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PubMed1995

Effect of choline supplementation on fatigue in trained cyclists.

The availability of choline, the precurser of the neurotransmitter, acetylcholine, in the diet is sufficient to provide the body's requirements under normal conditions. However, preliminary evidence indicates that depletion of choline may limit performance, while oral supplementation may delay fatigue during prolonged efforts. A double-blind cross-over design was used to determine the relationship between plasma choline and fatigue during supramaximal brief and submaximal prolonged activities. Twenty male cyclists (ages 23-29) with maximal aerobic power (VO2max) between 58 and 81 ml.min-1.kg-1 were randomly divided into BRIEF (N = 10) and PROLONGED (N = 10) groups. One hour after drinking a beverage with or without choline bitartrate (2.43 g), cyclists began riding at a power output equivalent to approximately 150% (BRIEF) and 70% (PROLONGED) of VO2max at a cadence of 80-90 rpm. Time to exhaustion, indirect calorimetry and serum choline, lactate, and glucose were measured. Increases in choline levels of 37 and 52% were seen within one hour of ingestion for BRIEF and PROLONGED groups, respectively. Neither group depleted choline during exercise under the choline or placebo conditions. Fatigue times and work performed under either test condition for the BRIEF or PROLONGED groups were similar. Consequently, trained cyclists do not deplete choline during supramaximal brief or prolonged submaximal exercise, nor do they benefit from choline supplementation to delay fatigue under these conditions.

Administration, Oral↗

PubMed1987

Influence of pregnancy and lactation on serum and breast fluid estrogen levels: implications for breast cancer risk.

We investigated estrogen (estrone and estradiol) levels in serum and in nipple aspirates of breast fluid in relation to reproductive and menopausal characteristics in 104 normal women. In general, breast fluid and serum estrogen levels were not correlated and breast fluid estrogen levels were approximately 5 to 45 times higher than serum levels. Serum estrogen levels were lower in post-menopausal than in pre-menopausal women. In contrast, breast fluid estrogen levels were approximately the same in pre- and post-menopausal women. Breast fluid estrogen mean levels were lower in pre-menopausal parous women than in nulligravidous or nulliparous women whereas serum estrogen levels did not differ in these 3 groups. Breast fluid estrogen levels were positively correlated with months since last birth or since last breast-feeding. Estrogen levels were low in nipple aspirates of breast milk but gradually increased in breast fluid of non-lactating women over a period of several years after cessation of lactation. Serum estrogen levels did not increase with months since last breast-feeding. We were unable to evaluate the post-partum effect of pregnancy without lactation due to the small numbers of these subjects. The high concentrations of estrogen in breast fluid and the absence of a relationship to serum estrogen levels may explain why prior serum studies have failed to link variations in serum estrogens with breast cancer risk. The prolonged low levels of breast fluid estrogens following full-term birth and lactation may, in part, provide a mechanism by which parity reduces breast cancer risk.

Body Fluids↗

PubMed1986

Cardiorespiratory response to exercise before and after acute beta-adrenoreceptor blockade in nonsmokers and chronic smokers.

To evaluate the effects of chronic smoking on exercise performance we studied 5 smokers and 7 nonsmokers of comparable age and physical characteristics. The resting heart rate in smokers (75 +/- 3 beats/min; mean +/- SD) was significantly (P less than 0.01) higher than in nonsmokers (64 +/- 5). During exercise on a bicycle ergometer the heart rate remained significantly (P less than 0.01) higher in smokers than in nonsmokers. After exercise, the heart rate in nonsmokers settled to 78 +/- 9 beats/min at 10 minutes compared with 105 +/- 11 (P less than 0.01) in smokers. Oxygen consumption was similar in both groups throughout. Beta-adrenergic blockade reduced the exercise tachycardia in both groups but the heart rate for the same workload remained significantly (P less than 0.01) higher in smokers. Beta-blockade significantly reduced (P less than 0.05) oxygen consumption in nonsmokers but not in smokers who also incurred a significantly (P less than 0.05) greater oxygen debt and had higher serum lactate levels. These differences were attributed mainly to carboxyhaemoglobinaemia and partly to the effect of prolonged smoking on the heart and on intermediary metabolism.

Adult↗

PubMed2004

Bisphenol-A exposure during pregnancy and lactation affects maternal behavior in rats.

In mammals, endogenous estrogens are crucial for sexual differentiation during the perinatal period, and the modulation in adulthood of many neuroendocrine and behavioral functions involved in reproduction. In rats, the estrogenic environment during pregnancy and lactation affects directly maternal behavior. This experiment was aimed to test whether the exposure to the estrogenic compound bisphenol-A (BPA; 0.040 mg/kg/die, orally) of adult female rats, from mating to weaning of the pups, could alter maternal behavior. An appropriate methodology was applied to reveal differences in the behavior of dams directed to male and female pups, testing the dams on postnatal days 3-4 and 8-9. Results show different maternal behavioral patterns towards male and female pups of control mothers, with more ano-genital licking to males than to females. Exposure of mothers to BPA modified their behavior, reducing specific components of maternal behavior, both active and passive, irrespective of the sex of pups and the period of observation. This experiment shows that maternal behavior is affected by a prolonged exposure to a low dose of BPA during pregnancy and lactation, thus suggesting an effect on neural circuits in adulthood.

Animals↗

PubMedDate not supplied

Biochemical and physiologic consequences of carnitine palmityltransferase deficiency.

A patient with a long history of exercise-unduced pain developed myoglobinuria and respiratory failure following extensive exercise (football). Although muscle histochemistry was normal, tissue oxidation of 14C-labeled palmitate was decreased, and muscle carnitine palmityltransferase (CPT) activity was one-tenth of normal. During fasting, his creatine kinase (CK) rose from 127 mu/ml to 278 mu/ml and blood ketones failed to exhibit a normal rise. Triglycerides were normal, as was fatty-acid mobilization. Prolonged exercise resulted in an inordinately increased CK with only moderate elevations in lactate. Treatment with medium-chain triglycerides did not alter his symptoms or improve exercise performance. Pain on exercise is a common complaint, but the occurrence of myoglobinuria points to a defect of energy metabolism; Screening for defects of fat utilization may be accomplished by the prolonged-exercise test, invitro oxidation of 14C-labeled substrates, and prolonged fasting.

Acyltransferases↗

PubMed1999

Decreased exercise blood lactate concentrations after respiratory endurance training in humans.

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (VO2) during exercise and their relationship to performance, 20 healthy, active subjects underwent 30 min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1 (SD 4.0) min (P < 0.001) and cycling endurance time was prolonged from 20.9 (SD 5.5) to 26.6 (SD 11.8) min (P < 0.01) after respiratory training. The VO2 did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8 (SD 1.9) mmol x l(-1), P < 0.001] as well as at the end of the endurance exercise [10.4 (SD 3.6) vs 9.6 (SD 2.7) mmol x l(-1), P < 0.01] test after respiratory training. We speculate that the reduction in blood lactate concentration was most likely caused by an improved lactate uptake by the trained respiratory muscles. However, reduced exercise blood lactate concentrations per se are unlikely to explain the improved cycling performance after respiratory endurance training.

Adult↗

PubMed1975

Systemic hypotension in neurosurgery.

The authors review the intraoperative use of elective hypotension to reduce the probability of hemorrhage, to increase pliability of the aneurysmal sac for ease of clip application, and to control hemorrhage. The optimum agent and techniques for lowering systemic blood pressure remain controversial, but trimethaphan, sodium nitroprusside, and halothane have been found most useful. When cerebral blood flow falls below the brain's capacity to autoregulate, distinct time-related alterations occur biochemically and histologically. The profile of prolonged reduced adenosine triphosphate (ATP), low phosphocreatine, low glucose, and elevated lactate and lactate/pyruvate ratio is associated with swelling of perivascular astrocytes and "blebbing" of vascular endothelial cells with subsequent cerebral damage. To prevent permanent alteration it is desirable to observe time constraints and to employ other means of protection such as hypothermia, although the authors believe the latter unnecessary for short hypotensive periods. It has been proposed, but not substantiated, that anesthetics which depress rate of cerebral oxygen consumption but do not affect cerebral ATP level protect the brain from hypotension. Several investigations suggest that halothane, a vasodiltor, satisfies the safety requirement. The most prominent contraindication to halothane, however, is elevation of intracranial pressure. At present hypotensive surgery for aneurysmorrhapy is usually performed when intracranial pressure has returned to normal. Experimentally the electroencephalogram has been observed to show alterations prior to biochemical parameters for following brain vulnerability, so that it conceivably could be an effective monitoring technique during prolonged profound hypotension.

Adenosine Triphosphate↗

PubMed2005

Prognostic value of procalcitonin in children with meningococcal sepsis.

OBJECTIVE: To compare procalcitonin, lactate, and C-reactive protein as prognostic markers in children with meningococcal septic shock. DESIGN: Prospective observational study. SETTING: Alder Hey Children's Hospital, Liverpool, UK. PATIENTS: Children admitted to our hospital during a 16-month period with a diagnosis of meningococcal sepsis. RESULTS: Plasma procalcitonin at admission was significantly higher in children with septic shock (median, 73.80 vs. 16.44 ng/mL), those requiring ventilation (median, 47.02 vs. 12.00 ng/mL), and those with a duration of hospital stay >10 days (median, 131.35 vs. 19.26 ng/mL). Both procalcitonin and lactate reliably discriminated between those children with septic shock (area under the curve [AUC] = 0.85 and 0.84, respectively) and durations of hospital stay exceeding 10 days (AUC = 0.87 and 0.79, respectively) and those without, but C-reactive protein did not. Procalcitonin alone reliably discriminated between those children requiring ventilation and those who did not (AUC = 0.72). CONCLUSION: Procalcitonin is a reliable prognostic marker of septic shock, requirement for ventilation, and prolonged hospital stay in children with meningococcal sepsis and performs better than lactate and C-reactive protein.

C-Reactive Protein↗

PubMedDate not supplied

[Effect of large doses of progesterone on pregnancy, lactation and morphology of the corpora lutea].

Cells of the corpora lutea of albino rats were examined histochemically after the administration of high perogesteron doses at various periods of pregnancy and lactation. Before the prepartum exogenous progesteron failed to influence the fetal development, during the prepartum--led to prolongation of the periods of pregnancy, and by the 25th day--to the intrauterine death of the fetuses in 100% of cases. Progesteron administration during the lactation increased the lactic acid function. Saturation of the organism with exogenous progesteron was accompanied by depression of the secretory activity of the lutein cells without any functional changes in the interstitial cells. Metabolic processes were disturbed in the lutein cells, this being expressed in the interruption of formation of the secretory vacuoles, reduction of the plate complex of Golgi function and a sharp depression of the lipid synthesis. Mitochondria are subject to disintegration. A comparative morphofunctional analysis of the corpus luteum cells under conditions of directed changed hormonal balance confirmed the concept on the separate production of progestins and estrogens by two types of the secretory cells.

Alkaline Phosphatase↗

PubMed1993

Synthesis-secretion coupling of insulin: effect of pregnancy and lactation.

Synthesis-secretion coupling of insulin was determined using perfused pancreata taken from either control, pregnant, or lactating female Sprague-Dawley rats. The pancreata were stimulated for 3 h with one of the two glucose concentrations used: either 150 or 300 mg/dl. In the case of pregnancy, the pancreata exhibited a twofold hypersecretory activity in response to the physiological glucose level of 150 mg/dl. Net insulinogenesis did not occur in response to the normoglycemic glucose concentration, and, as with the controls, there was an overall depletion of insulin stores. There was no insulin hypersecretion at the hyperglycemic level of 300 mg/dl, but net insulinogenesis did occur; however, it matched that of the controls. Therefore, the hypersecretion of insulin ascribed to pregnancy appears to be a function of the secretory process only, to be most demonstrable under normoglycemic conditions, and not to be due to enhanced synthesis-secretion coupling. In the case of pancreata from lactating rats, just the converse was observed. Compared with controls, there was no substantial difference in insulin secretion by pancreata from lactating rats at either glucose level or of insulinogenesis under normoglycemia conditions. However, when glucose was at a hyperglycemic load in the lactating group, not only was there no net insulinogenesis, but this condition actually resulted in a depletion of intracellular insulin stores (as opposed to both the control and the pregnant groups). This suggests that the hypoinsulinemia noted during lactation may be related to a reduced capacity of those beta-cells to synthesize insulin the face of prolonged hyperglycemic stimulation.

Animals↗

PubMed2003

[Metformin-associated lactic acidosis precipitated by acute renal failure].

In type II diabetes treated with metformin, lactic acidosis is a rare but severe complication. Commonly patients with lactic acidosis show signs of shock, tissue hypoxia, acute hepatic or renal failure and the link between metformin therapy and lactic acidosis may be coincidental, associated or causal. Excessive plasma metformin concentrations show that lactic acidosis is due to a toxicological mechanism. The case of a 65-year-old woman with type II diabetes, in whom severe type B2 lactic acidosis secondary to metformin was precipitated by acute renal failure, is presented. The association of diuretics with non-steroidal anti-inflammatory drugs and colchicine was responsible for a volume depletion and an acute renal failure. Initial serum creatinine was 643 micromol x l(-1) and arterial blood gas analysis revealed a pH of 7.01. Aggressive volume expansion and correction of the acidosis with intravenous bicarbonate therapy failed. At the intensive care unit, calculated anion gap was 35 mmol x l(-1) (normal range 10-18) and lactate concentration was 12.4 mmol x l(-1), liver profile was normal. Prolonged haemodialysis using bicarbonate dialysate resulted in a favourable outcome. Toxicology confirmed retrospectively the presence of a plasma concentration of metformine of 20 mg x l(-1) (normal <2). One month after this episode she has made a recovery of tubular necrosis, although no longer prescribed metformin. Metformin should be temporally stopped when acute renal failure occurs or is anticipated; patient with acute renal failure and high calculated anion gap should benefit from lactate measurements. Early bicarbonate haemodialysis is an adequate treatment of lactic acidosis caused by accumulation of metformin associated with acute renal failure

Acidosis, Lactic↗

PubMed1984

Cell proliferation in bone marrow cells of severely malnourished animals.

The cell proliferation of bone marrow cells in rats, suffering from severe malnutrition during the lactation period, was investigated by using bromodeoxyuridine (BdUr) mixed with 100 mg of activated charcoal injected i.p. The undernourished rats had significantly more mitosis in the first generation (82.6%) than did well-nourished rats (44.6%) at 18 hours after the BdUr injection, whereas there were more cells in second division metaphase in the well-nourished (54.7%) than in the undernourished group (13.7%). Our results seem to indicate that malnutrition produces a prolongation in the time of proliferation of bone marrow cells during the lactation period. This agrees with other reports that used other cell systems in experimental animals and severely malnourished children.

Animals↗

PubMed1998

Opposite fluxes of glutamine and alanine in the splanchnic area are an efficient mechanism for nitrogen sparing in rats.

Glutamine release by the liver constitutes a process of nitrogen salvage through the recycling of a part of the nitrogen, which prevents irreversible nitrogen losses as urea. The aim of this work was to study the nitrogen cycling in the splanchnic bed under different nutritional conditions: fed state, postabsorptive state (16 h food deprivation) or prolonged starvation (24 or 40 h). Rats were adapted to a 15% casein diet for 15 d and then sampled. The digestive, hepatic and splanchnic balances of glucose, lactate, ketone bodies, urea and amino acids were determined. There was a net release of lactate and alanine by the digestive tract, due to the high rate of glycolysis and glutaminolysis. During prolonged starvation, ketone bodies became major energy fuel for the intestine. In fed rats, there was a net uptake of most amino acids by the liver, except for glutamine and glutamate. Urea, glutamine and glutamate released represented 33, 24 and 6% of total nitrogen taken up by the liver, respectively. In postabsorptive rats, compared with fed rats, there was a significant reduction of ureagenesis, and glutamine became the major form of nitrogen released by the liver. In fact, nitrogen cycling in the form of glutamine or glutamate in the liver may be interpreted as a nitrogen salvage process, rather than as an acid-base control process. In the splanchnic area, in parallel with a highly active cycling of glucose as lactate, there exists a nitrogen cycling involving opposite fluxes of glutamine and alanine.

Alanine↗

PubMed1974

Substrate turnover during prolonged exercise in man. Splanchnic and leg metabolism of glucose, free fatty acids, and amino acids.

Arterial concentrations and substrate exchange across the leg and splanchnic vascular beds were determined for glucose, lactate, pyruvate, glycerol, individual acidic and neutral amino acids, and free fatty acids (FFA) in six subjects at rest and during 4 h of exercise at approximately 30% of maximal oxygen uptake. FFA turnover and regional exchange were evaluated using (14)C-labeled oleic acid. The arterial glucose concentration was constant for the first 40 min of exercise, but fell progressively thereafter to levels 30% below basal. The arterial insulin level decreased continuously, while the arterial glucagon concentration had risen fivefold after 4 h of exercise. Uptake of glucose and FFA by the legs was markedly augmented during exercise, the increase in FFA uptake being a consequence of augmented arterial levels rather than increased fractional extraction. As exercise was continued beyond 40 min, the relative contribution of FFA to total oxygen metabolism rose progressively to 62%. In contrast, the contribution from glucose fell from 40% to 30% between 90 and 240 min. Leg output of alanine increased as exercise progressed. Splanchnic glucose production, which rose 100% above basal levels and remained so throughout exercise, exceeded glucose uptake by the legs for the first 40 min but thereafter failed to keep pace with peripheral glucose utilization. Total estimated splanchnic glucose output was 75 g in 4 h, sufficient to deplete approximately 75% of liver glycogen stores. Splanchnic uptake of gluconeogenic precursors (lactate, pyruvate, glycerol, alanine) had increased 2- to 10-fold after 4 h of exercise, and was sufficient to account for 45% of glucose release at 4 h as compared to 20-25% at rest and at 40 min of exercise. In the case of alanine and lactate, the increase in precursor uptake was a consequence of a rise in splanchnic fractional extraction. It is concluded that during prolonged exercise at a low work intensity (a) blood glucose levels fall because hepatic glucose output fails to keep up with augmented glucose utilization by the exercising legs; (b) a large portion of hepatic glycogen stores is mobilized and an increasing fraction of the splanchnic glucose output is derived from gluconeogenesis; (c) blood-borne substrates in the form of glucose and FFA account for a major part of leg muscle metabolism, the relative contribution from FFA increasing progressively; and (d) augmented secretion of glucagon may play an important role in the metabolic adaptation to prolonged exercise by its stimulatory influence on hepatic glycogenolysis and gluconeogenesis.

Abdomen↗

PubMed2002

Increases in muscle MCT are associated with reductions in muscle lactate after a single exercise session in humans.

To investigate the effects of a single session of prolonged cycle exercise [60% peak O2 uptake (VO2 peak) for 5-6 h] on metabolic adaptations in working vastus lateralis muscle, nine untrained males (peak O2 uptake = 47.2 +/- 1.1 ml x kg(-1) x min(-1), means +/- SE) were examined before (Pre) and at 2 (Post-2), 4 (Post-4), and 6 (Post-6) days after the training session. On the basis of 15 min of cycle exercise at 59% VO2 peak, it was found that training reduced (P < 0.05) exercise muscle lactate (mM) at Post-2 (6.65 +/- 0.69), Post-4 (7.74 +/- 0.63), and Post-6 (7.78 +/- 1.2) compared with Pre (10.9 +/- 1.3). No effect of training was observed on exercise ATP, phosphocreatine, and glycogen levels. After the single session of training, plasma volumes were elevated (P < 0.05) at Post-2 (6.7 +/- 1.7%), Post-4 (5.86 +/- 1.9), and Post-6 (5.13 +/- 2.5). The single exercise session also resulted in elevations (P < 0.05) in the monocarboxylate transporters MCT1 and MCT4 throughout the 6 days after exercise. Although epinephrine and norepinephrine both increased with exercise, only norepinephrine was reduced (P < 0.05) with training and only at Post-4. These results indicate that regulation of cellular lactate levels occurs rapidly and independently of other metabolic adaptations. It is proposed that increases in MCT and plasma volume are at least partly involved in the lower muscle lactate content observed after the training session by increasing lactate membrane transport and removal, respectively.

Adult↗

PubMed1997

Respective oxidation of 13C-labeled lactate and glucose ingested simultaneously during exercise.

The purpose of this experiment was to measure, by using 13C labeling, the oxidation rate of exogenous lactate (25 g, as Na+, K+, Ca2+, and Mg2+ salts) and glucose (75 g) ingested simultaneously (in 1,000 ml of water) during prolonged exercise (120 min, 65 +/- 3% maximum oxygen uptake in 6 male subjects). The percentage of exogenous glucose and lactate oxidized were similar (48 +/-3 vs. 45 +/- 5%, respectively). However, because of the small amount of oral lactate that could be tolerated without gastrointestinal discomfort, the amount of exogenous lactate oxidized was much smaller than that of exogenous glucose (11.1 +/- 0.5 vs. 36.3 +/- 1.3 g, respectively) and contributed to only 2.6 +/- 0.4% of the energy yield (vs. 8.4 +/- 1.9% for exogenous glucose). The cumulative amount of exogenous glucose and lactate oxidized was similar to that observed when 100 g of [13C]glucose were ingested (47.3 +/- 1.8 vs. 50.9 +/- 1.2 g, respectively). When [13C]glucose was ingested, changes in the plasma glucose 13C/12C ratio indicated that between 39 and 61% of plasma glucose derived from exogenous glucose. On the other hand, the plasma glucose 13C/12C ratio remained unchanged when [13C]lactate was ingested, suggesting no prior conversion into glucose before oxidation.

Adult↗

PubMed1985

[Suppression of the adrenal cortex by infusion of etomidate in general anesthesia].

The effects of anaesthesia with fentanyl and prolonged etomidate infusion (0.8 mg/kg/h) on the peroperative and postoperative change in blood concentrations of aldosterone, cortisol, dehydroepiandrosterone, ACTH, epinephrine, norepinephrine, dopamine, glucose, lactate and free fatty acids (FFA) were investigated in connection with major abdominal surgery. During surgery and anaesthesia with prolonged etomidate infusion no significant alterations in plasma catecholamine concentrations were observed. In contrast, basal plasma levels of ACTH (20.0 +/- 9.5 pg/ml----352.8 +/- 150.8 pg/ml) were elevated in all patients. Despite this endogenous ACTH stimulus, aldosterone (121.8 +/- 19.4 pg/ml----58.4 +/- 10.4 pg/ml) and cortisol (12.3 +/- 2.84 micrograms/dl----5.79 +/- 1.2 micrograms/dl) and dehydroepiandrosterone (2.28 +/- 1.09 ng/ml----1.27 +/- 0.25 ng/ml) levels were markedly depressed in every patient during the perioperative period. Twenty-four hours after surgery the basal steroid values were within or above normal limits.

Abdomen↗

PubMed1965

Constitution, viability, and lactate dehydrogenase in stationary-phase L-cell suspension cultures.

Starved suspension cultures of L cells exhibit a plateau phase of short duration followed by loss of key cellular constituents and rapidly decreasing viability. In contrast, regularly fed,. undiluted cultures remain stationary at a high cell density for prolonged periods without structural alterations or loss of viability. The L cells contain a single lactate dehydrogenase isozyme with an electrophoretic mobility similar to that of lactate-dehydrogenase-5. High-density stationary cultures show a tenfold increase of the specific activity of this enzyme and a recurrent biphasic pattern of carbohydrate utilization with, first, production and, later, consumption of lactate.

Culture Media↗