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 (VO(2 peak)) levels during exercise. Control and clamped trials (LC) were performed at rest pre- (P(R)R, P(R)R-LC) and posttraining (P(O)R, P(O)R-LC) and during exercise pre- (P(R)E(X)) and posttraining at absolute (P(O)A(B), P(O)A(B)-LC) and relative (P(O)R(L), P(O)R(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(O)R (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 P(O)R(L)-LC (P(R)R, 32%; P(R)R-LC, 22%; P(O)R, 27%; P(O)R-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).
Miller
Benjamin F
BF
Department of Integrative Biology, University of California, Berkeley, California 94720, USA.
Fattor
Jill A
JA
Jacobs
Kevin A
KA
Horning
Michael A
MA
Suh
Sang-Hoon
SH
Navazio
Franco
F
Brooks
George A
GA
D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005990:Glycerol / Q000097:blood; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology*; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007328:Insulin / Q000097:blood; D019344:Lactic Acid / Q000097:blood / Q000493:pharmacokinetics*; D008297:Male; D010101:Oxygen Consumption / Q000502:physiology; D005082:Physical Exertion / Q000187:drug effects / Q000502:physiology*; D012119:Respiration; D012146:Rest / Q000502:physiology; D015431:Weight Loss / Q000502:physiology
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D019344:Lactic Acid; D005990:Glycerol