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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The value of the adenylate energy charge, i.e. ([ATP] + 1/2[ADP])/([ATP] + [ADP] + [AMP]), during batch culture of Beneckea natriegens remained relatively constant during the exponential and early stationary phases of the growth cycle. During exponential growth the intracellular ATP content remained constant, the amount of ATP in the culture increasing proportionally with growth; these conditions were unaltered during growth in the presence of added cyclic AMP. On cessation of growth, significant variation in bacterial ATP content was observed depending on whether growth of the cultures terminated due to exhaustion of carbon or nitrogen from the medium, and on the presence or absence of added cyclic AMP.
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PMID:Adenylate energy charge during batch culture of Beneckea natriegens. 1 48

Purine nucleotides (ATP, ADP, AMP, IMP), creatine, phosphocreatine, lactate, pyruvate and glycogen were measured in rainbow trout (Oncorhynchus mykiss) white muscle following exercise to exhaustion. Estimates of intracellular pH permitted calculation of free concentrations of nucleotides ([nucleotide]f) required for most models of control of energy metabolism. Creatine charge, [PCr]/([PCr]+[Cr]), fell from 0.49 +/- 0.05 (mean +/- S.E.M.) to 0.08 +/- 0.02 with exercise but recovered completely by the first sample (2 h). Although [ATP] declined to 24% of resting levels and recovered very slowly, RATP, [ATP]/([ATP]+[ADP]f+[AMP]f), and energy charge, EC, ([ATP]+0.5[ADP]f)/([ATP]+[ADP]f+[AMP]f), recovered as quickly as creatine charge. Changes in [IMP] mirrored those in [ATP], suggesting that AMP deaminase is responsible for maintaining RATP and EC. Recovery of carbon status was much slower than recovery of energy status. Lactate increased from 4 mumol g-1 at rest to 40 mumol g-1 at exhaustion and did not recover for more than 8 h. Glycogen depletion and resynthesis followed a similar time course. During the early stages of recovery, calculated [ADP]f declined by more than 10-fold relative to the resting values. The resulting high [ATP]/[ADP]f ratios may limit the rate at which white muscle mitochondria can produce ATP to fuel glycogenesis in situ. It is postulated that the high [ATP]/[ADP]f ratios are required to drive pyruvate kinase in the reverse direction for glyconeogenesis in recovery.
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PMID:Integrating metabolic pathways in post-exercise recovery of white muscle. 160 73

This study examined the dynamics for ammonia (NH3) metabolism in human skeletal muscle during and after intense one-legged exercise. Subjects (n = 8) performed dynamic leg extensor exercise to exhaustion (3.2 min). Muscle NH3 release increased rapidly to a maximum of 314 +/- 42 mumol/min and declined immediately on cessation of exercise. Recovery was complete in approximately 20 min. Arterial [NH3] increased less rapidly and reached its maximum 2-3 min into recovery. These data demonstrate that NH3 clearance is more sensitive to the cessation of exercise than is NH3 release from skeletal muscle. Muscle [NH3] increased three to fourfold during exercise and represented 74 +/- 8% of the total net NH3 formation. Thus the change in muscle [NH3] alone underestimates the NH3 production. There was no evidence that the muscle-to-venous blood NH3 ratio shifts in accordance with the H+ data. Thus other factors must contribute to the NH3 release from active muscle. The total net NH3 formed corresponded with the intramuscular inosine 5'-monophosphate accumulation, suggesting that the NH3 was derived from AMP deamination. Changes in the known modulators of AMP deaminase (ATP, ADP, H+) were moderate, so the mechanisms initiating the deamination remain obscure.
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PMID:Ammonia metabolism during intense dynamic exercise and recovery in humans. 238 11

1. Modulation of fast and slow Ca2+ channels of frog skeletal muscle by adrenaline (10(-6) to 10(-5) M) and cyclic AMP was investigated using intracellular voltage recordings in intact fibres and a voltage-clamp technique in cut fibres. 2. In tetraethylammonium (TEA), Cl(-)-free Ringer solution, adrenaline increased the maximum rate of rise of Ca2+ spikes by 85% and in a similar solution, peak slow Ca2+ current (ICa,s) by 51%. 3. Application of cyclic AMP to the cut ends of fibres, produced a relative increase of ICa,s of ca. 24%. The effect was maintained for ca. 2 h. 4. Changes in the time course of ICa,s were produced by adrenaline and cyclic AMP: the limiting values of time-to-peak current measured as a function of membrane potential were lower (ca. 41% in adrenaline and ca. 34% in cyclic AMP) than those found in control experiments. Also, ICa,s decayed faster in the presence of adrenaline or cyclic AMP. These changes can be explained by exhaustion of Ca2+ in the lumen of transverse tubular system and do not require the assumption of kinetic variations. 5. Fast Ca2+ currents (ICa,f) which could not be blocked by nifedipine were also recorded. Cyclic AMP greatly increased the amplitude of ICa,f but had no obvious effects on ICa,f kinetics. 6. Application of catalytic subunit of cyclic AMP-dependent protein kinase by diffusion or by pressure injection also increased the amplitude of ICa,s and ICa,f. Pressure injection brought about modifications in the time course of ICa,s that cannot be explained by depletion of Ca2+. 7. Mechanical experiments were performed on single fibres. Nominally Ca2+-free solutions prevented the development and the maintenance of positive inotropic effect of adrenaline on twitch tension. Development of twitch potentiation was dependent upon the frequency of stimulation. Adrenaline was practically ineffective if no stimulation was applied. 8. It is concluded that both populations of Ca2+ channels are modulated by adrenergic stimulation probably via cyclic AMP, and that twitch potentiation may be mediated by a Ca2+ entry through Ca2+ channels.
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PMID:Modulation of calcium channels of twitch skeletal muscle fibres of the frog by adrenaline and cyclic adenosine monophosphate. 245 39

The release of Ca2+ from vesicles of heavy sarcoplasmic reticulum after its accumulation due to hydrolysis of ATP, GTP, CTP, UTP or ITP has been studied using Antipyrylazo III, a metal-chromic Ca-indicator. All the studied substrates of the Ca-pump provide Ca2+ accumulation inside the heavy sarcoplasmic reticulum vesicles, the spontaneous Ca2+ outflux rate being different for different nucleoside triphosphates. It is only ATP that provides Ca-(caffeine)-induced Ca2+ release, however AMP, ADP, beta, gamma-methylene-ATP induce Ca2+ ejection in the presence of nonadenylic nucleotides. The ruthenium red (10(-7M) inhibits the induced ejection of Ca2+ from vesicles of the heavy sarcoplasmic reticulum, but does not prevent the spontaneous release of Ca2+ in the same concentrations. A conclusion is drawn that besides Ca-channels sensitive to Ca2+ and caffeine in the presence of ATP (or to AMP, ADP, beta, gamma-methylene-ATP in the presence of nonadenylic nucleotides) and possessing high sensitivity to the ruthenium red there is another pathway for Ca2+ in the heavy reticulum membranes along which its spontaneous release occurs after the substrate exhaustion. It is supposed that this release is provided by the presence of the Ca-ATPase protein.
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PMID:[Calcium release from vesicles of heavy sarcoplasmic reticulum of rabbit skeletal muscles]. 247 98

Phosphorescence of protein tryptophan was analyzed in sarcoplasmic reticulum vesicles, and in the purified Ca2+ transport ATPase in deoxygenated aqueous solutions at room temperature. Upon excitation with light of 295 nm wavelength, the emission maxima of fluorescence and phosphorescence were at 330 nm and at 445 nm, respectively. The phosphorescence decay was multiexponential; the lifetime of the long-lived component of phosphorescence was approximately equal to 22 ms. ATP and vandate significantly reduced the phosphorescence in the presence of either Ca2+ or EGTA; ADP was less effective, while AMP was without effect. The quenching by ATP showed saturation consistent with the idea that the ATP-enzyme complex had a lower phosphorescence yield. Upon exhaustion of ATP, the phosphorescence returned to starting level. Significant quenching of phosphorescence with a decrease in phosphorescence lifetime was also caused by NaNO2, methylvinyl ketone and trichloroacetate, without effect on ATPase activity; this quenching did not show saturation and was therefore probably collisional in nature.
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PMID:Tryptophan phosphorescence of the Ca2+-ATPase of sarcoplasmic reticulum. 297 55

Candida albicans was examined for a glucose effect and showed typical diauxic growth on a mixture of glucose and mannitol, in which mannitol utilization occurred only after exhaustion of glucose. The activity of NAD-linked mannitol dehydrogenase was very low while glucose was present in the medium, but started to increase after consumption of glucose. This increase in activity was fully prevented by trichodermin, an inhibitor of protein synthesis. The uptake of mannitol was detected in the cells grown on mannitol, but not in those grown on glucose with or without mannitol. Mannitol uptake by mannitol-grown cells was not affected by the presence of glucose (0.2 g l-1). These findings indicate that in C. albicans glucose represses the inducible syntheses of mannitol dehydrogenase and a mannitol transport system, and that the involvement of inducer exclusion in this effect is unlikely. Fructose, and to lesser extents galactose, mannose and sucrose, also exhibited similar effects on mannitol metabolism. No correlation was found between the intracellular cyclic AMP levels and the glucose effect.
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PMID:Regulation of mannitol catabolism in Candida albicans: evidence for cyclic AMP-independent glucose effect. 301 28

To study changes in muscle energy state during prolonged exercise, especially in relation to fatigue, muscle biopsies were obtained from seven healthy males working until exhaustion on a cycle ergometer at 68% (63-74%) of their maximal oxygen uptake. Biopsies were taken at rest, after 15 and 45 min of exercise and at exhaustion, and analysed for ATP, ADP, AMP, inosine monophosphate (IMP) and hypoxanthine content by high performance liquid chromatography (HPLC), and for creatine phosphate (CP), lactate and glycogen by enzymatic fluorometric techniques. Glycogen content at exhaustion was approximately 30% of the pre-exercise level. The CP content decreased steeply during the first 15 min of exercise (P less than 0.01) and continued to decrease during the rest of the exercise period (P less than 0.05). Pronounced increases in contents of IMP (64% P less than 0.001) and hypoxanthine (69%, P less than 0.05) were found when exhaustion was approaching. Furthermore, energy charge [EC; (ATP + 0.5 ADP)/(ATP + ADP + AMP)] was decreased at exhaustion (P less than 0.05). The increases in IMP and hypoxanthine which occurred when exhaustion was approaching during prolonged submaximal exercise together with the decrease in EC during this phase of exercise suggest a failure of the exercising skeletal muscle to regenerate ATP at exhaustion.
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PMID:ATP breakdown products in human skeletal muscle during prolonged exercise to exhaustion. 342 83

Measurements of metabolite concentrations before and immediately after swimming of trout to exhaustion indicate that all three potential endogenous fuels of anaerobic metabolism [glycogen, phosphocreatine (PCr) and adenosine triphosphate (ATP)] are utilized during anaerobic white muscle work. Lactate, H+, creatine Pi, NH4+ and inosine monophosphate (IMP) are formed in the process. Glycolysis is considered to be functionally (if loosely) coupled to adenylate depletion by setting up conditions favouring AMP-deaminase-catalysed formation of IMP and NH3. During recovery under these experimental conditions, glycolysis appears to outcompete oxidative metabolism as an ADP acceptor; therefore, in this kind of white muscle, glycolysis is also linked to IMP reconversion to AMP and thus to adenylate replenishment. The net process generates H+, which is why ATP replenishment must be completed before PCr concentrations can be returned to pre-exercise values.
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PMID:Role of glycolysis in adenylate depletion and repletion during work and recovery in teleost white muscle. 358 38

The muscle contents of high-energy phosphates and their derivatives [ATP, ADP, AMP, creatine phosphate (CrP), and creatine], glycogen, some glycolytic intermediates, pyruvate, and lactate were compared in 11 dogs performing prolonged heavy exercise until exhaustion (at ambient temperature 20.0 +/- 1.0 degrees C) without and with trunk cooling using ice packs. Without cooling, dogs were able to run for 57 +/- 8 min, and their rectal (Tre) and muscle (Tm) temperatures increased to 41.8 +/- 0.2 and 43.0 +/- 0.2 degrees C, respectively. Compared with noncooling, duration of exercise with cooling was longer by approximately 45% while Tre and Tm at the time corresponding to the end of exercise without cooling were lower by 1.1 +/- 0.2 and 1.2 +/- 0.2 degrees C, respectively. The muscle contents of high-energy phosphates (ATP + CrP) decreased less, the rate of glycogen depletion was lower, and the increases in the contents of AMP, pyruvate, and lactate as well as in the muscle-to-blood lactate ratio were smaller. The muscle content of lactate was positively correlated with Tm. The data indicate that with higher body temperature equilibrium between high-energy phosphate breakdown and resynthesis was shifted to the lower values of ATP and CrP and glycolysis was accelerated. The results suggest that hyperthermia developing during prolonged muscular work exerts an adverse effect on muscle metabolism that may be relevant to limitation of endurance.
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PMID:Exercise hyperthermia as a factor limiting physical performance: temperature effect on muscle metabolism. 405 65


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