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PubMed1996

Short endurance training improves lactate removal ability in patients with heart transplants.

Eight male patients with heart transplants at least a year after the operation were submitted to a 6-wk endurance training program and explored for their blood lactate kinetics before and after exercise. The tests consisted of a bicycle exercise upgraded by 20 W every 2 min until volitional fatigue. Training induced a significant (P < 0.025) decrease in lactate concentrations from the 40-W to the 120-W exercise step and a significant increase (P < 0.025) in the time into exercise (9.87 +/- 0.87 min vs 7.17 +/- 0.90 min) at which a lactate concentration of 2 mmol.l-1 was reached. Lactate recovery curves were significantly lower (P < 0.036) after training than before training, except at minutes 1, 2, 8, and 60. The fits of a biexponential mathematical model to the lactate recovery curves reveal a significant (P < 0.036) training-induced increase (+71%) in the slow-velocity constant gamma 2v of the model. In view of the functional meaning given to this parameter, namely the ability to remove lactate, it is concluded that training lowers blood lactate concentrations during exercise and recovery in patients with heart transplants at least in part by raising the efficiency with which lactate is removed, and that the ability to remove lactate can be a valuable criterion to evaluate physical fitness.

Adult↗
PubMed2000

Relationship between plasma lactate parameters and muscle characteristics in female cyclists.

PURPOSE: In a previous study, we showed that when six different plasma lactate parameters (LPs) were compared, the LP determined by the Dmax method was the best predictor of 1-h cycling performance in women. The present study extended these findings to determine whether or not the relationship between the following six LPs and endurance performance could be explained by their relationship with muscle fiber characteristics: 1) lactate threshold (LT; the power output at which plasma lactate concentration begins to increase above the resting level during an incremental exercise test), 2) LT1 (the power output at which plasma lactate increases by 1 mmol x L(-1) or more), 3) LT(D) (the lactate threshold calculated by the Dmax method), 4) LT(MOD) (the lactate threshold calculated by a modified Dmax method), 5) L4 (the power output at which plasma lactate reaches a concentration of 4 mmol x L(-1)), and 6) LT(LOG) (the power output at which plasma lactate concentration begins to increase when the log([La-]) is plotted against the log(power output)). METHODS: Twelve trained female cyclists (27.3 +/- 5.4 yr) first completed an incremental cycle test to determine both their LPs and peak VO2. One week later, endurance performance was assessed as the average absolute power output maintained during a 1-h endurance test (OHT). Resting muscle was sampled by needle biopsy from m. vastus lateralis and analyzed for fiber type diameter, fiber type percentage, 2-oxoglutarate dehydrogenase (OGDH) activity, and phosphofructokinase (PFK) activity. RESULTS: OHT performance was more strongly correlated with all LPs (r = 0.71-0.89, P < 0.05) than with peak VO2 (L x min(-1), r = 0.65, P < 0.05). OGDH activity, PFK activity, and the percentage of Type I fibers were not related to peak VO2, any of the LPs, or OHT performance. The diameter of the Type II fibers, however, was negatively related to OHT performance (r = -0.77, P < 0.01) and to four of the LPs (r = -59 to -0.86, P < 0.001). CONCLUSIONS: These correlations, which indicate that large Type II fibers may impair endurance performance, may be the result of greater production and/or reduced removal of lactate from the larger, glycolytic Type II fibers. LPs most strongly correlated with Type II fiber diameter were also most strongly correlated with OHT performance.

Adult↗
PubMed2003

Increased plasma D-lactate is associated with the severity of hemorrhagic/traumatic shock in rats.

D-lactate is produced by indigenous bacteria in the gastrointestinal tract. Mammals do not have the enzyme systems to metabolize D-lactate rapidly. The present study was designed to determine the kinetics of circulating D-lactate levels and to examine whether the severity of shock affects circulating D-lactate levels in rats subjected to hemorrhagic/traumatic shock. Anesthetized rats underwent midline laparotomy (duration 30 min) and were bled to 30-35 mmHg mean arterial pressure (MAP). After the onset of decompensation, MAP was either increased to 40-45 mmHg immediately by administration of Ringer's solution (moderate shock) or after 40% of shed blood volume had been re-infused as Ringer's solution (severe shock). MAP was then maintained at 40-45 mmHg for 40 min by further administration of Ringer's solution (inadequate resuscitation). Subsequently, adequate resuscitation was performed for 60 min with shed blood and additional Ringer's solution. Metabolic acidosis was significantly more pronounced in severe than in moderate hemorrhagic/traumatic shock. Plasma D-lactate levels were already significantly increased at the end of severe hemorrhagic/traumatic shock and remained high during inadequate resuscitation. D-lactate levels were significantly higher after severe than after moderate shock. Endotoxin levels did not correlate with shock severity. Damage to the intestinal mucosa was more profound in severe shock than in moderate shock. Our data suggest that hemorrhagic/traumatic shock is associated with mucosal damage and increased plasma D-lactate levels. The severity of shock affects D-lactate concentrations in plasma. Plasma D-lactate may be a useful marker of intestinal injury after hemorrhagic/traumatic shock.

Animals↗
PubMed2005

Lactate and base deficit in trauma: does alcohol or drug use impair their predictive accuracy?

BACKGROUND: Abnormal blood lactate and base deficit (BD) reflect hypoperfusion and have been documented to predict outcome in trauma. Alcohol and drug use may also induce metabolic acidosis in trauma victims, potentially diminishing the predictive accuracy of lactate and BD. We, therefore, sought to examine the effect of alcohol and drug use on the predictive accuracy of admission blood lactate and BD in trauma. METHODS: Prospective data were collected on 15,179 patients admitted to the R Adams Cowley Shock Trauma Center over a 3-year period from 1998 to 2000. Patients were stratified by age, gender, race, injury severity score (ISS), Glasgow coma score (GCS), alcohol concentration and illicit drug use. Multiple regression analyses were used to assess admission blood lactate and BD as independent risk factors for mortality, intensive care unit (ICU) admission, and ICU and hospital length of stay (LOS) controlling for alcohol and drug use [cocaine, phencyclidine and methamphetamines] by measured serum concentrations. RESULTS: The mean age of the study cohort was 37 +/- 19 years, mean ISS was 9 +/- 10, mean GCS 14.1 +/- 2.7, 71% were male and 77% sustained blunt trauma. Alcohol testing was completed in 13,102 of 15,179 (86.3%) of patients. Alcohol screen was positive in 27% (n = 3536) of the total cohort tested (n = 13,102) with a mean blood alcohol concentration of 141 +/- 95 mg/dL; 7% (n = 992) had positive drug screens. Increasing injury severity was associated with significantly increased admission blood lactate and BD (p < 0.001). Patients with positive alcohol and drug screens had significantly increased admission blood lactate, BD and injury severity compared with patients with negative alcohol and drug screens (p < 0.01). Patients with positive alcohol and drug screens had a significant increase in admission to the ICU (p < 0.05), but no significant increase in mortality, ICU or hospital LOS compared with patients with negative screens. Multiple logistic and linear regression analyses confirmed admission lactate and BD as significant independent predictors of mortality, ICU and hospital LOS (p < 0.01). These results were unchanged after controlling for alcohol and drug use as covariates in the logistic and linear regression analyses. CONCLUSION: Alcohol and drug use are common in trauma, but do not impair the predictive accuracy of admission lactate and BD in trauma outcome. Admission lactate and BD are therefore confirmed as significant independent predictors of trauma outcome in patients with acute alcohol and drug use in this largest clinical study to date.

Acid-Base Imbalance↗
PubMed2005

Lactate is mainly fermented to butyrate by human intestinal microfloras but inter-individual variation is evident.

AIM: To assess the role of lactate as a precursor for butyrate biosynthesis in human colonic microflora. METHODS AND RESULTS: Three human faecal microfloras were incubated in vitro with media supplemented with 30 mmol l(-1) unenriched or 13C-enriched lactate. Lactate metabolism and short-chain fatty acid (SCFA) production were quantified. Lactate conversion to butyrate was investigated by gas chromatography-mass spectrometry and the pathways involved were identified by 13C nuclear magnetic resonance spectroscopy. All human faecal microfloras rapidly and completely fermented lactate, yielding approx. 19 mmol l(-1) total SCFAs. However, the SCFA composition varied markedly between microfloras. Butyrate was the main end-product for two microfloras but not for the third (60 and 61%vs 27% of the net concentration of SCFA produced respectively). The latter was typified by its ability to produce propionate as a major product (37%), and valerate (3%). 13C-Labelling showed that butyrate was produced through the acetyl-CoA pathway and that the three microfloras possessed significant differences in their metabolic pathways for lactate consumption. CONCLUSIONS: In contrast to the ruminal microflora, the human intestinal microflora can utilize both d- and l-lactate as precursors for butyrate synthesis. Inter-individual variation is found. SIGNIFICANCE AND IMPACT OF THE STUDY: This study suggests that the butyrogenic capability of colonic prebiotics could be related to lactate availability. These findings will direct the development of selection strategies for the isolation of new butyrate-producing bacteria among the lactate-utilizing bacteria present in the human intestinal microfloras.

Adult↗
PubMed2004

Stimulus-induced brain lactate: effects of aging and prolonged wakefulness.

Both aging and sleep deprivation disturb the functions of the frontal lobes. Deficits in brain energy metabolism have been reported in these conditions. Neurons use not only glucose but also lactate as their energy substrate. The physiological response to elevated neuronal activity is a transient increase in lactate concentrations in the stimulated area. We have previously shown that cognitive stimulation increases brain lactate. To study the effect of prolonged wakefulness on the lactate response we designed an experiment to assess brain lactate levels during a 40-h sleep deprivation period in young (19-24 years old; n = 13) and in aged (60-68 years old; n = 12) healthy female volunteers. Brain lactate levels were assessed with proton MR-spectroscopy ((1)H MRS) during the performance of a silent word generation task. The (1)H MRS voxel location was individually selected, using functional magnetic resonance imaging, to cover the activated area in the left frontal lobe. The degree of sleepiness was verified using vigilance tests and self-rating scales. In the young alert subjects, the silent word generation test induced a 40% increase in lactate, but during the prolonged wakefulness period this response disappeared. In the aged subjects, the lactate response could not be detected even in the alert state. We propose that the absence of the lactate response may be a sign of malfunctioning of normal brain energy metabolism. The behavioral effects of prolonged wakefulness and aging may arise from this dysfunction.

Adult↗
PubMed2005

Synergistic cytotoxicity of acidity and 3,4-Dideoxyglucosone-3-ene under the existence of lactate in peritoneal dialysis fluid.

Of the non-physiological compounds in glucose-rich peritoneal dialysis fluid, we investigated the synergistic cytotoxicity of acidity and 3,4-Dideoxyglucosone-3-ene(3,4-DGE) under the existence of lactate using human peritoneal mesothelial cells (HPMC). The effect of pH on cell viability at various levels of pH (5.5, 6.7, 7.15), with or without lactate was examined by adding 1N-HCl to phosphate buffer solution. We also examined the cytotoxic effects of 3,4-DGE and pH (5.5, 6.7 or 7.15). Additionally, we compared the cytotoxic effects of 3,4-DGE and pH (5.5, 6.7 or 7.15) under existence of lactate (40 meq/L) or absence of lactate. The cells were exposed to these solutions for 2 or 4 h. Cell viability was determined by MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenylterazolium bromide) assay. 3,4-DGE or acidic solution alone had no significant effects on MTT viability under the absence of lactate. However, acidic solutions containing 3,4-DGE significantly decreased MTT viability under the existence of lactate. The MTT viability of HPMC was not decreased by 3,4-DGE or acidity alone under the absence of lactate. However, the combination of acidity and 3,4-DGE markedly decreased MTT viability under the existence of lactate, strongly suggesting the synergistic cytotoxicity of 3,4-DGE and acidity under the existence of lactate.

Cell Survival↗
PubMed1999

Muscle characteristics and plasma lactate and ammonia response after racing in Standardbred trotters: relation to performance.

Blood samples from the jugular vein and muscle biopsies (gluteus medius) in 25 Standardbred trotters were obtained 5-10 min after racing. The biopsies were analysed for fibre type composition and enzymatic profile and blood samples for plasma lactate and ammonia concentrations. Muscle characteristics, plasma lactate and ammonia concentrations after racing were compared with each horse's individual performance index (IPI). The IPI is calculated annually from the individual horse's racing performance (% placing 1, 2 or 3, total annual earnings, average earning per start, and best racing record), respectively, converted to and expressed as a percentage deviation from the average record of the same sex and age group. The IPI values were 100-116. Plasma lactate concentrations were 15.0-42.7 mmol/l (mean 31.3 mmol/l) and ammonia concentrations 65-210 micromol/l (mean 141 micromol/l) after racing. Fibre type composition varied among horses (range 9-27% for Type I, 32-54% for Type IIA, and 27-46% for Type IIB). Fibre type composition, enzyme activities, plasma lactate and ammonia responses to racing were not correlated to IPI. Ten of the horses also performed a submaximal test on the track, consisting of 5 incremental 1000 m heats at approximate speeds of 9.1, 9.5, 10.0, 10.5, and 11.1 m/s. Immediately after each heat a blood sample was drawn from the jugular vein for plasma lactate analysis. Plasma lactate response to exercise differed between horses, but no correlation was seen with IPI. Muscle characteristics, plasma lactate and ammonia concentrations after racing and lactate response to a submaximal track test did not correlate with current race performance expressed as IPI in a group of horses with average or better performance capacity at the time of testing. Analysis of lactate and ammonia in blood after racing is not a valuable tool to predict an individual performance index.

Age Factors↗
PubMed2003

A reduced cerebral metabolic ratio in exercise reflects metabolism and not accumulation of lactate within the human brain.

During maximal exercise lactate taken up by the human brain contributes to reduce the cerebral metabolic ratio, O(2)/(glucose + 1/2 lactate), but it is not known whether the lactate is metabolized or if it accumulates in a distribution volume. In one experiment the cerebral arterio-venous differences (AV) for O(2), glucose (glc) and lactate (lac) were evaluated in nine healthy subjects at rest and during and after exercise to exhaustion. The cerebrospinal fluid (CSF) was drained through a lumbar puncture immediately after exercise, while control values were obtained from six other healthy young subjects. In a second experiment magnetic resonance spectroscopy ((1)H-MRS) was performed after exhaustive exercise to assess lactate levels in the brain (n = 5). Exercise increased the AV(O2) from 3.2 +/- 0.1 at rest to 3.5 +/- 0.2 mM (mean +/-s.e.m.; P < 0.05) and the AV(glc) from 0.6 +/- 0.0 to 0.9 +/- 0.1 mM (P < 0.01). Notably, the AV(lac) increased from 0.0 +/- 0.0 to 1.3 +/- 0.2 mm at the point of exhaustion (P < 0.01). Thus, maximal exercise reduced the cerebral metabolic ratio from 6.0 +/- 0.3 to 2.8 +/- 0.2 (P < 0.05) and it remained low during the early recovery. Despite this, the CSF concentration of lactate postexercise (1.2 +/- 0.1 mM; n= 7) was not different from baseline (1.4 +/- 0.1 mM; n= 6). Also, the (1)H-MRS signal from lactate obtained after exercise was smaller than the estimated detection limit of approximately 1.5 mM. The finding that an increase in lactate could not be detected in the CSF or within the brain rules out accumulation in a distribution volume and indicates that the lactate taken up by the brain is metabolized.

Adult↗
PubMed1981

Anaerobic Degradation of Lactate by Syntrophic Associations of Methanosarcina barkeri and Desulfovibrio Species and Effect of H(2) on Acetate Degradation.

When grown in the absence of added sulfate, cocultures of Desulfovibrio desulfuricans or Desulfovibrio vulgaris with Methanobrevibacter smithii (Methanobacterium ruminantium), which uses H(2) and CO(2) for methanogenesis, degraded lactate, with the production of acetate and CH(4). When D. desulfuricans or D. vulgaris was grown in the absence of added sulfate in coculture with Methanosarcina barkeri (type strain), which uses both H(2)-CO(2) and acetate for methanogenesis, lactate was stoichiometrically degraded to CH(4) and presumably to CO(2). During the first 12 days of incubation of the D. desulfuricans-M. barkeri coculture, lactate was completely degraded, with almost stoichiometric production of acetate and CH(4). Later, acetate was degraded to CH(4) and presumably to CO(2). In experiments in which 20 mM acetate and 0 to 20 mM lactate were added to D. desulfuricans-M. barkeri cocultures, no detectable degradation of acetate occurred until the lactate was catabolized. The ultimate rate of acetate utilization for methanogenesis was greater for those cocultures receiving the highest levels of lactate. A small amount of H(2) was detected in cocultures which contained D. desulfuricans and M. barkeri until after all lactate was degraded. The addition of H(2), but not of lactate, to the growth medium inhibited acetate degradation by pure cultures of M. barkeri. Pure cultures of M. barkeri produced CH(4) from acetate at a rate equivalent to that observed for cocultures containing M. barkeri. Inocula of M. barkeri grown with H(2)-CO(2) as the methanogenic substrate produced CH(4) from acetate at a rate equivalent to that observed for acetate-grown inocula when grown in a rumen fluid-vitamin-based medium but not when grown in a yeast extract-based medium. The results suggest that H(2) produced by the Desulfovibrio species during growth with lactate inhibited acetate degradation by M. barkeri.

Journal Article↗
PubMed2006

Lactate acquisition promotes successful colonization of the murine genital tract by Neisseria gonorrhoeae.

Previous studies on Neisseria gonorrhoeae have demonstrated that metabolism of lactate in the presence of glucose increases the growth rate of the bacterium and enhances its resistance to complement-mediated killing. Although these findings in vitro suggest that the acquisition of lactate promotes gonococcal colonization, the significance of this carbon source to the survival of the gonococcus in vivo remains unknown. To investigate the importance of lactate utilization during Neisseria gonorrhoeae genital tract infection, we identified the gene lctP, which encodes the gonococcal lactate permease. A mutant that lacks a functional copy of lctP was unable to take up exogenous lactate and did not grow in defined medium with lactate as the sole carbon source, in contrast to the wild-type and complemented strains; the mutant strain exhibited no growth defect in defined medium containing glucose. In defined medium containing physiological concentrations of lactate and glucose, the lctP mutant demonstrated reduced early growth and increased sensitivity to complement-mediated killing compared with the wild-type strain; the enhanced susceptibility to complement was associated with a reduction in lipopolysaccharide sialylation of the lctP mutant. The importance of lactate utilization during colonization was evaluated in the murine model of lower genital tract infection. The lctP mutant was significantly attenuated in its ability to colonize and survive in the genital tract, while the complemented mutant exhibited no defect for colonization. Lactate is a micronutrient in the genital tract that contributes to the survival of the gonococcus.

Animals↗
PubMed1997

Serum lactate as a predictor of mortality after paediatric cardiac surgery.

OBJECTIVE: To assess the value of sequential lactate measurement in predicting postoperative mortality after surgery for complex congenital heart disease in children. DESIGN: Prospective observational study. SETTING: Sixteen bedded paediatric intensive care unit (PICU). SUBJECTS: Ninety nine children (90 survivors, nine non-survivors). MEASUREMENTS: Serum lactate and base deficit were measured on admission and every six hours thereafter. Data were analysed by Mann-Whitney and Fisher's exact tests. RESULTS: There was considerable overlap in initial lactate values between the survivor and non-survivor groups. Initial lactate was significantly raised in non-survivors (median 8.7, range 1.9-17.6 mmol/l) compared with survivors (median 2.4, range 0.6-13.6 mmol/l) (p = 0.0002). Twenty one patients (21.1%) with initial lactate concentrations greater than 4.5 mmol/l survived to PICU discharge. Using receiver operating characteristic analysis an initial lactate of 6 mmol/l had the optimum predictive value for mortality. Initial postoperative serum lactate > 6 mmol/l predicted mortality with sensitivity 78%, specificity 83%, and positive predictive value of only 32%. CONCLUSION: Initial lactate concentrations have poor positive predictive value for mortality. The routine measurement of lactate for this purpose cannot be justified in clinical practice.

Biomarkers↗
PubMed1998

Effects of lactate on force production by mouse EDL muscle: implications for the development of fatigue.

Numerous studies suggest that the accumulation of lactate during exercise contributes to the fatigue process. This notion is based on close negative correlations between force and intracellular muscle lactate concentrations during fatigue and recovery. In this investigation, we attempted to determine if lactate directly affects muscle force output. This was accomplished by incubating mouse extensor digitorum longus muscles in extracellular concentrations of 10, 20, 30 and 50 mM L-(+)-lactate at 21 and 37 degrees C and monitoring force output. At 21 degrees C, 30 and 50 mM, extracellular lactate significantly reduced tetanic force (Po 250 ms, 100 Hz) to 95 and 93% of initial, respectively. In addition, the rate of force development (+dP/dt) was reduced to 93 and 89% of initial. At 37 degrees C, the effects of extracellular lactate were augmented as Po was reduced to 73 and 62% of initial and +dP/dt was reduced to 55 and 44% of initial at 30 and 50 mM, respectively. We next sought to determine if the reduction in Po was due to altered sarcoplasmic reticulum (SR) function using a muscle homogenate fraction. The rate of AgNO3-induced SR Ca2+ release was depressed by 31% in the presence of 25 mM lactate. These results suggest that elevated lactate depresses force production by whole muscle and may play some role in the fatigue process. In addition, it appears that lactate depresses force production, in part, by inhibiting Ca2+ release from the SR.

Animals↗
PubMed2003

Effect of high-intensity intermittent training on lactate and H+ release from human skeletal muscle.

The study investigated the effect of training on lactate and H+ release from human skeletal muscle during one-legged knee-extensor exercise. Six subjects were tested after 7-8 wk of training (fifteen 1-min bouts at approximately 150% of thigh maximal O2 uptake per day). Blood samples, blood flow, and muscle biopsies were obtained during and after a 30-W exercise bout and an incremental test to exhaustion of both trained (T) and untrained (UT) legs. Blood flow was 16% higher in the T than in the UT leg. In the 30-W test, venous lactate and lactate release were lower in the T compared with the UT leg. In the incremental test, time to fatigue was 10.6 +/- 0.7 and 8.2 +/- 0.7 min, respectively, in the T and UT legs (P < 0.05). At exhaustion, venous blood lactate was 10.7 +/- 0.4 and 8.0 +/- 0.9 mmol/l in T and UT legs (P < 0.05), respectively, and lactate release was 19.4 +/- 3.6 and 10.6 +/- 2.0 mmol/min (P < 0.05). H+ release at exhaustion was higher in the T than in the UT leg. Muscle lactate content was 59.0 +/- 15.1 and 96.5 +/- 14.5 mmol/kg dry wt in the T and UT legs, and muscle pH was 6.82 +/- 0.05 and 6.69 +/- 0.04 in the T and UT legs (P = 0.06). The membrane contents of the monocarboxylate transporters MCT1 and MCT4 and the Na+/H+ exchanger were 115 +/- 5 (P < 0.05), 111 +/- 11, and 116 +/- 6% (P < 0.05), respectively, in the T compared with the UT leg. The reason for the training-induced increase in peak lactate and H+ release during exercise is a combination of an increased density of the lactate and H+ transporting systems, an improved blood flow and blood flow distribution, and an increased systemic lactate and H+ clearance.

Adult↗
PubMed2005

Extracellular lactate as a dynamic vasoactive signal in the rat retinal microvasculature.

We tested the hypothesis that extracellular lactate regulates the function of pericyte-containing retinal microvessels. Although abluminally positioned pericytes appear to adjust capillary perfusion by contracting and relaxing, knowledge of the molecular signals that regulate the contractility of these mural cells is limited. Here, we focused on lactate because this metabolic product is in the retinal extracellular space under both physiological and pathophysiological conditions. In microvessels freshly isolated from the adult rat retina, we used perforated-patch pipettes to monitor ionic currents, fura-2 to measure calcium levels, and time-lapse photography to visualize changes in mural cell contractility and lumen diameter. During lactate exposure, pericyte calcium rose; these cells contracted, and lumens constricted. This contractile response appears to involve a cascade of events resulting in the inhibition of Na+/Ca2+ exchangers (NCXs), the decreased of which function causes pericyte calcium to increase and contraction to be triggered. On the basis of our observation that gap junction uncouplers minimized the lactate-induced rise in pericyte calcium, we propose that the NCXs inhibited by lactate are predominately located in the endothelium. Indicative of the importance of endothelial/pericyte gap junctions, uncouplers of these junctions switched the pericyte response to lactate from contraction to relaxation. In addition, we observed that hypoxia, which closes microvascular gap junctions, also switched lactate's effect from vasocontraction to vasorelaxation. Thus the response of pericyte-containing retinal microvessels to extracellular lactate is metabolically modulated. The ability of lactate to serve as a vasoconstrictor when energy supplies are ample and a vasodilator under hypoxic conditions may be an efficient mechanism to link capillary function with local metabolic need.

Animals↗
PubMed2000

Inner medullary lactate production and accumulation: a vasa recta model.

Since anaerobic glycolysis yields two lactates for each glucose consumed and since it is reported to be a major source of ATP for inner medullary (IM) cell maintenance, it is a likely source of "external" IM osmoles. It has long been known that such an osmole source could theoretically contribute to the "single-effect" of the urine concentrating mechanism, but there was previously no suggestion of a plausible source. I used numerical simulation to estimate axial gradients of lactate and glucose that might be accumulated by countercurrent recycling in IM vasa recta (IMVR). Based on measurements in other tissues, anaerobic glycolysis (assumed to be independent of diuretic state) was estimated to consume approximately 20% of the glucose delivered to the IM. IM tissue mass and axial distribution of loops and vasa recta were according to reported values for rat and other rodents. Lactate (P(LAC)) and glucose (P(GLU)) permeabilities were varied over a range of plausible values. The model results suggest that P(LAC) of 100 x 10(-5) cm/s (similar to measured permeabilities for other small solutes) is sufficiently high to ensure efficient lactate recycling. By contrast, it was necessary in the model to reduce P(GLU) to a small fraction of this value (1/25th) to avoid papillary glucose depletion by countercurrent shunting. The results predict that IM lactate production could suffice to build a significant steady-state axial lactate gradient in the IM interstitium. Other modeling studies (Jen JF and Stephenson JL. Bull Math Biol 56: 491-514, 1994; and Thomas SR and Wexler AS. Am J Physiol Renal Fluid Electrolyte Physiol 269: F159-F171, 1995) have shown that 20-100 mosmol/kgH(2)O of unspecified external, interstitial, osmolytes could greatly improve IM concentrating ability. The present study gives several plausible scenarios consistent with accumulation of metabolically produced lactate osmoles, although only to the lower end of this range. For example, if 20% of entering glucose is consumed, the model predicts that papillary lactate would attain about 15 mM assuming vasa recta outflow is increased 30% by fluid absorbed from the nephrons and collecting ducts and that this lactate gradient would double if IM blood flow were reduced by one-half, as may occur in antidiuresis. Several experimental tests of the hypothesis are indicated.

Animals↗
PubMed1999

Active muscle and whole body lactate kinetics after endurance training in men.

We evaluated the hypotheses that endurance training decreases arterial lactate concentration ([lactate](a)) during continuous exercise by decreasing net lactate release () and appearance rates (R(a)) and increasing metabolic clearance rate (MCR). Measurements were made at two intensities before [45 and 65% peak O(2) consumption (VO(2 peak))] and after training [65% pretraining VO(2 peak), same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative intensity (RLT)]. Nine men (27.4 +/- 2.0 yr) trained for 9 wk on a cycle ergometer, 5 times/wk at 75% VO(2 peak). Compared with the 65% VO(2 peak) pretraining condition (4.75 +/- 0.4 mM), [lactate](a) decreased at ABT (41%) and RLT (21%) (P < 0.05). decreased at ABT but not at RLT. Leg lactate uptake and oxidation were unchanged at ABT but increased at RLT. MCR was unchanged at ABT but increased at RLT. We conclude that 1) active skeletal muscle is not solely responsible for elevated [lactate](a); and 2) training increases leg lactate clearance, decreases whole body and leg lactate production at a given moderate-intensity power output, and increases both whole body and leg lactate clearance at a high relative power output.

Adult↗
PubMed2004

Injections of recombinant human erythropoietin increases lactate influx into erythrocytes.

Previous studies showed that erythropoietin not only increases erythrocyte production but is also essential in both the synthesis and the good functioning of several erythrocyte membrane proteins, including band 3. It is still unknown whether anion and/or H(+) fluxes are modified by erythropoietin. This study aimed to evaluate the effect of recombinant human erythropoietin (rHuEPO) injections on lactate transport into erythrocytes via band 3 and H(+)-monocarboxylate transporter MCT-1, two proteins involved in lactate exchange. Nine athletes received subcutaneous rHuEPO (50 U/kg body mass 3 times a week for 4 wk), and seven athletes received a saline solution (placebo group). All subjects were also supplemented with oral iron and vitamins B(9) and B(12). Lactate transport into erythrocytes was studied before and after the rHuEPO treatment at different lactate concentrations (1.6, 8.1, 41, and 81.1 mM). After treatment, MCT-1 lactate uptake was increased at 1.6, 41 (P < 0.01), and 81.1 mM lactate concentration (P < 0.001) although lactate uptake via band 3 and nonionic diffusion were unchanged. MCT-1 maximal velocity increased in the rHuEPO group (P < 0.05), reaching higher values than in the placebo group (P < 0.05) after treatment. Our results show that rHuEPO injections increased MCT-1 lactate influx at low and high lactate concentrations. The increase in MCT-1 maximal velocity suggests that rHuEPO may stimulate MCT-1 synthesis during erythrocyte formation in bone marrow.

Adult↗