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PubMed1994

Kidney function during exercise in healthy and diseased humans. An update.

Exercise induces profound changes in renal haemodynamics and protein excretion. The rate of ultrafiltration across the glomerular capillary is determined by the imbalance between the transcapillary hydraulic and colloid osmotic pressure gradients. Despite a major reduction in the renal plasma flow, the filtration fraction can double with maximal exercise, preserving the transfer of metabolites or substances through the glomerulus. Tubular processes and excretion rates are modified by exercise. Despite large increases in plasma lactate during strenuous exercise, renal excretion plays a limited role in lactate metabolism. Apparently, the mechanism of transcellular transport of lactate is saturated during severe exercise. Urea reabsorption is enhanced during prolonged exercise, and this process may act to limit the dehydration of an individual. As uric acid transport is also carrier-mediated, it appears that there is no saturation of the carrier system during prolonged exercise. Postexercise proteinuria is directly related to the intensity of exercise rather than to its duration. This excretion of excess proteins is a transient state with a half-time decay of about 1 hour. The increased clearance of plasma proteins suggests an increased glomerular permeability and a partial inhibition of tubular reabsorption. Studies suggest that exercise decreases the glomerular electrostatic barrier and facilitates transfer of macromolecules. Postexercise proteinuria appears to be age-dependent. Nephropathy is a common observation in the diabetic patient. In young and adult diabetic patients, exhaustive physical exercise does not provoke an enhanced dysfunction of the kidney to what is already found in healthy individuals. Heart and kidney transplant patients have a lesser postexercise proteinuria as compared with healthy individuals.

Adolescent↗

PubMed1995

[Effect of DL-butylphthalide (NBP) on mouse brain energy metabolism in complete brain ischemia induced by decapitation].

The effects of NBP on gasping and brain energy metabolism after complete brain ischemia in mice subjected to decapitation were investigated. The levels of ATP, phosphocreatine (PCr) and lactate were determined by the method of Lowry. The data indicated that NBP at 112.5 or 250 mg.kg-1 sc can significantly prolong the duration of gasping and at the dose of 150 or 200 mg.kg-1 sc reduce the level of lactate and increase the levels of ATP and PCr after complete brain ischemia. The results suggest that NBP may have brain protective action and improve ischemic brain energy metabolism.

Adenosine Triphosphate↗

PubMedDate not supplied

[Structure and functional changes in the gastric intramural nervous plexus in emotionally stressed rats exposed to low doses of long-term ionizing irradiation and lead].

Changes in the catecholamine content in adrenergic fibres, acetylcholinesterase activity, and in the energy metabolism enzymes lactate dehydrogenase and succinate dehydrogenase in neurons of the gastric intramural plexus during emotional stress in rats a day after combined exposure to prolonged (30 days) ionizing radiation in a total dose 1.0 Gy and 0.6 mg/kg lead were studied. A decrease in catecholamines in adrenergic fibres and acetylcholinesterase and lactate dehydrogenase activity in neurons was observed. An enhanced sensitivity of the gastric intramural plexus after the prolonged exposure to small doses of ionizing radiation and lead in conditions of emotional stress was suggested.

Animals↗

PubMed2002

Tolerance against ischemic neuronal injury can be induced by volatile anesthetics and is inducible NO synthase dependent.

BACKGROUND AND PURPOSE: We tested whether volatile anesthetics induce neuroprotection that is maintained for a prolonged time. METHODS: Rats were pretreated for 3 hours with 1 minimal anesthetic concentration of isoflurane or halothane in normal air (anesthetic preconditioning [AP]). The animals were subjected to permanent middle cerebral artery occlusion (MCAO) at 0, 12, 24, or 48 hours after AP. Halothane-pretreated animals were subjected to MCAO 24 hours after AP. Histological evaluation of infarct volumes was performed 4 days after MCAO. Cerebral glucose utilization was measured 24 hours after AP with isoflurane. Primary cortical neuronal cultures were exposed to 1.4% isoflurane for 3 hours. Oxygen-glucose deprivation (OGD) was performed 24 hours after AP. Injury was assessed 24 hours later by measuring the release of lactate dehydrogenase into the medium 24 hours after OGD. RESULTS: Isoflurane anesthesia at 0, 12, and 24 hours before MCAO or halothane anesthesia 24 hours before MCAO significantly reduced infarct volumes (125+/-42 mm3, P=0.024; 118+/-51 mm3, P=0.008; 120+/-49 mm3, P=0.009; and 121+/-48 mm3, P=0.018, respectively) compared with control volumes (180+/-51 mm3). Three hours of isoflurane anesthesia in rats did not have any effect on local or mean cerebral glucose utilization measured 24 hours later. Western blot analysis from cortical extracts of AP-treated animals revealed an increase of the inducible NO synthase (iNOS) protein beginning 6 hours after AP. The iNOS inhibitor aminoguanidine (200 mg/kg IP) eliminated the infarct-sparing effect of AP. In cultured cortical neurons, isoflurane exposure 24 hours before OGD decreased the OGD-induced release of lactate dehydrogenase by 49% (P=0.002). CONCLUSIONS: Pretreatment with volatile anesthetics induces prolonged neuroprotection in vitro and in vivo, a process in which iNOS seems to be critically involved.

Anesthetics, Inhalation↗

PubMed1985

Maternal and fetal metabolic effects of prolonged ritodrine infusion.

To investigate metabolic and endocrine changes in the fetus during prolonged maternal tocolysis with beta sympathomimetic drugs, ritodrine hydrochloride (2.1 micrograms/kg per minute) was infused into pregnant sheep near term. Confirming earlier studies, maternal plasma metabolite and hormone levels changed greatly during the first six to eight hours of infusion. Changes in the fetus paralleled these closely: glucose, lactate, and insulin increased sharply, but glucagon and alpha-amino acid nitrogen decreased. After this, most maternal and fetal plasma metabolite and hormone levels returned to the normal range and were unchanged by infusion for 72 to 96 hours. Fetal lactate levels, however, remained elevated. Similar changes occurred during interrupted maternal infusions of ritodrine. Prolonged infusion of ritodrine leads to diminished responsiveness in beta-adrenergic mechanisms regulating maternal plasma metabolite and hormone levels. Comparable unresponsiveness of fetal beta-adrenergic mechanisms, though less certain, could increase hazards during delivery and adaptation to postnatal life.

Adrenal Cortex Hormones↗

PubMed1992

A comparative evaluation of the individual anaerobic threshold and the critical power.

The individual anaerobic threshold (IAT) is defined as the highest metabolic rate where blood lactate (La) concentrations are maintained at a steady-state during prolonged exercise. The asymptote of the hyperbolic relationship between power output and time to fatigue has been defined as the critical power (CP), which, in theory, represents the highest metabolic rate where a steady-state response can be achieved during prolonged exercise. Since IAT and CP may define the same power output, the purpose of this study was to compare the gas exchange, blood La, and acid-base responses during exercise at the metabolic rates defined as IAT and CP. Fourteen males performed a maximal incremental cycle exercise test that was followed by a light active recovery period to determine IAT. Subsequently, subjects exercised to fatigue at five power outputs (calculated to elicit from 90% to 110% VO2max) to determine CP. IAT occurred at a significantly lower power output and VO2 (235 +/- 44 W and 2.97 +/- 0.47 l.min-1, respectively) compared with CP (265 +/- 39 W and 3.35 +/- 0.41 l.min-1, respectively). During 30 min of exercise at IAT, blood La levels increased during the initial 10 min to 3.9 +/- 1.9 mmol.l-1 but did not change during the final 15 min. Blood pH decreased to 7.32 +/- 0.04 at 5 min and did not change thereafter, while PCO2 fell from 41.5 +/- 3.2 mm Hg at 5 min to 36.2 +/- 3.6 mm Hg at 30 min. Only one subject completed 30 min of exercise at CP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Incremental test protocol, recovery mode and the individual anaerobic threshold.

The individual anaerobic threshold (IAT) is defined as the highest metabolic rate at which blood lactate (LA) concentrations are maintained at a steady-state during prolonged exercise. The purpose of this study was to compare the effects of active and passive recovery on the determination of IAT following both a submaximal or maximal incremental exercise test. Seven males (VO2max = 57.6 +/- 5.8 ml.kg-1.min -1) did two submaximal, incremental cycle exercise tests (30 W and 4 min per step) and two maximal incremental tests. Blood was sampled repeatedly during exercise and for 12 min during the subsequent recovery period, which was passive for one submaximal and one maximal test and active (approximately 35% VO2max) during the other tests. An IAT metabolic rate and power output were calculated for the submax-passive (IATsp, LA = 1.85 +/- 0.42 mmol.l-1), max-passive (IATmp, LA = 3.41 +/- 1.14 mmol.l-1), submax-active (IATsa, LA = 2.13 +/- 0.45 mmol.l-1) and max-active (IATma, LA = 3.44 +/- 0.73 mmol.l-1) protocols. At weekly intervals, the subjects exercised for 30 min at one of the four IAT metabolic rates. Active recovery did not affect the calculation of IAT, but following the maximal incremental tests, IAT occurred at a higher (p less than 0.05) power output, absolute VO2 and %VO2max (71% VO2max) compared with the IAT determined with the submaximal incremental tests (61% VO2max).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Adaptations to training at the individual anaerobic threshold.

The individual anaerobic threshold (Th(an)) is the highest metabolic rate at which blood lactate concentrations can be maintained at a steady-state during prolonged exercise. The purpose of this study was to test the hypothesis that training at the Th(an) would cause a greater change in indicators of training adaptation than would training "around" the Th(an). Three groups of subjects were evaluated before, and again after 4 and 8 weeks of training: a control group, a group which trained continuously for 30 min at the Th(an) intensity (SS), and a group (NSS) which divided the 30 min of training into 7.5-min blocks at intensities which alternated between being below the Th(an) [Th(an) -30% of the difference between Th(an) and maximal oxygen consumption (VO2max)] and above the Th(an) (Th(an) +30% of the difference between Th(an) and VO2max). The VO2max increased significantly from 4.06 to 4.27 l.min-1 in SS and from 3.89 to 4.06 l.min-1 in NSS. The power output (W) at Th(an) increased from 70.5 to 79.8% VO2max in SS and from 71.1 to 80.7% VO2max in NSS. The magnitude of change in VO2max, W at Th(an), % VO2max at Th(an) and in exercise time to exhaustion at the pretraining Th(an) was similar in both trained groups. Vastus lateralis citrate synthase and 3-hydroxyacyl-CoA-dehydrogenase activities increased to the same extent in both trained groups. While all of these training-induced adaptations were statistically significant (P < 0.05), there were no significant changes in any of these variables for the control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1981

The effect of compensation of acidosis on survival in endotoxin shock.

IP injection of 10 mg E. coli endotoxin in fasted female rats causes 100% mortality while hemodynamic effects are absent. A progressive fall in blood glucose to extremely low values with a concomitant rise in plasma lactate is recorded. Plasma pH falls below 7.00. Infusion of glucose or glucose and insulin does not prolong the survival time. An infusion of 5% NaHCO3 preventing the terminal acidosis has no effect on the survival time and dose not affect the blood glucose and plasma lactate concentrations. Artificial ventilation has no effect on survival time or on blood glucose and plasma lactate concentrations.

Acidosis↗

PubMed1987

The effect of mild hypoxemia maintained for twenty-four hours on maternal and fetal glucose, lactate, cortisol, and arginine vasopressin in pregnant sheep at 122 to 139 days' gestation.

The effects of prolonged mild hypoxemia on the fetus have received little attention. We investigated the response to a decrease in fetal arterial Po2 of 5 mm Hg or less sustained for a period of 24 hours in the chronically instrumented fetal lamb. Hypoxemia was induced by an infusion of nitrogen via the maternal trachea for 24 hours in 13 pregnant sheep at 122 to 139 days' gestation. Two control periods of air infusion via the maternal trachea for 24 hours were alternated with hypoxemia. Fetal hypoxemia was not associated with any change in fetal pH. During the first and second exposures to hypoxemia, there was an increase in fetal plasma lactate of 22.8 +/- 22.3 and 15.3 +/- 14.6 mg.dl-1 (mean +/- SD) above preliminary values (p less than 0.05) compared with the control period. Fetal plasma cortisol also increased by 5.7 +/- 6.1 and 9.5 +/- 5.4 ng.ml-1 (mean +/- SD) (p less than 0.05) compared with the control period. These results suggest that the fetal lamb at 122 to 139 days' gestation is highly sensitive to small decrements in Po2 of 5 mm Hg or less.

Animals↗

PubMed1988

Skeletal muscle glucose uptake during dynamic exercise in humans: role of muscle mass.

To study the role of muscle mass in glucoregulation, six subjects worked with the knee extensors of one leg on a specially constructed cycle ergometer. The knee extensors of one leg worked either alone or in combination with the knee extensors of the other leg and/or with the arms. Substrate usage was measured across both knee extensors by femoral arterial and venous catheterization and measurement of femoral venous blood flow. Glucose uptake by the working knee extensors was absolutely (by approximately 20%) or relatively decreased when arm cranking was added to knee extensions. The decrease in glucose uptake was not compensated for by increased uptake of free fatty acids but was accompanied by decreases in plasma insulin and increases in plasma epinephrine and norepinephrine. During work with large muscle masses, arterial lactate increased to approximately 6 mM, and net leg lactate release reverted to net lactate uptake. Decreased glucose uptake could not be explained by decreased perfusion. It is concluded that thigh muscle glucose uptake is affected by the size of the total muscle mass engaged in exercise. The decrease in thigh glucose uptake, when arm cranking was added and O2 uptake was increased above 50% of maximum aerobic capacity, may be elicited by neuroendocrine adjustments or lactate-induced inhibition of glycolysis and may represent a mechanism for protecting against premature hypoglycemia during prolonged exercise.

Adult↗

PubMed1993

Protective effect of R(-)-1-(benzo[b]thiophen-5-yl)- 2-[2-(N,N-diethylamino)ethoxy]ethanol hydrochloride (T-588), a novel cerebral activator, against experimental cerebral anoxia.

Effects of R(-)-1-(benzo[b]thiophen-5-yl)-2-[2- (N,N-diethylamino)ethoxy]ethanol hydrochloride (T-588) on normobaric hypoxia, histotoxic anoxia by KCN and complete ischemia by decapitation were investigated in mice. T-588 (30-100 mg/kg, p.o.) showed a significant and dose-dependent prolongation of the survival time in all of the models studied. Bifemelane (100-300 mg/kg, p.o.) was also protective against all the models. Tacrine was protective against hypoxia but had no effect on anoxia and ischemia. Imipramine was protective against anoxia, but shortened the survival time of hypoxic mice. It had no effect on ischemia. The anti-hypoxic effect of T-588 was completely inhibited by pretreatment with scopolamine (1 mg/kg, i.p.), while the anti-anoxic effect was partially inhibited. Its effect on the ischemia was not affected by scopolamine. Hypoxia decreased the cerebral contents of ATP, phosphocreatine and glucose and increased the contents of lactate in mice. T-588 had no effect on these changes. Bifemelane prolonged pentobarbital-induced sleeping time in mice with the doses inducing anti-anoxic action, but T-588 did not. These results suggest that the activation of the CNS cholinergic system is involved as one of the mechanisms for the anti-anoxic action of T-588.

Animals↗

PubMed1991

Effects of tromethamine and hyperventilation on brain injury in the cat.

The metabolic brain acidosis after trauma has been thought to be harmful and to contribute to neurological deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore with magnetic resonance (MR) spectroscopy the metabolic changes in brain that occur with the use of hyperventilation, THAM (tromethamine; tris[hydroxymethyl]aminomethane), and a combination (THAM and hyperventilation) therapy in experimental fluid-percussion injury. Brain lactate, brain pH, inorganic phosphate (Pi), and adenosine triphosphate levels were measured by 1H and 31P MR spectroscopy. Arterial and cerebrovenous lactate and water content in brain tissue was determined in 29 cats using the specific gravimetric technique. Following injury, the phosphocreatine (PCr)/Pi ratio, which is an index of cerebral energy depletion, decreased to 76% in four untreated animals, to 79% in 11 THAM-treated animals, to 68% in seven animals receiving hyperventilation, and to 66% in seven animals with combination THAM and hyperventilation therapy. The PCr/Pi ratio returned to a normal level in 8 hours in animals treated with THAM and THAM in combination with hyperventilation. The brain lactate index increased to 157% in the hyperventilation group after trauma. In cats receiving THAM plus hyperventilation, the brain lactate index was reduced to 142%, while the minimum rise of 126% was associated with treatment of THAM alone. In the THAM-treatment and combination-treatment groups, the water content of the white and gray matter was significantly decreased compared with that in untreated cat brains. Prolonged hyperventilation provided relative ischemia in brain tissue and promoted more production of brain lactate, no recovery of the PCr/Pi ratio, and no decrease in brain edema. On the other hand, administration of THAM decreased production of brain lactate and brain edema and promoted the recovery of cerebral energy dysfunction. It was found that THAM ameliorates the deleterious effects of hyperventilation by minimizing energy disturbance and that it also decreases brain edema. The authors conclude that THAM may be effective in reducing brain tissue acidosis and helpful as a metabolic stabilizing agent following severe head injury.

Acidosis, Lactic↗

PubMedDate not supplied

Iron lactate-induced osteopenia in male Sprague-Dawley rats.

Osteopenia was induced in rats fed a diet containing 50,000 ppm (5%) iron lactate for 2 or 4 weeks. Blood chemistry, urinalysis, and bone histomorphometry of the proximal tibial metaphysis were performed. Urinary pyridinoline and deoxypyridinoline and the osteoclast number per bone surface were selected for the measurement of dynamic resorption. The osteoclast surface, eroded surface, and osteoblast surface increased at both ends of the exposure periods, and bone resorption and formation both increased. The bone volume, trabecular thickness, and trabecular number decreased, and the secondary spongiosa of proximal metaphysis showed a marked bone loss. However, no mineralization defect was observed. At the end of the 2-week exposure period, biomarkers of osteoclasts and osteoblasts had increased the most, and the osteoblast surface, osteoclast surface, and osteoclast number per bone surface increased with prolonged exposure. The pathological changes of the bone lesion in iron lactate-overloaded rats were similar to those in rats of the osteoporotic model, because they consisted of changes reflecting the increase of bone resorption and formation without an osteomalacic change. However, the decline of serum parathyroid hormone (PTH) levels was different from that of the osteoporosis model rat. We concluded iron-induced bone lesions probably differ from those of low turnover bone diseases.

Administration, Oral↗

PubMed2005

Effects of week of lactation and genetic selection for milk yield on milk fatty acid composition in Holstein cows.

Control (CL) and select line (SL) dairy cows (n = 22) managed identically but differing in milk yield (>4100 kg/305 d) were used to determine differences in milk fatty acid profile as lactation progressed. Milk yield was recorded daily and milk samples were collected during wk 1, 4, 8, 12, and 16 postpartum for milk composition analysis. Milk samples from wk 1, 8, and 16 were also analyzed for fatty acid composition. Select-line cows produced more milk (44.4 vs. 31.2 kg/d) and milk components than CL cows during the 16-wk period. There was no difference in rate of milk yield increase, but peak milk yield for SL cows was greater and occurred later in lactation. There were no differences in milk SCC or milk fat, protein, or lactose content. Selection for milk yield did not affect the content of most individual milk fatty acids; however, compared with CL, SL cows had a reduced Delta(9)-desaturase system and tended to produce milk with lower monounsaturated fatty acid content. Selection for milk yield did not affect milk fatty acid origin but the percentage of de novo fatty acids increased and preformed fatty acids decreased as lactation progressed. Milk fat trans-11 18:1 and cis-9,trans-11 conjugated linoleic acid increased with progressing lactation (10.7 vs. 14.1 and 3.1 vs. 5.4 mg/g, or 31 and 76%, respectively) and were correlated strongly among wk 1, 8, and 16 of lactation. Temporal changes in the Delta(9)-desaturase system occurred during lactation but these changes were not correlated with milk fat cis-9,trans-11 conjugated linoleic acid content. Results indicate prolonged genetic selection for milk yield had little effect on milk fatty acid composition, but milk fatty acid profiles varied markedly by week of lactation.

Animals↗

PubMed1993

Minimum inhibitory concentration (MIC) of sodium lactate for pathogens and spoilage organisms occurring in meat products.

Pathogens and spoilage organisms occurring in meat products were screened in laboratory media, according to a method of Eklund (1983), in order to determine the specific inhibitory effect of lactate on growth of these microorganisms under optimum growth conditions (pH 6.5, 20 degrees C). In general, Gram-positive bacteria were more sensitive towards lactate than Gram-negative bacteria. It was shown especially, that strains that were able to grow at water activities of 0.95 and below in the presence of NaCl (Staphylococcus aureus, Listeria monocytogenes, Brochothrix thermosphacta) were inhibited by sodium lactate (NaL). It appeared, that yeasts were resistant to large amounts of NaL (> 10% w/v). However, NaL had a specific inhibitory effect on growth of these organisms when compared to the effect of NaCl. These results indicate that lactate addition to food products with a pH near neutrality offers good prospects for shelf life prolongation.

Animals↗

PubMed2004

Validity of the heart rate deflection point as a predictor of lactate threshold concepts during cycling.

This paper examines the validity of the heart rate deflection point (HRDP) obtained with the "updated" Conconi test. Eleven male road cyclists performed 2 progressive incremental cycling tests and a 30-minute prolonged exercise test (PET). From the data obtained, comparisons were made and correlation coefficients were calculated between HRDP, the lactate threshold (LT), and the 3 mmol.L(-1) threshold (AT3). The PET at HRDP demonstrated whether or not a steady state in blood lactate concentration (BLaSS) could be maintained. Significantly lower values for power output (p < 0.01) and heart rate (HR) (p < 0.01) were found at LT compared with HRDP. No differences were found between HRDP and AT3. Only a moderate correlation for power output between HRDP and AT3 (rs = 0.69; p < 0.05) could be observed. During the PET, only 6 out of 11 cyclists reached the target time of 30 minutes, and only 4 cyclists maintained a BLaSS. We conclude that the updated Conconi test is not a valid method for assessing LT or AT3. Therefore, this method seems not suitable to evaluate endurance performance and prescribe exercise intensities in road cycling.

Adult↗

PubMed1980

Thermoregulatory ability of female rats during pregnancy and lactation.

Thermoregulatory ability of female rats was examined before pregnancy, during gestation, and during lactation. Thermoregulatory pattern, colonic temperature, evaporative water loss, and survival time were monitored during terminal heating (39.5 +/- 0.9 degrees C) designed to allow prolonged survival (3-4 h) with a sustained thermoregulatory effort. Results confirmed our previously reported observation of decreased thermoregulatory ability in lactating dams, with evidence suggesting thermoregulatory impairment during late gestation. Lactating dams displayed a type III thermoregulatory pattern, and established a rate of evaporative water loss effective for thermostasis at an elevated colonic temperature. However, survival time was significantly decreased compared to nonreproducing females. In contrast, prior heat acclimation tended to increase the survival time of lactating dams. It was concluded that the reduction in thermoregulatory ability observed in lactating dams was related to their inability to maintain a rate of evaporative water loss effective for thermostasis at an elevated colonic temperature.

Adaptation, Physiological↗