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PubMed2006

Effects of length of dry period on yields of milk fat and protein, fertility and milk somatic cell score in the subsequent lactation of dairy cows.

The objective was to utilize data from modern US dairy cattle to determine the effect of days dry on fat and protein yield, fat and protein percentages, days open, and somatic cell score in the subsequent lactation. Field data collected through the dairy herd improvement association from January 1997 to December 2003 and extracted from the Animal Improvement Programs Laboratory national database were used for analysis. Actual lactation records calculated from test-day yields using the test-interval method were used in this study. The model for analyses included herd-year of calving, year-state-month of calving, previous lactation record, age at calving, and days dry as a categorical variable. Fat and protein yield was maximized in the subsequent lactation with a 60-d dry period. Dry periods of 20 d or less resulted in substantial losses in fat and protein yield in the subsequent lactation. In contrast to yields, a short dry period was beneficial for fat and protein percentages. Short dry periods also resulted in fewer days open in the subsequent lactation; however, this was entirely due to the lower milk yield associated with shortened dry period. When adjusted for milk yield, short dry periods actually resulted in poorer fertility in the subsequent lactation. Long days dry improved somatic cell score in the subsequent lactation. Herds with mastitis problems should be cautious in shortening days dry because short dry periods led to higher cell scores in the subsequent lactation compared with 60-d dry.

Animals↗

PubMed2000

Effect of environmental factors and of the proportion of Holstein blood on the milk yield and lactation length of crossbred dairy cattle on smallholder farms in north-east Tanzania.

A study was carried out on the lactation performance of crossbred dairy cattle in a smallholder farming system in north-east Tanzania. Data were collected from the records for 6 years and the factors considered were district, proportion of Holsteins, season of calving, year of calving and herd size. The data were considered separately for animals with a single lactation record. The least-square means for first lactation length and yield were 331 days (SD 77.0) and 2332 L (SD 283.0), respectively, while for cows with data on more than one lactation record the yield was 2477 L (SD 840.1) in 324 days (SD 74.0). First lactation yield was significantly affected by year of calving. For repeated records, the lactation yield was significantly affected by district, proportion of Holsteins and herd size, while lactation length was significantly affected by district and herd size. The calculated repeatabilities for lactation yield and length were 0.27 and 0.12, respectively. For the pooled data, the correlation between lactation length and yield gave r = 0.569 (p < 0.0001).

Animals↗

PubMed1999

Hormonal and dietary regulation of changes in bone density during lactation and after weaning in women.

Lactating women secrete approximately 250 mg of calcium in breast milk each day. Some of the calcium used for milk production comes from bone as women experience a transient 3-9% decrease in bone density during lactation. This loss appears to be obligatory and under hormonal regulation as lactation-induced bone loss occurs even when calcium intake is high. Bone mineral is recovered after lactation ceases or menses resume. Recovery of bone mineral appears to be complete even when pregnancies and lactations are closely spaced, and lactation does not increase future risk of osteoporotic fracture. Current data point to estrogen and parathyroid hormone-related peptide as regulating bone mobilization during lactation. The typical calcium regulatory hormones, parathyroid hormone, calcitriol and calcitonin, do not appear to stimulate bone resorption during lactation. Restoration of ovarian hormone production and decreased production of PTHrP2 are likely to result in the recovery of bone mineral after lactation has ceased.

Amenorrhea↗

PubMed2005

Comparison of immunosuppression in dry and lactating Awassi ewes due to water deprivation stress.

In seminomadic farming practice, dry and lactating ewes are exposed to different degrees of water deprivation, leading to stress followed by various disease outbreaks. This study compares quantitatively the immunosuppression to Salmonella Enteritidis (SE) fimbriae (14 and 21 kDa) and other major polypeptides (28.9, 37.7, 42.9, 68.0, 92.6 and 96.8 kDa) in water-deprived dry and lactating ewes. Sixteen dry and lactating multiparous Awassi ewes were divided into four treatment groups (A, A', B and B'). Ewes in groups A and B were lactating, whereas ewes in groups A' and B' were dry. All ewes were administered a killed SE vaccine, subcutaneously in the neck, at the initiation of the experiment. The water availability for ewes in groups B (lactating) and B' (dry) was ad libitum, while that for ewes in groups A (lactating) and A' (dry) was once every 4 days. A serum sample was collected from the jugular vein of each ewe at zero time (initiation of the experiment, when SE bacterin was delivered) and at 2, 9, 12, 15 and 18 days post SE vaccination. The percentage reduction in the level of humoral antibody response to polypeptides of > or = 21 kDa was more apparent in water-deprived lactating ewes of group A between 9 and 18 days post initiation of thirst. In this period, immunosuppression to polypeptides > or = 21 kDa was present in 14 out of 16 observations in group A (water-deprived lactating), with significant immunosuppression in 9 observations in relation to the respective control (p<0.05), while it was present in only 4 out of 16 observations in group A' (water-deprived dry), with significant immunosuppression in 2 observations (p <0.05). In conclusion, immunosuppression to polypeptides of > or =21 kDa is more significant in lactating water-deprived ewes in the period 9-18 days post initiation of thirst, a result that will influence our future sheep welfare awareness programmes targeting an elimination of the practice of water deprivation in seminomadic sheep farming.

Animals↗

PubMed1987

Effect of probenecid on cerebral and cisternal cerebrospinal fluid lactate content.

In this study, the cisternal CSF contents of lactate and glucose were sequentially measured in free-moving rats that had been administered probenecid, 200 mg/kg-1, drug diluent, or no injections. In animals receiving either no injections or injections of drug diluent, CSF lactate and glucose were constant over a 6-h period (93-106% of control), whereas rats receiving probenecid showed increased lactate at 1 and 2 h (170 and 125% control, respectively) and increased glucose at 1, 2, and 3 h (169, 141 and 129% control, respectively). Cerebral cortex content of energy metabolites and lactate and blood lactate levels were statistically unaltered at 0.5-6 h exposure to probenecid, whereas cerebral and blood glucose contents were increased after 1 and 2 h exposure to probenecid. Rats exposed to 5% O2 and probenecid for 0.5 h showed a statistically higher CSF lactate at 0.5 and 1.5 h reoxygenation (169 and 168% control, respectively). A similar effect was also seen in rats exposed to 5% O2 and the 5-hydroxyindoleacetic acid (5-HIAA) transport inhibitor Na divalproate. The results suggested that the increase in CSF glucose was secondary to a probenecid-induced elevation of blood glucose, whereas the increase in CSF lactate seemed to be secondary to a reduced rate of efflux of lactate from the CSF. It is suggested that it may be possible to increase the CSF lactate content by mechanisms that are independent of direct effects on the processes of cerebral energy metabolism.

Animals↗

PubMed1994

Evaluation of lactate production and clearance kinetics by 1H NMR in a model of brief repetitive cerebral ischemia.

Pilots of high-performance aircraft are subject to repeated transient cerebral ischemia during high-gravitational stress maneuvers. Previously we have demonstrated that repeated episodes of transient cerebral ischemia and reflow are cumulative and lactate accumulations appear to be exponential. To evaluate the metabolic events determining the kinetics of lactate accumulation, and therefore the rates of substrate utilization, we have used in vivo 1H nuclear magnetic resonance with a 5-s time resolution to measure lactate production and clearance. The individual rates for each animal were then used to predict the accumulation of lactate in the same animal during 30 episodes of ischemia and reflow. Lactate accumulation was modeled as the balance between a zero-order production process during the ischemic period and a first-order clearance process. The predicted lactate accumulation showed excellent agreement with the observed time course, validating the predictive power of the simple model used. The highly reproducible nature of this model and its accuracy in predicting lactate accumulation should enable more accurate studies of the deleterious effects of lactate accumulation in cerebral ischemia by providing a highly reproducible means for generating a specific level of lactate accumulation.

Animals↗

PubMed1974

The effect of lysine on gluconeogenesis from lactate in rat hepatocytes.

1. In freshly prepared isolated rat liver cells there is a lag in gluconeogenesis from lactate. The magnitude of the lag increases with increasing lactate concentration. 2. The lag is virtually abolished by lysine. 3. A few other amino acids (tyrosine, arginine, asparagine, ornithine) and NH(4)Cl had effects similar to, but less pronounced than, lysine during the early stage of incubation. Lysine was unique in accelerating gluconeogenesis beyond the lag period. 4. The effects of the accelerators are not additive. 5. Glycine, serine, threonine, cysteine, tryptophan and histidine at 2mm markedly inhibit (>20%) gluconeogenesis from lactate. 6. Oleate, which promotes gluconeogenesis from lactate by supplying acetyl-CoA required for the pyruvate carboxylase reaction, had no effect on the lag, yet oleate oxidation showed no lag. 7. Preincubation of cells decreased the lag and decreased the magnitude of the lysine effect. 8. Pyruvate (added at 1mm to give an initial [lactate]/[pyruvate] ratio of 10) also abolished the lag and decreased the lysine effect by about 50%. 9. Lysine reversed the inhibition by ethanol of gluconeogenesis from lactate. 10. All accelerators increased the rate of re-oxidation of cytosolic NADH as shown by a rapid re-adjustment of the [lactate]/[pyruvate] ratio on addition of 10mm-lactate. 11. The accelerated rates of gluconeogenesis are associated with an increased formation of aspartate and glutamate and especially alanine. 12. The existence of the lag period can be explained on the basis of the fact that the accumulation of pyruvate during the lag diverts oxaloacetate from gluconeogenesis to malate formation, i.e. that the re-oxidation of cytosolic NADH takes precedence over gluconeogenesis. This means that much oxaloacetate formed by the pyruvate carboxylase reaction has to be transferred twice from the mitochondria to the cytosol by the aspartate shuttle. Under these conditions the operation of the shuttle limits the rate of gluconeogenesis from lactate. Lysine and other accelerators may increase the effectiveness of the shuttle by providing components of the aspartate aminotransferases involved. The question of why lysine specifically accelerates gluconeogenesis beyond the lag period is discussed.

Alanine↗

PubMed1977

Effects of lactation of ketogenesis from oleate or butyrate in rat hepatocytes.

1. Rates of ketogenesis from endogenous butyrate or oleate were measured in isolated hepatocytes prepared from fed rats during different reproductive states [virgin, pregnant, early-lactating (2-4 days) and peak-lactating (10-17 days)]. In the peak-lactation group there was a decrease (25%) in the rate of ketogenesis from butyrate, but there were no differences in the rates between the other groups. Wth oleate, the rate of ketogenesis was increased in the pregnant and in the early-lactation groups compared with the virgin group, whereas the rate was 50% lower in the peak-lactation group. 2. Experiments with [1-(14)C]oleate indicated that these differences in rates of ketogenesis were not due to alterations in the rate of oleate utilization, but to changes in the amount of oleoyl-CoA converted into ketone bodies. 3. Although the addition of carnitine increased the rates of ketogenesis from oleate in all groups of rats, it did not abolish the differences between the groups. 4. Measurements of the accumulation of glucose and lactate showed that hepatocytes from rats at peak lactation had a higher rate of glycolytic flux than did hepatocytes from the other groups. After starvation, the rate of ketogenesis from oleate was still lower in the peak-lactation group compared with the control group. This suggests that the alteration in ketogenic capacity in the former group is not merely due to a higher glycolytic flux. 5. It is concluded that livers from rats at peak lactation have a lower capacity to produce ketone bodies from long-chain fatty acids which is due to an alteration in the partitioning of long-chain acyl-CoA esters between the pathways of triacylglycerol synthesis and beta-oxidation. The physiological relevance of this finding is discussed.

Animals↗

PubMed1978

Lactate-stimulated ethanol oxidation in isolated rat hepatocytes.

1. Hepatocytes isolated from starved rats and incubated without other substrates oxidized ethanol at a rate of 0.8-0.9mumol/min per g wet wt. of cells. Addition of 10mm-lactate increased this rate 2-fold. 2. Quinolinate (5mm) or tryptophan (1mm) decreased the rate of gluconeogenesis with 10mm-lactate and 8mm-ethanol from 0.39 to 0.04-0.08mumol/min per g wet wt. of cells, but rates of ethanol oxidation were not decreased. From these results it appears that acceleration of ethanol oxidation by lactate is not dependent upon the stimulation of gluconeogenesis and the consequent increased demand for ATP. 3. As another test of the relationship between ethanol oxidation and gluconeogenesis, the initial lactate concentration was varied from 0.5mm to 10mm and pyruvate was added to give an initial [lactate]/[pyruvate] ratio of 10. This substrate combination gave a large stimulation of ethanol oxidation (from 0.8 to 2.6mumol/min per g wet wt. of cells) at low lactate concentrations (0.5-2.0mm), but rates remained nearly constant (2.6-3.0mumol/min per g wet wt. of cells) at higher lactate concentrations (2.0-10mm). 4. In contrast, owing to the presence of ethanol, the rate of glucose synthesis was only slightly increased (from 0.08 to 0.12mumol/min per g wet wt. of cells) between 0.5mm- and 2.0mm-lactate and continued to increase (from 0.12 to 0.65mumol/min per g wet wt. of cells) with lactate concentrations between 2 and 10mm. 5. In the presence of ethanol, O(2) uptake increased with increasing substrate concentration over the entire range. 6. Changes in concentrations of glutamate and 2-oxoglutarate closely paralleled changes in the rate of ethanol oxidation. 7. In isolated hepatocytes, rates of ethanol oxidation are lower than those in vivo apparently because of depletion of malate-aspartate shuttle intermediates during cell preparation. Rates are returned to those observed in vivo by substrates that increase the intracellular concentration of shuttle metabolites.

Animals↗

PubMed1986

Phosphoribosyl pyrophosphate and phosphoribosyl pyrophosphate synthetase in rat mammary gland. Changes in the lactation cycle and effects of diabetes, insulin and phenazine methosulphate.

Changes in the tissue content of phosphoribosyl pyrophosphate (PPRibP), glucose 6-phosphate, ribose 5-phosphate (Rib5P), RNA and DNA, of the activity of PPRibP synthetase (EC 2.7.6.1) and the conversion of [1-14C]- and [6-14C]-glucose into 14CO2 were measured at mid-lactation in the normal and diabetic rat and in pregnancy, lactation and mammary involution in the normal rat. The PPRibP, glucose 6-phosphate and Rib5P contents increase during pregnancy and early lactation to reach a plateau value at mid-lactation, before falling sharply during weaning. The PPRibP content, PPRibP synthetase activity and flux of glucose through the oxidative pentose phosphate pathway (PPP) all change in parallel during the lactation cycle. Similarly, after 3 and 5 days duration of streptozotocin-induced diabetes, ending on day 10 of lactation, there were parallel declines in PPRibP content, PPRibP synthetase and PPP activity. The effect of streptozotocin was prevented by pretreatment with nicotinamide and partially reversed by insulin administration. Addition of insulin to lactating rat mammary-gland slices incubated in vitro significantly raised the PPRibP content (+47%) and the activity of the PPP (+40%); phenazine methosulphate, which gives a 2-fold increase in PPP activity, raised the PPRibP content of lactating mammary gland slices by approx. 3-fold. It is concluded that Rib5P, generated in the oxidative segment of the PPP, is an important determinant of PPRibP synthesis in the lactating rat mammary gland and that insulin plays a central role in the regulation of the bioavailability of this precursor of nucleotide and nucleic acid synthesis.

Animals↗

PubMed1990

Amino acid metabolism and protein synthesis in lactating rats fed on a liquid diet.

1. Amino acid metabolism was studied in control virgin rats, lactating rats and virgin rats protein-pair-fed with the lactating rats (high-protein virgin rats). 2. Urinary excretion of nitrogen and urea was higher in lactating than in control virgin rats, and in high-protein virgin rats it was higher than in lactating rats. 3. The activities of urea-cycle enzymes (units/g) were higher in high-protein virgin than in lactating rats, except for arginase. In lactating rats the activities of carbamoyl-phosphate synthase, ornithine carbamoyltransferase and argininosuccinate synthase were lower than in control virgin rats. When the liver size is considered, the activities in lactating rats were similar to those in high-protein virgin rats, except for arginase. 4. N-Acetylglutamate content was higher in high-protein virgin rats than in the other two groups. 5. The rate of urea synthesis from precursors by isolated hepatocytes was higher in high-protein virgin rats than in the other two groups. 6. The flooding-dose method (L-[4-3H]phenylalanine) for measuring protein synthesis was used. The absolute synthesis rates of mammary gland, liver and small-intestinal mucosa were higher in lactating rats than in the other two groups, and in high-protein virgin rats than in control virgin rats 7. These results show that the increased needs for amino acids during lactation are met by hyperphagia and by a nitrogen-sparing mechanism.

Amino Acids↗

PubMed1991

Effects of lactate on pathways of glycogen formation in the perfused rat liver.

In order to investigate the roles of lactate as substrate and regulator of hepatic glycogen synthesis, two groups of rat livers were perfused with oxygenated blood for 2 h. The initial perfusate glucose and lactate concentrations of Group I and II were 245 +/- 6.8 and 254 +/- 12.9 mg/dl and 49 +/- 2.6 and 54 +/- 2.2 mg/dl respectively. Labelled glucose was added to the perfusate to assess direct glycogen formation. Either additional glucose (Group I) or lactate (Group II) was added (1 mg/min) to a recirculating liver-perfusion system. Initial lactate uptake and glucose formation was identical in the two groups of studies. For Group I, both glucose and lactate uptake by the liver fell to nearly zero, in spite of increasing glucose concentrations. However, with lactate infusion (Group II), its uptake by the liver was maintained at 0.89 +/- 0.14 mg/min after 120 min. In total, 6.2 +/- 0.7 mg (Group I) or 20.2 +/- 3.9 mg (Group II) of glycogen was formed, 4.0 +/- 0.7 mg or 9.2 +/- 2.0 mg by direct synthesis from glucose and 2.2 +/- 0.3 mg or 11.0 +/- 2.1 mg by gluconeogenic formation, in Groups I and II respectively. With the provision of additional lactate, its uptake by the perfused liver tripled, as did glycogen synthesis. Glucose production doubled when lactate was added instead of glucose. Gluconeogenic formation of glycogen increased by 400%. Surprisingly, direct synthesis from glucose also rose by 130%. These data indicate that continued lactate uptake by the liver with gluconeogenic glycogen formation determines the amount of glycogen formed not only by this route, but also by direct synthesis from glucose.

Animals↗

PubMed2002

Chronic neuropeptide Y Y5 receptor stimulation suppresses reproduction in virgin female and lactating rats.

Continuous infusion of neuropeptide Y (NPY) disrupts cyclicity and delays the onset of puberty in female rats indicating that NPY can suppress reproduction. Central application of NPY also reliably increases food intake in rats. States with heavy demands on energy resources where reproduction is also inhibited, such as lactation, are similarly accompanied by elevations in central NPY expression. In previous studies, we have shown that, compared to lactating rats fed ad libitum, food-restricted lactating rats exhibit a longer period of lactational diestrus that is correlated with increased central NPY expression. These studies link NPY to the inhibition of reproduction that is mediated by low availability of energy resources. Here, we examine the effect of chronic 7-day infusion of the mixed Y1/Y4/Y5 agonist (Leu31, Pro34) NPY and selective agonists to the Y2 (NPY13-36) and Y5 (D-Trp32 NPY and D-Trp34 NPY) receptors on food intake and the oestrous cycle of virgin female rats. We also investigated the effect of chronic infusion from day 8-15 postpartum (pp) of D-Trp32 NPY and D-Trp34 NPY on food-intake and the length of lactational diestrus in lactating rats fed ad libitum. In virgin females, infusion of (Leu31, Pro34) NPY and both the Y5 agonists lengthened the period between consecutive oestrus days while the Y2 agonist NPY13-36 was without effect. Selective Y5 receptor activation alone caused an increase in food intake in virgin females. In lactating females, D-Trp32 NPY extended the length of lactational diestrus, while D-Trp34 NPY had no effect on this parameter. These data suggest that Y5 receptor activation suppresses the reproductive axis in both virgin and lactating rats and that Y5 receptor activation enhances food-intake in virgin females.

Animals↗

PubMed2002

Cytokines gene expression patterns of bovine milk during middle and late stages of lactation.

The cytokine mRNA profiles of the bovine mammary gland were investigated using newly developed TaqMan real-time polymerase chain reaction systems (Applied Biosystems, Foster City, CA, USA). Transcriptional activity of six cytokines, interleukin (IL)-2, IL-6, IL-12, interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and granulocyte-macrophage colony stimulating factor (GM-CSF) was studied during the mid- and late-lactation stages. Transcripts for TNF-alpha, GM-CSF, and IFN-gamma were detected in all samples of both stages. However, IL-12 was only detected in 80 and 58 % of late- and mid-lactation samples, respectively. IL-12 expression was up-regulated in late lactation in comparison with the corresponding level in mid-lactation. The cytokines interaction in late lactation was more co-ordinated and their transcriptional levels were significantly correlated among each other, whereas, in mid-lactation significant correlation of the cytokines transcription was only seen with the TNF-alpha, GM-CSF, and IFN-gamma. Cytokine mRNA profiles between mid- and late lactation showed significant differences, which can be attributed to the dramatic changes that the mammary gland is subjected to during late lactation. The significant elevation of IL-12 transcriptional activity in late lactation and its relevance to the mammary gland immunity is discussed.

Animals↗

PubMed1989

Iodine nutrition in ewes: effects of low to high iodine intake on iodine content of biological fluids in pregnant and lactating ewes.

In a first experiment, 2 groups of 46 and 47 multiparous ewes received diets which provided an iodine intake of 0.36 and 0.26 mg/kg dry matter (group C) and, 2.01 and 1.94 mg/kg (group D), respectively, for pregnancy and lactation. In a second experiment, 3 groups of 10 nulliparous ewes received diets which provided an I intake of 0.13 and 0.12 mg/kg dry matter (group A), 0.22 and 0.20 mg/kg dry matter (group B), and 10.77 and 8.88 mg/kg dry matter (group E), respectively, for pregnancy and lactation. Observations and sampling were carried out on the ewes from the first third of pregnancy to the 2nd and the 6th week of lactation. The diets provided adequate nutrition for pregnant and lactating ewes. Dietary I content had no effect on the dry matter intake, the size or the weight of the litter and the length of pregnancy. Plasma inorganic iodine (PII) was less affected by the I intake during lactation than during pregnancy. The excretion of I in milk induced a decrease in PII between pregnancy and lactation. The I in urine expressed as microgram I/g creatinine was largely affected by the intake. Colostrum I was 6.7, 4.0, 1.2, 1.3 and 1.5 times higher in groups A, B, C, D and E than the I in milk collected 1 week postpartum. Milk iodine (MI) content and the ratio MI/PII were markedly dependent on the I intake. During pregnancy, plasma T4 concentration decreased for each group. Plasma T4 concentration remained low during lactation in the low I intake group, whereas it increased at the same time in the other groups. The plasma T3 concentration decreased at the 6th week of lactation in the highest I intake group. Experimental values showed that 0.12 mg I/kg dry matter induced depletion in the I stocks of pregnant and lactating ewes, whereas an I intake above 10 mg I/mg dry matter disturbed the metabolism of thyroid hormones.

Animals↗

PubMedDate not supplied

Leptin and the adaptations of lactation in rodents and ruminants.

Lactation markedly increases nutrient requirements in both rodents and ruminants. This is met mostly by increased food intake, but there are also adaptations to increase metabolic efficiency. Despite such changes, lactating animals usually experience periods of negative energy balance. This is not due to a physical constraint on food intake, at least in the rat. Leptin, a hormone secreted by adipocytes, plays an important role in the regulation of appetite and energy balance. During lactation, serum leptin concentration is decreased in both rodents and ruminants, and the nocturnal rise in concentration is lost in rats. Hypoleptinaemia in lactation is primarily a result of negative energy balance. There is also increased clearance of serum leptin, and the attenuation of the nocturnal rise in leptin in rats is at least partly due to the suckling stimulus. Hypoleptinaemia is not the major factor driving hyperphagia in lactating rats, but it probably facilitates the increased food intake. Leptin may play a more important role in this respect in lactating ruminants. Leptin is probably involved in other adaptations that increase metabolic efficiency during lactation. The ability of hypothalamic neuropeptides to respond to leptin does not appear to be altered by lactation in either rodents or ruminants. The reason why lactating animals do not respond to hypoleptinaemia with a further increase in appetite, thereby achieving energy balance, appears to be due to a failure to respond to changes in neuropeptides which mediate the effects of leptin.

Adaptation, Physiological↗

PubMed1984

Placental contribution to lactate production by the human fetoplacental unit.

Umbilical cord blood levels of lactate, base deficit, and pH were measured in 452 liveborn infants. In vigorous newborns, the mean umbilical arterial and venous concentrations of lactate were lowest with elective cesarean section, higher with cesarean section performed during labor, and highest with vaginal delivery (P less than .001). This suggests a rise in the fetal lactate level in response to labor. However, there was no concomitant increase in the mean umbilical arteriovenous lactate differences, indicating that both fetus and placenta increase their lactate production proportionately with labor. Depressed newborns had higher umbilical lactate levels than vigorous newborns irrespective of the method of delivery (P less than .001). Depressed newborns also had a higher mean umbilical arteriovenous lactate difference than vigorous newborns (P less than .001). This suggests that, under conditions that lead to neonatal depression, the fetus is the major source of the increased lactate produced, with a smaller contribution from the placenta. The fetal lactate level may be a good indicator of fetal stress in labor.

Acidosis↗

PubMed1997

Lactate and ammonia concentration in blood and sweat during incremental cycle ergometer exercise.

It is known that the concentrations of ammonia and lactate in blood increase during incremental exercise. Sweat also contains lactate and ammonia. The aim of the present study was to investigate the physiological response of lactate and ammonia in plasma and sweat during a stepwise incremental cycle ergometer exercise test in ten subjects. During this test lactate and ammonia were measured in blood obtained from the earlobe and in sweat collected in a bag attached to the back of the subject. At the end of each interval this bag was emptied for measuring lactate and ammonia. A disproportional increase in the concentration of lactate and ammonia in blood was found, in sweat a disproportional decrease. The lactate concentrations in sweat were higher than those in blood. We hypothesise that lactate in sweat is produced from glycogen granules of the clear cell of the eccrine gland. This lactate production results in acidification of sweat, which facilitates the diffusion of ammonia from eccrine duct cell to duct lumen. It is uncertain how far duct cell ammonia originates from plasma, the duct cell itself might produce ammonia. Part of the ammonia in sweat could come from the breakdown of urea by skin bacteria.

Adult↗