.5-4.0 mM during rest and to pretraining 65% peak O-2 consumption ((V) over dotO(2peak)) levels during exercise. Control and clamped trials (LC) were performed at rest pre( PRR, PRR-LC) and posttraining (PoR, PoR-LC) and during exercise pre- (PREX) and posttraining at absolute (P(o)A(B), P(o)A(B)- 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(-1) . min(-1)) and P(o)A(B) (3.82 +/- 0.51 vs. 5.0 +/- 0.62 mg . kg(-1) . min(-1)). Percent glucose R-d oxidized decreased with all LC except PoRL-LC (PRR, 32%; PRR-LC, 22%; PoR, 27%; PoR-LC, 20%; P(o)A(B), 95%; P(o)A(B)- LC, 77%), which resulted in a significant increase in oxidation from alternative carbohydrate (CHO) sources at rest and P(o)A(B). We conclude that 1) increased arterial [lactate] did not increase glucose R-r 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 R-ox.