PMID- 12376315
OWN - NLM
STAT- MEDLINE
DCOM- 20021108
LR  - 20131121
IS  - 0193-1849 (Print)
IS  - 0193-1849 (Linking)
VI  - 283
IP  - 5
DP  - 2002 Nov
TI  - Metabolic and cardiorespiratory responses to "the lactate clamp".
PG  - E889-98
AB  - 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).
FAU - Miller, Benjamin F
AU  - Miller BF
AD  - Department of Integrative Biology, University of California, Berkeley, California 
      94720, USA.
FAU - Fattor, Jill A
AU  - Fattor JA
FAU - Jacobs, Kevin A
AU  - Jacobs KA
FAU - Horning, Michael A
AU  - Horning MA
FAU - Suh, Sang-Hoon
AU  - Suh SH
FAU - Navazio, Franco
AU  - Navazio F
FAU - Brooks, George A
AU  - Brooks GA
LA  - eng
GR  - AR-42906/AR/NIAMS NIH HHS/United States
PT  - Clinical Trial
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (Blood Glucose)
RN  - 0 (Fatty Acids, Nonesterified)
RN  - 0 (Insulin)
RN  - 33X04XA5AT (Lactic Acid)
RN  - PDC6A3C0OX (Glycerol)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Blood Glucose/*metabolism
MH  - Blood Pressure/drug effects/*physiology
MH  - Energy Metabolism/drug effects/physiology
MH  - Fatty Acids, Nonesterified/blood
MH  - Glycerol/blood
MH  - Heart Rate/drug effects/*physiology
MH  - Homeostasis/drug effects/physiology
MH  - Humans
MH  - Insulin/blood
MH  - Lactic Acid/blood/*pharmacokinetics
MH  - Male
MH  - Oxygen Consumption/physiology
MH  - Physical Exertion/drug effects/*physiology
MH  - Respiration
MH  - Rest/physiology
MH  - Weight Loss/physiology
EDAT- 2002/10/12 04:00
MHDA- 2002/11/26 04:00
CRDT- 2002/10/12 04:00
PHST- 2002/10/12 04:00 [pubmed]
PHST- 2002/11/26 04:00 [medline]
PHST- 2002/10/12 04:00 [entrez]
AID - 10.1152/ajpendo.00266.2002 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2002 Nov;283(5):E889-98. doi: 
      10.1152/ajpendo.00266.2002.