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 O₂ consumption (Vo_{2 peak}) levels during exercise. Control and clamped trials (LC) were performed at rest pre-(P_RR, P_RR-LC) and posttraining (P_oR, P_oR-LC) and during exercise pre- (P_RE_x) and posttraining at absolute (P_oA_B, P_oA_B-LC) and relative (P_oR_L, P_oR_L-LC) intensities. Glucose R_r was not different in any rest or exercise condition. Glucose R_a did not differ as a result of LC. Glucose R_ox was significantly decreased with LC at P_oR (0.38 ± 0.03 vs. 0.56 ± 0.04 mg·kg^-1·min^-1) and P_oA_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 P_oR_L-LC (P_RR, 32%; P_RR-LC, 22%; P_oR, 27%; P_oR-LC, 20%; P_oA_B, 95%; P_oA_B-LC, 77%), which resulted in a significant increase in oxidation from alternative carbohydrate (CHO) sources at rest and P_oA_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.