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Asymmetry in the transport of lactate by basolateral and brush border membranes of rat kidney cortex.

The uptake of L(+)lactate into rat renal cortical brush border (BBV) and basolateral (BLV) membrane vesicles, isolated through differential centrifugation and free flow electrophoresis, were studied using a rapid filtration technique. In contrast to the lactate transport into the BBV, that into the BLV: 1) was found to proceed only towards equilibrium, 2) showed Na+ -independent coupling of the influx of L(+)lactate and the efflux of L(+) but not to the efflux of D(-)lactate, 3) was not inhibited by D(-)lactate, 2-thiolactate or 3-phenyl-lactate, but 4) was inhibited by 3-thiolactate and alpha-hydroxybutyrate and 5) was accelerated by changes in inwardly directed ionic gradients or by increases in cation conductance both of which led to increased intravesicular positivity. The latter changes had the opposite effect on the uptake of L(+)lactate by BBV. Thus, while the L(+)lactate transport system present in BBV showed the characteristics of Na-dependent electrogenic cotransport system, that in the BLV was consistent with a carrier mediated Na-dependent, facilitated diffusion system.

Animals↗

The influence of extracellular buffer concentration and propionate on lactate efflux from frog muscle.

Lactate efflux from frog sartorius muscles was measured following a lactate load of about 18 mumol X g-1 induced by a 4-min period of stimulation. Lactate efflux rate was buffer concentration dependent. The initial efflux rate increased from about 150 nmol X g-1 X min-1 in 1 mM MOPS buffer to 400 nmol X g-1 X min-1 in 25 mM MOPS buffer. The addition of 20 mM propionate reduced mean intracellular pH by about 0.2 units and increased lactate efflux rate by 70% at the highest buffer concentration and 400% at the lowest buffer concentration. The observed results are in reasonable agreement with predictions based on a model in which net efflux is limited by diffusion of both buffer and lactate in the extracellular space. Transmembrane lactate efflux appears to consist of two components, one of which is proton linked and carried either by undissociated lactic acid or coupled proton-lactate transport, the other being carried by independent lactate ions.

Animals↗

Response of left ventricular diastolic filling to graded exercise relative to the lactate threshold.

During incremental exercise, the left ventricular ejection fraction increases up to the intensity of the anaerobic threshold and tends to level off at higher exercise intensities. Since there is a correlation between the response of peak filling rate and ejection fraction to exercise, this study was conducted to determine whether the response of left ventricular diastolic function is similar to the response of systolic function relative to lactate threshold. Twelve healthy men performed two exercise tests on a cycle ergometer. In the first test, lactate threshold and maximal power output were determined. In the second exercise test, gated radionuclide ventriculography was performed at rest, at the lactate threshold intensity, and at peak exercise to measure ejection fraction and peak filling rate. Ejection fraction increased significantly from rest [mean (SD): 62 (5)%] to lactate threshold [76 (7)%] and did not change significantly from lactate threshold to peak exercise [77 (7)%]. Likewise, peak filling rate (normalized for stroke counts) increased from resting [6.1 (0.9) VS.s-1] to lactate threshold [9.4 (1.8) VS.s-1] and did not change significantly from lactate threshold to peak exercise [9.6 (2.9) VS.s-1]. There was no correlation between the change in peak filling rate and the change in ejection fraction from rest to lactate threshold. Thus, during incremental exercise, left ventricular diastolic function responds qualitatively similar to systolic function.

Adult↗

Effect of momentary stress on brain energy metabolism in weanling mice: apparent use of lactate as cerebral metabolic fuel concomitant with a decrease in brain glucose utilization.

The hypothesis that the anxiety induced by repeated injections affects brain energy metabolism was tested. Normal 19- to 21-day-old mice were stressed by two sham intraperitoneal injections within 4 min, at which time they were decapitated. Noninjected, control littermates were quickly decapitated. Momentary stress increased plasma glucose (12%), glycerol (85%), beta-hydroxybutyrate (108%), and lactate (153%)--a reflection of elevated plasma cortisol (25%) and glucagon (45%). In brain, stress increased levels of glucose-6-P (15%) and fructose-6-P (17%). The brain pyruvate concentration increased 74%; lactate 76%. Citrate, alpha-ketoglutarate, and malate increased 15, 95, and 37%, respectively. Levels of glycogen, glucose, phosphocreatine, ATP, ADP, and AMP were unchanged. The brain lactate/pyruvate ratio was normal but the brain/plasma lactate ratio fell 32%. Metabolite changes in the stressed animals were compatible with a decrease in the glycolytic flux at the phosphofructokinase step and a paradoxical increased flux in the Krebs citric acid cycle. The decreased brain/plasma lactate ratio supported increased uptake of lactate from plasma and increased brain lactate oxidation. Metabolite changes similar to those described above occurred in unstressed mice injected with lactate. Findings confirm a positive effect of stress on brain metabolism, support a role for lactate as an oxidative fuel for brain, and caution that the rate of cerebral glucose utilization may not always reflect brain energy (oxidative) metabolism accurately.

Animals↗

Blood lactate production and recovery from anaerobic exercise in trained and untrained boys.

Blood lactate production and recovery from anaerobic exercise were investigated in 19 trained (AG) and 6 untrained (CG) prepubescent boys. The exercises comprised 3 maximal test performances; 2 bicycle ergometer tests of different durations (15 s and 60 s), and running on a treadmill for 23.20 +/- 2.61 min to measure maximal oxygen uptake. Blood samples were taken from the fingertip to determine lactate concentrations and from the antecubital vein to determine serum testosterone. Muscle biopsies were obtained from vastus lateralis. Recovery was passive (seated) following the 60 s test but that following the treadmill run was initially active (10 min), and then passive. Peak blood lactate was highest following the 60 s test (AG, 13.1 +/- 2.6 mmol.1-1 and CG, 12.8 +/- 2.3 mmol.1-1). Following the 15 s test and the treadmill run, peak lactate values were 68.7 and 60.6% of the 60 s value respectively. Blood lactate production was greater (p less than 0.001) during the 15 s test (0.470 +/- 0.128 mmol.1-1.s-1) than during the 60 s test (0.184 +/- 0.042 mmol.1-1.s-1). Although blood lactate production was only nonsignificantly greater in AG, the amount of anaerobic work in the short tests was markedly greater (p less than 0.05-0.01) in AG than CG. Muscle fibre area (type II%) and serum testosterone were positively correlated (p less than 0.05) with blood lactate production in both short tests. Blood lactate elimination was greater (p less than 0.001) at the end of the active recovery phase than in the next (passive) phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaerobiosis↗

Lactate transport by skeletal muscle sarcolemmal vesicles.

Recent studies have indicated that lactate traversal of the sarcolemmal membrane of skeletal muscle could be a carrier mediated process. In the present study, the initial rates of L(+)-lactate flux (Jlact) were measured in highly purified rat hindlimb skeletal muscle sarcolemmal vesicles. Fluxes were determined by the vesicle uptake of L(+)-[U-14C]lactate from the extra-vesicular medium. Jlact was saturable with respect to increasing concentrations of L(+)-lactate. Regression of these data to the Michaelis-Menten equation yielded a Km of 12.5 mM. Jlact was inhibited 81% by 10 mM pyruvate and 83% by 5mM alpha-cyano 4 hydroxycinnamate (p < 0.05), but not by D-lactate, indicating the presence of a stereoselective monocarboxylate transporter in the sarcolemmal membrane. Preincubation of the vesicles with the protein modifier, N-ethylmaleimide (20mM), inhibited Jlact by 86% (p < 0.05). An inhibitor of the inorganic anion exchanger, SITS (1mM), had no effect on Jlact. However, Jlact was markedly sensitive to an inwardly directed proton gradient (p < 0.05), and the flux was more closely related to the concentration of external ionic L(+)-lactate than to the protonated (HLa) form. These studies suggest that skeletal muscle sarcolemmal membranes possess a specific transport system for L-lactate and other monocarboxylates, which has similar properties to the lactate carrier described for several other tissues.

Animals↗

Microregional distributions of glucose, lactate, ATP and tissue pH in experimental tumours upon local hyperthermia and/or hyperglycaemia.

Microregional distributions of glucose, lactate and ATP concentrations as well as tissue pH values were determined in subcutaneous rat tumours during normothermia and normoglycaemia, and upon local hyperthermia (HT) and/or hyperglycaemia (HG). Experiments were performed in order to investigate whether, and to what extent, these adjuvant therapeutic measures applied alone or in combination can modify the bioenergetic and metabolic status, parameters that are known to markedly influence the therapeutic response of tumours to heat. Local HT was performed in a saline bath (44 degrees C/2 h) and HG was induced by i.v. infusion of glucose for 2.5 h (blood glucose levels during heating: 35-40 mM). Immediately after treatment, the microregional distributions of glucose, lactate and ATP concentrations were assessed using quantitative bioluminescence and single-photon counting. In corresponding histological sections the fraction of tumour tissue with changes indicating cellular damage was determined. For comparison, global levels of glucose, lactate, ATP, ADP and AMP were measured using enzymatic assays or HPLC. Tumour tissue pH values were recorded immediately after treatment with miniaturised needle glass pH electrodes. Upon HT alone, the microregional glucose distribution remained unchanged. Lactate concentrations significantly increased, resulting in a pH drop of about 0.20 pH units. Mean ATP concentrations decreased without an obvious change in the shape of the distribution curve. The fraction of tumour tissue showing cellular damage increased from 18% (in control tumours) to 27%. Upon HG alone, mean glucose and lactate levels in the tumours increased. Glucose, lactate and pH distributions became broader. Lactate accumulation results in a severe tumour acidosis (mean pH = 6.22). Mean ATP concentrations marginally decreased despite a higher glucose availability, probably because of poorer ATP yield resulting from changes in metabolic channelling (Crabtree effect). The fraction of tumour tissue exhibiting cellular damage was 23%. Following the combined treatment (HT/HG), glucose and lactate levels, and tissue pH were similar to those seen upon HG alone. However, ATP concentrations were lowest under this condition. The variation of tumour ATP concentrations is substantially reduced with only a few tumour areas remaining with ATP levels of at least 0.6 mumol/g. The ATP depletion upon HT/HG is accompanied by a drastic increase in the fraction of tissue areas exhibiting cellular damage to 61%. It may therefore be concluded that only the combined treatment can deplete ATP to such an extent that a pronounced cytotoxic effect is achieved.

Adenosine Triphosphate↗

D-lactate concentrations in blood, urine and sweat before and after exercise.

The purpose of this study was to investigate changes in the concentrations of D-lactate, L-lactate, pyruvate and methylglyoxal (MG) in body fluids after exercise. Eight untrained male students and five male students who were boat club members engaged in the exercise. Each subject performed runs of short and long duration. Compared to pre-exercise values plasma concentrations of D-lactate, L-lactate and pyruvate increased after running; in trained men by 3.6, 5.0, 3.4 times after short runs and by 1.5, 4.6, 2.0 times after long runs, and in untrained men by 3.0, 12.0, 1.6 times after short runs and 2.5, 5.6, 1.6 times after long runs, respectively. In all cases, the increase of L-lactate was always higher than that of D-lactate after running. The MG contents in red blood cells decreased markedly after running, especially in the untrained students. After short runs the MG concentration had decreased to 13% in the untrained men and 30% in the trained men, and after long runs the concentration had decreased to 41% in the untrained and 60% in the trained men. The MG in plasma and red blood cells appeared to have been utilized during relatively anaerobic exercise, especially by the untrained subjects. The D-lactate and related substances were also determined in urine, but the concentration of these substances showed no relationship to exercise. The D-lactate concentration in sweat samples tripled after short periods of running but the relative concentration to sodium ion concentration was not altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Transport of L-lactate by cultured rat brain astrocytes.

Several reports indicate that lactate can serve as an energy substrate for the brain. The rate of oxidation of this substrate by cultured rat brain astrocytes was 3-fold higher than the rate with glucose, suggesting that lactate can serve as an energy source for these cells. Since transport into the astrocytes may play an important role in regulating nutrient use by individuals types of brain cells, we investigated the uptake of L-[U-14C]lactate by primary cultures of rat brain astrocytes. Measurement of the net uptake suggested two carrier-mediated mechanisms and an Eadie-Hofstee type plot of the data supported this conclusion revealing 2 Km values of 0.49 and 11.38 mM and Vmax values of 16.55 and 173.84 nmol/min/mg protein, respectively. The rate of uptake was temperature dependent and was 3-fold higher at pH 6.2 than at 7.4, but was 50% less at pH 8.2. Although the lactate uptake carrier systems in astrocytes appeared to be labile when incubated in phosphate buffered saline for 20 minutes, the uptake process exhibited an accelerative exchange mechanism. In addition, lactate uptake was altered by several metabolic inhibitors and effectors. Potassium cyanide and alpha-cyano-4-hydroxycinnamate inhibited lactate uptake, but mersalyl had little or no effect. Phenylpyruvate, alpha-ketoisocaproate, and 3-hydroxybutyrate at 5 and 10 mM greatly attenuated the rate of lactate uptake. These results suggest that the availability of lactate as an energy source is regulated in part by a biphasic transport system in primary astrocytes.

Animals↗

Cerebrospinal fluid lactate in 78 cases of adult meningitis.

In a retrospective study of 78 cases of adult meningitis, the CSF lactate was measured on the first spinal tap (ST); 25 had a bacterial meningitis, 28 a viral meningitis; 22 other cases had been on antibiotics prior to admission; 3 cases had meningitis of rare aetiology. The median CSF lactate level among the 25 bacterial cases amounted to 13.6 mmol/l (range: 3.5-24.5) whereas it remained low in the 28 viral cases: 2.7 mmol/l (range: 1.4-4.2). These differences are highly significant. The comparison of the CSF lactate level with the other tests routinely performed showed that the CSF lactate level had the highest sensitivity, specificity and predictive values. The CSF lactate level on the first ST had no prognostic value, but a rapid decrease of the CSF lactate during the treatment is indicative of good prognosis. Among the pretreated cases, a high lactate level could be an indication that bacteria were the causal agents. In conclusion, the measurement of the CSF lactate, quickly performed and inexpensive, is worth performing when a meningitis is suspected, as it appears to be the best way of distinguishing bacterial from non-bacterial meningitis.

Adolescent↗

The mechanism of lactate transport in human erythrocytes.

Lactate accumulates in human erythrocytes stored at 4 degrees C in the presence of glucose. Efflux of lactate exhibits an activation energy of 22kcal/mole and is markedly stimulated with increasing medium pH. Lactate influx into erythrocytes that were depleted of intracellular lactate by incubation at 37 degrees at pH 8.0 was stimulated by decreasing medium pH. Under appropriate conditions the pH-dependent lactate flux was insensitive to 4-acet-amido-4'-isothiocyano-2,2'-disulfonic stilbene or 4,4'-diisothiocyano-2,2'-disulfonic stilbene, inhibitors of the inorganic anion channel, while, e.g., inorganic phosphate transport was fully sensitive. These experiments as well as measurements of H+ movements associated with lactate fluxes demonstrate that lactate transport takes place via a specific monocarboxylate transporter (distinct from the inorganic ion channel) by a H+-lactate symport mechanism.

Biological Transport, Active↗

Oxygen deficit and blood lactate in prepubertal boys during exercise above the anaerobic threshold.

Recent studies have shown that in boys a steady-state of blood lactate is maintained at exercise levels above the anaerobic threshold. Therefore, the explanation hitherto provided for the steeper increase in blood lactate beyond the anaerobic threshold, i.e. the onset of anaerobic metabolism, needs modification. Investigations were carried out in ten boys, aged 11-12 years, during treadmill running. Maximal oxygen uptake (VO2max) and maximal blood lactate were determined during incremental exercise. Subsequently each boy performed four runs at different high constant speeds of 16 min duration, in order to determine maximal steady-state blood lactate. The underlying data also served to estimate roughly the lactate anaerobic threshold. Oxygen uptaken (VO2) was measured at 0.5 min intervals during the initial 7.5 min of each constant-speed run. Maximal steady-state blood lactate was 5.6 mmol/l corresponding to 92% of VO2max. The mean blood lactate at which the anaerobic threshold was reached or just exceeded was 2.7 mmol/l corresponding to 82% of VO2max. Oxygen transport transient kinetics were computed from the mean 0.5 min VO2-values during the constant-speed runs near the maximal steady-state blood lactate and from runs near the anaerobic threshold. Half-times of VO2 response were shorter than values previously reported for adults due to a faster increase in VO2 at the onset of exercise. Half-times increased with increasing work rates as did the oxygen deficit, due to a slower increase in VO2 along with a longer time required to attain a steady-state at higher work rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗

Neurocardiac toxicity of racemic D,L-lactate fluids.

Racemic D,L-lactate has long been used in burn therapy as Ringer's lactate and in peritoneal dialysis fluid for treatment of renal failure. The D-lactate component of this racemic mixture is known to cause two forms of neurological toxicity in patients: encephalopathy and, in a subset of the population, panic reaction. Here we demonstrate that coma, similar in degree to that produced by blood levels of 75 mM ethanol was induced in rats by the intraperitoneal infusion of sodium D-lactate sufficient to raise serum D-lactate concentration to 25 mM, whereas infusion of equal quantities of sodium L-lactate produced no observable neurological effect. We further demonstrate that the intravenous infusion of racemic D,L-lactic acid into 48-hour fasted rats produced serious disturbances of cardiac rate and rhythm leading to death. When serum D-lactate concentration had reached 1-2 mM there was bradycardia, at 2-3 mM prolongation of QT interval, at 6-7 mM AV block with ectopic escape rhythms, and at 11 mM death in ventricular standstill or fibrillation. In contrast, intravenous infusion of L-lactic acid to blood levels of 25 mM failed to produce any change in cardiac rhythm. On the other hand, the isolated working heart, free of influence from the central nervous system, displayed no change of cardiac rhythm or physiological function when perfused with 25 mM sodium D,L-lactate.

Adult↗

Lactate blood levels in the perioperative period of orthotopic liver transplantation.

To investigate whether early postoperative changes in blood lactate concentration indicate the functional recovery of the newly grafted liver, changes in oxygen supply, oxygen consumption, acid-base equilibrium, and blood lactate concentrations were prospectively studied in a group of 53 postnecrotic cirrhotic patients during the various phases of orthotopic liver transplantation (preanhepatic, anhepatic, neohepatic) and for the first 48 h following reperfusion. The patients were divided into two groups according to the quality of the early graft function, as indicated by alanine aminotransferase, bile flow, and prothrombin activity: group A (49 patients), good immediate graft function and group B (4 patients), immediate graft non-function. Lactate levels rose in the same manner during the preanhepatic and anhepatic stages and peaked after revascularization of the graft. Following reperfusion, however, distinctly different blood lactate profiles were recorded in the two groups of patients. A fall in lactate concentration was recorded in group A patients, whereas a continuous rise occurred in group B patients: the difference becoming significant by the end of surgery (P < or = 0.05). During the first 48 h following revascularization of the graft, opposite trends in lactate concentration, bile flow, alanine aminotransferase, and prothrombin activity were evident in the two groups of patients: 24 h after reperfusion, lactate levels were below 2 mmol/l in 47 of 49 patients from group A, while they plateaued above 4 mmol/l in all patients from group B. Group A patients had lower alanine aminotransferase levels (P < or = 0.001), higher prothrombin activity, (P < or = 0.01), and greater bile flow (P < or = 0.02). If validated in larger series, the blood lactate profile, probably more than the absolute level, appears to be a useful indicator of the early recovery of liver metabolic capacities in the immediate postoperative period of orthotopic liver transplantation.

Alanine Transaminase↗

Pregnancy and lactation confer reversible bone loss in humans.

The influence of pregnancy on bone mineral density (BMD) was evaluated by dual-energy X-ray absorptiometry (DXA) in 73 women (mean age 29 years, range 20-44 years) postpartum. Fifty-five age-matched women served as controls. The influence of lactation was evaluated in 65 of the delivered women who were followed with repeated measurements, a mean of 4.5 +/- 0.1 and 11.5 +/- 0.1 months after the delivery. The influence of multiple pregnancies was evaluated in 39 premenopausal women (mean age 38 years, range 31-54 years) with a minimum of four pregnancies (range 4-7). Fifty-eight age-matched healthy premenopausal women with a maximum of two pregnancies (range 0-2) served as controls. Data are presented as mean +/- SEM. BMD data are adjusted for differences in total fat mass and total lean mass. Lumbar spine BMD was 7.6 +/- 0.1% and total body BMD 3.9 +/- 0.1% lower in women postpartum compared with controls (both p<0.001). BMD did not decrease significantly in non-breastfeeding mothers. Mothers breastfeeding for 1-6 months decreased femoral neck BMD by 2.0 +/- 1.0% during the first 5 months postpartum (p<0.001). No further BMD loss was seen between 5 and 12 months postpartum. Femoral neck BMD 12 months after delivery was 1.3 +/- 0.8% lower than after delivery in mothers breastfeeding for 1-6 months (p = 0.05). Mothers breastfeeding for more than 6 months decreased Ward's triangle BMD by 8.5 +/- 1.0% and lumbar spine BMD by 4.1 +/- 0.8% during the first 5 months postpartum (both p<0.05). No further BMD loss was seen between 5 and 12 months postpartum. Femoral neck BMD 12 months after delivery was 4.0 +/- 1.1% lower and Ward's triangle BMD 5.3 +/- 1.9% lower than after delivery in mothers breastfeeding for more than 6 months (both p<0.05). BMD loss was higher during the first 5 months following delivery in the lactating women compared with the non-lactating women (p<0.05 comparing lumbar spine BMD loss in lactating mothers versus non-lactating mothers). However, in women with a minimum of four pregnancies the BMD was no lower than in age-matched women with fewer pregnancies. Total duration of lactation was not correlated with the present BMD. In summary, pregnancy seem to confer a low BMD with additional BMD loss during 5 months of lactation. Even if complete restoration in BMD was not reached within 5 months of weaning, women with four pregnancies or more had a BMD no lower than women with two pregnancies or fewer. We conclude that neither an extended lactation period nor multiple pregnancies could be used as a risk factor when predicting women at risk for future osteoporosis.

Absorptiometry, Photon↗

Inhibition of puerperal lactation with 2-mercaptopropionyl-glycine.

OBJECTIVES: Thiols (sulfydryl compounds) have a prolactin-lowering effect in animals. The purpose of our study was to evaluate the effects of orally administered N-2-mercaptopropionyl-glycine (tiopronin) on suppression of lactation and plasma prolactin (PRL) levels in a group of women in the puerperium. METHODS: One hundred women aged 17-37 years were studied. We divided our population in four groups (25 patients in each group). In group I, no medication was administered but only conservative measures were taken (restriction of fluid intake, ice-bags applied on the breasts, tight breast binders). Subjects in group II received tiopronin (200 mg/day) for 14 days. In group III, tiopronin (500 mg/day) was administered for 14 days. Subjects in group IV, took bromocriptine (5 mg/day) for 14 days. Assessment of suppression of lactation was performed clinically and laboratory determinations were obtained before and after 1, 2, 3, 4, and 14 days of treatment. Furthermore, in seven healthy women plasma PRL responses to thyrotropin-releasing hormone (TRH) before and after one week of tiopronin therapy (500 mg/day) were studied. RESULTS: Statistically significant higher percentages of success of lactation suppression were obtained with tiopronin (84% and 88%) and bromocriptine (96%) compared to conservative treatment (60%). In the four groups a significant decrease of PRL was observed. However, in women who received tiopronin and bromocriptine, the levels of PRL after 14 days of therapy were lower compared to the conservative treatment group. Moreover, in the tiopronin groups and the bromocriptine group, lactation was stopped earlier. In the first group (conservative measures) the lactation was suppressed after 13.3+/-5.4 days of treatment. In the groups who received tiopronin (200 mg/day and 500 mg/ day) lactation was suppressed after 4.4+/-1.7 and 4.3+/-1.6 days of treatment. In the bromocriptine group the lactation was stopped after 1.2+/-0.4 days. Bromocriptine treatment was associated with more frequent side effects than the tiopronin. CONCLUSION: Administration of tiopronin in low to moderate doses is effective in suppression of puerperal lactation.

Adolescent↗

Factors influencing the radiative surface temperature of grey seal (Halichoerus grypus) pups during early and late lactation.

The aim of this study was to examine the variation in body surface temperature of grey seal (Halichoerus grypus) pups throughout lactation in response to different environmental conditions. Radiative surface temperatures (T (r), degrees C) of pups were measured on the Isle of May (56 degrees 11'N, 02 degrees 33'W), southeast Scotland from 29 October to 25 November 2003. Records were obtained from a total of 60 pups (32 female and 28 male) from three different pupping sites during early and late lactation. Pups were sheltered from high wind speeds but air temperature, humidity and solar radiation at pupping sites were similar to general meteorological conditions. The mean T (r) of all pups was 15.8 degrees C (range 7.7-29.7 degrees C) at an average air temperature of 10.2 degrees C (range 6.5-13.8 degrees C). There was no difference in the mean T (r) of pups between early and late lactation. However, the T (r) varied between different regions of the body with hind flippers on average 2-6 degrees C warmer than all other areas measured. There was no difference in mean T (r) of male and female pups and pup body mass did not account for the variation in T (r) during early or late lactation. Throughout the day there was an increase in the T (r) of pups and this explained 20-28% of the variation in T (r) depending on stage of lactation. There was no difference in the mean T (r) of pups between pupping sites or associated with different substrate types. Wind speed and substrate temperature had no effect on the T (r) of pups. However, solar radiation, air temperature and relative humidity accounted for 48% of the variation in mean T (r) of pups during early lactation. During late lactation air temperature and solar radiation alone accounted for 43% of the variation in T (r). These results indicate that environmental conditions explain only some of the variation in T (r) of grey seal pups in natural conditions. Differences in T (r) however indicate that the cost of thermoregulation for pups will vary throughout lactation. Further studies examining intrinsic factors such as blubber thickness and activity levels are necessary before developing reliable biophysical models for grey seals.

Animals↗

Effects of 30 versus 60 min of low-load work on intramuscular lactate, pyruvate, glutamate, prostaglandin E(2) and oxygenation in the trapezius muscle of healthy females.

The aim of this study was to investigate the effects of duration of low-load repetitive work on intramuscular lactate, pyruvate, glutamate and prostaglandin E(2) (PGE(2)), and oxygen saturation in the trapezius muscle. Twenty healthy females were studied during baseline rest, during low-load repetitive work for either 30 (REP 30) or 60 min (REP 60) and 60 min recovery. Intramuscular microdialysate (IMMD) samples were obtained, and local muscle tissue oxygenation (%StO(2)) assessed with near-infrared spectroscopy (NIRS). Subjects rated their perceived exertion (Borg CR-10 scale) and capillary blood was sampled for lactate analysis. The results showed a significant increase in IMMD lactate in response to both REP 30 and REP 60 (P < 0.05 and P < 0.01, respectively) and glutamate (P < 0.0001), but no progressive increase with increasing work duration. Both IMMD pyruvate and lactate tended to be significantly increased during the recovery period. No corresponding increase in blood lactate was found. Local muscle %StO(2) did not change significantly in response to work and was not correlated to the IMMD lactate concentration. The ratings of perceived exertion increased in response to work, and remained increased after recovery for REP 60. In conclusion, the results of this study show significantly increased IMMD lactate and, glutamate concentrations in the trapezius muscle of healthy females in response to low-load work, but no progressive increase with increased work duration. Further, they do not indicate that the increased IMMD lactate concentration was caused by a locally decreased or insufficient muscle tissue oxygenation.

Adult↗