Sodium-free fluid ingestion decreases plasma sodium during exercise in the heat.
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This study assessed whether replacing sweat losses with sodium-free fluid can lower the plasma sodium concentration and thereby precipitate the development of hyponatremia. Ten male endurance athletes participated in one 1-h exercise pretrial to estimate fluid needs and two 3-h experimental trials on a cycle ergometer at 55% of maximum O2 consumption at 34 degrees C and 65% relative humidity. In the experimental trials, fluid loss was replaced by distilled water (W) or a sodium-containing (18 mmol/l) sports drink, Gatorade (G). Six subjects did not complete 3 h in trial W, and four did not complete 3 h in trial G. The rate of change in plasma sodium concentration in all subjects, regardless of exercise time completed, was greater with W than with G (-2.48 +/- 2.25 vs. -0.86 +/- 1.61 mmol. l-1. h-1, P = 0.0198). One subject developed hyponatremia (plasma sodium 128 mmol/l) at exhaustion (2.5 h) in the W trial. A decrease in sodium concentration was correlated with decreased exercise time (R = 0.674; P = 0.022). A lower rate of urine production correlated with a greater rate of sodium decrease (R = -0. 478; P = 0.0447). Sweat production was not significantly correlated with plasma sodium reduction. The results show that decreased plasma sodium concentration can result from replacement of sweat losses with plain W, when sweat losses are large, and can precipitate the development of hyponatremia, particularly in individuals who have a decreased urine production during exercise. Exercise performance is also reduced with a decrease in plasma sodium concentration. We, therefore, recommend consumption of a sodium-containing beverage to compensate for large sweat losses incurred during exercise. (+info)
Incorporation and utilization of [3-13C]lactate and [1,2-13C]acetate by rat skeletal muscle.
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Skeletal muscle can utilize many different substrates, and traditional methodologies allow only indirect discrimination between oxidative and nonoxidative uptake of substrate, possibly with contamination by metabolism of other internal organs. Our goal was to apply 1H- and 13C-nuclear magnetic resonance spectroscopy to monitor the patterns of [3-13C]lactate and [1,2-13C]acetate (model of simple carbohydrates and fats, respectively) utilization in resting vs. contracting muscle extracts of the isolated perfused rat hindquarter. Total metabolite concentrations were measured by using NADH-linked fluorometric assays. Fractional oxidation of [3-13C]lactate was unchanged by contraction despite vascular endogenous lactate accumulation. Although label accumulated in several citric acid cycle (CAC) intermediates, contraction did not increase the concentration of CAC intermediates in any muscle extracts. We conclude that 1) the isolated rat hindquarter is a viable, well-controlled model for measuring skeletal muscle 13C-labeled substrate utilization; 2) lactate is readily oxidized even during contractile activity; 3) entry and exit from the CAC, via oxidative and nonoxidative pathways, is a component of normal muscle metabolism and function; and 4) there are possible differences between gastrocnemius and soleus muscles in utilization of nonoxidative pathways. (+info)
Effect of artemether on glyceraldehyde-3-phosphate dehydrogenase, phosphoglycerate kinase, and pyruvate kinase of Schistosoma japonicum harbored in mice.
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AIM: To study the effect of artemether (Art) on glyceraldehyde-phosphate dehydrogenase (GAPDH), phosphoglycerate kinase (PGK), and pyruvate kinase (PK) of S japanicum. METHODS: Mice infected with schistosome cercariae for 32-38 d were treated ig with Art 100-300 mg.kg-1 and killed 24-72 h after medication for collection of schistosomes. The activities of GAPDH, PGK, and PK of the worms were determined by measuring the formation of NADH or consumption of NAD. The lactate content of the worms was also measured. RESULTS: After the infected mice were treated ig with Art 300 mg.kg-1 for 24 h, the inhibition rates of GAPDH were 13% (Male) and 21% (Female), and 48 h later the inhibition rates of the enzyme were 6% (Male) and 28% (Female). When Art 300 mg.kg-1 was given to infected mice for 24 h and 48 h, the inhibition rates of PGK were 60% (Male) and 48% (Female) as well as 75% (Male) and 62% (Female), respectively. Similar results were seen in PK activity. At 72 h after treatment the reduction rate of lactate content in Female worm was 72%, while that of Male was 48%. CONCLUSION: In the glycolytic pathway of both Male and Female schistosomes, PGK and PK activities were inhibited by Art. The GAPDH activity of Female worms was also susceptible to Art, While that of Male worms showed only temporary inhibition after treatment with Art. The Art reduced lactate content more in Female than in Male worms. (+info)
Improvement of spermatogenesis in adult cryptorchid rat testis by intratesticular infusion of lactate.
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In order to test the hypothesis that a lack of energy could be a cause of germ cell death at high temperatures, cryptorchid rats testes were infused with lactate, delivered by osmotic pumps over 3-15 days. In cryptorchid testes, the spermatids and spermatocytes were lost between 3 and 8 days. In cryptorchid testes supplemented with lactate, elongated spermatids persisted in a few seminiferous tubules at Day 15. Elimination of round spermatids occurred progressively between 3 and 15 days, mostly at stage VIII. The loss of spermatocytes increased after 8 days, and 30% of seminiferous tubules still contained meiotic or meiotic plus spermiogenetic cells at Day 15. After 8 days, the chromatin of step 8 round spermatids was abnormal and nuclear elongation did not commence. The Sertoli cell cytoplasm that was retracted toward the basal compartment of the seminiferous epithelium could not hold the germ cells of the adluminal compartment. Therefore, attachment of germ cells to Sertoli cells and the supply of lactate seem necessary for the development of germ cells at high temperatures. The improvement in spermatogenesis in cryptorchid supplemented testes for several days is a new finding. (+info)
Quinupristin/dalfopristin attenuates the inflammatory response and reduces the concentration of neuron-specific enolase in the cerebrospinal fluid of rabbits with experimental Streptococcus pneumoniae meningitis.
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The inflammatory response following initiation of antibiotic therapy and parameters of neuronal damage were compared during intravenous treatment with quinupristin/dalfopristin (100 mg/kg as either a short or a continuous infusion) and ceftriaxone (10 mg/kg/h) in a rabbit model of Streptococcus pneumoniae meningitis. With both modes of administration, quinupristin/dalfopristin was less bactericidal than ceftriaxone. However, the concentration of proinflammatory cell wall components (lipoteichoic acid (LTA) and teichoic acid (TA)) and the activity of tumour necrosis factor (TNF) in cerebrospinal fluid (CSF) were significantly lower in the two quinupristin/dalfopristin groups than in ceftriaxone-treated rabbits. The median LTA/TA concentrations (25th/75th percentiles) were as follows: (i) 14 h after infection: 133 (72/155) ng/mL for continuous infusion of quinupristin/dalfopristin and 193 (91/308) ng/mL for short duration infusion, compared with 455 (274/2042) ng/mL for ceftriaxone (P = 0.002 and 0.02 respectively); (ii) 17 h after infection: 116 (60/368) ng/mL for continuous infusion of quinupristin/dalfopristin and 117 (41/247) ng/mL for short duration infusion, compared with 694 (156/2173) ng/mL for ceftriaxone (P = 0.04 and 0.03 respectively). Fourteen hours after infection the median TNF activity (25th/75th percentiles) was 0.2 (0.1/1.9) U/mL for continuous infusion of quinupristin/dalfopristin and 0.1 (0.01/3.5) U/mL for short duration infusion, compared with 30 (4.6/180) U/mL for ceftriaxone (P = 0.02 for each comparison); 17 h after infection the TNF activity was 2.8 (0.2/11) U/mL (continuous infusion of quinupristin/dalfopristin) and 0.1 (0.04/6.1) U/mL (short duration infusion), compared with 48.6 (18/169) U/mL for ceftriaxone (P = 0.002 and 0.001). The concentration of neuron-specific enolase (NSE) 24 h after infection was significantly lower in animals treated with quinupristin/dalfopristin: 4.6 (3.3/5.7) microg/L (continuous infusion) and 3.6 (2.9/4.7) microg/L (short duration infusion) than in those treated with ceftriaxone (17.7 (8.8/78.2) microg/L) (P = 0.03 and 0.009 respectively). In conclusion, antibiotic treatment with quinupristin/dalfopristin attenuated the inflammatory response within the subarachnoid space after initiation of antibiotic therapy. The concentration of NSE in the CSF, taken as a measure of neuronal damage, was lower in quinupristin/dalfopristin-treated rabbits than in ceftriaxone-treated rabbits. (+info)
Assessment of long-distance running performance in elite male runners using onset of blood lactate accumulation.
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The purpose of this study was to evaluate the relationship between onset of blood lactate accumulation (OBLA) and long-distance running performance in order to examine whether OBLA can be a good predictor of long-distance running performance even in elite male runners with similar performance levels. Eleven highly-trained male long-distance runners participated in this study. The average running velocities of the individuals' running performance were 5.918 +/- 0.084 m.s-1 and 5.672 +/- 0.095 m.s-1 for 5000 m (V5000) and 10,000 m (V10000), respectively. The blood lactate concentrations and heart rate responses were measured immediately after field running, and the average value of running velocity corresponding to OBLA (VOBLA) was 5.447 +/- 0.132 m.s-1. Variations of these three velocities expressed as a coefficient of variance (CV) ranged from 1.4 to 2.4%. A strong inverse relationship between heart rate corresponding to OBLA (HROBLA) and performance was observed (r = -0.709, p < 0.02 for V5000 and r = -0.830, p < 0.01 for V10000), while there was a lack of significant relationship between VOBLA and performance (r = 0.293, NS for V5000 and r = 0.130, NS for V10000). Furthermore, the average value of HROBLA obtained in this study (174.5 +/- 8.2 b.min-1) was quite similar to that of the heart rate threshold reported by some previous researchers. In conclusion, VOBLA alone could not explain the small variation of long-distance running performance, and HROBLA should be used in place of VOBLA for evaluating long-distance running performance in elite runners with quite similar performance levels. (+info)
Nisin production by a mixed-culture system consisting of Lactococcus lactis and Kluyveromyces marxianus.
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To control the pH during antimicrobial peptide (nisin) production by a lactic acid bacterium, Lactococcus lactis subsp. lactis (ATCC11454), a novel method involving neither addition of alkali nor a separation system such as a ceramic membrane filter and electrodialyzer was developed. A mixed culture of L. lactis and Kluyveromyces marxianus, which was isolated from kefir grains, was utilized in the developed system. The interaction between lactate production by L. lactis and its assimilation by K. marxianus was used to control the pH. To utilize the interaction of these microorganisms to maintain high-level production of nisin, the kinetics of growth of, and production of lactate, acetate, and nisin by, L. lactis were investigated. The kinetics of growth of and lactic acid consumption by K. marxianus were also investigated. Because the pH of the medium could be controlled by the lactate consumption of K. marxianus and the specific lactate consumption rate of K. marxianus could be controlled by changing the dissolved oxygen (DO) concentration, a cascade pH controller coupled with DO control was developed. As a result, the pH was kept constant because the lactate level was kept low and nisin accumulated in the medium to a high level compared with that attained using other pH control strategies, such as with processes lacking pH control and those in which pH is controlled by addition of alkali. (+info)
A general method for relieving substrate inhibition in lactate dehydrogenases.
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The mutation S163L in human heart lactate dehydrogenase removes substrate inhibition while only modestly reducing the turnover rate for pyruvate. Since this is the third enzyme to show this behaviour, we suggest that the S163L mutation is a general method for the removal of substrate inhibition in L-LDH enzymes. Engineering such enzymatic properties has clear industrial applications in the use of these enzymes to produce enantiomerically pure alpha-hydroxy acids. The mutation leads to two principal effects. (1) Substrate inhibition is caused by the formation of a covalent adduct between pyruvate and the oxidized form of the cofactor. The inability of S163L mutants to catalyse the formation of this inhibitory adduct is demonstrated. However, NMR experiments show that the orientation of the nicotinamide ring in the mutant NAD+ binary complex is not perturbed. (2) The mutation also leads to a large increase in the KM for pyruvate. The kinetic and binding properties of S163L LDH mutants are accounted for by a mechanism which invokes a non-productive, bound form of the cofactor. Molecular modelling suggests a structure for this non-productive enzyme-NADH complex. (+info)