Endurance training enhances lactate clearance during hyperlactatemia

Constant infusions of cold molar lactate (178.0 +/- 1.6 mumol.kg-1.min-1), [U-14C]lactate (0.50 muCi/min), and [6-3H]glucose (0.5 muCi/min) were employed to study the effects of endurance training (running 1 h/day, at 38 m/min, 10% grade) on lactate clearance in resting, hyperlactatemic rats. Before infusion, resting blood lactate levels were not significantly different between controls, 1.10 +/- 0.04 mM, and trained animals, 1.16 +/- 0.04 mM. Lactate levels increased significantly during the infusion period, attaining steady-state mixed venous concentrations of 11.32 +/- 0.24 mM and 5.44 +/- 0.09 mM, respectively, for controls and trained animals. Lactate clearance rates, based on net lactate removal (i.e., not tracer-estimated lactate removal), were twofold greater in trained animals vs. controls, 33.0 +/- 0.7 and 15.4 +/- 0.4 ml.kg-1. min-1, respectively. Lactate specific activity values during the infusion period were not significantly different between controls, 22,243 +/- 236 dpm/mumol, and trained animals, 21,270 +/- 374 dpm/mumol, indicating similar endogenous dilution of the pyruvate-lactate pool. For both control and trained animals, essentially 100% of the 14C infused as lactate was recovered as either glucose or CO2; however, trained animals demonstrated a 25% greater rate of gluconeogenesis. At a given lactate production rate, trained animals maintain lower lactate levels through enhanced clearance via gluconeogenesis and oxidation.

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Endurance training affects lactate clearance, not lactate production

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1983.244.1.e83 ◽

1983 ◽

Vol 244 (1) ◽

pp. E83-E92 ◽

Cited By ~ 43

Author(s):

C. M. Donovan ◽

G. A. Brooks

Keyword(s):

Endurance Training ◽

Blood Lactate ◽

Lactate Production ◽

Lactate Clearance ◽

Metabolic Clearance ◽

Lactate Metabolism ◽

Turnover Rates ◽

Lactate Turnover ◽

Metabolic Conditions ◽

Lactate Levels

Primed-continuous infusion of [2-3H]- and [U-14C]lactate was used to study the effects of endurance training (running 2 h/day at 29.4 m/min up a 15% gradient) on lactate metabolism in rats. Measurements were made under three metabolic conditions: rest (Re), easy exercise (EE, 13.4 m/min, 1% gradient) and hard exercise (HE, 26.8 m/min, 1% gradient). Blood lactate levels in trained animals increased from 1.0 +/- 0.09 mM in Re to 1.64 +/- 0.21 in EE and 2.66 +/- 0.38 in HE. Control animals also demonstrated an increase in blood lactate with increasing work rate, but values were 1.93 +/- 0.21 and 4.62 +/- 0.57 mM at EE and HE, respectively. Lactate turnover rates (RtLA) measured with [U-14C]lactate increased from 214.0 +/- 17.0 mumol.kg-1.min-1 in Re to 390.3 +/- 31.6 in EE and 518.1 +/- 56.4 in HE. No significant differences in RtLA were observed between controls and trained animals under any condition. Identical relationships between RtLA and exercise or training were obtained with [2-3H]lactate; however, the values obtained were consistently 90% higher than those observed with [U-14C]lactate. Metabolic clearance rate (MCR) for 14C was not significantly different in Re between controls and trained animals (180.6 +/- 27.7 ml.kg-1.min-1). Metabolic clearance of lactate in trained animals was 37 and 107% greater than in controls during EE and HE, respectively. Results indicate that the effect of endurance training is not on production of lactate but on its clearance from the blood.

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Serial blood lactate levels as a prognostic factor for sepsis mortality

Paediatrica Indonesiana ◽

10.14238/pi54.3.2014.168-73 ◽

2014 ◽

Vol 54 (3) ◽

pp. 168

Author(s):

Keswari Aji Patriawati ◽

Nurnaningsih Nurnaningsih ◽

Purnomo Suryantoro

Keyword(s):

Blood Lactate ◽

Lactate Clearance ◽

Major Health Problem ◽

Major Health ◽

Serial Blood ◽

Factors Associated ◽

Relative Risks ◽

Increased Risk ◽

Lactate Levels ◽

Blood Lactate Levels

Background Sepsis is a major health problem in children and aleading cause of death. In recent decades, lactate has been studiedas a biomarker for sepsis, and as an indicator of global tissuehypoxia, increased glycolysis, endotoxin effect, and anaerobicmetabolism. Many studies h ave shown both high levels andincreased serial blood lactate level measurements to be associatedwith increased risk of sepsis mortality.Objective To evaluate serial blood lactate levels as a prognosticfactor for sepsis mortality.Methods We performed an observational, prospective study in thePediatric Intensive Care Unit (PICU) at DR. Sardjito Hospital,Yogyakarta from July to November 2012. We collected serialblood lactate specimens of children with sepsis, first at the time ofadmission, followed by 6 and 24 hours later. The outcome measurewas mortality at the end ofintensive care. Relative risks and 95%confidence intervals of the factors associated with mortality werecalculated using univariate and multivariate analyses.Results Sepsis was found in 91 (50.3%) patients admitted tothe PIW , of whom 75 were included in this study. Five patients(6. 7%) died before the 24-hour lactate collection and 39 patients(52.0%) died during the study. Blood lactate levels of ~ 4mmol;Lat the first and 24-hour specimens were associated with mortality(RR 2.9; 95%CI 1.09 to 7 .66 and RR 4.92; 95%CI 1.77 to 13.65,respectively). Lactate clearance of less than 10% at 24 hours(adjusted RR 5.3; 95% CI 1.1 to 24.5) had a significantly greaterrisk fo llowed by septic shock (adjusted RR 1.54; 95%CI 1.36 to6.4 7) due to mortality.Conclusion In children with sepsis there is a greater risk of mortalityin those with increasing or persistently high serial blood lactatelevels, as shown by less than 10% lactate clearance at 24-hours afterPIW admission.

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Oxamate Enhances the Anti-Inflammatory and Insulin-Sensitizing Effects of Metformin in Diabetic Mice

Pharmacology ◽

10.1159/000478909 ◽

2017 ◽

Vol 100 (5-6) ◽

pp. 218-228 ◽

Cited By ~ 2

Author(s):

Mu-chao Wu ◽

Wei-ran Ye ◽

Yi-jia Zheng ◽

Shan-shan Zhang

Keyword(s):

Blood Lactate ◽

Cell Mass ◽

Lactate Production ◽

Beta Cell Mass ◽

Serum Lactate ◽

Blood Levels ◽

Anti Inflammatory ◽

Lactate Levels ◽

Blood Lactate Levels

Metformin (MET) is the first-line drug for treating type 2 diabetes mellitus (T2DM). However, MET increases blood lactate levels in patients with T2DM. Lactate possesses proinflammatory properties and causes insulin resistance (IR). Oxamate (OXA), a lactate dehydrogenase inhibitor, can decrease tissue lactate production and blood lactate levels. This study was conducted to examine the effects of the combination of OXA and MET on inflammation, and IR in diabetic db/db mice. Supplementation of OXA to MET led to lowered tissue lactate production and serum lactate levels compared to MET alone, accompanied with further decreased tissue and blood levels of pro-inflammatory cytokines, along with better insulin sensitivity, beta-cell mass, and glycemic control in diabetic db/db mice. These results show that OXA enhances the anti-inflammatory and insulin-sensitizing effects of MET through the inhibition of tissue lactate production in db/db mice.

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Role of glucose in corneal metabolism

AJP Cell Physiology ◽

10.1152/ajpcell.1985.249.5.c409 ◽

1985 ◽

Vol 249 (5) ◽

pp. C409-C416 ◽

Cited By ~ 20

Author(s):

R. S. Thies ◽

L. J. Mandel

Keyword(s):

Oxygen Consumption ◽

Steady State ◽

Specific Activity ◽

Krebs Cycle ◽

Lactate Production ◽

Minor Component ◽

Acid Oxidation ◽

Endogenous Fatty Acid ◽

Nonsteady State ◽

A Minor

Glucose catabolism by glycolysis and the Krebs cycle was examined in the isolated rabbit cornea incubated with [6-14C]glucose. The production of [14C]lactate and 14CO2 from this substrate provided minimal values for the fluxes through these pathways since the tissue was in metabolic steady state but not isotopic steady state during the 40-min incubation. The specific activity of lactate under these conditions was one-third of that for [6-14C]glucose, and label dilution by exchange with unlabeled alanine was minimal, suggesting that glycogen degradation was primarily responsible for this dilution of label in the Embden-Meyerhof pathway. In addition, considerable label accumulation was found in glutamate and aspartate. Calculations revealed that these endogenous amino acid pools were not isotopically equilibrated after the incubation period, suggesting that they were responsible for the isotopic nonsteady state by exchange dilution through transaminase reactions with labeled intermediates. An estimate of glucose oxidation by the Krebs cycle, which was corrected for label dilution by exchange, indicated that glucose could account for most of the measured corneal oxygen consumption that was coupled to oxidative phosphorylation. A minor component of this respiration could not be accounted for by glucose or glycogen oxidation. Additional experiments suggested that endogenous fatty acid oxidation was probably also active under these conditions. Finally, reciprocal changes in plasma membrane Na+-K+-ATPase activity induced by ouabain and nystatin were found to concomitantly alter oxygen consumption rates and [14C]lactate production from [6-14C]glucose. These results demonstrated the capacity for regulating glycolysis and the Krebs cycle in response to changing energy demands in the cornea.

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Lactate kinetics in resting and exercising forearms during moderate-intensity supine leg exercise

Journal of Applied Physiology ◽

10.1152/jappl.1993.74.1.435 ◽

1993 ◽

Vol 74 (1) ◽

pp. 435-443 ◽

Cited By ~ 13

Author(s):

P. G. Catcheside ◽

G. C. Scroop

Keyword(s):

Skeletal Muscle ◽

Blood Lactate ◽

Lactate Production ◽

Voluntary Contraction ◽

Moderate Intensity ◽

Arterial Blood ◽

Exercise Period ◽

Leg Exercise ◽

Lactate Removal ◽

Lactate Levels

Arterial blood lactate was elevated by supine leg exercise (20 min at approximately 65% maximal oxygen uptake) in five untrained male subjects, and the contribution to blood lactate removal from passive uptake vs. metabolic disposal was compared in resting and lightly exercising (15% maximal voluntary contraction static handgrip) forearm skeletal muscle. An integrated form of the Fick equation was used to predict venous lactate levels resulting solely from passive equilibration of lactate between incoming arterial blood and the forearm muscles. In the resting forearm, predicted and measured venous lactate levels were closely correlated during the exercise period (r = 0.995, P < 0.001), indicating that lactate removal could be accounted for in terms of passive uptake alone. In the lightly exercising forearm, measured venous lactate levels were higher than both the arterial and predicted venous levels, indicating net lactate production. It was concluded that most of the blood lactate generated by moderate-intensity supine leg exercise is taken up passively and not metabolized by resting skeletal muscle and that the rate of lactate disposal is unlikely to be enhanced in lightly exercising muscle.

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Relationship Among Recovery Oxygen, Oxygen Missed, Lactate Production and Lactate Removal During and Following Severe Hypoxia in the Unanesthetized Dog

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1958.192.3.585 ◽

1958 ◽

Vol 192 (3) ◽

pp. 585-591 ◽

Cited By ~ 7

Author(s):

Norman R. Alpert ◽

Herbert Kayne ◽

Winona Haslett

Keyword(s):

Oxygen Consumption ◽

Significant Relationship ◽

Recovery Period ◽

Lactate Production ◽

Severe Hypoxia ◽

Plasma Lactate ◽

Oxygen Oxygen ◽

Lactate Removal ◽

Lactate Levels ◽

Removal And Recovery

An experiment was designed to test the ‘O2debt’ hypothesis. Oxygen consumption and plasma lactate were measured before, during and following hypoixa in unanesthetized spinally transected dogs. The O2 consumption was depressed during hypoxia and returned toward control levels during recovery. Lactate levels increased during the hypoxia and returned to the control during recovery. Oxygen missed was correlated with the excess consumption of recovery. A highly significant relationship was found which indicated that the larger the depression in O2 consumption during hypoxia, the greater was the depression during the recovery period and the more prolonged the return to control levels. Oxygen missed during hypoxia was compared to lactate production. A significant relationship was found. Lactate removal was compared to excess consumption of recovery. No correlation existed between lactate removal and recovery O2 consumption. The authors postulate the presence of a metabolic governor which controls the rate of O2 uptake.

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Effect of endurance training on activators of glycolysis in muscle during exercise

Journal of Applied Physiology ◽

10.1152/jappl.1994.76.2.846 ◽

1994 ◽

Vol 76 (2) ◽

pp. 846-852 ◽

Cited By ~ 12

Author(s):

C. Duan ◽

W. W. Winder

Keyword(s):

Endurance Training ◽

Blood Lactate ◽

Lactate Concentration ◽

Lactate Production ◽

Blood Lactate Concentration ◽

Quadriceps Muscle ◽

Muscle Lactate ◽

Cyclic Monophosphate ◽

Lactate Levels ◽

Exercise Induced

Endurance training attenuates exercise-induced increases in blood lactate at the same submaximal work rate. Three intramuscular compounds that influence muscle lactate production were measured in fasted non-trained (NT) and endurance-trained (T) rats. The T rats were subjected to a progressive endurance-training program. At the end of the program (11 wk), they were running 2 h/day at 31 m/min up a 15% grade 5 days/wk. NT and T rats were fasted for 24 h and then anesthetized (pentobarbital, iv) at rest or after running for 30 min at 21 m/min (15% grade). Blood lactate levels were significantly lower in the T rats than in the NT rats after 30 min of running (2.3 +/- 0.2 vs. 3.9 +/- 0.2 mM). The lower blood lactate concentration was accompanied by lower plasma epinephrine (2.8 +/- 0.4 vs. 6.0 +/- 0.8 nM), adenosine 3′, 3′,5′-cyclic monophosphate (0.36 +/- 0.02 vs. 0.50 +/- 0.03 pmol/mg), mg), glucose 1,6-diphosphate (26 +/- 2 vs. 40 +/- 5 pmol/mg), and fructose 2,6-diphosphate (3.2 +/- 0.2 vs. 4.3 +/- 0.3 pmol/mg) in white quadriceps muscle in T than in NT rats. Red quadriceps muscle glucose 1,6-diphosphate and adenosine 3′,5′-cyclic monophosphate were also lower in T than in NT rats. These adaptations may be responsible in part for the lower exercise-induced blood lactate in fasted rats as a consequence of endurance training.

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Is fetal acidosis in the human fetus maternogenic during labor? A reanalysis

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1991.261.5.r1294 ◽

1991 ◽

Vol 261 (5) ◽

pp. R1294-R1299 ◽

Cited By ~ 2

Author(s):

F. Piquard ◽

A. Schaefer ◽

P. Dellenbach ◽

P. Haberey

Keyword(s):

Steady State ◽

Acute Stress ◽

Lactate Production ◽

Regression Coefficients ◽

Labor And Delivery ◽

Maternal Contribution ◽

Acid Base Status ◽

Lactate Levels ◽

Fetal Acidosis ◽

Net Transfer

The purpose of this study was to investigate whether maternogenic fetal acidosis can occur at the time of labor and delivery and to evaluate the extent of the possible maternal contribution to fetal acidosis. We have therefore determined fetal and maternal lactate concentrations and acid-base status under various conditions in 589 women at the end of gestation and during labor. The results show that metabolic acidosis develops in all fetuses because of increased production of lactic acidosis is primarily of fetal origin: 1) the umbilical arteriovenous lactate differences were positive and large in steady-state conditions as well as in depressed newborns; 2) the conditions that could produce a net transfer of lactate from the mother to the fetus, namely a positive maternofetal gradient of lactate and proton, were rarely observed; and 3) the correlation between fetal and maternal lactate levels was very weak, with regression coefficients decreasing from near steady-state conditions to acute stress conditions, indicating that the increase in lactate in the fetus and mother occurs independently. This correlation indicates also that increased maternal lactate production under conditions of labor and delivery can make a contribution by affecting the rate of net transfer from fetus to mother. This is possible in approximately 6% of the fetuses.

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Prognostic Significance of Blood Lactate and Lactate Clearance in Trauma Patients

Anesthesiology ◽

10.1097/aln.0b013e318273349d ◽

2012 ◽

Vol 117 (6) ◽

pp. 1276-1288 ◽

Cited By ~ 100

Author(s):

Marie-Alix Régnier ◽

Mathieu Raux ◽

Yannick Le Manach ◽

Yves Asencio ◽

Johann Gaillard ◽

...

Keyword(s):

Blood Lactate ◽

Injury Severity ◽

Prognostic Significance ◽

Lactate Clearance ◽

Trauma Patients ◽

Operating Characteristics ◽

Additional Information ◽

Lactate Levels ◽

Initial Blood ◽

Blood Lactate Levels

Background Lactate has been shown to be a prognostic biomarker in trauma. Although lactate clearance has already been proposed as an intermediate endpoint in randomized trials, its precise role in trauma patients remains to be determined. Methods Blood lactate levels and lactate clearance (LC) were calculated at admission and 2 and 4 h later in trauma patients. The association of initial blood lactate level and lactate clearance with mortality was tested using receiver-operating characteristics curve, logistic regression using triage scores, Trauma Related Injury Severity Score as a reference standard, and reclassification method. Results The authors evaluated 586 trauma patients (mean age 38±16 yr, 84% blunt and 16% penetrating, mortality 13%). Blood lactate levels at admission were elevated in 327 (56%) patients. The lactate clearance should be calculated within the first 2 h after admission as LC0-2 h was correlated with LC0-4 h (R=0.55, P<0.001) but not with LC2-4 h (R=0.04, not significant). The lactate clearance provides additional predictive information to initial blood lactate levels and triage scores and the reference score. This additional information may be summarized using a categorical approach (i.e., less than or equal to -20 %/h) in contrast to initial blood lactate. The results were comparable in patients with high (5 mM/l or more) initial blood lactate. Conclusions Early (0-2 h) lactate clearance is an important and independent prognostic variable that should probably be incorporated in future decision schemes for the resuscitation of trauma patients.

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