Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Characterization and quantification of the Hxt2 (hexose transport) protein of Saccharomyces cerevisiae indicate that it is one of a set of differentially expressed high-affinity glucose transporters. The protein product of the HXT2 gene was specifically detected by antibodies raised against a synthetic peptide encompassing the 13 carboxyl-terminal amino acids predicted by the HXT2 gene sequence. Hxt2 migrated in sodium dodecyl sulfate-polyacrylamide gel electrophoresis as a broad band or closely spaced doublet with an average M(r) of 47,000. Hxt2 cofractionated with the plasma membrane ATPase, Pma1, indicating that it is a plasma membrane protein. Hxt2 was not solubilized by high pH or urea but was solublized by detergents, which is characteristic of an integral membrane protein. Expression of the Hxt2 protein was measured under two different conditions that produce expression of high-affinity glucose transport: a medium shift from a high (2.0%) to a low (0.05%) glucose concentration (referred to below as high and low glucose) and growth from high to low glucose. Hxt2 as measured by immunoblotting increased 20-fold upon a shift from high-glucose to low-glucose medium, and the high-affinity glucose transport expressed had a strong HXT2-dependent component. Surprisingly, Hxt2 was not detectable when S. cerevisiae growing in high glucose approached glucose exhaustion, and the high-affinity glucose transport expressed under these conditions did not have an HXT2-dependent component. The role of Hxt2 in growth during aerobic batch culture in low-glucose medium was examined. An hxt2 null mutant grew and consumed glucose significantly more slowly than the wild type, and this phenotype correlated directly with appearance of the Hxt2 protein.
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PMID:Physiological characterization of putative high-affinity glucose transport protein Hxt2 of Saccharomyces cerevisiae by use of anti-synthetic peptide antibodies. 824 39

The present study was undertaken in order to establish the possible involvement of GABAergic and/or opioid pathways in the mechanism underlying the arginine-vasopressin (AVP) response to physical exercise. After fasting overnight, seven subjects were tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3 min intervals until exhaustion and lasted about 15 min in all subjects. Tests were carried out under administration of placebo, the opioid antagonist naloxone (10 mg as an i.v. bolus injection), the GABAergic agonist sodium valproate (600 mg in three divided doses orally) or naloxone plus sodium valproate. Plasma AVP levels rose 4-fold during exercise. The administration of naloxone did not modify, whereas sodium valproate completely abolished the plasma AVP rise during exercise. When naloxone was given together with sodium valproate, AVP rose 3-fold in response to exercise. These data suggest the involvement of a GABAergic mechanism in regulation of the AVP response to physical exercise in men. Furthermore, the data argue against a role of naloxone sensitive endogenous opioids in the control of AVP during exercise, whereas they suggest a partial opioid mediation of the GABAergic inhibitory action.
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PMID:Role of GABA and opioids in the regulation of the vasopressin response to physical exercise in normal men. 827 34

Many researchers have investigated the effects of induced metabolic alkalosis, by ingestion of sodium bicarbonate, on anaerobic exercise performance. But the results have been inconsistent and often contradictory. The purpose of this review was to synthesize the varied findings using a meta-analytic approach. Twenty-nine investigations met our inclusion criteria. Results show that NaHCO3 ingestion clearly results in a more alkaline extracellular environment. The dosage, however, was only moderately related to the increase in pH and HCO3-. Overall, performance was enhanced but the range of effect sizes was large, -0.12 to 2.87. In studies that measured time to exhaustion, there was a mean 27 +/- 20% increase in duration. The treatment effect, however, was only weakly related to the degree of induced alkalosis. But in comparing the 19 studies that showed a positive treatment effect with the 16 that showed no effect, the former were associated with a greater increase in pH following ingestion of a somewhat larger dosage, and a greater decrease in pH with exercise.
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PMID:Effects of sodium bicarbonate ingestion on anaerobic performance: a meta-analytic review. 838 67

1. Heat acclimation was induced in eight subjects by asking them to exercise until exhaustion at 60% of maximum oxygen consumption rate (VO2) for 9-12 consecutive days at an ambient temperature of 40 degrees C, with 10% relative humidity (RH). Five control subjects exercised similarly in a cool environment, 20 degrees C, for 90 min for 9-12 days; of these, three were exposed to exercise at 40 degrees C on the first and last day. 2. Acclimation had occurred as seen by the increased average endurance from 48 min to 80 min, the lower rate of rise in the heart rate (HR) and core temperature and the increased sweating. 3. Cardiac output increased significantly from the first to the final heat exposure from 19.6 to 21.4 l min-1; this was possibly due to an increased plasma volume and stroke volume. 4. The mechanism for the increased plasma volume may be an isosmotic volume expansion caused by influx of protein to the vascular compartment, and a sodium retention induced by a significant increase in aldosterone. 5. The exhaustion coincided with, or was elicited when, core temperature reached 39.7 +/- 0.15 degrees C; with progressing acclimation processes it took progressively longer to reach this level. However, at this point we found no reduction in cardiac output, muscle (leg) blood flow, no changes in substrate utilization or availability, and no recognized accumulated 'fatigue' substances. 6. It is concluded that the high core temperature per se, and not circulatory failure, is the critical factor for the exhaustion during exercise in heat stress.
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PMID:Human circulatory and thermoregulatory adaptations with heat acclimation and exercise in a hot, dry environment. 848 4

This study was conducted to determine the efflux of specific ions, including fluoride, from a deionization (DI) water purification system (WPS) when the WPS was operated beyond exhaustion of the DI resin. Effluent from the DI WPS was monitored for resistivity, total dissolved solids, pH, and concentrations of silica, fluoride, potassium, and sodium. After 16,000 L of water was purified, the resistivity declined to 0.492 omega Ohm-cm, and silica was released from the DI WPS. Fluoride ions were released after an additional 8,000 L water was treated, and the resistivity fell to 0.07 omega Ohm-cm. The fluoride efflux reached a peak of 32 mg/L, 28 times greater than the original fluoride concentration in the city water. Sodium and potassium ions were released after approximately 26,000 and 32,000 L of water had been treated and reached peaks of 76 and 47 mg/L, respectively. This study confirms that the minimum resistivity standard of 1 omega Ohm-cm for DI water used for hemodialysis should provide an adequate safety margin. Once resistivity fell to 1 omega Ohm-cm, more than 8,000 L of water was treated before fluoride efflux occurred. Accordingly, hemodialysis centers should be attentive to the calculated capacity of their DI WPS and reliably monitor the resistivity to prevent patient illness related to exhaustion of DI resins.
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PMID:Potential hazards of deionization systems used for water purification in hemodialysis. 864 25

Onset of exercise leads to a sudden increase in [K+] in venous plasma from the exercising muscles. Delayed by about 10 s. the arterial [K+] rises nearly at the same rate as the venous concentration. At exercise intensities below 100% of Vo2max, both venous and arterial [K+] stabilize at a steady-state value. At higher intensities, venous and arterial plasma [K+] continue to rise until exhaustion. During the first 5 min of exercise the contracting muscles always lose K+, with a peak in loss rate after 1-2 min. During steady state, the loss rate is minimized or may even be reduced to zero. The loss is caused by an exercise-induced afflux of K+ from the contracting cells which exceeds the exercise-induced influx mediated by the Na, K pump. The Na, K pump is stimulated by catecholamines in vitro and in resting tissue in vivo. However, the loss rate of K+ from steady-state exercising muscles does not show any increase during beta -adrenergic blockade or decrease during beta-adrenergic stimulation. This is probably due to a compensatory change in intracellular [Na+]. During low exercise intensity, arterial [K+] does not increase after 1-2 min. while the exercising muscles lose K+, showing that the extracellular pool of K+ is redistributed. During beta-adrenergic blockade this redistribution is impaired so that the rise in plasma [K+] is accentuated. Conversely alpha-adrenergic blockade reduces the exercise-induced hyperkalaemia. Hence, the adrenergic system plays an important role in regulation of whole-body K+ balance during exercise but its significance in exercising muscles is not clear.
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PMID:K+ balance in humans during exercise. 872 88

Blood flow to skeletal muscle during exercise is greater in the trained state. We hypothesized that intrinsic vasomotor reactivity of arteries to active muscle during training bouts would be altered to favor a relative vasodilation after training. To test this hypothesis, miniature swine were pen confined (Sed; n = 30) or treadmill trained for 5 days/wk over 16-20 wk (Trn; n = 32). Efficacy of training was indicated by myocardial hypertrophy (4.84 +/- 0.11 and 5.81 +/- 0.12 g/kg body wt for Sed and Trn, respectively, P < 0.0005), training bradycardia at several submaximal running speeds of a maximal exercise test, increased running time to exhaustion (26 +/- 1 and 35 +/- 1 min for Sed and Trn, respectively, P < 0.0005), and increased oxidative capacities of several locomotory skeletal muscles. Segments of femoral, brachial, mesenteric, renal, and hepatic arteries were isolated from Sed and Trn swine. Isometric contractile and relaxation properties of vascular rings cut from these segments were determined in vitro. Contractile responses to KCl and norepinephrine (NE) were determined, as were relaxation responses to sodium nitroprusside and adenosine, agents acting directly on vascular smooth muscle, and the endothelium-dependent agents bradykinin and the calcium ionophore A-23187. Responses to vasocontractile and vasorelaxation agents were not different between Sed and Trn swine for vessels serving active muscles (i.e., femoral, brachial). On the other hand, renal arterial rings from Trn swine exhibited lesser contractile responses than those from Sed swine across a range of NE concentrations (P < 0.05) and approximately 25% less maximal contractile response to NE (32.7 +/- 2.6 and 24.2 +/- 2.1 g for Sed and Trn, respectively, P < 0.01). Responses of other vessels serving viscera (i.e., mesenteric, hepatic) were unchanged with training. These data indicate that vasomotor reactivity of porcine conduit-type arteries generally does not change with exercise training. An exception is the lesser contractile response to NE in renal artery, which could permit better preservation of renal blood flow during acute exercise in trained animals.
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PMID:Effects of exercise training on responses of peripheral and visceral arteries in swine. 884 6

We examined the effects of sodium bicarbonate (BIC) and sodium citrate (CIT) ingestion on distance running performance. Seven male runners [mean VO2max = 61.7 (SEM 1.7) ml.kg-1.min-1] performed three 30-min treadmill runs at the lactate threshold (LT) each followed by a run to exhaustion at 110% of LT. The runs were double-blind and randomly assigned from BIC (0.3 g.kg body mass-1), CIT (0.5 g.kg body mass-1) and placebo (PLC, wheat flour, 0.5 g.kg body mass-1). Venous blood samples were collected at 5, 15 and 25 min during the run and immediately post-exhaustion (POST-EX) and analysed for pH, and the concentrations of lactate ([la-]b) and bicarbonate ([HCO3-]). Performance was measured as running time to exhaustion at 110% of LT (TIME-EX). The pH was significantly higher (P < or = 0.05) for the BIC and CIT trials during exercise, but not POST-EX compared to PLC. The [la-]b was significantly higher (P < or = 0.05) for the CIT trial compared to PLC during exercise, and for both CIT and BIC compared to PLC at POST-EX. Blood [HCO3-] was significantly higher (P < or = 0.05) during exercise for BIC compared to PLC. TIME-EX was not significantly different among treatments: BIC 287 (SEM 47.4)s; CIT 172.8 (SEM 29.7)s; and PLC 222.3 (SEM 39.7)s. Despite the fact that buffer ingestion produced favourable metabolic conditions during 30 min of high intensity steady-state exercise, a significant improvement in the subsequent maximal exercise run to exhaustion did not occur.
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PMID:The effects of buffer ingestion on metabolic factors related to distance running performance. 885 7

Manipulations of pH and electrical gradients in a perfused preparation were used to analyze the factors controlling ammonia distribution and flux in trout white muscle after exercise. Trout were exercised to exhaustion, and then an isolated-perfused white muscle preparation with discrete arterial inflow and venous outflow was made from the posterior portion of the tail. The tail-trunks were perfused with low (7.4)-, medium (7.9)-, and high (8.4)-pH saline, achieved by varying HCO3- concentration ([HCO3-]) at constant Pco2. Intracellular and extracellular pH, ammonia, CO2, K+, Na+, and Cl- were measured. Muscle intracellular pH was not affected by changes in extracellular pH. Increasing extracellular pH caused a decrease in the transmembrane NH3 partial pressure (PNH3) gradient and a decrease in ammonia efflux. When extracellular K+ concentration was increased from 3.5 to 15 mM in the medium-pH group, a depolarization of the muscle cell membrane potential from -92 to -60 mV and a 0.1-unit depression in intracellular pH occurred. Ammonia efflux increased despite a marked reduction in the PNH3 gradient. Amiloride (10(-4) M) had no effect, indicating that Na+/H(+)-NH4+ exchange does not participate in ammonia transport in this system. A comparison of observed intracellular-to-extracellular ammonia distribution ratios with those modeled according to either pH or Nernst potential distributions supports a model in which ammonia distribution across white muscle cell membranes is affected by both pH and electrical gradients, indicating that the membranes are permeable to both NH3 and NH4+. Membrane potential, acting to retain high levels of NH4+ in the intracellular compartment, appears to have the dominant influence during the postexercise period. However, at rest, the pH gradient may be more important, resulting in much lower intracellular ammonia levels and distribution ratios. We speculate that the muscle cell membrane NH3-to-NH4+ permeability ratio in trout may change between the rest and postexercise condition.
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PMID:Ammonia movement and distribution after exercise across white muscle cell membranes in rainbow trout. 885 99

It is well established that the ingestion of carbohydrate-containing drinks can improve the performance of prolonged exercise. The present study examined the effects of ingestion of water and two dilute glucose-electrolyte drinks on exercise performance and on cardiovascular and metabolic responses to exercise. Twelve subjects exercised to exhaustion on a cycle ergometer at a workload corresponding to 70% of maximum oxygen uptake (VO2,max) on five occasions each separated by 1 week. The first trial served to accustom subjects to experimental conditions. On one trial, no drinks were given and on the others subjects drank 100 ml every 10 min. Drinks consisted of water, an isotonic glucose-electrolyte solution (I: 200 mmol/l glucose; 35 mmol/l NA2; 310 mosmol/kg) and a hypotonic glucose-electrolyte solution (H: 90 mmol/l glucose; 60 mmol/l Na+; 240 mosmol/kg). Treatment order was randomized. Blood and expired air samples were taken and heart rate and rectal temperature measured at intervals during exercise. Median exercise time was greatest for treatment H (110.3 min) followed by treatment I (107.3 min), water (93.1) and no drink (80.7). Endurance times differed significantly overall, and for pairwise comparisons (P < 0.01) between the no-drink trial and both treatments H and I: a difference between water and no drink was seen at the 5% level. At exhaustion, a significant treatment difference was found for the change in plasma volume, with the greatest decrease (6.7%) on the no-drink trial and the smallest decrease (0.5%) on treatment H. Significant treatment effects were also observed for heart rate, rectal temperature and serum osmolality. The results suggest that the ingestion of glucose-electrolyte drinks can improve exercise performance even when the amount of added glucose is small, and that performance may also be enhanced, albeit to a lesser degree, by ingestion of water.
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PMID:Effects of ingested fluids on exercise capacity and on cardiovascular and metabolic responses to prolonged exercise in man. 888 82


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