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PubMed2003

The aerobic brain: lactate decrease at the onset of neural activity.

The metabolic events of neuronal energetics during functional activity are still partially unexplained. In particular, lactate (and not glucose) was recently proposed as the main substrate for neurons during activity. By means of proton magnetic resonance spectroscopy, lactate was reported to increase during the first minutes of prolonged stimulation, but the studies reported thus far suffered from low temporal resolution. In the present study we used a time-resolved proton magnetic resonance spectroscopy strategy in order to analyse the evolution of lactate during the early seconds following a brief visual stimulation (event-related design). A significant decrease in lactate concentration was observed 5 s after the stimulation, while a recovering of the baseline was observed at 12 s.

Adult↗
PubMed1978

Metabolic changes associated with intake by cows of complete diets containing straw and concentrates in different proportions.

1. Pelleted diets containing concentrates and 0, 200, 400 or 600 g chopped straw/kg were fed ad lib, for 5 h daily to four cows. Concentrations of various energy-yielding metabolites were measured in samples of rumen fluid and jugular blood taken before feeding and at intervals after food was offered. 2. After feeding, the pH of rumen fluid decreased rapidly and the total concentration of volatile fatty acids (VFA) increased; the changes were greatest in the diet containing no roughage. The changes were essentially complete by 135 min at approximately the time feeding stopped. Rumen lactate concentrations were always low and increased significantly only in cows given no roughage. 3. There were highly significant relationships between the peak rumen acetate concentration after a meal and the apparent digestibility of the dry matter of that meal, and the amount of material in the rumen at the end of a meal. The latter relationship resulted in there being no difference between treatments in the total amount of acetate present in the rumen after feeding. 4. In the blood, concentrations of acetate, propionate, beta-hydroxybutyrate (BHB) and lactate all increased after feeding. The increase was prolonged and maximum values were rarely reached before 4-5 h. The highest concentrations of acetate and BHB were found in cows given 20 g roughage/kg and were twice as great as those in cows given no roughage; lower concentrations were found in cows given 400 or 600 g roughage/kg. This information, together with the rumen concentrations of acetate and butyrate, was interpreted as indicating an inhibition of VFA absorption from the rumen of cows given no roughage. 5. Plasma glucose concentrations decreased rapidly for 4 h after feeding, the decrease being greatest in cows given 200 g roughage/kg. Non-esterified fatty acid concentrations also decreased after feeding 200 and 0 g roughage/kg rations, but concentrations were not high at any time. 6. It is concluded that chemical changes in the rumen correspond to feeding behaviour much more closely than changes in blood and therefore any chemostatic regulation of food intake probably occurs at the former site, with acetate playing a major role. Monitoring energy balance at tissue level is likely to be mediated hormonally, with insulin an important factor.

Acetates↗
PubMed1998

Preconditioning in rat hearts is independent of mitochondrial F1F0 ATPase inhibition.

Mitochondrial F1F0 adenosinetriphosphatase (ATPase) is responsible for the majority of ATP synthesis during normoxic conditions, but under ischemic conditions it accounts for significant ATP hydrolysis. A previous study showed that preconditioning in isolated rat hearts is mediated by inhibition of this ATPase during ischemia. We tested this hypothesis in our isolated rat heart model of preconditioning. Preconditioning was accomplished by three 5-min periods of global ischemia separated by 5 min of reperfusion. This was followed by 20 min of global ischemia and 30 min of reperfusion. Preconditioning significantly enhanced reperfusion contractile function and reduced lactate dehydrogenase release but paradoxically reduced the time to onset of contracture during global ischemia. Myocardial ATP was depleted at a faster rate during the prolonged ischemia in preconditioned than in sham-treated hearts, which is consistent with the reduced time to contracture. ATP during reperfusion was repleted more rapidly in preconditioned hearts, which is consistent with their enhanced contractile function. Preconditioning significantly reduced lactate accumulation during the prolonged ischemia. We were not able to demonstrate that mitochondrial F1F0 ATPase (measured in submitochondrial particles) was inhibited by preconditioning before or during the prolonged ischemia. The mitochondrial ATPase inhibitor oligomycin significantly conserved ATP during ischemia and increased the time to the onset of contracture, which is consistent with inhibition of the mitochondrial ATPase. Our results show that preconditioning in rat hearts can be independent of mitochondrial ATPase inhibition as well as ATP conservation.

Adenosine Triphosphate↗
PubMed1979

Age-related differences in lactate distribution kinetics following maximal exercise.

Lactate concentrations were determined at 3, 5, and 7 min of recovery following maximal, continuous, multi-stage treadmill work in 180 men, aged 20-80 years, who were participants of the Baltimore Longitudinal Study of Aging. Each subject was placed into one of six age groups, e.g., 20-29, 30-39, etc. As expected, average concentrations decreased consistently with age. All three sampling times were similar in characterizing maximal lactates for the youngest men. For each older group, except for the oldest, the later values were significantly (p less than 0.01) higher than the 3-min values. For subjects in their 50's and 60's mean concentrations continued to rise through the 7th min. These data suggest that in man there is a progressive, age-related diminution of ability to diffuse lactate from muscle and/or distribute it into its space. This may result in decreased endurance and work capacity and a prolongation of recovery. As an alternative to multiple sampling and analyses for maximal lactate, single blood samples should be obtained no sooner than 5 min of recovery for men up to age 50, and at 7 min for those between 50 and 70 years. Variability among the men over 70 years of age was large enough to preclude single-sample alternatives.

Adult↗
PubMed1997

Sympathetic outflow to the skeletal muscle in humans increases during prolonged light exercise.

To investigate the effects of exercise duration on muscle sympathetic nerve activity (MSNA), heart rate, blood pressure (BP), tympanic temperature, blood lactate concentration, and thigh electromyogram were measured in eight volunteers during 30 min of cycling in the sitting position at an intensity of 40% of maximal oxygen uptake. MSNA burst frequency increased 18 min after exercise was begun (25 +/- 4 bursts/min at baseline and 36 +/- 5 bursts/min at 21 min of exercise), reaching 41 +/- 5 bursts/min at the end of exercise. Heart rate and systolic BP increased during exercise. Twenty minutes after commencement of exercise, however, both systolic and diastolic BP values tended to drop compared with the initial period of exercise. Tympanic temperature increased in a time-dependent manner, and the increment was significant 12 min after exercise was begun. Blood lactate concentration and integrated electromyogram showed no significant changes during exercise. The increased MSNA during prolonged light-intensity exercise may be a secondary effect of the drop in BP as a result of blood redistribution caused by thermoregulation rather than by metaboreflex.

Adult↗
PubMed2000

Oxygen-dependent energetics of anoxia-tolerant and anoxia-intolerant hepatocytes.

The oxygen-dependence of cellular energetics was investigated in hepatocytes from goldfish Carassius auratus (anoxia-tolerant) and rainbow trout Oncorhynchus mykiss (anoxia-intolerant). In goldfish hepatocytes, an approximately 50 % reduction in the rate of oxygen consumption was observed in response to both acute and prolonged hypoxia, the latter treatment shifting the threshold for this reduction to a higher oxygen level. A concomitant increase in the rate of lactate production did not compensate for the decreased aerobic ATP supply, resulting in an overall metabolic depression of 26 % during acute hypoxia and of 42 % during prolonged hypoxia. Trout hepatocytes showed a similar suppression of cellular respiration after prolonged hypoxia but were unresponsive to acute hypoxia. Similarly, the rate of lactate production was unaltered during acute hypoxia but was increased during prolonged hypoxia, metabolic depression amounting to 7 % during acute hypoxia and 30 % during prolonged hypoxia. In both species, the affinity of hepatocytes for oxygen decreased during hypoxia, but this alteration was not sufficient in absolute terms to account for the observed decrease in aerobic ATP supply. Protein synthesis was suppressed in both cell types under hypoxia, whereas Na(+)/K(+)-ATPase activity decreased in trout but not in goldfish hepatocytes, emphasising the importance of membrane function in these cells during conditions of limited energy supply.

Adenosine Triphosphate↗
PubMed2003

Issues concerning the construction of a metabolic model for neuronal activation.

The metabolic events underlying neuronal activity still remain the object of intense debate, in spite of the considerable amount of information provided from different experimental techniques. Indeed, several attempts at linking the cellular metabolic phenomena with the macroscopic physiological changes have not yet attained foolproof conclusions. The difficulties in drawing definitive conclusions are due primarily to the heterogeneity of the experimental procedures used in different laboratories, and also given the impossibility of extrapolating the findings obtained under stationary conditions (prolonged stimulation) to dynamic and transient phenomena. Recently, lactate has received much attention, following its proposal by Pellerin and Magistretti (1994; Proc. Natl. Acad. Sci. USA 91:10625-10629), instead of glucose, as the main substrate for neurons during activity. Several challenging aspects suggest the return to a more conventional view of neuronal metabolism, in which neurons are able to metabolize ambient glucose directly as their major substrate, also during activation.

Animals↗
PubMed1995

Gel-entrapment bioartificial liver therapy in galactosamine hepatitis.

A need exists for an effective, safe bioartificial liver to support patients in fulminant hepatic failure (FHF). The purpose of this study was to determine the treatment efficacy of the novel gel-entrapment porcine hepatocyte bioartificial liver (BAL) in a fatal model of canine hepatic failure. FHF was produced in 27- to 30-kg halothane-anesthetized dogs by bolus infusion of the hepatotoxin D-galactosamine (D-Gal). Three groups were studied during the 48-hr experiment: Group D-Gal (n = 5) received galactosamine, 1.0 g/kg, iv at Time O, Group HepBAL (n = 5) received D-Gal followed by continuous hemoperfusion with the BAL device loaded with approximately 6 billion viable pig hepatocytes starting at Time 24 hr, and three dogs served as healthy controls (Group Control) and received no galactosamine. The primary endpoints were survival and coma development. Group D-Gal demonstrated 100% mortality from liver failure by 42 hr, characterized by a progressive rise in liver enzymes, total bilirubin, ammonia, and lactate and associated with coagulopathy, hypoglycemia, coma, and brain death. BAL therapy significantly delayed the onset of coma and improved survival (median 47 hr vs D-Gal median 36 hr). A significant delay in the rise of lactate and ammonia was also noted. BAL therapy prolonged survival and improved both laboratory and clinical markers of fatal liver failure. These data indicate that this BAL may have clinical utility in supporting human liver failure.

Animals↗
PubMed1997

[High altitude training: sense, nonsense, trends].

Athletes who need high endurance capacity often use training at moderately high altitude (1500-3000 m) to improve oxygen delivery and utilization because of a hypoxia-induced increase of the red blood cell volume and adaptations at the muscular level. As maximal heart rates decrease at high altitude and plasma lactate levels for a given workload change during prolonged exposure to high altitude, it can be difficult to control and adapt the intensity and duration of the work-outs. Furthermore, maximal performance capacity decreases and therefore training intensity at high altitude is usually reduced compared to training at sea level. To avoid these disadvantages at high altitude a concept of living at moderately high altitude and training at lower elevations, termed "live high-train low" evolved, opposing the conventional concept of "live high-train high". A third option using a hypobaric chamber ("live low-train low") is hardly used anymore for training athletes. Studies on the effects of conventional high-altitude training for the improvement of athletic performance often lack a rigorous controlled design and yield controversial results. Regarding the new concept of "live high-train low" there is only one controlled study on college athletes and it shows a minor advantage of this new approach compared to conventional high-altitude training. However, training concepts are especially important for elite competitive athletes, and controlled studies with such individuals are very difficult to perform. Therefore, it appears that today we cannot answer the question of whether altitude-specific physiologic factors or non-altitude-related benefits of training camps account for the success of individual athletes.

Altitude↗
PubMed2004

Perinatal hypothyroidism effects on step-through passive avoidance task in rats.

Previous studies have documented a decrease in the ability of neonatal hypothyroid animals to learn and habituate to maze tests, and an increase in spontaneous activity. However, there is little information about the effects of perinatal (i.e., prenatal and postnatal) hypothyroidism on behaviour. The present study was designed to assess whether perinatal hypothyroidism in rats induces alteration on acquisition and/or short- and long-term retention of a learned response in male Wistar rats. Perinatal hypothyroidism was induced by prolonged (E9-P21) exposure of pregnant and lactating dams to methimazole (administered orally in drinking water, 0.2 mg/ml). Cognitive function was tested at 50 days by means of a step-through passive avoidance task. The effects of perinatal hypothyroidism on the retention of the passive avoidance response are long lasting being, however, highly dependent on the retention after the original training. Our results showed that methimazole-treated rats performed more poorly when retention was tested at long-term (24 h and 7 days) retention interval. Instead, methimazole-treated rats showed longer retrieval latencies than the control ones did when retention was tested at short term (1 h).

Animals↗
PubMed2000

Mastoparan transiently permeabilizes Swiss 3T3 cells and induces c-fos proto-oncogene expression. Role of calcium and G protein activation.

Mastoparan, a widely used tetradecapeptide activator of Gi/Go G proteins, has been reported to be a potent co-mitogen for Swiss 3T3 fibroblasts. However, we have previously shown that the peptide promotes the release of lactate dehydrogenase from Swiss 3T3 cells and evokes only a modest and delayed increase in DNA. We suggested that the ability of the peptide to permeabilise these cells may account for its mitogenic action. Here we show that mastoparan caused a rapid release of fluorescein from cells which had been pre-incubated with fluorescein diacetate, indicating that the peptide increases membrane permeability to small molecules. Furthermore, the release of lactate dehydrogenase evoked by mastoparan was lost after prolonged (24 h) incubation of cells with the peptide. Together, these data indicate that mastoparan-induced cell permeabilisation is both rapid and transient. We have also shown that mastoparan increased c-fos mRNA accumulation and that this response was not influenced by pertussis toxin or indomethacin. Although mastoparan increased the intracellular calcium concentration, the removal of extracellular calcium had no effect on mastoparan stimulated c-fos mRNA accumulation. These data show that mastoparan-induced c-fos mRNA accumulation is not mediated by activation of a G protein and subsequent activation of phospholipase D nor by a non-selective increase in calcium influx. The data have significance for the interpretation of studies in which mastoparan is, or has been, used as an activator of Gi/Go.

3T3 Cells↗
PubMed2006

Crimean-Congo haemorrhagic fever.

Crimean-Congo haemorrhagic fever (CCHF) is an often fatal viral infection described in about 30 countries, and it has the most extensive geographic distribution of the medically important tickborne viral diseases, closely approximating the known global distribution of Hyalomma spp ticks. Human beings become infected through tick bites, by crushing infected ticks, after contact with a patient with CCHF during the acute phase of infection, or by contact with blood or tissues from viraemic livestock. Clinical features commonly show a dramatic progression characterised by haemorrhage, myalgia, and fever. The levels of liver enzymes, creatinine phosphokinase, and lactate dehydrogenase are raised, and bleeding markers are prolonged. Infection of the endothelium has a major pathogenic role. Besides direct infection of the endothelium, indirect damage by viral factors or virus-mediated host-derived soluble factors that cause endothelial activations and dysfunction are thought to occur. In diagnosis, enzyme-linked immunoassay and real-time reverse transcriptase PCR are used. Early diagnosis is critical for patient therapy and prevention of potential nosocomial infections. Supportive therapy is the most essential part of case management. Recent studies suggest that ribavirin is effective against CCHF, although definitive studies are not available. Health-care workers have a serious risk of infection, particularly during care of patients with haemorrhages from the nose, mouth, gums, vagina, and injection sites. Simple barrier precautions have been reported to be effective.

Africa↗
PubMed2000

Functional significance of endothelin B receptors in mediating sinusoidal and extrasinusoidal effects of endothelins in the intact rat liver.

Endothelins (ET) are important regulators of the hepatic microcirculation that act through different receptor subtypes. We investigated functional significance of ET(B) receptors in mediating microhemodynamic effects of ETs in normal and endotoxin (lipopolysaccharide [LPS])-primed rat liver. LPS priming (Escherichia coli O26:B6; 1 mg. kg(-1)) selectively increased ET(B) mRNA and led to a shift in available receptors to the ET(B) subtype. IRL 1620 (an ET(B) agonist) increased portal pressure in a dose-dependent manner, and the increase in ET(B) expression was associated with prolonged portal pressor response in isolated livers. However, lactate dehydrogenase (LDH) release was attenuated and sinusoidal blood flow was better maintained upon ET(B) stimulation in vivo. In isolated livers, portal constriction as well as release of LDH, were substantially increased in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS). In vivo microscopic assessment of sinusoidal perfusion during ET(B) stimulation revealed a disruption of the flow pattern including frequent reversal of the flow direction without significant sinusoid constriction. Sinusoidal flow decreased even further after discontinuation of IRL 1620. Both effects were mediated at extrasinusoidal sites that probably included postsinusoidal sites. However, after pretreatment with L-NAME, IRL 1620 evoked a significant sinusoidal constriction that colocalized with the body of the stellate cell. We propose that ET(B1)-induced NOS activity attenuates ET(B2) (and presumably ET(A))-mediated portal pressor response and stellate cell constriction. Transcriptional activation of the ET(B) gene may have a permissive effect on liver blood flow and protect against hepatocellular damage under pathophysiological conditions associated with endotoxemia.

Animals↗
PubMed2000

New and old in pediatric exercise physiology.

Researchers in pediatric exercise physiology sometimes overlook previously published findings that are similar, or even identical, to their own. The intent of this review is to provide examples for the above pattern. These examples relate to the following topics: 1) is the O2 uptake plateau a necessary criterion for the establishment of maximal O2 uptake in children? 2) children's greater utilization of fat during prolonged exercise, 3) children's lower maximal blood lactate levels, 4) the higher metabolic energy cost of locomotion in children and the possible causes for this phenomenon, and 5) the lower cardiac output and stroke volume in children, at any given O2 uptake.

Child↗
PubMed1988

Skin to skin contact for very low birthweight infants and their mothers.

Separation between mothers and very low birthweight infants is often prolonged with subsequent psychological distress, behaviour problems, and lactation failure. Babies as small as 700 g, who no longer require oxygen, can be safely and enjoyably held naked, except for a nappy, between the mother's breasts for up to four hours a day. We have carried out a randomised trial among babies less than 1500 g. Seventy one infants were randomised. In 35, the mother was helped to hold her baby in skin to skin contact and encouraged to do so whenever she visited the baby. In 36, the mother was encouraged to handle her baby but without skin to skin contact. Mothers using skin to skin contact lactated for four weeks longer on average than the control group. At 6 months of age the infants who had skin to skin contact cried significantly less than the control group. Skin to skin contact can safely and enjoyably be offered to very low birthweight infants especially in developing countries where the mother's lactation is vital.

Child Behavior↗
PubMed2006

Effects of neonatal resveratrol exposure on adult male and female reproductive physiology and behavior.

Resveratrol (RES) is a phytoestrogen that has the ability to bind to estrogen receptors (ERs) and evoke biological effects that parallel those exerted by endogenous and synthetic estrogens. We have shown in previous studies that adult female rats acutely exposed to RES exhibit estrous cycle irregularity, ovarian hypertrophy, and alterations in sociosexual behavior. The present experiment characterizes the prolonged effects of maternal RES exposure throughout the lactational period on subsequent behavior, reproductive tissues, and brain morphology of the adult offspring. During adulthood, female offspring exposed to RES throughout nursing exhibited reduced body weight and increased ovarian weight, but exhibited normal estrous cyclicity and sociosexual behavior, without changes in the volume of the sexually dimorphic nucleus of the preoptic area or the anteroventral periventricular nucleus of the hypothalamus. During adulthood, males exposed to RES throughout nursing exhibited decreased body weight and plasma testosterone concentration, increased testicular weight, and reduced sociosexual behavior. These males also had significantly smaller sexually dimorphic nucleus of the preoptic area volumes and larger anteroventral periventricular nucleus volumes compared to male controls. These data suggest that postnatal exposure to RES may affect estrogenic activity in specific peripheral tissues (e.g., the gonads), while inducing antiestrogenic effects in the brain. Thus, the present study supports recent in vitro and in vivo findings that RES differs from most other phytoestrogens by acting as a possible mixed ER agonist/antagonist, depending on the tissue-specific availability of ER subtypes that are preferentially localized in specific brain regions and throughout the reproductive tract. More importantly these data indicate that maternal consumption of phytoestrogens during lactation can have lasting effects on the offspring that may not become apparent until they reach adulthood.

Animals↗
PubMed1996

Attenuated glycogenolysis reduces glycolytic catabolite accumulation during ischemia in preconditioned rat hearts.

Prior transient episodes of ischemia ("ischemic preconditioning") reduce lactate accumulation and attenuate acidosis during a subsequent prolonged ischemic insult. The mechanisms responsible for attenuated glycolytic catabolite accumulation have not been established but may include earlier exhaustion of glycogen stores, slowed glycogenolysis before complete glycogen depletion, and/or inhibition of glycolysis. Simultaneous repeated measures of myocardial glycogen and the rates of glycolysis, glycogenolysis, glucose utilization, and glycolytic ATP production were obtained during total ischemia by 13C nuclear magnetic resonance spectroscopy in control and ischemia-preconditioned isolated rat hearts. Both [13C]glycolytic and [13C]glycogenolytic rates were significantly lower during total ischemia in preconditioned compared with control hearts (0.77 +/- 0.04 versus 1.06 +/- 0.06 mumol/min per gram wet weight [P < .01] for glycolysis and 0.15 +/- 0.07 versus 0.78 +/- 0.12 mumol/ min per gram wet weight [P < .001] for glycogenolysis, respectively, at 2.5 minutes of ischemia). Slowed glycolysis was present even during the early minutes of ischemia, when significant amounts of available [13C]glycogen were still present. Importantly, the reduction in the rate of glycogenolysis was larger and out of proportion to the reduction in glycolysis and occurred despite an increase in glucose utilization in preconditioned hearts (2.23 +/- 0.15 versus 1.5 +/- 0.10 mumol/min per gram wet weight at 1.25 minutes, P < .01). During early ischemia, conversion of glycogen phosphorylase to the a or "active" form was less in preconditioned than in control hearts (29.1 +/- 2.6% versus 41.2 +/- 9.8%, respectively; P < .05). Taken together, these findings demonstrate that ischemic preconditioning significantly depresses glycolytic catabolite accumulation during sustained ischemia not by more severe glycolytic inhibition or exhaustion of glycogen stores but by depressed glycogenolysis from the onset of ischemia.

Animals↗