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

Although exponential growth of Bacillus subtilis 168 in a phosphate-limited medium halted with the exhaustion of inorganic phosphate, the bacteria continued to grow at a slower rate for a further 3 to 4 h at 37 degrees C. This postexponential growth in the absence of an exogenous phosphate supply was accompanied by a loss of teichoic acid from the cell walls of the bacteria. Quantitative analysis of walls and culture fluids showed that the phosphate loss from the walls could not be accounted for by an increase in phosphate-containing compounds in the medium, which implied that the cells were using their own wall teichoic acids to supply phosphate necessary for growth. Addition of exogenous teichoic acid to phosphate-starved cultures resulted in stimulation of growth and in the simultaneous disappearance of teichoic acid phosphate from the medium. It is proposed that teichoic acids, which can contain more than 30% of the total phosphorus of exponential-phase cells, can be used as a reserve phosphate source when the bacteria are starved for inorganic phosphate.
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PMID:Cell wall teichoic acid as a reserve phosphate source in Bacillus subtilis. 10 66

Conditions causing cyanide-resistant respiration were studied in the yeast Candida lipolytica. This type of respiration was found when the culture growing on glucose, glycerol, hexadecane, or acetate exhuasted the substrate and passed from the logarithmic to stationary growth phase; the same phenomenon can be induced by exhaustion of phosphorus or nitrogen in the glucose medium. The yeast culture growing on lactate, ethanol, pyruvate, alpha-ketoglutarate, malate, or succinate is characterized by cyanide-resistant respiration even at the beginning of the logarithmic growth phase. The values of pH in the incubation medium have no effect on the time of manifestation of cyanide-resistant respiration.
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PMID:[Detection of cyanide resistant respiration among Candida lipolytics yeasts]. 94 Apr 87

The toxicity of FUT-187, a synthetic protease inhibitor, was investigated in Sprague-Dawley rats. FUT-187 was given orally to the rats at doses of 2, 10, 50, 250 and 1250 mg/kg/day for 13 weeks, then the drug was withdrawn for 5 weeks for recovery. The results are summarized as follows: In the 1250 mg/kg/day group, 9 out of 20 males died with decreased body weight and exhaustion. Histopathological examination revealed renal papillary necrosis, ulcer in the urinary bladder, hemostatic lesions in the lungs and liver, ulcer or erosion in the stomach, duodenum and jejunum. The surviving animals in this group showed swelling of the limbs due to synovitis, transient salivation immediately after administration, suppression of growth with decreased food consumption. Urinalysis revealed a low pH, increased ketones and bilirubin excretion, dark yellowish change in color, the appearance of "leaflet-shaped" crystals and increased red blood cells and epithelial cells in the urinary sediment, increased water intake, decreased specific gravity and decreased sodium, potassium and chloride in the urine. Hematologically, there was an increase in the white blood cell count. A biochemical analysis of the blood revealed decreased amylase activity, glucose and total protein levels and increased GOT activity and inorganic phosphorus levels. Pathological changes were observed in the pancreas, kidney, digestive tract, urinary bladder and liver. The pancreas showed macroscopical enlargement and increased organ weight. Histopathologically, there were several alterations in the acinar cells, such as vacuolization due to increased fat droplets, nuclear irregularity, prominent nucleoli, irregular arrangement and vesiculation of rough endoplasmic reticulum (rER), dilatation of developed Golgi apparatus and increased free ribosomes. In the kidney, increased weight and pigmentation in the proximal tubular epithelium were noted. Electron microscopically, these pigments were recognized as secondary lysosomes containing filamentous material and electron dense granules within a lucent matrix. In the digestive tract, ulcer or erosion in the stomach and duodenum, and villous proliferation in the small intestine were observed. Furthermore, hyperplasia and vacuolization were noted in the mucosal epithelium of the urinary bladder. In addition, loss of perilobular fat droplets in the liver and increased adrenal weight without histological change were observed. After a 5-week recovery period, these changes disappeared almost completely. In the 250 mg/kg/day group, slight suppression of growth the appearance of "leaflet-shaped" crystals in the urinary , sediment, increased water intake and decreased sodium in the urine were observed. The pancreas showed enlargement, increased weight, acinar cell hypertrophy with increased zymogen granules, fine vacuolization, slight derangement and vesicular of rER, and dilatation of Golgi apparatus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 13-week subacute oral toxicity study of 6-amidino-2-naphthyl 4-[(4,5-dihydro-1H-imidazol-2-yl) amino] benzoate dimethanesulfonate (FUT-187) in rats]. 129 23

To examine the respective roles of malnutrition and phosphate depletion on muscle exercise capacity and bioenergetics, phosphate-depleted, either underfed or partly refed rats; phosphate-supplemented, either underfed or partly refed rats; and well-nourished control animals were studied, using swim time to exhaustion and 31P NMR spectroscopy measurements of muscle phosphocreatine, inorganic phosphate, adenosine triphosphate and intracellular pH. Only partly refed rats displayed hypophosphataemia. Swim time to exhaustion was lower in non-refed rats than in controls. Among the four groups, both refeeding and phosphate depletion positively affected swim time to exhaustion (both with P less than 0.02), and swim time to exhaustion was negatively correlated with phosphataemia (P less than 0.05). At rest, the ratio of muscle phosphocreatine/inorganic phosphate was lower in the phosphate-supplemented rats than in controls, whereas muscle phosphocreatine/adenosine triphosphate and intracellular pH were comparable. After non-tetanic stimulation, the muscle phosphocreatine recovery was slower in the four groups than in controls and closely correlated with exhaustion (P less than 0.01). These findings suggest that malnutrition alters the capacity of muscular work, mainly because of a reduced cell oxidative energy availability. These patterns are improved by partial refeeding and clearly influenced by the level of phosphorus intake, whether depletion is capable of improving metabolic alterations or uncontrolled supplementation is deleterious in malnourished animals.
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PMID:Respective effects of malnutrition and phosphate depletion on endurance swimming and muscle metabolism in rats. 159 46

To assess exercise energy metabolism of forearm flexor muscles in rowers, six male student rowers and six control subjects matched for age and sex were studied using phosphorus-31 magnetic resonance spectroscopy (31P-MRS). Firstly, to adjust for the effect of differences in cross-sectional muscle area, the maximal cross-sectional area (CSAmax) of the forearm flexor muscles was estimated in each individual using magnetic resonance imaging. Multistage exercise was then carried out with an initial energy production of 1 J.cm-2 CSAmax for 1 min and an increment of 1 J.cm-2 CSAmax every minute to the point of muscle exhaustion. A series of measurements of 31P-MRS were performed every minute. The CSAmax was significantly greater in the student rowers than in the control subjects [19.8 (SD 2.2) vs 17.1 (SD 1.2) cm2, P less than 0.05]. The absolute maximal exercise intensity (J.min-1) was greater in the rowers than in the control subjects. However, the maximal exercise intensity per unit of muscle cross sectional area (J.min-1.cm-2) was not significantly different between the two groups. During mild to moderate exercise intensities, a decrease in phosphocreatine and an increase in inorganic phosphate before the onset of acidosis were significantly less in the rowers, indicating a requirement of less adenosine 5'-diphosphate to drive adenosine 5'-triphosphate production. The onset of acidosis was also significantly delayed in the rowers. No difference was observed in forearm blood flow between the two groups at the same exercise intensity (J.min-1.cm-2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phosphorus-31 magnetic resonance spectroscopy of forearm flexor muscles in student rowers using an exercise protocol adjusted for differences in cross-sectional muscle area. 161 91

To assess forearm exercise capacity and exercise energy metabolism in relationship to forearm muscle mass and blood flow in patients with chronic heart disease, 22 patients (NYHA class I (C1) 8, class II(C2) 10, class III (C3) 4) and 10 normal subjects were studied using Phosphorus-31 magnetic resonance spectroscopy (31P-MRS). First, the maximal cross sectional area (MCA) of the forearm flexor muscles was estimated in each individual using magnetic resonance imaging. Then, during multistage forearm flexor exercise, 31P-MRS was performed to estimate phosphocreatine (PCr), inorganic P (Pi), and intracellular pH. Forearm blood flow was measured by plethysmography. An initial work load of forearm exercise was decided by MCA as 1 J/cm2, and multistage exercise was done with an increment of 1 J/min/cm2 to the point of maximal muscle exhaustion. The maximal load (J/min) was decreased in cardiac groups as NYHA class advanced. However, the difference among all groups except group C3 was not significant when the max load was adjusted for muscle MCA. As the work load was increased during forearm exercise, PCr and intracellular pH decreased, and Pi increased in every group. Standardized PCr [PCr/(PCr + Pi)] was lower in group C2 and C3 than in group N at each work load. At high work loads, intracellular pH tended to be lower in group C2 and C3 than in group N and C1. Forearm blood flow during forearm exercise was not different among the four groups. In the maximal exercise test using upright ergometer, peak oxygen uptake and anaerobic threshold were lower in group C1, C2 and C3 than in group N.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A study of forearm muscle metabolism in patients with chronic heart disease]. 188 57

The purpose of this study was to investigate the ergogenic effect of oral inosine (IN) supplementation (6,000 mg.d-1 for 2 d) upon 3-mile run time (3MTIME) and VO2 peak. Nine highly trained endurance runners participated in a double-blind, placebo (PL), crossover study. Each subject undertook an IN or PL trial, consisting of three exercise tests: a submaximal warm-up run (SUBRUN), a competitive 3-mile treadmill run (3MRUN), and a maximal treadmill run (MAXRUN) to determine VO2 peak and time to exhaustion (MAXTIME). Additional measurements during the 3MRUN and MAXRUN included oxygen uptake (VO2), ventilation (VE), respiratory exchange ratio (R), and ratings of perceived exertion (RPE); blood samples were also taken prior (PRERUN) to the SUBRUN test and following the SUBRUN, 3MRUN, and MAXRUN tests in order to assess glucose, pyruvate, lactate, phosphorus, 2,3-DPG, hemoglobin, and uric acid. Analyses of the data revealed no significant effect of oral IN supplementation either upon 3MTIME (IN = 18.31 +/- 1.21; PL = 18.33 +/- 1.15 min) or VO2 peak (IN = 58.6 +/- 5.1; PL = 60.7 +/- 4.5 ml O2.kg-1.min-1) or upon other dependent variables. MAXTIME was significantly longer during the PL trial (P less than 0.05), suggestive of a possible impairment effect of oral IN supplementation. Based upon our data, we conclude that IN is not an effective ergogenic aid to enhance athletic performance of an aerobic nature.
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PMID:Effect of inosine supplementation on 3-mile treadmill run performance and VO2 peak. 240 14

N-methyl-D-aspartate (NMDA) is an agonist used to identify neuronal receptive sites for dicarboxylic amino acid neurotransmitters; NMDA receptors are implicated in neuronal damage of ischemic or hypoglycemic origin in newborns although involved mechanisms remain to be identified. In the present study, 31P magnetic resonance spectroscopy with fast (6/min) data acquisition was used in newborn rat brain slices to measure changes of intracellular phosphocreatine and nucleotide triphosphate levels following extracellular NMDA applications. The rapid exhaustion of phosphocreatine stores in 50% of the total population of brain cells was induced in all cases by application of NMDA (30-45 s, 25-100 mM). It was not reproduced by other excitatory agents: potassium ions (24.6 mM, 4 min), isobutylxanthine (1mM), muscarine (10 mM), serotonin (0.1 mM) or substance P (10 microM). Such an effect of NMDA was not modified after tetrodotoxin (1 microM) and was reduced by extracellular 2-amino-5-phosphonovalerate (50 microM) or magnesium ions (2.2 mM). However it did develop during NMDA-induce neuronal excitations and was reversible within 10-30 min. This action of NMDA was followed by an irreversible decrease of phosphorus metabolites if mitochondrial creatine kinase and adenosine triphosphatase were decoupled by atractyloside (50 microM). Experiments revealed a link between selective NMDA action at neuronal plasma membranes, neurotoxicity and energy production by mitochondria.
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PMID:Metabolic action of N-methyl-D-aspartate in newborn rat brain ex vivo: 31p magnetic resonance spectroscopy. 268 43

Hypophosphoremia may interfere with respiratory function in chronic obstructive pulmonary diseases (COPD) through different mechanisms: muscular exhaustion and weakness. Accordingly, the frequency and magnitude of hypophosphoremia was studied in 36 consecutive patients with acute respiratory failure and mechanical ventilation. Initial phosphoremia was normal (1,32 +/- 0,12 mmol/l) but often and rapidly decreased in all patients after mechanical ventilation had been started (0,54 +/- 0,14 mmol/l after 24 h). After this, phosphoremia remained low, slowly increasing with continued enteral nutrition (2000 Kcal, 276 g of glucides, 33 mmol/l of phosphorus). Four patients had severe hypophosphoremia after 24 h of mechanical ventilation (less than 0,30 mmol/l). Phosphoremia returned to a normal level 36 h after extubation. Hypophosphoremia was closely linked to pH improvement (r = + 0,67, P less than 0,001) and was paralleled by a drop in phosphaturia, suggesting intra-cellular penetration of phosphorus.
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PMID:[Hypophosphoremia during mechanical ventilation for chronic obstructive bronchopathies]. 316 18

Quantitative probing of heterogeneous regions in muscle is feasible with phosphorus-31 magnetic resonance spectroscopy because of the differentiation of metabolic patterns of glycolytic and oxidative fibers. A differential recruitment of oxidative and glycolytic fibers during exercise was demonstrated in 4 of 10 untrained young men by following changes in phosphate metabolites. Concentrations of inorganic phosphate (Pi), phosphocreatine, and ATP were estimated in the wrist flexor muscles of the forearm at rest, during two cycles of three grades of exercise, and in recovery. At high work levels (40% of maximum strength), two distinct Pi peaks were observed and identified with Pi pools at pH 6.9 and pH 5.9-6.4, respectively. These could be accounted for as follows. At the lowest level of work (using 20% of maximum strength), early recruitment primarily of oxidative (type I) and possibly some intermediate (type IIA) muscle fibers occurs with relatively little net lactate production and consequently little decrease in pH. At higher work loads, however, primarily glycolytic (type IIB) muscle fibers are recruited, which have relatively high net lactate production and therefore generate a second pool of Pi at low pH. ATP depletion (35-54%) and Pi losses accompanied the reduction in ability to perform during the first exercise cycle. When the cycle of graded exercise was repeated immediately, the total Pi remained high but gave rise to only one peak at pH 6.8-7.0. These observations indicated exhaustion of glycolytic type IIB fibers, removal of lactate by high local blood flow, and sustained contractions largely by oxidative type I and IIA fibers. A functional differentiation of fiber types could also be demonstrated during recovery if exercise was stopped while two pools of Pi were still apparent. In the first 3 min of recovery, the Pi peak at pH 6.8-6.9 disappeared almost entirely, whereas the Pi peak at pH 6.0 remained unaltered, reflecting the faster recovery of oxidative type I fibers. The potential of magnetic resonance spectroscopy to characterize oxidative and glycolytic fibers, predict capacity for aerobic performance, and signal the presence of muscle pathology is discussed.
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PMID:Functional pools of oxidative and glycolytic fibers in human muscle observed by 31P magnetic resonance spectroscopy during exercise. 348 May 22


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