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PubMed1995

Lactate and pyruvate isotopic enrichments in plasma and tissues of postabsorptive and starved rats.

It has been proposed that plasma pyruvate isotopic enrichment (IE) during infusion of labeled lactate could be used to estimate the intracellular IE of lactate and pyruvate and thus to calculate their turnover rate. We determined the relations of plasma and tissue IE of lactate and pyruvate in anesthetized rats infused with [3-13C]lactate in an artery and sampled from a vein (A-V mode) or infused in a vein and sampled from an artery (V-A mode). In both groups of rats, the ratio of tissue to plasma lactate IE was < 1 with large differences between tissues: the highest ratio was observed in heart and the lowest in soleus. With the exception of liver, this ratio was higher in the A-V than in the V-A mode. Pyruvate IE was lower than lactate IE in tissues, with a few exceptions, and in plasma. This ratio of pyruvate to lactate IE was approximately 0.70 in plasma in A-V and V-A modes. Moreover pyruvate IE was also always higher in plasma than in tissues. This seemingly surprising result could be explained by the production of labeled pyruvate from labeled lactate inside the circulation by erythrocytes, because we observed a rapid isotopic equilibrium between lactate and pyruvate in blood "in vitro." Apparent lactate turnover was higher in the A-V than in the V-A mode when it was calculated using lactate as well as pyruvate IE. Therefore plasma pyruvate IE cannot be used in rats to estimate tissue IE and did not reconcile turnover rates measured using the A-V or V-A mode.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Lactate stimulates progesterone secretion via an increase in cAMP production in exercised female rats.

The effect of exercise on the production of ovarian progesterone was examined in female rats. During in vivo experiments, diestrous rats were catheterized via the right jugular vein (RJV), and blood samples were collected before and after 10, 15, 30, and 60 min of swimming. In addition, blood samples were collected from the RJV before and 2, 5, 10, 15, 30, 60, and 120 min after 10 min of infusion of lactate (13 mg.kg-1.min-1) through the left femoral vein. To explore if lactate modulates progesterone secretion by acting directly on rat ovary or on anterior pituitary gland (AP), an in vitro experiment that mimicked the in vivo condition was performed. The ovarian tissue was challenged with lactate (0.01-10 mM) or porcine follicle-stimulating hormone (1 microgram/ml) and 3-isobutyl-1-methylxanthine (1 mM) for 60 min, and the AP was challenged with lactate ranging from 0.1 to 10 mM or 10 nM gonadotropin-releasing hormone for 30 min. The postexercise levels of plasma glucose, lactate, and progesterone at 10, 15, and 30 min were significantly higher than the corresponding basal levels. Plasma luteinizing hormone (LH) did not change after exercise. An elevation of plasma lactate and progesterone was found at 15 and 30 min subsequent to 10 min of infusion of lactate. Lactate ranging from 0.01 to 10 mM significantly increased ovarian adenosine 3',5'-cyclic monophosphate (cAMP) and progesterone production in a dose-dependent manner. LH concentration in plasma was not changed subsequent to lactate infusion. LH level in media samples was not altered after incubation of AP with lactate. These results suggest that the increase of plasma progesterone level in rats during exercise is independent of LH secretion and at least in part is due directly to a stimulatory effect of lactate on the production of ovarian cAMP.

1-Methyl-3-isobutylxanthine↗
PubMed1975

Uptake of lactate by dog skeletal muscle in vivo and the effect of free fatty acids.

These experiments were designed to determine: 1) if lactate can be extracted from the arterial blood and utilized by resting skeletal muscle of the dog, and 2) if lactate uptake or production by skeletal muscle is influenced by the level of circulating free fatty acids. Skeletal muscle arteriovenous differences in lactate were measured at several arterial lactate and free fatty acid concentrations. With sodium pentobarbital anesthesia and a low concentration of free fatty acids, arterial lactate concentrations of 1-2 mM were associated with extraction of lactate; however, when circulating free fatty acids were elevated (greater than 1 mM), no extraction of lactate occurred at these lactate concentrations. The relationship between arterial free fatty acids and uptake or release of lactate demonstrated in these in vivo studies suggest that the inhibition of free fatty acid release from adipose tissue that occurs when the arterial lactate concentration increases may function facilitate the metabolism of lactate by skeletal muscle.

Albumins↗
PubMed1986

Disposal of blood [1-13C]lactate in humans during rest and exercise.

Lactate irreversible disposal (RiLa) and oxidation (RoxLa) rates were studied in six male subjects during rest (Re), easy exercise [EE, 140 min of cycling at 50% of maximum O2 consumption (VO2max)] and hard exercise (HE, 65 min at 75% VO2max). Twenty minutes into each condition, subjects received a Na+-L(+)-[1-13C]lactate intravenous bolus injection. Blood was sampled intermittently from the contralateral arm for metabolite levels, acid-base status, and enrichment of 13C in lactate. Expired air was monitored continuously for determination of respiratory parameters, and aliquots were collected for determination of 13C enrichment in CO2. Steady-rate values for O2 consumption (VO2) were 0.33 +/- 0.01, 2.11 +/- 0.03, and 3.10 +/- 0.03 l/min for Re, EE, and HE, respectively. Corresponding values of blood lactate levels were 0.84 +/- 0.01, 1.33 +/- 0.05, and 4.75 +/- 0.28 mM in the three conditions. Blood lactate disposal rates were significantly correlated to VO2 (r = 0.78), averaging 123.4 +/- 20.7, 245.5 +/- 40.3, and 316.2 +/- 53.7 mg X kg-1 X h-1 during Re, EE, and HE, respectively. Lactate oxidation rate was also linearly related to VO2 (r = 0.81), and the percentage of RiLa oxidized increased from 49.3% at rest to 87.0% during exercise. A curvilinear relationship was found between RiLa and blood lactate concentration. It was concluded that, in humans, 1) lactate disposal (turnover) rate is directly related to the metabolic rate, 2) oxidation is the major fate of lactate removal during exercise, and 3) blood lactate concentration is not an accurate indicator of lactate disposal and oxidation.

Adult↗
PubMed1987

Lactate as substrate for glycogen resynthesis after exercise.

Muscle glycogen levels in the perfused rat hemicorpus preparation were reduced two-thirds by electrical stimulation plus exposure to epinephrine (10(-7) M) for 30 min. During the contraction period muscle lactate concentrations increased from a control level of 3.6 +/- 0.6 to a final value of 24.1 +/- 1.6 mumol/g muscle. To determine whether the lactate that had accumulated in muscle during contraction could be used to resynthesize glycogen, glycogen levels were determined after 1-3 h of recovery from the contraction period during which time the perfusion medium (flow-through system) contained low (1.3 mmol/l) or high (10.5 or 18 mmol/l) lactate concentrations but no glucose. With the low perfusate lactate concentration, muscle lactate levels declined to 7.2 +/- 0.8 mumol/g muscle by 3 h after the contraction period and muscle glycogen levels did not increase (1.28 +/- 0.07 at 3 h vs. 1.35 +/- 0.09 mg glucosyl U/g at end of exercise). Lactate disappearance from muscle was accounted for entirely by output into the venous effluent. With the high perfusate lactate concentrations, muscle lactate levels remained high (13.7 +/- 1.7 and 19.3 +/- 2.0 mumol/g) and glycogen levels increased by 1.11 and 0.86 mg glucosyl U/g, respectively, after 1 h of recovery from exercise. No more glycogen was synthesized when the recovery period was extended. Therefore, it appears that limited resynthesis of glycogen from lactate can occur after the contraction period but only when arterial lactate concentrations are high; otherwise the lactate that builds up in muscle during contraction will diffuse into the bloodstream.

Animals↗
PubMed1993

Training does not affect zero-trans lactate transport across mixed rat skeletal muscle sarcolemmal vesicles.

Hindlimb muscle sarcolemmal vesicles were purified from three age-matched groups of female Sprague-Dawley rats: sedentary control (CON; n = 10), sprint trained (ST; n = 8), and endurance trained (ET; n = 9). Membrane isolations from the three groups were not significantly different in protein yield or purification index. Blood lactate concentration was determined in resting CON rats and running ET and ST rats during the final week. Both the ST and ET groups were significantly higher in citrate synthase (vs. CON) in the soleus and mid-vastus lateralis. The time course of 1 mM L-(+)-lactate uptake in vesicles from the three groups showed no significant difference at any of the five time points tested under zero-trans conditions. Saturation kinetics were examined at nine lactate concentrations, and Lineweaver-Burk plots revealed no difference between groups in apparent Michaelis-Menten constant or maximal transport velocity. Vesicles from CON and ET rats were used to investigate cis inhibition of 0.1 mM L-(+)-lactate transport by four unlabeled monocarboxylates: L-(+)-lactate, D-(-)-lactate, pyruvate, and alpha-cyanohydroxycinnamate at 0.1, 1.0, and 10 mM. Under pH gradient-stimulated L-(+)-lactate transport conditions, cis inhibition was affected by neither D-(-)-lactate nor endurance training. We conclude that the lactate transporter has distinct cis-inhibitory specificity, is stereospecific, and is stimulated when confronted with parallel lactate and proton gradients but that spring and endurance training do not alter lactate transport rate or capacity under these conditions.

Acidosis, Lactic↗
PubMed1998

Evidence supporting the existence of an activity-dependent astrocyte-neuron lactate shuttle.

Mounting evidence from in vitro experiments indicates that lactate is an efficient energy substrate for neurons and that it may significantly contribute to maintain synaptic transmission, particularly during periods of intense activity. Since lactate does not cross the blood-brain barrier easily, blood-borne lactate cannot be a significant source. In vitro studies by several laboratories indicate that astrocytes release large amounts of lactate. In 1994, we proposed a mechanism whereby lactate could be produced by astrocytes in an activity-dependent, glutamate-mediated manner. Over the last 2 years we have obtained further evidence supporting the notion that a transfer of lactate from astrocytes to neurons might indeed take place. In this article, we first review data showing the presence of mRNA encoding for two monocarboxylate transporters, MCT1 and MCT2, in the adult mouse brain. Second, by using monoclonal antibodies selectively directed against the two distinct lactate dehydrogenase isoforms, LDH1 and LDH5, a specific cellular distribution between neurons and astrocytes is revealed which suggests that a population of astrocytes is a lactate 'source' while neurons may be a lactate 'sink'. Third, we provide biochemical evidence that lactate is interchangeable with glucose to support oxidative metabolism in cortical neurons. This set of data is consistent with the existence of an activity-dependent astrocyte-neuron lactate shuttle for the supply of energy substrates to neurons.

Animals↗
PubMed1989

Lactate influx and efflux in the 'Streptococcus mutants group' and Streptococcus sanguis.

Lactate influx was measured in Streptococcus sanguis and in several strains of Streptococcus mutans by comparing the intra- and extracellular distribution of (14C)-lactate. Lactate efflux was followed enzymatically against rising external lactate concentration. The glucose concentration was monitored in the same way. With S. sanguis OMZ 9, lactate was transported into the cells when a high external lactate concentration and a pH gradient were established. The transport rate was approximately 1,000 nmol lactate per minute and milligram protein. No lactate influx could be measured with four strains of the 'S. mutans group' (OMZ 51, 634, T3/13 and NCTC 10449). Metabolizing cells of S. mutans NCTC 10449 were able to transport lactate even against an external lactate concentration of 92 mmol/l at pH = 7. The transport rates ranged from 1,200 to 750 nmol lactate/min mg protein decreasing with increasing external lactate concentration. While an external pH = 9 had little influence on transport, transport rates decreased to 440 nmol/min mg protein at pH = 5.

Biological Transport↗
PubMed1994

Lactate transport in mammalian ventricle. General properties and relation to K+ fluxes.

Net cellular L-lactate efflux associated with accelerated anaerobic glycolysis has been implicated as a potential cause of the marked cellular K+ loss contributing to lethal cardiac arrhythmias in ischemic heart and to impaired function of fatigued skeletal muscle. To examine the mechanisms of transsarcolemmal L-lactate movement in the heart, isolated guinea pig ventricular myocytes were loaded with the fluorescent H+ or K+ indicators, carboxy SNARF-1 or PBFI, respectively, under whole-cell patch-clamp conditions. With H+ as the only permeable monovalent cation, a rapid increase in extracellular L-lactate concentration ([L-]o) from 0 to 30 mmol/L at constant pHo (7.35) caused an intracellular acidification averaging 0.18 +/- 0.02 pH units in 60 seconds (n = 7), reflecting L-lactate influx in association with H+ influx (or OH- efflux). Under voltage-clamp conditions, no significant electrogenic current was associated with H(+)-coupled L-lactate influx, and membrane potential (-75 to +75 mV) had no effect on the degree of acidification produced by 30 mmol/L [L-]o, indicating that L-lactate influx was predominantly nonelectrogenic. Acidification in response to increased [L-]o was saturable (Km, approximately 5 mmol/L), partially stereospecific for L-lactate over D-lactate, and inhibited by 55 +/- 7% and 82 +/- 7% by the monocarboxylate carrier inhibitors alpha-cyano-4-hydroxycinnamate and mersalyl acid, respectively, consistent with a carrier-mediated transport mechanism. Extracellular K+ inhibited H(+)-coupled L-lactate influx by 36 +/- 2%, suggesting that K+ either inhibited or substituted for H+ in cotransport with L-lactate. However, in myocytes loaded with PBFI, no significant increase in [K+]i was detected during exposure to 30 mmol/L [L-]o, suggesting that only a minor component, if any, of L-lactate influx was cotransported or codiffused with K+.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2003

Effect of intravenous administration of sodium-lactate on retinal blood flow in healthy subjects.

PURPOSE: The present study was designed to investigate the effect of intravenously administered sodium lactate on ocular blood flow. METHODS: Twelve healthy male volunteers received either sodium lactate (0.6 mol/L) or physiologic saline solution in a randomized, double-masked, two-way crossover study. Sodium lactate or placebo were administered at an infusion speed of 500 and 1000 mL/h for 30 minutes each. Blood flow measurements were performed in the last 10 minutes of the infusion periods. Retinal blood flow was calculated based on the measurement of maximum erythrocyte velocity, assessed with bidirectional laser Doppler velocimetry, and retinal vessel diameter obtained with a retinal vessel analyzer. Choroidal blood flow was assessed with laser Doppler flowmetry and laser interferometric measurement of fundus pulsation amplitude. RESULTS: Administration of lactate increased blood lactate concentration from 1.3 +/- 0.4 to 3.9 +/- 0.7 mmol/L (P < 0.001) and to 7.1 +/- 1.4 mmol/L (P < 0.001) at infusion speeds of 500 and 1000 mL/h, respectively. At these blood lactate concentrations, retinal blood flow increased by 15% +/- 20% and by 24% +/- 37% (ANOVA, P = 0.01). Fundus pulsation amplitude increased by 3% +/- 6% and 10% +/- 5% (ANOVA, P = 0.04) at the two plasma lactate concentrations. Subfoveal choroidal blood flow measured with laser Doppler flowmetry tended to increase by 10% +/- 15% and 13% +/- 20% (ANOVA, P = 0.19), but this effect was not significant. Infusion of sodium lactate induced alkalosis in arterial blood taken from the earlobe (7.41 +/- 0.03 at baseline; 7.50 +/- 0.03 during lactate infusion; P = 0.001). CONCLUSIONS: The data indicate that intravenously administered sodium lactate increases retinal blood flow. Whether this is related to a cytosolic redox impairment or to other hitherto unidentified mechanism remains to be clarified. Further studies are needed to determine whether lactate plays a role in regulation of choroidal blood flow.

Alkalosis↗
PubMed1982

Blood-brain barrier permeability to lactic acid in the newborn dog: lactate as a cerebral metabolic fuel.

The arteriovenous difference (A-V) method was utilized to assess the permeability of the blood-brain barrier to lactic acid in paralyzed and artificially ventilated newborn dogs. A femoral artery and the sagittal sinus were cannulated to sample arterial and cerebral venous blood simultaneously for measurements of glucose and lactate during normoglycemia, normoglycemia and hyperlactatemia insulin-induced hypoglycemia, or hypoglycemia and hyperlactatemia. During normoglycemia, arterial lactate concentrations remained less than 2 mmoles/liter for up to 2 h; mean A-V lactate was essentially zero. Arterial lactate increased up to 8 mmoles/liter during intravenous infusion of neutralized 10 mM L-lactic acid. During hyperlactatemia, the A-V lactate was directly proportional to the arterial concentration of the metabolite, a finding which is consistent with transport into brain either by simple diffusion or via a carrier with saturability greater than 8 simple diffusion or via a carrier with saturability greater than 8 mmoles/liter. During hypoglycemia (mean arterial glucose=27 mg/dl), A-V glucose was reduced by 71% with a significant increase in A-V lactate at an arterial lactate level of 1.3 mmoles/liter. Hyperlactatemia combined with hypoglycemia resulted in A-V lactate which was 2-3 fold greater than during normoglycemia at similar arterial lactate concentrations. Brain/blood lactate ratios declined by 83% during hypoglycemia compared with normoglycemic ratios, indicating that, once in brain, lactic acid was actively consumed for oxidative processes. These experimental observations may have clinical relevance in newborn human infants when concentrations of lactate in blood often approach or even exceed those of glucose.

Animals↗
PubMed1975

The role of LH in the luteotrophic process of lactating rats.

The role of LH in the leuteotrophic process was examined by evaluating progesterone secretion in pregnant, lactating, and pregnant lactating rats, and the response of these rats to antisera against LH (LHAS) was observed. Ovarian venous progesterone concentration in lactating rats was elevated as litter size increased. Treatment with LHAS on day 8 postpartum of rats nursing 12 pups significantly decreased peripheral progesterone levels within 24 hr. Treatment with LHAS on days 8 and 9 of pregnancy terminated gestation in all normal pregnant animals by in similarly treated pregnant lactating rats gestation was maintained until day 14 in 4 of 10 rats. If the litter was removed from pregnant lactating dams at the time of initiation of LHAS treatment, pregnancy was interrupted in all 12 animals. Ovarian venous progesterone concentration was reduced by greater than 90% 24 hr after LHAS treatment on day 8 of normal pregnant rats and 20alpha-OH-P increased such that the concentration of total progestins remained constant. Ovarian venous progesterone concentration 24 hr after LHAS treatment of pregnant lactating rats was reduced by 50% in animals receiving daily estradiol treatment by LHAS had little effect in pregnant lactating animals which received a single injection of estradiol on day 4 postpartum. The level of 20alpha-OH-P in pregnant lactating animals was not affected by LHAS. The results of these studies demonstrate that in lactating rats nursing a large litter (12 pups) LH is part of the luteotrophic complex, and the data obtained from studies in pregnant lactating rats suggest that when pregnancy and lactation are superimposed the role of LH in the luteotrophic process on day 8 of gestation is diminished.

Animals↗
PubMed1993

Lactation alters neuropeptide-Y and proopiomelanocortin gene expression in the arcuate nucleus of the rat.

To identify possible factors associated with lactation that may be involved in the suppression of GnRH neuronal function, we have examined whether lactation induces changes in arcuate nucleus neuronal function, focusing on changes in neuropeptide-Y (NPY) and POMC neuronal activity. Animals were studied during diestrous day 1 of the estrous cycle or during day 10 postpartum. Lactating animals had their litters adjusted to eight pups on day 2 postpartum. Brain tissue was removed to measure NPY peptide content in the median eminence (ME) or the ME-arcuate nucleus (ME-ARC) and to quantify NPY or POMC mRNA by in situ hybridization, using 35S-labeled antisense riboprobes. The NPY peptide content was significantly increased in the ME (1.8-fold) and ME-ARC (1.5-fold) during lactation compared to those on diestrus. The NPY mRNA content throughout the ARC did not differ between diestrous and lactating animals. However, if specific subdivisions of the ARC were examined, a significant increase (1.8-fold) in NPY mRNA in the ARC-C region of the ARC (at the plane of the dorsal medial hypothalamic nucleus) was observed during lactation. Dorsal to the ARC in this same plane, there was also an induction of NPY expression in cells lateral to the dorsal medial hypothalamic nucleus. The increases in NPY mRNA in the ARC-C region of the arcuate nucleus persisted for at least 24 h after removal of the suckling stimulus. The other subdivisions of the ARC did not show any differences in NPY mRNA between diestrus and lactation. The POMC mRNA content was decreased by 20-30% during lactation compared with that on diestrus. The effects of lactation to decrease POMC mRNA content were not specific to any subdivision of the ARC, but were observed throughout the entire ARC. Given that lactation is an estrogen-deficient state, the increase in NPY neuronal activity, as indicated by increased gene expression in the caudal portion of the ARC and increased content in the ME, could play an inhibitory role in the regulation of GnRH secretion. However, the decrease in POMC neuronal activity, as suggested by the decrease in gene expression throughout the ARC, would not appear to be involved in the suppression of GnRH neuronal activity. These changes in ARC neuronal function could be related to hormonal changes or metabolic signals regulating food intake during lactation.

Animals↗
PubMed1997

Regulation of growth hormone (GH) gene expression and secretion during pregnancy and lactation in the rat: role of insulin-like growth factor-I, somatostatin, and GH-releasing hormone.

GH appears to play an important metabolic role during late pregnancy and in lactation maintenance. In this study, pregnant (days 8, 15, and 20 of gestation) and postpartum (days 3 and 8 postpartum, including lactating and nonlactating dams) Wistar rats were used to investigate pituitary GH gene expression and hormone secretion, and the potential alterations of the major signals regulating GH secretion and action [somatostatin (SS) and GH-releasing hormone (GHRH), GH receptor (GH-R), and insulin-like growth factor-I (IGF-I)]. GH and SS messenger RNA (mRNA) were quantitated by Northern blot, and both IGF-I and GH-R mRNA were analyzed by the ribonuclease protection assay technique. Pituitary IR-GH content and GH mRNA increased at midpregnancy. IR-GH content was decreased in lactating rats. Plasma GH levels progressively increased during pregnancy, whereas no significant alterations were shown during lactation. Elevated GH levels persisted during lactation. Levels at this time were higher in nonsuckling compared with suckling dams. Liver GH-R mRNA progressively decreased during pregnancy, but it remained unchanged during lactation. Plasma IGF-I and liver IR-IGF-I constantly decreased during pregnancy, and no significant modifications were seen either in suckling or in nonsuckling animals. IGF-I mRNA accumulation in the liver decreased during pregnancy. After delivery, a progressive decrease of liver IGF-I mRNA occurred. At the hypothalamic level, a progressive increase in the IR-SS content was found during pregnancy, with no SS mRNA modification. After delivery, a higher hypothalamic IR-SS content was found in lactating than in nonlactating rats, with no changes in SS mRNA levels. Hypothalamic IR-IGF-I also showed a progressive increase during pregnancy with no significant alterations during lactation. Hypothalamic IR-GHRH presented a nonsignificant mild increase during pregnancy with no modifications during lactation. In the pituitary, IR-IGF-I content progressively increased during gestation, reaching its highest concentration at day 20. During lactation, pituitary IGF-I did not change. In summary, our data show that the mechanisms of the increase in plasma GH levels occurring during pregnancy include an increase in GH gene expression in the pituitary, a decrease in SS secretion from the hypothalamus, an increase in IR-IGF-I content in the hypothalamus and in the pituitary, and a significant decrease in circulating IGF-I. Plasma and liver IR-IGF-I and IGF-I mRNA in the liver decreased throughout gestation due to a lower GH-R gene expression in the liver. This state of GH resistance with a higher GH/IGF-I ratio could be important in providing supplementary nutrients to the fetus. During lactation, GH and its regulatory machinery did not show important modifications.

Animals↗
PubMed1999

Suppression of leptin during lactation: contribution of the suckling stimulus versus milk production.

Lactation in the rat is characterized by the suppression of pulsatile LH secretion, a large increase in food intake, and changes in energy balance due to the metabolic drain of milk production. The change in energy balance may be a major component in altering reproductive function. A number of factors may contribute to changing energy balance of a lactating animal; one is leptin, the product of adipose tissue, which is known to act partly as a satiety factor to decrease food intake. The aims of the present study were to determine whether there are changes in leptin levels during lactation, a state of high energy demand, and during periods of acute suckling in the presence or absence of changes in energy demand. Our goals were to determine whether lactation and the suckling stimulus influenced serum leptin levels and whether there was a potential role for leptin in the suppression of LH secretion during lactation. The first experiment was performed during diestrus of the estrous cycle, and chronic lactation, (day 9 post partum) in animals suckling 8 pups. The results showed that leptin levels were significantly decreased in both ovarian intact or ovariectomized lactators; this decrease parallels the suppression of pulsatile LH secretion. Serum insulin levels were not altered in the lactating animals. The second experiment was performed in ovariectomized lactators whose 8 pup litters were removed for 48 h, starting on day 9. On day 11, mothers received no pups or pups that were either nonfostered (resulting in no milk production) or fostered (resulting in milk production). The pups were allowed to suckle for 24 h. Following 24 h of acute suckling, serum leptin, and insulin levels correlated with the energy drain on the mother. The levels of leptin were normal and of insulin were elevated in mothers producing no milk. Conversely, leptin levels were suppressed and insulin levels normal in mothers producing milk. The third experiment used the same groups as described for the second experiment except that serial blood samples were collected for measurement of pulsatile LH secretion following 24 h of acute suckling. The results showed that regardless of whether leptin levels remained normal or were suppressed in response to acute suckling, pulsatile LH secretion was significantly inhibited compared with the nonsuckled control animals. In summary, these data suggest that the metabolic drain of milk production, and not the suckling stimulus itself, is the most likely factor responsible for the suppression of leptin secretion during lactation. Furthermore, although the decreased levels of leptin may be causally related to the inhibition of pulsatile LH secretion during chronic lactation, changes in leptin are not a prerequisite for the suppression of LH secretion in response to suckling.

Animals↗
PubMed1985

The concentration of hypoxanthine and lactate in the blood of healthy and hypoxic newborns.

This work examines the correlation between the concentration of hypoxanthine and lactate, the clinical course, and the parameters of the acid-base metabolism in newborns. In order to obtain normal values in mature, healthy newborns (Group A) 136 determinations of hypoxanthine and 126 determinations of lactate in blood were performed in the first five postnatal days. In well prematures (Group B) hypoxanthine was determined 18 times and lactate 16 times. In newborns requiring oxygen therapy including ventilator support (Group C) hypoxanthine and lactate were determined 36 and 31 times respectively. Hypoxanthine levels in the blood of mature healthy newborns decreased with increasing age. A similar course is known for lactate levels. In the group of well prematures (Group B), hypoxanthine and lactate levels have an age dependent course similar to that in group A. Correlations between hypoxanthine and lactate concentrations were observed in all three groups but were not noted to be as well defined as has been seen experimentally (e.g., by SAUGSTAD) and thus confirm the clinical results of other authors. Among the newborns requiring oxygen therapy (Group C) 7 of 36 hypoxanthine values were more than two standard deviations above those in the normal group. For lactate group C infants were in 12 of 31 cases above the two standard deviation range. The hypoxanthine and lactate concentrations of group C newborns were correlated with clinical and biochemical indicators of hypoxia. Infants with unequivocal signs of hypoxia showed elevated as well as normal hypoxanthine and lactate levels. Conversely, infants without clinical, pathological or biochemical hypoxia indicators showed in some cases elevated hypoxanthine and lactate values.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMedDate not supplied

Prognostic value of plasma L-lactate concentration measured cow-side with a portable clinical analyzer in Holstein dairy cattle with abomasal disorders.

BACKGROUND: L-Lactate has been used as a prognostic indicator for ill humans and animals. A portable analyzer that measures L-lactate could help veterinarians decide to proceed with correction of a displaced abomasum. HYPOTHESES: The likelihood of a dairy cow with a displaced abomasum remaining in the herd can be predicted by lactate concentration and other variables. ANIMALS: Thirty-four healthy early-lactation dairy cows, and 131 cows with abomasal displacements (DA) presented to Cornell University, Ithaca, NY. METHODS: Plasma L-lactate was measured using a commercial analyzer (i-STAT). A cow had a positive outcome (PO) if she remained in the herd 30 days after surgical correction of the displaced abomasum and a negative outcome (NO) if she was culled or died in that time. A multivariable model with physical examination and clinicopathologic variables for predicting NO for cows with right-sided abomasal displacements was constructed. RESULTS: The median plasma L-lactate was 0.54 mM/L (interquartile range, 0.42-0.74) in healthy lactating Holstein cows. In cows with right-sided displaced abomasa, median plasma L-lactate concentrations were higher in cows with NO (5.88 mM/L) versus PO (3.23 mM/L) (P = .002). In a multivariable model, which identified chloride, heart rate, and L-lactate as the best fitting variables for cows with right-sided displacements, the probability of NO increased as L-lactate increased. CONCLUSIONS AND CLINICAL IMPORTANCE: Plasma L-lactate concentration might be a useful predictor of productive outcomes in cows with right-sided abomasal disorders.

Abomasum↗
PubMedDate not supplied

Blood lactate. Implications for training and sports performance.

The blood lactate response to exercise has interested physiologists for over fifty years, but has more recently become as routine a variable to measure in many exercise laboratories as is heart rate. This rising popularity is probably due to: the ease of sampling and improved accuracy afforded by recently developed micro-assay methods and/or automated lactate analysers; and the predictive and evaluative power associated with the lactate response to exercise. Several studies suggest that the strong relationship between exercise performance and lactate-related variables can be attributed to a reflection by lactate during exercise of not only the functional capacity of the central circulatory apparati to transport oxygen to exercising muscles, but also the peripheral capacity of the musculature to utilise this oxygen. For example, several studies contrast the relationship between VO2max and endurance running performance with that between a lactate variable and the same running performance. In every study, the lactate variable is more highly correlated with performance. Similarly, prescribing training intensity as a function of the lactate concentration elicited by the training may prove to be a means of obtaining a more homogeneous adaptation to training in a group of athletes or subjects than is obtained by setting intensity as a function of maximal heart rate or % VO2max. A review of the recent literature shows that the lactate response to supramaximal exercise is a sensitive indicator of adaptation to 'sprint training' and is correlated with supramaximal exercise performance. This review also describes the possible applications of lactate measurements to enhance the rate of recovery from high intensity exercise. Although the lactate response to exercise is reproducible under standardised conditions it can be influenced by the site of blood sampling, ambient temperature, changes in the body's acid-base balance prior to exercise, prior exercise, dietary manipulations, or pharmacological interpretation.

Adolescent↗