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PubMed1990

Time-related changes in the diagnostic utility of total lactate dehydrogenase, lactate dehydrogenase isoenzyme-1, and two lactate dehydrogenase isoenzyme-1 ratios in serum after myocardial infarction.

Using receiver-operating characteristic (ROC) curve and likelihood ratio analysis, we examined the diagnostic utility of total lactate dehydrogenase (LD; EC 1.1.1.27) activity (I). LD isoenzyme-1 activity (II), and the LD-1 percentage of total LD activity (III), LD-1 LD-2 (IV), and LD-1/LD-4 (V) in 347 persons admitted to the Cardiac Care Unit (of whom 173 were subsequently proven to have had myocardial infarction). Blood was sampled from these subjects at about 6-h intervals for up to 96 h from the onset of chest pain. Defining an "effective" test as one having an area under the ROC curve of greater than or equal to 0.9, we determined the ranked utility (greatest to least) of these tests as V = IV greater than III greater than II greater than I. Tests III, IV, and V had by this criterion, diagnostic effectiveness equivalent to measurements of creatine kinase-2 in serum but in samples obtained at later time intervals. The decision thresholds for both high (constant) test sensitivity and specificity varied with time, to differing extents, over the entire 96-h period, a finding with important diagnostic implications. We document positive and negative likelihood ratio values for each of these tests throughout the entire period of study.

Adult↗
PubMed1986

Lactate extraction during net lactate release in legs of humans during exercise.

Lactate metabolism was studied in six normal males using a primed continuous infusion of lactate tracer during continuous graded supine cycle ergometer exercise. Subjects exercised at 49, 98, 147, and 196 W for 6 min at each work load. Blood was sampled from the brachial artery, the iliac vein, and the brachial vein. Arteriovenous differences were determined for chemical lactate concentration and L-[1-14C]-lactate. Tracer-measured lactate extraction was determined from the decrease in lactate radioactivity per volume of blood perfusing the tissue bed. Net lactate release was determined from the change in lactate concentration across the tissue bed. Total lactate release was taken as the sum of tracer-measured lactate extraction and net (chemical) release. At rest the arms and legs showed tracer-measured lactate extraction, as determined from the isotope extraction, despite net chemical release. Exercise elicited an increase in both net lactate release and tracer-measured lactate extraction by the legs. For the legs the total lactate release (net lactate release + tracer-measured lactate extraction) was roughly equal to twice the net lactate release under all conditions. The tracer-measured lactate extraction by the exercising legs was positively correlated to arterial lactate concentration (r = 0.81, P less than 0.001) at the lower two power outputs. The arms showed net lactate extraction during exercise, which was correlated to the arterial concentration (r = 0.86). The results demonstrate that exercising skeletal muscle extracts a significant amount of lactate during net lactate release and that the working skeletal muscle appears to be a major site of blood lactate removal during exercise.

Adult↗
PubMed1991

Conversion of oral glucose to lactate in dogs. Primary site and relative contribution to blood lactate.

We evaluated the relative contribution of oral glucose to arterial lactate and the relative role of the splanchnic bed in converting glucose to lactate in normal healthy dogs. After an oral glucose load (1.2 g/kg) spiked with [U-14C]glucose (16.9 muCi/kg; protocol 1, n = 7), arterial blood lactate increased from 0.43 +/- 0.03 mM at basal to a peak of 1.04 +/- 0.07 mM at 45 min and then slowly decreased to 0.47 +/- 0.07 mM at 240 min. Arterial blood [14C]lactate peaked at 60 min and then decreased slowly to approximately 35% of the peak at 4 h. When arterial blood lactate peaked at 45 min, the proportion of arterial lactate that was derived from oral glucose was 34 +/- 3%. The integrated area under the curve of lactate derived from exogenous glucose was 40 +/- 2% of that of total lactate. The splanchnic bed released lactate and [14C]lactate during the initial 2 h after oral [14C]glucose. Thus, the splanchnic bed apparently contributed to the conversion of exogenous glucose to lactate. In the matched experiments (protocol 2, n = 5), dogs were given the same amount of oral glucose but no [14C]glucose, and [U-14C]lactate was infused into the right atrium to match the splanchnic [14C]lactate release from the first experiment. Despite a well-matched splanchnic [14C]lactate contribution, arterial concentrations of [14C]lactate were markedly lower in protocol 2 compared with protocol 1. The integrated area under the [14C]lactate profile in protocol 2 was only 11 +/- 1% of that in protocol 1. These results indicate that the splanchnic bed is responsible for only 11% of arterial blood lactate that was derived from oral glucose. We concluded that 1) after oral glucose loading, a major portion of circulating lactate has its origin not in exogenous glucose but in endogenous sources, and 2) the splanchnic bed is not the major site of oral glucose conversion to lactate after glucose ingestion.

Administration, Oral↗
PubMed1999

Are arterial, muscle and working limb lactate exchange data obtained on men at altitude consistent with the hypothesis of an intracellular lactate shuttle?

The "Lactate Shuttle" Hypothesis posits that lactate removal requires exchange among producing and consuming cells. The "Intra-cellular Lactate Shuttle" hypothesis posits that lactate exchange occurs among compartments within cells, and that mitochondria are the major sites of cellular lactate disposal. Thus, cells with high mitochondrial densities (cardiocytes, myocytes, hepatocytes) are those which participate in lactate clearance. The model of an Intracellular Lactate Shuttle recognizes that the Keq for LDH is 3.6 x 10(4) M-1; thus, glycolysis results in cytosolic lactate production regardless of the intracellular PO2. The model also requires presence of a mitochondrial monocarboxylate transporter (MCT) that allows uptake of lactate as well as pyruvate, and intra-mitochondrial LDH whose function is linked to the ETC, and which permits lactate-->pyruvate conversion and oxidation. Recently, we have shown that liver, heart and muscle mitochondria readily oxidize lactate and contain LDH and MCT1. Accordingly, we have concluded that lactate is the predominant monocarboxylate oxidized by mitochondria in vivo. The model of an "Intra-cellular Lactate Shuttle" is consistent with many of the observations on men at sea level and altitude. The observations include: oxidation is the primary fate of lactate disposal during rest and exercise; lactate production and oxidation occur simultaneously within resting and working muscle; increasing [lactate]a increases muscle lactate extraction, and that by increasing SaO2 acclimatization reduces blood [lactate].

Animals↗
PubMed1984

Hepatic and extrahepatic lactate metabolism in sheep: effects of lactate loading and pH.

Hepatic lactate metabolism was studied in five sheep receiving infusions of either lactic acid or sodium lactate using an arteriovenous difference technique. Hepatic uptake of lactate was a saturable process with second order (Michaelis-Menten) kinetics. Although lactic acid infusion decreased blood pH, hepatic saturation of lactate uptake occurred before changes in pH could influence hepatic lactate metabolism. The Vmax for hepatic lactate metabolism is 5.72 mmol X kg-0.75 X h-1 and the Km 3.06 mmol/l. These findings have therapeutic relevance. In acidosis, the hepatic response to therapeutic administration of sodium lactate during fluid therapy will be variable. If plasma lactate is low, lactated fluids may increase hepatic uptake and produce an alkalizing effect. If plasma lactate is already high, hepatic lactate metabolism is nearly saturated, and additional lactate will not produce a hepatic alkalizing response. Extrahepatic tissues switch from lactate production to lactate utilization under conditions of lactate loading. They remove more lactate than liver at high plasma lactate concentrations. Muscle may be important in lactate removal in certain types of exercise.

Animals↗
PubMed1980

Net hepatic and splanchnic metabolism of lactate, pyruvate and propionate in dairy cows in vivo in relation to lactation and nutrient supply.

1. Circulating concentrations of glucose, propionate, lactate and pyruvate, and net exchange of these compounds across the liver and gut, were measured in lactating and non-lactating dairy cows (a) in the normal fed state, (b) before, during and after intravenous infusion of an aqueous solution of glucose, propionate or lactate (lactating cows only) in fed animals, and (c) before and during 6 days of food deprivation. 2. In the normal fed state, gut output of propionate, hepatic output of glucose and hepatic uptake of lactate were all higher in the lactating group. There was a net uptake of pyruvate across the liver in the lactating cows and a net output in the non-lactating cows. In the lactating cows there was a net uptake of lactate and pyruvate by the splanchnic bed (i.e. gut and liver combined). 3. In the lactating cows, the glucose and propionate infusions had the following effects: decrease in net hepatic uptake of lactate; a switch in pyruvate exchange across the liver from uptake to output; suppression of uptake of lactate and pyruvate by the splanchnic bed; increase in the magnitude of the liver (propionate uptake)/(glucose output) ratio. Lactate infusion did not affect hepatic propionate uptake. 4. Food deprivation increased hepatic extraction of lactate and pyruvate and decreased the liver (propionate uptake)/(glucose output) ratio in both groups. 5. It is concluded that mechanisms exist to ensure an inverse relationship between the availability to the cow of glucose or propionate and utilization by the splanchnic bed of endogenously derived lactate and pyruvate.

Animals↗
PubMed1983

Tissue glucose and lactate metabolism and interconversions in pregnant and lactating sheep.

Continuous infusions of [14C]glucose and [14C]lactate on separate days, and measurements of blood flow-rate, were used to obtain values for rates of unidirectional metabolism and of interconversion of glucose and lactate in the portal-drained viscera, liver and hind-quarters of ewes during late pregnancy and early lactation. All infusions were made within 5 h after the morning meal, when steady-state conditions appeared to exist. Use was made of ewes that had been appropriately catheterized during pregnancy, and whose catheters remained patent through into lactation. The liver was the main source of glucose production (67-70%) during both pregnancy and lactation. Other sources were the portal-drained viscera (absorbed glucose) and, presumably, the kidneys. Over 80% of the glucose was utilized by the peripheral tissues with approximately 35-40% of utilization being attributable to the hind-quarters. Of the total lactate production, 76% occurred in the peripheral tissues during pregnancy but only 36% during lactation. While the liver utilized 73% of lactate during pregnancy, this value fell to only 42% during lactation, at which time the portal-drained viscera utilized 26% of the lactate. During pregnancy, approximately 80% of the lactate arose from glucose, chiefly in peripheral tissues, while at least 12% of the glucose arose from lactate, chiefly in the liver. During lactation the extent of these interconversions was decreased. Despite the interconversions, whole-body turnover rates for glucose and lactate were under- or overestimated by only 4-10% and 2-5% respectively. Furthermore, a comparison of turnover rates obtained with [U-14C]- and [6-3H]glucose indicated that there was only 6 and 2% recycling of glucose-C during pregnancy and lactation respectively. Under the conditions employed in this study, lactate does not appear to be a major precursor of glucose in the ruminant, and most of the lactate taken up by the liver must be used for purposes other than gluconeogenesis, such as oxidation or alternative anabolic pathways.

Animals↗
PubMed1997

Effect of intravenous lactated Ringer's solution infusion on the circulating lactate concentration: Part 3. Results of a prospective, randomized, double-blind, placebo-controlled trial.

OBJECTIVES: We previously discovered that small amounts of lactated Ringer's solution, which are inadequately cleared from an intravenous catheter, falsely increase the circulating lactate concentration in blood samples collected from that catheter. That finding prompted us to test the hypothesis that intravenous lactated Ringer's solution, infused at a rate used in resuscitation, would increase the circulating lactate concentration. DESIGN: A prospective, randomized, double-blinded, placebo-controlled study. SETTING: A critical care research laboratory. SUBJECTS: Twenty-four normal, healthy, adult volunteer subjects. INTERVENTIONS: Two intravenous catheters were placed. One was used for the infusion of the test solution and the other catheter was used for blood sampling. Blood samples were serially collected for the determination of blood lactate concentrations. MEASUREMENTS AND MAIN RESULTS: Twenty-four healthy adult volunteers were randomized to receive a 1-hr infusion of either lactated Ringer's solution (n = 6), 0.9% saline (n = 6), 5% dextrose in lactated Ringer's solution (D5RL) (n = 6), or 5% dextrose in water (D5W) (n = 6). Each subject received nothing by mouth after midnight. At 0800 hrs, catheters were inserted and each subject received 1 L of the assigned solution over 1 hr. Throughout the study, the subjects were at rest. Three-milliliter samples of venous blood were collected before, during (at 15, 30, 45, and 60 mins), and after (at 90, 120, and 240 mins) the infusion. Blood samples were placed on ice immediately after collection and analyzed within 5 mins of collection. Lactate concentrations were determined using an ion-selective, amperometric electrode, which we have previously validated. Lactate concentrations were compared between subjects receiving lactated Ringer's solution vs. subjects receiving normal saline. A similar comparison was made between subjects receiving D5RL vs. D5W at similar time points during the study. There were no clinically or statistically significant differences in lactate values at the time points studied in those subjects receiving lactated Ringer's solution vs. those persons receiving normal saline (p > .05; n = 12; Student-Newman-Keuls' multiple comparison test) or those subjects receiving D5W vs. those subjects infused with D5RL (p > .05; n = 12; Student-Newman-Keuls' multiple comparison test). In no case did the circulating lactate values exceed 2 mmol/L (the upper limit of normal). CONCLUSIONS: The short-term infusion of lactated Ringer's solution in normal adults (hemodynamically stable) does not falsely increase circulating lactate concentrations when 1 L is given over 1 hr. Therefore, clinicians should not disregard increased lactate concentrations in patients receiving a rapid infusion of lactated Ringer's solution.

Adult↗
PubMed1993

Dose-response effects of lactate infusions on gluconeogenesis from lactate in normal man.

Lactate is the predominant gluconeogenic precursor in man. To determine the dose-response relationships between plasma lactate concentration and rates of lactate incorporation in plasma glucose (lactate gluconeogenesis, LGN), we infused 17 normal volunteers with sodium lactate for 180 min at rates ranging from 6 to 40 mumol kg-1 min-1 and measured [U-14C]lactate incorporation into plasma glucose, as well as rates of lactate and glucose appearance in plasma. With the highest lactate infusions, plasma lactate increased up to 7 mM (compared to 1.1 +/- 0.13 mM during control sodium bicarbonate infusions, n = 10) and LGN averaged 4.73 +/- 0.23 mumol kg-1 min-1 (compared to 1.57 +/- 0.26 mumol kg-1 min-1 in bicarbonate control experiments, P < 0.001). The data relating plasma lactate concentration to LGN best fit a sigmoidal curve which plateaued at plasma lactate concentrations of approximately 6 mM and yielded an ED50 of 2.04 +/- 0.20 (SD) mM and a Vmax (6.25 +/- 1.2) (SD) (mumol kg-1 min-1). The sum of the basal rate of lactate appearance and the rate of lactate infusion was not significantly different from the overall rates of lactate appearance during the lactate infusions (35.8 +/- 2.2 vs. 34.8 +/- 2.9 mumol kg-1 min-1, P = 0.23). Thus, our results support the view that infusion of exogenous lactate does not suppress endogenous lactate appearance in plasma.

Adult↗
PubMed1998

Lactate clamp: a method to measure lactate utilization in vivo.

A lactate clamp method has been developed to quantify the whole body lactate utilization in conscious, unstressed rats. Dichloroacetate (DCA), a known lactate utilization enhancer, was used to validate the method. Fasting blood lactate concentrations before the clamps were identical for DCA-treated (1 mmol/kg) and control groups (1.65 +/- 0.37 vs. 1.65 +/- 0.19 mM). The animals received a primed continuous lactate infusion for 90 min at variable rates to clamp the blood lactate concentration at 2 mM. The steady-state (60-90 min) lactate infusion rate, which represents the whole body lactate utilization in DCA-treated animals, was 144% higher than that in the control animals (13.2 +/- 1.0 vs. 5.4 +/- 1.1 mg . kg-1 . min-1; P < 0.001). The markedly increased lactate infusion rate indicates an enhanced lactate flux by DCA. To determine whether the increased lactate infusion by DCA reflected reduced endogenous lactate production, lactate production was measured. The results indicate that endogenous lactate production was not affected by DCA. In conclusion, the lactate clamp provides a sensitive and reliable method to assess lactate utilization in vivo, a dynamic measurement that may not be clearly demonstrated by blood lactate concentrations per se.

Animals↗
PubMed2003

Lactate carbon does not enter the sugars of lipopolysaccharide when gonococci are grown in a medium containing glucose and lactate: implications in vivo.

In media containing glucose, lactate stimulates the metabolism of gonococci at concentrations that simulate conditions in vivo. Nuclear magnetic resonance (NMR) spectroscopy of (13)C-labelled lipids obtained from gonococci grown in a synthetic medium with (13)C-labelled lactate and unlabelled glucose (culture A), (13)C-labelled glucose alone (culture B) or (13)C-labelled glucose and unlabelled lactate (culture C) showed lactate carbon was not present in glycerol/ethanolamine residues of lipids from culture A. This indicated that, in the presence of glucose, lactate gluconeogenesis is shut down. Hence, the stimulation of metabolism could result from the production of extra energy because lactate is used solely for conversion to acetyl-CoA, the precursor of fatty acid synthesis and the components of the tricarboxylic acid cycle. In this paper, additional evidence for lack of gluconeogenesis has been sought using a different approach. The carbohydrate moieties of lipopolysaccharide (LPS) have been examined for lactate carbon after gonococci were grown with lactate and glucose. Two methods were used: NMR spectroscopy of (13)C-labelled lipopolysaccharide purified from the three cultures described above showed that, in the presence of glucose, lactate carbon, in contrast to glucose carbon, was not in the carbohydrate moiety. Also, (14)C-labelled lactate was added to a culture containing unlabelled glucose and lactate (culture A) and [(14)C]glucose to cultures containing unlabelled glucose without unlabelled lactate (culture B) and with unlabelled lactate (culture C). When LPS samples purified from these cultures were subjected to hydrazinolysis, the ratio of the radioactivity of water-soluble products (carbohydrate moieties) to those of chloroform-soluble products (fatty acids) was much lower when [(14)C]lactate was used in culture A, than when [(14)C]glucose was used in cultures B and C. Thus, in the presence of glucose, lactate carbon, unlike glucose carbon, is incorporated predominantly into fatty acids of LPS, not into its carbohydrate moieties. There is no doubt, therefore, that gluconeogenesis is shut off when lactate is present with glucose and there is a consequent stimulation of metabolism. This probably occurs in vivo on mucous surfaces, where gonococci are surrounded by a mixture of glucose and lactate in the secretions.

Carbohydrates↗
PubMed2000

Effects of lactate-buffered and lactate-free dialysate in CAVHD patients with and without liver dysfunction.

BACKGROUND: Continuous modalities of renal replacement deplete patients of bicarbonate, which is traditionally replaced indirectly by lactate in dialysate or replacement fluids. We have compared a new lactate-free dialysate (unbuffered dialysate with separate bicarbonate replacement of dialytic bicarbonate loss) with standard lactate-buffered dialysate in terms of acid-base control, lactate accumulation, and hemodynamic stability in patients undergoing continuous renal replacement therapy in an intensive care unit. METHODS: A nonrandomized crossover cohort study involving 54 patients with multi-organ failure (of whom 19 had significant hepatic dysfunction) was performed. All patients completed 24-hour continuous hemodiafiltration against both lactate-buffered and lactate-free dialysate. Arterial pH, blood gases, bicarbonate, and lactate, venous sodium, blood pressure, and inotrope requirements were measured before and at six hourly intervals during the first 24 hours of dialysis against each dialysate. RESULTS: Lactate-free dialysate provided more rapid control of acidosis than lactate buffered with less total administration of buffer than that given during the lactate-buffered period (total mmol bicarbonate vs. total mmol lactate + bicarbonate). Lactate accumulation was slight in both periods, but was higher during lactate-buffered continuous venovenous hemodiafiltration (CVVHD). The mean arterial pressure rose during lactate-free dialysis with decreased inotrope doses and fell during lactate-buffered dialysis with increased inotrope requirement. Results in patients with liver dysfunction were not significantly different from those without it. CONCLUSIONS: Over the time scale of 24 hours, lactate derived from continuous dialysis circuits is efficiently cleared from the blood of most patients with multi-organ failure, but with less effect on systemic acidosis than is produced by equivalent amounts of bicarbonate.

APACHE↗
PubMed1995

Chronic oral lactate supplementation does not affect lactate disappearance from blood after exercise.

This study tested the hypothesis that a 3-week oral lactate supplementation affects postexercise blood lactate disappearance in untrained male subjects. Fifteen men were randomly assigned to either a lactate supplementation (n = 8) or a placebo (n = 7) treatment. During the treatment period they drank an oral lactate or a maltodextrin (placebo) supplement twice a day. The lactate drink contained 10 g of lactate as calcium, sodium, and potassium salts. Blood lactate concentrations were studied before, during, and immediately after three exercise tests, both pre- and posttreatment. Peak lactate values for placebo (PL) or lactate (L) treatment groups during different tests were as follows: Test 1 PL, 13.49 +/- 3.71; L, 13.70 +/- 1.90; Test 2 PL, 12.64 +/- 2.32; L, 12.00 +/- 2.23; Test 3 PL, 12.29 +/- 2.92; L, 11.35 +/- 1.38 and were reached 3 min postexercise. The decrease in blood lactate during the long (30- to 45-min) recovery periods amounted to / 10 mmol/L. Blood lactate changes were highly reproducible. However, a 3-week oral lactate supplementation did not result in differences in lactate disappearance. This study does not support the hypothesis that regular oral lactate intake at rest enhances the removal of lactate during and following exercise, that is, not with the given lactate load and supplementation period.

Administration, Oral↗
PubMed2002

Lactate metabolism in resting and contracting canine skeletal muscle with elevated lactate concentration.

This study was undertaken to quantitatively account for the metabolic disposal of lactate in skeletal muscle exposed to an elevated lactate concentration during rest and mild-intensity contractions. The gastrocnemius plantaris muscle group (GP) was isolated in situ in seven anesthetized dogs. In two experiments, the muscles were perfused with an artificial perfusate with a blood lactate concentration of ~9 mM while normal blood gas/pH status was maintained with [U-(14)C]lactate included to follow lactate metabolism. Lactate uptake and metabolic disposal were measured during two consecutive 40-min periods, during which the muscles rested or contracted at 1.25 Hz. Oxygen consumption averaged 10.1 +/- 2.0 micromol. 100 g(-1). min(-1) (2.26 +/- 0.45 ml. kg(-1). min(-1)) at rest and 143.3 +/- 16.2 micromol. 100 g(-1). min(-1) (32.1 +/- 3.63 ml. kg(-1). min(-1)) during contractions. Lactate uptake was positive during both conditions, increasing from 10.5 micromol. 100 g(-1). min(-1) at rest to 25.0 micromol. 100 g(-1). min(-1) during contractions. Oxidation and glycogen synthesis represented minor pathways for lactate disposal during rest at only 6 and 15%, respectively, of the [(14)C]lactate removed by the muscle. The majority of the [(14)C]lactate removed by the muscle at rest was recovered in the muscle extracts, suggesting that quiescent muscle serves as a site of passive storage for lactate carbon during high-lactate conditions. During contractions, oxidation was the dominant means for lactate disposal at >80% of the [(14)C]lactate removed by the muscle. These results suggest that oxidation is a limited means for lactate disposal in resting canine GP exposed to elevated lactate concentrations due to the muscle's low resting metabolic rate.

Animals↗
PubMed1992

Effects of sodium L-lactate and sodium racemic lactate on intraoperative acid-base status.

Lactated Ringer's solution is frequently used to avoid metabolic acidosis during fluid resuscitation. The standard lactated Ringer's solution contains racemic lactate, an equal mixture of the D- and L-stereoisomers. We investigated whether sodium L-lactate or sodium racemic lactate (DL-lactate) is more effective for increasing buffering capacity in body fluids. For the purpose of this comparison, Ringer's solutions containing no lactate, sodium L-lactate, or racemic lactate at a concentration of 84 mEq/L (three times more than the ordinary level) were infused in patients under general anesthesia during tympanoplasty. Although differences occurred among the three groups in blood concentrations of L-lactate, D-lactate, and the L-lactate/pyruvate ratio, no differences occurred between the two lactate groups in either bicarbonate ion concentration or base excess. The amount of buffering capacity increased significantly in both lactate groups, compared with preinfusion levels, and was more than the values in the nonlactated Ringer's solution group. We conclude that sodium racemic lactate is metabolized at nearly the same rate as that of sodium L-lactate.

Acid-Base Equilibrium↗
PubMed1995

Is lactate-induced myocardial ischaemic injury mediated by decreased pH or increased intracellular lactate?

The detrimental effect of exogenous lactate during ischaemia on post-ischaemic contractile function may be mediated either by a lactate-induced intracellular H+ load or by an increase in intracellular lactate. To distinguish between these two mechanisms, isolated rat hearts were perfused with lactate or pyruvate during low flow ischaemia, the rationale being that both would decrease H+ efflux via lactate/H+ cotransport and lead to decreased pH, but only exogenous lactate would decrease lactate efflux and lead to increased intracellular lactate. 31P NMR spectra were acquired sequentially while hearts were subjected to 32 min low flow (0.5 ml/min) ischaemia and 32 min reperfusion. During ischaemia, hearts were perfused with Krebs-Henseleit buffer containing 11 mM glucose (controls) or 11 mM glucose plus either 10 mM lactate or 10 mM pyruvate. Reperfusion of all hearts was with buffer containing only glucose. Intracellular volume, estimated to be 0.52 ml/heart using 31P NMR spectroscopy with phosphonate space markers, did not change under any of the ischaemic conditions during the protocol. Control and pyruvate hearts recovered approximately 85% of pre-ischaemic contractile function, but there was no recovery of function in lactate hearts. This lack of recovery correlated with a 57% loss of ATP during ischaemia, which was significantly greater (P < 0.001) than the 41% loss of ATP in control and pyruvate-perfused hearts. End-ischaemic intracellular pH was 6.60 in both lactate-perfused and control hearts, but significantly lower (P < 0.05) at pH 6.43 in pyruvate-perfused hearts. Both exogenous pyruvate and lactate should have decreased H+ efflux, however the higher pH in the lactate-perfused hearts could be explained by a 60% inhibition of glycolysis, determined by measurement of myocardial lactate production. Thus, the intracellular pH during ischaemia does not necessarily predict the extent of myocardial injury. We propose that lactate-induced damage is a consequence of increased intracellular lactate leading to inhibition of glycolysis, presumably via an increased NADH/NAD ratio. This study highlights the important role of glycolysis in the ischaemic rat heart.

Animals↗
PubMed1997

The effect of dietary energy source during mid to late lactation on liver triglyceride and lactation performance of dairy cows.

Control [1.61 Mcal of net energy for lactation (NEL)/kg of dry matter (DM)], high grain (1.70 Mcal of NEL)/kg of DM), or high fat [1.70 Mcal of NEL/kg of DM with 2.3% tallow (DM basis)] diets were fed to 43 cows (150 +/- 3.1 d in milk) during mid to late lactation to determine effects on performance characteristics, metabolic parameters, or both during mid to late lactation, the dry period, and the first 100 d of the next lactation. All cows received identical diets during the dry period and during early lactation. Increasing the energy density of the diets during mid to late lactation increased DM intake (DMI), plasma nonesterified fatty acid concentration, milk production, and milk protein yield. Compared with the high grain diets, fat supplementation decreased DMI and the percentage of milk protein but increased plasma nonesterified fatty acid concentration without causing elevation of liver triglyceride at the end of mid to late lactation. Increased energy density of the diets did not affect body condition score during mid to late lactation. There were no residual effects for any of the treatments on DMI, lactation performance, or body weight in the subsequent lactation. However, energy supplementation during mid to late lactation increased liver triglyceride content after calving. Compared with high fat diets, high grain diets fed during mid to late lactation increased plasma beta-hydroxy-butyrate concentration in the subsequent lactation. High energy diets fed during mid to late lactation may influence lipid metabolism during the following lactation.

3-Hydroxybutyric Acid↗
PubMed2002

Lactate and glucose interactions during rest and exercise in men: effect of exogenous lactate infusion.

To test the hypothesis that lactate plays a central role in the distribution of carbohydrate (CHO) potential energy for oxidation and glucose production (GP), we performed a lactate clamp (LC) procedure during rest and moderate intensity exercise. Blood [lactate] was clamped at approximately 4 mM by exogenous lactate infusion. Subjects performed 90 min exercise trials at 65 % of the peak rate of oxygen consumption (V(O(2))(,peak); 65 %), 55 % V(O(2))(,peak) (55 %) and 55 % V(O(2))(,peak) with lactate clamped to the blood [lactate] that was measured at 65 % V(O(2))(,peak) (55 %-LC). Lactate and glucose rates of appearance (R(a)), disappearance (R(d)) and oxidation (R(ox)) were measured with a combination of [3-(13)C]lactate, H(13)CO(3)(-), and [6,6-(2)H(2)]glucose tracers. During rest and exercise, lactate R(a) and R(d) were increased at 55 %-LC compared to 55 %. Glucose R(a) and R(d) were decreased during 55 %-LC compared to 55 %. Lactate R(ox) was increased by LC during exercise (55 %: 6.52 +/- 0.65 and 55 %-LC: 10.01 +/- 0.68 mg kg(-1) min(-1)) which was concurrent with a decrease in glucose oxidation (55 %: 7.64 +/- 0.4 and 55 %-LC: 4.35 +/- 0.31 mg kg(-1) min(-1)). With LC, incorporation of (13)C from tracer lactate into blood glucose (L GNG) increased while both GP and calculated hepatic glycogenolysis (GLY) decreased. Therefore, increased blood [lactate] during moderate intensity exercise increased lactate oxidation, spared blood glucose and decreased glucose production. Further, exogenous lactate infusion did not affect rating of perceived exertion (RPE) during exercise. These results demonstrate that lactate is a useful carbohydrate in times of increased energy demand.

Adult↗