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)

Acute and repeated exposure for 8-13 consecutive days to exercise in humid heat was studied. Twelve fit subjects exercised at 150 W [45% of maximum O2 uptake (V.O2,max)] in ambient conditions of 35 degrees C and 87% relative humidity which resulted in exhaustion after 45 min. Average core temperature reached 39.9 +/- 0.1 degrees C, mean skin temperature (T-sk) was 37.9 +/- 0.1 degrees C and heart rate (HR) 152 +/- 6 beats min-1 at this stage. No effect of the increasing core temperature was seen on cardiac output and leg blood flow (LBF) during acute heat stress. LBF was 5.2 +/- 0.3 l min-1 at 10 min and 5.3 +/- 0.4 l min-1 at exhaustion (n = 6). After acclimation the subjects reached exhaustion after 52 min with a core temperature of 39.9 +/- 0.1 degrees C, T-sk 37.7 +/- 0.2 degrees C, HR 146 +/- 4 beats min-1. Acclimation induced physiological adaptations, as shown by an increased resting plasma volume (3918 +/- 168 to 4256 +/- 270 ml), the lower exercise heart rate at exhaustion, a 26% increase in sweating rate, lower sweat sodium concentration and a 6% reduction in exercise V.O2. Neither in acute exposure nor after acclimation did the rise of core temperature to near 40 degrees C affect metabolism and substrate utilization. The physiological adaptations were similar to those induced by dry heat acclimation. However, in humid heat the effect of acclimation on performance was small due to physical limitations for evaporative heat loss.
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PMID:Acute and adaptive responses in humans to exercise in a warm, humid environment. 909 55

Brevetoxin-3 at nanomolar concentrations markedly enhanced spontaneous quantal transmitter release from neuromuscular junctions equilibrated in a Ca2+-free EGTA medium. After about 3 h, the sustained increase in miniature endplate potential frequency led to an exhaustion of transmitter release. This increase still occurred after loading the nerve terminals with the Ca2+ chelator bis-(aminophenoxy)ethanetetra-acetate or after pretreatment with various pharmacological agents known to prevent Ca2+ release from intracellular pools, but was completely prevented by the Na+ channel blocker tetrodotoxin. Brevetoxin-3 also increased miniature endplate potential frequency from junctions treated with botulinum type-A toxin, but to a smaller extent than at normal junctions. At normal junctions, brevetoxin-3 exposure for 2 h increased the three-dimensional projected area of living motor nerve terminals in situ by about 74% while at botulinum type-A poisoned junctions a similar toxin exposure caused only a 29% increase. Tetrodotoxin prevented such effects, indicating that they are related to both Na+ entry into the terminals and increased quantal transmitter release. Ultrastructural examination of nerve terminals from junctions exposed for 3 h to brevetoxin-3 revealed profound depletions of clear and large dense core synaptic vesicles and an increase in coated vesicles and axolemma infoldings. These results indicate that brevetoxin-3 impairs the recycling of clear synaptic vesicles and are consistent with our immunofluorescent observations showing that synaptophysin epitopes can be revealed without nerve terminal permeabilization. In contrast, no such changes were detected in nerve terminals poisoned with botulinum type-A toxin which, after 3 h exposure to brevetoxin-3, retained their synaptic vesicles and had a normal appearance. We conclude that tetrodotoxin-sensitive Na+ entry into motor nerve terminals induced by brevetoxin-3 triggers external Ca2+-independent asynchronous quantal transmitter release, blocks synaptic vesicle recycling and induces swelling of the terminals. We suggest that an excess of cytoplasmic Na+ per se can activate the asynchronous neurotransmitter release process.
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PMID:Sodium-dependent increase in quantal secretion induced by brevetoxin-3 in Ca2+-free medium is associated with depletion of synaptic vesicles and swelling of motor nerve terminals in situ. 915 66

Sodium is the major cation of the extracellular fluid and has a potent influence on fluid movement. Sodium has been likened to a sponge that draws fluids into the extracellular space, including the plasma volume, to equalize gradients in concentration. Conventional wisdom suggests limiting dietary intake of Na+ to decrease risk of hypertension. However, there are some extreme occupational or exercise-related conditions where sweat losses are great and Na+ losses may exceed normal dietary intake. This can occur acutely such as in an ultra-endurance event or chronically as in hard manual work in the hear. In such cases, additional Na+ in the form of a higher Na+ diet or adding Na+ to beverages used for fluid replacement may be warranted. A higher Na+ diet also appears to accelerate the cardiovascular and thermoregulatory adaptations that accompany heat acclimation or short term exercise training. Saline ingestion before exercise causes an expansion of plasma volume at rest and throughout the subsequent exercise bout. This expansion of plasma volume alters cardiovascular and thermoregulatory responses to exercise in ways that may lead to beneficial changes in endurance exercise performance. Plasma volume expansion also occurs with saline infusion during exercise, but exercise performance advantages have yet to be reported. The purpose of this article is to review the literature concerning dietary sodium and its influence on fluid balance, plasma volume and thermoregulation during exercise. It contains 2 major sections. First, we will discuss manipulations in daily Na+ intake initiated before or throughout an exercise regime. Second, we will examine studies where an acute Na+ load was administered immediately before or during an exercise trial. The dependent variables that we will discuss pertain to: (i) body water compartments, i.e. plasma volume; (ii) thermoregulatory variables, i.e. core temperature and sweat rate; (iii) cardiovascular variables, i.e. heart rate and stroke volume; and (iv) performance, i.e. time trial performance and time to exhaustion. Particular attention will be given to the route by which Na+ was administered, the environmental conditions, the level of acclimation of the participants and specifics relating to Na+ administration such as the osmolality of the Na(+)-containing beverage.
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PMID:Dietary sodium and plasma volume levels with exercise. 918 66

The effect of different rates of fluid ingestion on heart rate, rectal temperature, plasma electrolytes, hormones and performance was examined during prolonged strenuous exercise conducted at 21 degrees C. Seven well-trained males (24 +/- 1 yr; 68.6 +/- 2.9 kg; VO2 peak = 4.69 +/- 0.17 L min-1; mean +/- SEM) cycled for 2 h at 69 +/- 1% VO2 peak while receiving either no fluid replacement (NF), a volume of water estimated to prevent body weight loss (FR-100 = 2.32 +/- 0.10 L 2 h-1) or 50% of this volume (FR-60 = 1.16 +/- 0.05 L 2 h-1). The 2-h exercise bout was followed by a ride to exhaustion at a workload estimated to be 90% VO2 peak. After 2 h of exercise, NF was associated with a 3.2 +/- 0.1% weight loss, while FR-50 and FR-100 resulted in losses of 1.8 +/- 0.1 and 0.1 +/- 0.1%, respectively. Compared with FR-100, heart rate and rectal temperature were elevated (P < 0.05) during the second hour of exercise in NF, with FR-50 intermediate. Reductions in plasma volume during exercise were greater in NF and FR-50, compared with FR-100 and plasma sodium concentration was elevated in NF, decreased slightly in FR-100, with FR-50 intermediate. Plasma renin activity, aldosterone and atrial natriuretic peptide increased to similar extents in the three trials. Plasma vasopressin remained unchanged for FR-100, increased for NF, with intermediate values for FR-50. Exercise time to exhaustion at 90% VO2-peak was longer in FR-100 (328 +/- 93 s) than NF (171 +/- 75 s) with FR-50 (248 +/- 107 s) not significantly different from either FR-100 or NF. In conclusion, the responses of heart rate, rectal temperature, plasma sodium, and vasopressin during, and performance following, prolonged cycling exercise conducted at 21 degrees C are related to the amount of fluid ingested (i.e. the degree of dehydration).
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PMID:Influence of ingested fluid volume on physiological responses during prolonged exercise. 920 41

The aim of this investigation was to determine the relationship between muscle performance and the myosin heavy chain (MHC) composition and the reliability of electrophoretically determined MHC compositions. A total of thirty-one male subjects participated in the experiments. Maximal voluntary isometric contractions (MVC) of the knee extensors were performed at an arbitrary knee angle of 90 degrees and the following variables were recorded: maximal isometric force, muscle fibre conduction velocity (MFCV), electromechanical delay (EMD), maximal rate of force development (MRFD), median frequency of EMG (MF) and iEMG. Static isometric contractions of the knee extensors were held at an angle of 90 degrees using contractile forces of 10%, 50% and 100% MVC, respectively. These tests were conducted on separate days. Muscle biopsy samples were obtained from the left m. vastus lateralis before MVC and static endurance tests. MHC protein isoform differences were determined through sodium dodecyl-polyacrylamide gel electrophoresis (SDS-PAGE) followed by densitometric analysis. Type I-MHC compositions of the m. vastus lateralis ranged from 20-68% with a mean of 49 +/- 18%, mean type IIa-MHC and type IIb-MHC percentages were 35 +/- 16% and 16 +/- 10%, respectively. MHC compositions of duplicate biopsy samples were not significantly different from that of original samples. The coefficients of variation calculated for duplicate biopsy samples suggested reasonable reproducibility for MHC isoform differentiation for type I-MHC and type-II MHC composition (CV = 12.6%). Differentiation between type IIa-MHC and type IIb-MHC was not always clear using the densitometric traces. Subjects with higher percentages of type II-MHC displayed significantly faster MFCV (r = 0.67, P < 0.1), isometric force development (r = 0.68, P < 0.1) and shorter periods of EMD (r = -0.72, P < 0.05). There was also a tendency toward faster MRFD in these subjects although results did not reach significance. Endurance times for isometric contractions held at 10%, 50% and 100% MVC to exhaustion were not correlated with MHC composition. No relationships between II-MHC composition and MF or iEMG were observed. It was suggested that surface electromyographic recordings obtained during isometric MVC did not reflect underlying differences in muscle fibre composition.
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PMID:Electrophoretic separation of myosin heavy chain isoforms in the human m. vastus lateralis: references to reproducibility and relationships with force, electromechanical delay, fibre conduction velocity, endurance and electromyography. 922 41

The aim of this study was to examine whether the alkalosis-induced improvement in supramaximal performance could be explained by a less-altered muscle metabolic status. Eight subjects first performed exhausting exercise at 120% peak oxygen uptake after ingesting either a placebo (PLC) or sodium citrate (CIT) at a dose of 0.5 g.kg-1 body mass to determine exhaustion time (texh). They then, performed exercise (Lim-EX) at the same relative intensity lasting PLCtexh minus 20 s in both treatments. Samples were taken from vastus lateralis muscle at rest (90-min after the ingestion) and at the end of Lim-EX. Arterial blood samples were obtained at rest (immediately prior to and 90 min after ingesting the drug) and during the 20-min post-exercise recovery. The texh was significantly increased by CIT [PLC 258 (SD 29) s, CIT 297 (SD 45) s]. The CIT raised the rest [citrate] in blood [PLC 0.11 (SD 0.01) mmol.l-1, CIT 0.34 (SD 0.07) mmol.l-1] and in muscle [PLC 0.78 (SD 0.23) mmol.kg-1 dry mass, CIT 1.00 (SD 0.21) mmol.kg-1 dry mass]. Resting muscle pH and buffering capacity were unchanged by CIT. The same fall in muscle pH was observed during Lim-EX in the two conditions. This was associated with similar variations in both the cardio-respiratory response and muscle energy and metabolism status in spite of a better blood acid-base status after CIT. Thus, CIT would not seem to allow the alkalinization of the muscle cytosolic compartment. Though sodium citrate works in a similar way to NaHCO3 on plasma alkalinization and exercise performance, the exact nature of the mechanisms involved in the delay of exhaustion could be different and remains to be elucidated.
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PMID:Effect of sodium citrate on performance and metabolism of human skeletal muscle during supramaximal cycling exercise. 924 69

The effects of a 7-day period of daily physical stress (chasing until exhaustion) on the beta-adrenergic response of the rainbow trout (Oncorhynchus mykiss) red blood cell (rbc) were examined in vitro. Physical stress was associated with pronounced increases in the circulating levels of the catecholamine hormones (adrenaline and noradrenaline) measured on days 1, 3 and 7 of the stress regime. After 7 days, the numbers of high-affinity cell surface beta-adrenoceptors were reduced in the physically stressed fish when measured in vitro under conditions of normoxia (20 % reduction) or hypoxia (30 % reduction). Under hypoxic conditions, the binding affinity of the rbc beta-adrenoceptor was significantly higher in the stressed fish. Although the stressed fish had fewer beta-adrenoceptors, rbc adrenergic responsiveness was enhanced after 7 days of physical stress as determined from dose-response curves relating noradrenaline concentration to water and Na+ accumulation (indices of rbc adrenergic Na+/H+ exchange activity). The EC50 values (concentrations yielding half-maximal responses) for noradrenaline were lowered significantly by 1.7- to 3.9-fold in the blood from physically stressed fish. The enhanced adrenergic responsiveness of the rbcs appeared to be unrelated to changes in the initial steps of the beta-adrenergic signal transduction pathway leading to cyclic AMP production because physical stress was without effect on the magnitude or the dose-dependency of rbc cyclic AMP accumulation. To determine whether post-cyclic-AMP events were affected by physical stress, water and Na+ accumulation were measured in rbcs that had been incubated with the permeable cyclic AMP analogue 8-bromo cyclic AMP. The EC50 values for 8-bromo cyclic AMP were lowered by 1.6- to 1.7-fold in the blood from stressed fish. These experiments demonstrate that repeated physical stress significantly enhances the adrenergic responsiveness of the rainbow trout rbc, presumably by modifying the sensitivity of the Na+/H+ exchanger (or the steps immediately preceding exchanger activation) to cyclic AMP. The results are discussed with respect to the interrelationships between chronic and acute stress responses in fish.
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PMID:The effects of repeated physical stress on the b-adrenergic response of the rainbow trout red blood cell 931 46

Feeding a high-carbohydrate (CHO) diet and administration of alkalinizing agents have both been shown to improve performance in high-intensity exercise. The effect of these treatments in combination was investigated in the present study. Six healthy male subjects exercised to exhaustion on an electrically braked cycle ergometer at a power output equivalent to 100% of their maximum oxygen uptake (VO2,max) on four separate occasions. Each subject consumed either a diet with the same composition as his normal diet (termed the experimental normal (N) diet; 54 +/- 7% CHO, 13 +/- 2% protein, 33 +/- 7% fat) or a high-CHO diet (81 +/- 2% CHO, 13 +/- 2% protein, 6 +/- 1% fat) that had the same energy and protein content for the 3 days prior to the exercise tests. Subjects then ingested either a placebo (CaCO3) or trisodium citrate (0.3 g (kg body mass)-1) 3 h before exercise. Time to fatigue was not different between experimental conditions. Consumption of the high-CHO diet had no effect on blood acid-base status, but the ingestion of sodium citrate induced a mild metabolic alkalosis after both the N diet and the high-CHO diet. This alkalinizing effect was also evident after exercise, since blood pH, plasma bicarbonate and blood base excess were higher (P < 0.05) after the ingestion of sodium citrate than under the placebo conditions. The changes in blood lactate, pyruvate and glucose and plasma glycerol after exercise were similar for all experimental conditions. Blood lactate, glucose and pyruvate and plasma glycerol concentrations increased from resting values (P < 0.01) following exercise but this increase was similar under all experimental conditions. These data demonstrate that when the energy and protein content of the diets is the same, exercise capacity and the metabolic response to intense exercise are similar following consumption either of a high-CHO diet or a more normal diet. Acute ingestion of sodium citrate prior to exercise resulted in a reduction in post-exercise acidosis despite a blood lactate concentration that was similar to that observed after the ingestion of a placebo, but did not affect exercise performance under the conditions of this study.
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PMID:The effect of sodium citrate ingestion on the metabolic response to intense exercise following diet manipulation in man. 941 35

We examined the gastric emptying (GE) of oral rehydration solutions (ORS) at rest and after exercise in four Standardbred horses. In one study isotonic, cold isotonic (5 degrees C), isotonic containing glucose and hypertonic fluid were tested at rest. In another study, isotonic fluid was given following a bout of treadmill exercise at 70 per cent VO2 max until exhaustion or at rest. In both studies, a single dose of 8 litres was given via nasogastric tube. GE and electrolyte concentrations (Na+, K+ and Cl-) of the stomach content were measured at 15 minutes intervals for one hour. In both studies, 90 per cent of the fluid was emptied within 15 minutes of administration. There was no treatment effect on electrolyte concentrations in either study but significant changes did occur over time. The data showed that GE is unlikely to significantly affect rehydration.
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PMID:Gastric emptying of oral rehydration solutions at rest and after exercise in horses. 942 55

The aim of this study was to examine if the pattern of fluid intake with a carbohydrate-electrolyte solution during 4 h recovery from prolonged, submaximal running would influence the subsequent endurance capacity. Seven well-trained athletes aged 19.8 +/- 0.3 years (mean +/- s(mean)) took part in the study, which had university ethical committee approval. They ran at 70% VO2 max on a level treadmill for 90 min (T1), or until volitional fatigue, whichever came first, on two occasions, at least 7-10 days apart. Four hours later, the subjects ran at the same speed for as long as possible (T2), as a measure of their endurance capacity. During the 4 h rehydration recovery period, the runners were allowed to drink a carbohydrate-electrolyte solution (6.9% Lucozade-Sport; sodium, 24 mmol l(-1); potassium, 2.6 mmol l(-1); calcium, 1.2 mmol l(-1); osmolality, 300 mOsm kg(-1)) ad libitum on one occasion. On the other occasion, the volume of the same fluid was prescribed from calculations of the body mass loss during T1 (2.6% of pre-exercise body mass). All subjects completed the 90 min run during T1 on both trials. However, during T2, in the prescribed intake trial, the exercise time to exhaustion was 16% longer (P< 0.05) than during T2 in the ad libitum trial (69.9 +/- 9.1 vs 60.2 +/- 10.2 min). Although there was no difference between conditions in the total volume ingested (1499 +/- 155 vs 1405 +/- 215 ml), the volume of carbohydrate-electrolyte solution ingested in the fourth hour of the rehydration recovery period was greater in the prescribed intake trial than in the ad libitum trial (258 +/- 52 vs 78 +/- 34 ml; P< 0.05). The amount of glucose ingested in this period during the prescribed intake trial was also greater than during the ad libitum trial (17.8 +/- 3.6 vs 5.4 +/- 2.4 g; P< 0.05). There was a higher blood lactate concentration at the start of T2 in the prescribed intake trial than in the ad libitum trial (1.12 +/- 0.20 vs 0.94 +/- 0.09 mmol l(-1); P< 0.05), but there were no differences in blood glucose, plasma insulin, free fatty acid concentrations or urine volume between trials. The results of this study suggest that drinking a prescribed volume of a carbohydrate-electrolyte solution after prolonged exercise, calculated to replace the body fluid losses, restores endurance capacity to a greater extent than ad libitum rehydration during 4 h of recovery, even though the total volumes ingested were the same between trials.
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PMID:Influence of fluid intake pattern on short-term recovery from prolonged, submaximal running and subsequent exercise capacity. 953 Oct 3


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