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PubMed1996

PTH-related protein is released into the mother's bloodstream during lactation: evidence for beneficial effects on maternal calcium-phosphate metabolism.

Recent studies have indicated that parathyroid hormone-related protein (PTHrP) may have important actions in lactation, affecting the mammary gland, and also calcium metabolism in the newborn and the mother. However, there are as yet no longitudinal studies to support the notion of an endocrine role of this peptide during nursing. We studied a group of 12 nursing mothers, mean age 32 years, after they had been nursing for an average of 7 weeks (B) and also 4 months after stopping nursing (A). It was assumed that changes occurring between A and B correspond to the effect of lactation. Blood was assayed for prolactin (PRL), PTHrP (two-site immunoradiometric assay with sheep antibody against PTHrP(1-40), and goat antibody against PTHrP(60-72), detection limit 0.3 pmol/l), intact PTH (iPTH), ionized calcium (Ca2+), 25-hydroxyvitamin D3 (25(OH)D3) and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), alkaline phosphatase (alkP), as well as for creatinine (Cr), protein, phosphorus (P), and total calcium (Ca). Fasting 2-h urine samples were analyzed for Ca excretion (CaE) and renal phosphate threshold (TmP/GFR). PRL was significantly higher during lactation than after weaning (39 +/- 10 vs. 13 +/- 9 micrograms/l; p = 0.018) and so was PTHrP (2.8 +/- 0.35 vs. 0.52 +/- 0.04 pmol/l; p = 0.002), values during lactation being above the normal limit (1.3 pmol/l) in all 12 mothers. There was a significant correlation between PRL and PTHrP during lactation (r = 0.8, p = 0.002). Whole blood Ca2+ did not significantly change from A (1.20 +/- 0.02 mmol/l) to B (1.22 +/- 0.02, mmol/l), whereas total Ca corrected for protein (2.18 +/- 0.02 mmol/l) or uncorrected (2.18 +/- 0.02 mmol/l) significantly rose during lactation (2.31 +/- 0.02 mmol/l, p = 0.003 and 2.37 +/- 0.03 mmol/l, p = 0.002, respectively). Conversely, iPTH decreased during lactation (3.47 +/- 0.38 vs. 2.11 +/- 0.35 pmol/l, A vs. B, p = 0.02). Serum-levels of 25(OH)D3 and 1,25(OH)2D3 did not significantly change from A to B (23 +/- 2.3 vs. 24 +/- 1.9 ng/ml and 29.5 +/- 6.0 vs. 21.9 +/- 1.8 pg/ml, respectively). Both TmP/GFR and P were higher during lactation than after weaning (1.15 +/- 0.03 vs. 0.86 +/- 0.05 mmol/l GF, p = 0.003 and 1.25 +/- 0.03 vs. 0.96 +/- 0.05 mmol/l, p = 0.002, respectively) as was alkP (74.0 +/- 7.1 vs. 52.6 +/- 6.9 U/l, p = 0.003). CaE did not differ between A and B (0.015 +/- 0.003 vs. 0.017 +/- 0.003 mmol/l GF, A vs. B, NS). We conclude that lactation is accompanied by an increase in serum PRL. This is associated with a release of PTHrP into the maternal blood circulation. A rise in total plasma Ca ensues, probably in part by increased bone turnover as suggested by the elevation of alkP. PTH secretion falls, with a subsequent rise of TmP/GFR and plasma P despite high plasma levels of PTHrP.

Adult↗
PubMedDate not supplied

Cerebral lactate production and blood flow in acute stroke.

Eight stroke patients were examined serially in the acute phase and 1 week and 2-4 weeks after stroke with water-suppressed proton magnetic resonance spectroscopy. The time courses of lactate level and regional cerebral blood flow were studied. A high lactate level was found in the acute phase. The lactate content decreased to barely detectable levels during the following 3 weeks, while regional blood flow increased during this period. The inverse relationship between lactate level and cerebral blood flow suggests that lactate plays no substantial role in the vasodilatation underlying the hyperemia that follows reperfusion. The amount of lactate present in the acute phase reflects the severity of ischemia in the affected region. The lactate level was still above normal in the subacute phase with hyperemia, suggesting lactate production through aerobic glycolysis. Thus, the lactate level in the subacute phase probably does not reflect the degree of anaerobic glycolysis in hypoxic neuronal tissue.

Acute Disease↗
PubMed1994

Importance of the modulation of glycolysis in the control of lactate metabolism by fatty acids in isolated hepatocytes from fed rats.

In liver cells from fed rats, lactate utilization depends on its extracellular concentration and the threshold concentration at which lactate uptake equilibrates release is about 3 mM. Even-chain fatty acids (butyrate, octanoate, or oleate) played a crucial role (i) to depress the lactate release, from 40% (butyrate or oleate) to 72% (octanoate), and (ii) to lower the threshold concentration for lactate utilization (down to 1 mM with octanoate). The effects of fatty acids were connected to their inhibition of hepatic glycolysis, estimated by the detritiation of [6-3H]glucose (about -30% with butyrate or oleate and -45% with octanoate). Fatty acids depressed the cellular concentration of pyruvate which, at physiological concentration of lactate, favors its utilization. The rise in ketone bodies concentration in response to fatty acids reflected an enhanced acetyl CoA production, resulting in an accumulation of citrate. In parallel there was a drop of the cellular concentration of fructose 2,6-biphosphate. As a result, there was an inhibition of the flux through 6-phosphofructo-1 kinase (50, 75, or 40% inhibition with butyrate, octanoate, or oleate, respectively). The other regulatory glycolysis steps, catalyzed by glucokinase and pyruvate kinase, were not affected by fatty acids. Inhibition of hepatic glycolysis by fatty acids seems connected to acetyl-CoA generation since octanoate, readily metabolized to acetyl-CoA and ketone bodies by hepatocytes, had a more potent stimulatory effect on the hepatic uptake of lactate than butyrate or oleate. Propionate, which yields practically no acetyl CoA, slightly stimulated lactate release and elevated the threshold of lactate utilization. The present data suggest thus that, in hepatocytes from fed rats, fatty acids effectively inhibit glycolysis and switch liver cell metabolism toward gluconeogenic conditions, which promotes lactate utilization.

Acetyl Coenzyme A↗
PubMed1994

Proton-lactate cotransport in the apical membrane of frog retinal pigment epithelium.

We studied lactate- and pyruvate-dependent proton transport across the apical membrane of frog RPE. The epithelium was mounted in a modified Ussing-chamber that allowed measurement of transepithelial potential and resistance while intracellular pH was measured with either intracellular microelectrodes or a pH-sensitive dye, 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF). To estimate the rate of lactate influx from the change in intracellular pH, we used the NH4 pulse technique to measure intracellular buffering capacity and its dependence on intracellular pH. We found that the buffering capacity was 16 mM at pH1 = 7.28, and that it increased as intracellular pH decreased. Intracellular pH was monitored with the tissue bathed in nominally HCO3-free (Hepes buffered) Ringer. The perfusate on the apical side of the epithelium was then changed to a Ringer that contained between 5 and 100 mM lactate or pyruvate. When 10-100 mM lactate or pyruvate was added to the apical bath the cells acidified by 0.05-0.50 pH units. For each of these acidifications, the initial acid influx into the RPE cells was calculated from the intracellular buffering capacity and the initial rate of intracellular acidification. These influxes were plotted as functions of the concentrations of lactate or pyruvate and this relationship was analysed using Michaelis-Menten kinetics. The Km values were: 33 +/- 5 mM for lactate and 9 +/- 3 mM for pyruvate. There were no differences in the rates of acid influx caused by L- or D-lactate. The rates of acidification caused by 50 mM apical L-lactate were reversibly reduced by 56% after apical administration of probenecid (2 mM), and irreversibly reduced by 63% after apical administration of the SH-reagent mersalyl acid (2 mM). These results indicate the presence of a proton-lactate cotransport system in the apical membrane of the frog RPE.

Animals↗
PubMed1995

Role of the nutritional status of the litter and length and frequency of mother-litter contact bouts in prolonging lactational diestrus in rats.

Food restricting lactating rat dams over the first 2 weeks of lactation results in a prolongation of the period of lactational diestrus. Such food restriction has not only a direct effect on the dam but also the pups are undernourished, and the pattern of dam-litter contact is also changed. In a series of studies, we investigated the effects of nursing undernourished pups and the change in dam-litter interaction on the prolongation of lactational diestrus. While nursing undernourished pups in the last 2 weeks of lactation is sufficient to extend lactational diestrus in ad lib-fed dams nursing well-nourished pups in the last 2 weeks of lactation is not necessary for the prolongation of lactational diestrus seen in food-restricted dams. Further, neither nursing underfed pups nor increased nest time in the first 2 weeks postpartum are necessary factors for the prolongation of lactational diestrus in food-restricted dams.

Animals↗
PubMed1980

Water deprivation in lactating rats: changes in nucleolar dry mass of paraventricular and supraoptic neurones.

The separation of function between and within the paraventricular (PV) and supraoptic (SO) nuclei was investigated in the rat. Nucleolar dry mass of PV and SO neurones was measured to detect increased synthetic activity after water deprivation for 3 days, lactation for 8 days or water deprivation during days 5 to 8 of lactation. Lactation or water deprivation increased nucleolar dry mass in both PV and SO neurones. These stimuli caused similar nucleolar changes in PV neurones, but water deprivation caused greater changes in SO neurones than lactation. The effects of lactation and water deprivation were additive for both SO and PV neurones. Furosemide was used to intensify the dehydration stimulus to determine whether such intensification could have caused the greater nucleolar changes when lactation and water deprivation were combined. For PV neurones this was not the case, but remained a possibility for SO neurones. Measurements of serum osmolality in the experimental groups were ranked as follows: water deprivation + furosemide > lactation + water deprivation > water deprivation > lactation = virgin control. Loss of body weight was similar in the first two groups but less during water deprivation alone. Although milk yield fell, milk was obtained by the litters of lactating animals throughout the period of water deprivation.

Animals↗
PubMed1990

Blood lactate responses in older swimmers during active and passive recovery following maximal sprint swimming.

The purpose of this study was to determine the effect of age on three blood lactate parameters following maximal sprint swimming. The parameters examined were maximal blood lactate concentration, time to reach maximal blood lactate concentration, and half recovery time to baseline lactate concentration. These parameters were examined in 16 male competitive masters swimmers (n = 4 for each age group: 25-35, 36-45, 46-55, and 56 plus years) during both passive and active recovery following a maximal 100 m freestyle sprint. Passive recovery consisted of 60 min sitting in a comfortable chair and active recovery consisted of a 20-min swim at a self-selected pace. Capillary blood samples were obtained every 2 min up to 10 min of recovery then at regular intervals to the end of the recovery period. Curves of blood lactate concentration against time were drawn and the three parameters determined for each condition for each subject. There were no significant differences between age groups in any of the lactate parameters examined. A significant difference (P less than 0.05) was noted in each of the parameters between active and passive recovery over all age groups. As expected, active recovery produced lower maximal blood lactate concentrations, lower time to maximal blood lactate values, and lower half recovery times. These data suggest that intensive swimming training may prevent or delay the decline with age in the physiological factors affecting blood lactate values following a maximal sprint swim. Older sprint swimmers appeared to be capable of producing and removing lactic acid at the same rate as younger swimmers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

ATP-sensitive potassium channels are modulated by intracellular lactate in rabbit ventricular myocytes.

During myocardial ischemia, increased anaerobic glycolysis results in the accumulation of large amount of intracellular lactate. Effects of lactate on the ATP-sensitive potassium (KATP) channels were examined in rabbit ventricular myocytes, using the inside-out patch-clamp technique. Millimolar concentrations of lactate, applied to the cytosolic side of the patch membrane, induced openings of the KATP channel. This effect was inhibited by 0.1 mM glybenclamide. Lactate-induced openings of the channel were increased in a dose-dependent fashion. In dose-response relation for lactate, Kd (the lactate concentration producing half-maximal activation) and n (Hill coefficient) were 20 mM and 1.3, respectively (n = 5). Activation of KATP channels by lactate occurred even in the presence of 2 mM ATP. Lactate also caused a significant increase in Ki, the ATP concentration causing half-maximal inhibition, from 70 microM in control (n = 7) to 232 microM (n = 5). From the above results it could be concluded that intracellular lactate modulate KATP channels directly and such modulation may resolve the discrepancy between the low Ki in excised membrane patches and high levels of intracellular ATP concentration during myocardial ischemia or hypoxia.

Adenosine Triphosphate↗
PubMed1976

[Comparative studies of lactate concentration in the perilymph, blood and cerebrospinal fluid of normal and sound exposed guinea pigs (author's transl)].

The paper deals with comparative studies of lactate concentration in the perilymph (PL) of scala tympani and of scala vestibuli, arterial and venous blood, serum and cerebrospinal fluid (CSF) of normal and sound exposed guinea pigs, special consideration having been given to possible sources of error in the methods employed. Lactate was determined enzymatically using a micromodification of the Boehringer UV-test combination adapted to 1 mul PL. The lactate concentrations in the PL of scala tympani and scala vestibuli did not differ significantly. The mean values amounted to 4.5-5.2 mM/l in the case of the opened and of the unopened subarachnoid space (Table 1). The lactate concentrations in the PL of both cochlea scales were significantly higher already ten minutes post-mortem. In the exposure experiments the animals were unilaterally exposed to sound for 1 h in an acoustically isolated system using a wide-band noise at an intensity of 120 dB SPL for one series and 2-kHz pure-tone at intensities of 112 and 122 dB SPL for two other series. We did not detect any changes in the lactate concentrations neither in the PL nor in the blood and in the CSF, following sound exposure (Table 2 and 3). The lactate concentrations of arterial and venous blood and CSF did not differ significantly. The mean values amounted to 1.4-1.8 mM/l (Table 2). However, if blood was not deproteinized or centrifuged immediately after being taken, the lactate concentration increased markedly. A comparison of the present results has shown that the lactate concentration in the PL is about three times as high as in blood and in CSF. This difference in concentration suggests that the PL lactate is of intracochlear origin and that glycolytic processes take place in the inner ear also under normal conditions. Systematic studies of additional metabolic parameters must be conducted before a definitive physiological interpretation of the present analytical results can be given.

Animals↗
PubMed1991

Gentle exercise with a previously inactive muscle group hastens the decline of blood lactate concentration after strenuous exercise.

The aim of this study was to elucidate the mechanism by which the disappearance of blood lactate following severe exercise is enhanced during active recovery in comparison with recovery at rest. Rates of decline of arterialised venous blood lactate concentrations in man after maximal one-leg exercise were compared during four different modes of recovery: passive (PR), exercise of the muscles involved in the initial exercise (SL), exercise of the corresponding muscles in the hitherto-inactive leg (OL), or exercise of one arm (RA). Recovery exercise workloads were each 40% of the onset of blood lactate accumulation (OBLA) for the limb used. In comparison with PR, SL and OL accelerated the fall in blood lactate to similar extents whereas RA was without effect. The first-order rate constant (min-1) for decline of arterialised venous blood lactate concentration after the intense exercise was 0.027 (0.003) in PR, 0.058 (0.025) in SL, 0.034 (0.002) in OL, and in RA was 0.028 (0.002) [mean (SEM), n = 6 subjects]. Preliminary studies had shown that RA in isolation elevated blood lactate whereas SL and OL did not. Thus, with appropriate workloads, exercise of either hitherto active or passive muscles enhanced blood lactate decline during recovery from intense exercise. This suggests that the effect resulted principally from the uptake and utilisation of lactate in the circulation by those exercising muscles rather than from increased transport of lactate to other sites of clearance by sustained high blood flow through the previously active muscles.

Adult↗
PubMed1991

Anaerobic threshold and maximal steady-state blood lactate in prepubertal boys.

To elucidate further the special nature of anaerobic threshold in children, 11 boys, mean age 12.1 years (range 11.4-12.5 years), were investigated during treadmill running. Oxygen uptake, including maximal oxygen uptake (VO2max), ventilation and the "ventilatory anaerobic threshold" were determined during incremental exercise, with determination of maximal blood lactate following exercise. Within 2 weeks following this test four runs of 16-min duration were performed at a constant speed, starting with a speed corresponding to about 75% of VO2max and increasing it during the next run by 0.5 or 1.0 km.h-1 according to the blood lactate concentrations in the previous run, in order to determine maximal steady-state blood lactate concentration. Blood lactate was determined at the end of every 4-min period. "Anaerobic threshold" was calculated from the increase in concentration of blood lactate obtained at the end of the runs at constant speed. The mean maximal steady-state blood lactate concentration was 5.0 mmol.l-1 corresponding to 88% of the aerobic power, whereas the mean value of the conventional "anaerobic threshold" was only 2.6 mmol.l-1, which corresponded to 78% of the VO2max. The correlations between the parameters of "anaerobic threshold", "ventilatory anaerobic threshold" and maximal steady-state blood lactate were only poor. Our results demonstrated that, in the children tested, the point at which a steeper increase in lactate concentrations during progressive work occurred did not correspond to the true anaerobic threshold, i.e. the exercise intensity above which a continuous increase in lactate concentration occurs at a constant exercise intensity.

Anaerobic Threshold↗
PubMed1991

The effect of different blood sampling sites and analyses on the relationship between exercise intensity and 4.0 mmol.l-1 blood lactate concentration.

The aim of the study was to examine whether the difference in lactate concentration in different blood fractions is of practical importance when using blood lactate as a test variable of aerobic endurance capacity. Ten male firefighters performed submaximally graded exercise on a cycle ergometer for 20-25 min. Venous and capillary blood samples were taken every 5 min for determination of haematocrit and lactate concentrations in plasma, venous and capillary blood. At the same time, expired air was collected in Douglas bags for determination of the oxygen consumption. A lactate concentration of 4.0 mmol.l-1 was used as the reference value to compare the oxygen consumption and exercise intensity when different types of blood specimen and sampling sites were used for lactate analysis. At this concentration the exercise intensity was 17% lower (P less than 0.01) when plasma lactate was compared to venous blood lactate, and 12% lower (P less than 0.05) when capillary blood lactate was used. Similar discrepancies were seen in oxygen consumption. The results illustrated the importance of standardizing sampling and handling of blood specimens for lactate determination to enable direct comparisons to be made among results obtained in different studies.

Adult↗
PubMed1982

Effect of lactate and H+ on structure and function of rat intestine.

Segments of rat ileum and colon were infused in vivo to test if 0.1 M lactate, 10(-4) M H+, or both altered mucosal structure and function. In the first series of experiments, lactate concentration was kept at 0.1 M while H+ was varied from 10(-4) to 10(-7) M. Lactate and 10(-4) M H+ in the colon, and lactate and 10(-5) M H+ in the ileum depressed net water transport and caused sloughing of superficial absorptive cells. In the second series of experiments, H+ concentration was kept at 10(-4) by using carboxymethylcellulose, rather than organic acids, to buffer the infusion mixture; the concentration of lactate was varied from 0 to 0.1 M. Mucosa remained normal after infusions of 10(-4) M H+ alone. Addition to the 10(-4) M H+ infusion of 0.1 M lactate in the colon or 0.075 M lactate in the ileum caused increased mucosal sloughing. Thus lactate plus H+ (or unionized lactic acid) alters colonic and ileal mucosa. Because such high concentrations of lactate and H+ are found in subjects malabsorbing carbohydrates, the present experiments support the contention that H+ and organic acids are etiological factors in some cases of chronic fermentative diarrhea.

Animals↗
PubMed1993

Presence of lactate dehydrogenase-containing vesicles in an intramembranous ossifying tissue: new-born mouse calvaria.

Lactate dehydrogenase-containing vesicles have been isolated from the extracellular matrix of the calvaria of new-born mice. The calvariae, intramembranous ossification tissue, were removed from 2-day-old mice, followed by the separation of the extracellular matrix vesicle fraction after collagenase digestion. Lactate dehydrogenase-containing vesicles with a density different from that of matrix vesicles were detected in the matrix vesicle fraction. Lactate dehydrogenase in these vesicles did not result from cell lysis and vesicle capture during the preparation of the matrix vesicle fraction. The isoenzyme pattern of lactate dehydrogenase in lactate dehydrogenase-containing vesicles was nearly identical to that of cytosolic lactate dehydrogenase of the cell fraction. Other cytosolic enzymes were not detected in lactate dehydrogenase-containing vesicles, suggesting the presence of a mechanism for specific uptake of cytosolic lactate dehydrogenase during the in vivo formation of the vesicles. This is the first report on the presence of lactate dehydrogenase-containing vesicles in the intramembranous ossification site.

Animals↗
PubMed1995

Effects of endurance training on lactate removal by oxidation and gluconeogenesis during exercise.

This report describes the effects of 9 weeks of endurance-training on the relative rates of lactate removal via oxidation and gluconeogenesis in humans. Before and after training, eight subjects performed incremental (60 W plus 40 W every 6 min) exercise tests, while 14C-lactate was infused into one forearm vein and arterialized venous blood was sampled from the other forearm. During the trial, the volume of expired 14CO2 and circulating 14C-lactate and 14C-glucose specific radioactivities were measured. Such measurements revealed that training increased the estimated oxidation of equivalent venous blood lactate concentrations [VLa] of greater than 1.6 mmol/l. These increases in lactate oxidation were more than would be predicted from the approximately 40% higher O2 uptake values at any [VLa] after training. At a [VLa] of 6 mmol/l, rates of lactate oxidation were increased by some 100% following training, from 105 +/- 12 to 208 +/- 33 micromol/min/kg (P < 0.01). Improvements in lactate oxidation after training reduced the estimated rates of lactate-to-glucose conversion from 40 +/- 3 to 9 +/- 2 micromol/min/kg at a [VLa] of 2.5 mmol/l (P < 0.01). Thus, unlike in rats, human endurance-training does not increase gluconeogenesis. In the final stages of progressive exercise after training, more than 80% of lactate was oxidised and accounted for approximately 45% of overall carbohydrate oxidation.

Adult↗
PubMed1983

The mechanism of Na+-L-lactate cotransport by brush border membrane vesicles from horse kidney: analysis of rapid equilibrium kinetics in absence of membrane potential.

Membrane transport of lactate was studied using vesicles prepared from horse kidney brush border. It is shown that the carrier-mediated transport of L-lactate is Na dependent and the D-lactate Na dependence seems weaker than the L stereoisomer. Augmented transport rate is observed following imposition of an artificial chemical Na+ gradient of electrical potential difference. The effect of Na+ chemical gradient on the L-lactate uptake was analyzed using membrane vesicles incubated with 50 mM KCl and valinomycin in order to short circuit any contribution of transmembrane electrical potential to the transport. Kinetics results and principally the absence of linearity between l/v (lactate) versus l/Na+ show that the L-lactate transport mechanism fit the properties of an ordered process with two Na+ ions cotransported with one L-lactate anion. The L-lactate and sodium affinities (Km) determined under Na+ chemical gradient were 1.05 and 48 mM for L-lactate and Na, respectively. The sodium activation was shown to be highly cooperative with a Hill number of 2 although no "sigmoidal" activation effect was observed.

Animals↗
PubMed1988

Lactation performance of the White Fulani cattle in southern Nigeria.

Data on the lactation performance of the White Fulani cattle in Southern Nigeria were analysed. The first lactation yield over a mean lactation period of 230.68 +/- 2.25 days averaged 810.89 +/- 32.11 kg, while overall lactation yields averaged 1018.28 +/- 18.10 kg over a mean lactation period of 249.67 +/- 3.28 days. The year of calving was a significant source of variation in both first and overall lactation yields but season of calving had no significant effect on lactation yield. Lactation yield and length were positively correlated. Heritabilities of 0.26 +/- 0.06 and 0.51 +/- 0.05 were obtained for lactation yield and length respectively from half-sib analysis while the repeatability estimates were 0.32 +/- 0.04 and 0.21 +/- 0.04 respectively. There was little difference in performance of the White Fulani cattle under the humid conditions of Southern Nigeria compared to the semi-arid conditions of the north.

Age Factors↗
PubMed1986

Intraerythrocyte and plasma lactate concentrations during exercise in humans.

The purpose of this study was to examine plasma and intraerythrocyte lactate concentrations during graded exercise in humans. Seven adult volunteers performed a maximum O2 uptake (VO2max) test on a cycle ergometer. Plasma and intraerythrocyte lactate concentrations (mmol . L-1 of plasma or cell water) were determined at rest, during exercise, and at 15-min post-exercise. The results show that plasma and intraerythrocyte lactate concentrations were not significantly different from each other at rest or moderate (less than or equal to 50% VO2max) exercise. However, the plasma concentrations were significantly increased over the intraerythrocyte levels at 75% and 100% VO2max. The plasma to red cell lactate gradient reached a mean (+/- SE) 1.7 +/- 0.4 mmol . L-1 of H2O at exhaustion, and was linearly (r = 0.84) related to the plasma lactate concentration during exercise. Interestingly, at 15-min post-exercise the direction of the lactate gradient was reversed, with the mean intraerythrocyte concentration now being significantly increased over that found in the plasma. These results suggest that the erythrocyte membrane provides a barrier to the flux of lactate between plasma and red cells during rapidly changing blood lactate levels. Furthermore, these data add to the growing body of research that indicates that lactate is not evenly distributed in the various water compartments of the body during non-steady state exercise.

Adult↗