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)

To determine the extent of metabolite oxidation, rats were injected with [U-14C]lactate, -glucose, or -bicarbonate (n = 5, each) during rest or after continuous (CE) and intermittent (IE) exercises to exhaustion. Tissue analyses of resting rats, or rats killed following CE and IE and pulse injection with [14C]lactate or -glucose (n = 72, each), were used to determine the metabolic pathways of these two substrates. Oxygen consumption (VO2) declined rapidly for the first 15 min after exercise; thereafter, VO2 declined slowly and remained elevated above resting levels for 120 min. The slow phase of decline in VO2 during recovery did not coincide with lactate removal, which occurred within 15 min. Two-dimensional radiochromatograms produced from blood, kidney, liver, skeletal muscle, and heart indicated a rapid incorporation of 14C into several amino acid pools, including alanine, glutamine, glutamate, and aspartate. Four-hour postexercise recoveries (means of CE and IE) of injected [14C]lactate were lactate (0.75%), glucose (0.52%), protein (8.57%), glycogen (18.30%), CO2 (45.18%), and HCO3- (17.72%). Greater (P < 0.05) incorporation of 14C into protein and glycogen constituents after exercise, compared with rest, was demonstrated. Incorporation of [14C]lactate into glycogen represented a significant but only minor fraction of the metabolism of lactate after exhausting exercise. It is suggested that classical explanations of excess postexercise O2 consumption (i.e., "O2 debt") are too simplistic.
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PMID:End points of lactate and glucose metabolism after exhausting exercise. 744 Feb 96

In the present study, we investigated possible mechanisms behind exogenous phospholipase C-induced glycerol production in irreversibly damaged myocytes. Rat ventricular myocytes were preincubated for 60 min in substrate-free Krebs-Henseleit bicarbonate buffer equilibrated with 95% N2-5% CO2 (37 degrees C, pH = 7.4), resulting in exhaustion of cellular high energy phosphates and loss of rod-shaped morphology. At the end of the preincubation period, the incubation vials were divided into two groups; one receiving 10 mU/ml phospholipase C (PC-PLC), whereas the other received an equivalent volume of buffer (control incubations). Incubation was then continued for another 60 min under 95% air-5% CO2 atmosphere. Samples for measurement of metabolite levels were taken immediately after cell isolation, at the end of the preincubation period and at the end of the normoxic incubation period. During the 60 min incubation period following reoxygenation, glycerol output was markedly higher from PC-PLC treated than from control myocytes. However, the elevated glycerol output from these cells was not accompanied by a simultaneous rise in glycerol-3-phosphate, nor was it inhibited by inclusion of pyruvate in the incubation buffer. On the other hand, glycerol output from PC-PLC treated myocytes was effectively inhibited by a diacylglycerol lipase inhibitor (U-57908, The Upjohn Company). Analysis of cellular lipids revealed a 22% reduction of phospholipid in PC-PLC treated myocytes (P < 0.02), while the content of triacylglycerol, diacylglycerol and unesterified fatty acids increased by 76, 261 and 103%, respectively (P < 0.02). No significant changes were observed for these parameters in control myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phospholipid degradation in hypoxic/reoxygenated cardiomyocytes in response to phospholipase C from Bacillus cereus. 760 7

Buffering is a factor which influences performance in short and middle-term endurance by compensating exercise acidosis. The aim of the study was to establish whether respiration parameters are a relative measure of buffering capacity and to study the influence of buffering on specific performance parameters. Three groups (each of ten subjects) with defined degrees of adaptation [untrained (UT), aerobic-trained (AeT) and elite 400-m runners (AnT) with a best time of 48.47 +/- 0.98 s] were examined in an incremental multi-stage test on the treadmill. Breath-by-breath gas analysis was performed using mass spectrometry and computer routines. Serum lactate concentrations were determined at each exercise level until subjective exhaustion. A value for the relative functional buffering capacity (relFB) was calculated using exercise metabolic parameters. Running speed at the lactate threshold was used as the starting point of buffering. The start of respiratory compensation of acidosis (RCP) was taken as the endpoint of buffering. RCP was determined at the point of decrease in end-tidal CO2 content (CO2-ET). RelFB was given in percent of buffering to running speed at RCP. Group AnT attained the same maximum performance data (maximum running speed, maximum rate of O2 consumption) as group AeT. However, these values were attained in group AnT with a significantly higher relFB (AnT: 31.0 +/- 3.2% vs. AeT: 15.7 +/- 3.9%, P < 0.0001), while a higher lactate threshold indicated a greater oxidative capacity in AeT (AeT: 3.07 +/- 0.26 m.s-1 vs. AnT: 2.68 +/- 0.22 m.s-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relative functional buffering capacity in 400-meter runners, long-distance runners and untrained individuals. 807 24

In order to determine the level of hypoxemia which is sufficient to impair maximal performance, seven well-trained male cyclists [maximum oxygen consumption (VO2max) > or = 5 l.min-1 or 60 ml.kg-1.min-1] performed a 5-min performance cycle test to exhaustion at maximal intensity as controlled by the subject, under three experimental conditions: normoxemia [percentage of arterial oxyhemoglobin saturation (%SaO2) > 94%], and artificially induced mild (%SaO2 = 90 +/- 1%) and moderate (% SaO2 = 87 +/- 1%) hypoxemia. Performance, evaluated as the total work output (Worktot) performed in the 5-min cycle test, progressively decreased with decreasing % SaO2 [mean (SE) Worktot = 107.40 (4.5) kJ, 104.07 (5.6) kJ, and 102.52 (4.7) kJ, under normoxemia, mild, and moderate hypoxemia, respectively]. However, only performance in the moderate hypoxemia condition was significantly different than in normoxemia (P = 0.02). Mean oxygen consumption and heart rate were similar in the three conditions (P = 0.18 and P = 0.95, respectively). End-tidal partial pressure of CO2 was significantly lower (P = 0.005) during moderate hypoxemia compared with normoxemia, and ventilatory equivalent of CO2 was significantly higher (P = 0.005) in both hypoxemic conditions when compared with normoxemia. It is concluded that maximal performance capacity is significantly impaired in highly trained cyclists working under an % SaO2 level of 87% but not under a milder desaturation level of 90%.
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PMID:Arterial hypoxemia and performance during intense exercise. 816 27

We studied the influence of diaphragmatic fatigue on the control of ventilation and respiratory muscle contribution to pressure swings in six normal seated subjects. CO2 was rebreathed before and after diaphragmatic fatigue induced by breathing against an inspiratory resistance requiring 60% maximal transdiaphragmatic pressure with each breath until exhaustion. After diaphragmatic fatigue for a given level of end-tidal PCO2, we found that tidal volume, breathing frequency, minute ventilation, duty cycle, and mean inspiratory flow did not change; esophageal pressure swings were the same, but gastric and transdiaphragmatic pressure swings were decreased; and the slope of the transpulmonary pressure-gastric pressure relationship determined at zero flow points at end expiration and end inspiration was increased. End-expiratory transpulmonary pressure progressively decreased and end-expiratory gastric pressure progressively increased with increasing end-tidal PCO2 by the same magnitude before and after diaphragmatic fatigue. We conclude that diaphragmatic fatigue induces proportionately greater contributions of inspiratory rib cage muscles than of the diaphragm, which results in the preservation of ventilatory response to CO2 despite impaired diaphragmatic contractility.
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PMID:Effect of diaphragmatic fatigue on control of respiratory muscles and ventilation during CO2 rebreathing. 822 52

We evaluated the effect of global inspiratory muscle fatigue on ventilation and respiratory muscle control during CO2 rebreathing in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. CO2 response curves were measured before and after fatigue. During CO2 rebreathing, global fatigue caused a decreased tidal volume (VT) and an increased breathing frequency but did not change minute ventilation, duty cycle, or mean inspiratory flow. Both esophageal and transdiaphragmatic pressure swings were significantly reduced after global fatigue, suggesting decreased contribution of both rib cage muscles and diaphragm to breathing. End-expiratory transpulmonary pressure for a given CO2 was lower after fatigue, indicating an additional decrease in end-expiratory lung volume due to expiratory muscle recruitment, which leads to a greater initial portion of inspiration being passive. This, combined with the reduction in VT, decreased the fraction of VT attributable to inspiratory muscle contribution; therefore the inspiratory muscle elastic work and power per breath were significantly reduced. We conclude that respiratory control mechanisms are plastic and that the respiratory centers alter their output in a manner appropriate to the contractile state of the respiratory muscles to conserve the ventilatory response to CO2.
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PMID:Effect of global inspiratory muscle fatigue on ventilatory and respiratory muscle responses to CO2. 822 53

We hypothesized that augmented responses of glucoregulatory hormones in iron deficiency would enhance liver and muscle glycogenolysis, leading to increased gluconeogenic precursor (lactate) supply and upregulation of hepatic gluconeogenesis. Female weanling rats were randomly placed on either a mildly iron-deficient (-Fe; 15 mg Fe/kg diet) or an iron-sufficient (+Fe; 50 mg Fe/kg diet) diet for 4 wk and studied at rest and during exhaustive treadmill running. Hemoglobin was 9.0 +/- 0.2 and 13.1 +/- 0.3 g/dl in -Fe and +Fe, respectively, after 3.5 wk of dietary iron deficiency. Arterial plasma epinephrine (Epi), norepinephrine (NE), adrenocorticotropic hormone (ACTH), corticosterone, insulin, and glucagon levels were similar at rest in both groups, as were liver, gastrocnemius, and superficial and deep vastus medialis glycogen levels. Liver and kidney phosphoenolpyruvate carboxykinase (PEPCK) activities were similar in both groups. Maximum O2 consumption was decreased (22%) in -Fe. Respiratory exchange ratio (CO2 production/O2 consumption) was unaffected at rest but increased at maximum O2 consumption in -Fe. Time to exhaustion during a standardized running test (13.4 m/min, 0% grade) was decreased 45% in -Fe (63 +/- 5 vs. 116 +/- 10 min). During exercise, euglycemia was maintained in both groups, but blood lactate was elevated in -Fe. The mean net glycogen utilization during exercise was increased in liver (43%), soleus (33%), and superficial vastus medialis (106%) and decreased in the gastrocnemius (36%) in -Fe. Liver and kidney PEPCK activities were increased similarly at exhaustion in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmented glucoregulatory hormone concentrations during exhausting exercise in mildly iron-deficient rats. 823 58

1. Lactate and H+ efflux from skeletal muscles were studied with the one-legged knee extension model under conditions in which blood flow, arterial lactate and the muscle-blood lactate concentration gradient were altered. Subjects exercised one leg twice to exhaustion (EX1, EX2), separated by a 10 min recovery and a period of intense intermittent exercise. After 1 h of recovery the exercise protocol was repeated with the other leg. Low-intensity exercise was performed with one leg during the recovery periods, while the other leg was passive during its recovery periods. 2. Prior to, and immediately after, EX1 and EX2 and then 3 and 10 min after EX1, a biopsy was taken from the vastus lateralis of the exercised leg for lactate, pH, muscle water and fibre-type determinations. Measurements of leg blood flow and venous-arterial differences for lactate (whole blood and plasma), pH, partial pressure of CO2 (PCO2), haemoglobin, saturation and base excess (BE) were performed at the end of exercise and regularly during the recovery period after EX1. 3. The lactate release was linearly related (r = 0.96; P < 0.05) to the muscle lactate gradient over a range of muscle lactate from 0 to 45 mmol (kg wet wt)-1. The muscle lactate transport was evaluated from the net femoral venous-arterial differences (V-Adiff) for lactate. This rose with increases in the muscle lactate gradients, but as the gradient reached higher levels the V-Adiff lactate responded less than at smaller gradients. Thus, the lactate transport over the muscle membrane appears to be partly saturated at high muscle lactate concentrations. 4. The percentage of slow twitch (%ST) fibres was inversely related to the muscle lactate gradient, but it was not correlated to the lactate release at the end of the exercises. In spite of a significantly higher blood flow during active recovery, the lactate release was the same whether the leg was resting or performed low-intensity exercise in the recovery periods. In several other conditions the muscle lactate and H+ gradients would have predicted that the V-Adiff lactate would have been greater than it actually was. Thus, a variety of factors affect muscle lactate transport, including arterial lactate concentration, muscle perfusion, muscle contraction pattern and muscle morphology. 5. The muscle and femoral venous pH declined during EX1 to 6.73 and 7.14-7.15, respectively, and they increased to resting levels during 10 min of either passive or active recovery.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Lactate and H+ effluxes from human skeletal muscles during intense, dynamic exercise. 833 79

We have compared the results of a standard progressive maximal exercise test to those of an endurance exercise test in 22 healthy school children (13 girls, 9 boys, mean age 14.8 years) in order to examine whether it is possible to extrapolate results from a maximal test to predict their endurance capacity. All children performed a standard progressive maximal exercise test (15 W increments every minute until exhaustion) and an endurance test (individually calculated loads to mimic cycling at 20 km/h against a windforce 5 of Beaufort for 30 minutes) on 2 separate days. In both tests metabolic [oxygen uptake (VO2), CO2 production, blood lactate accumulation], ventilatory [minute ventilation (VE)], and circulatory variables were measured. From the maximal test the threshold of lactate accumulation (LT) was determined. Thirteen children were capable of enduring the 30 minute exercise (Group 1), and 9 could not complete the endurance test (Group 2). These two groups were comparable with respect to age, height, and baseline lung function. Children in Group 2 had a higher mean weight (P < 0.005) than those in Group 1. Eight of the 9 children in Group 2 were girls, whereas Group 1 consisted of 5 girls and 8 boys. There was no significant difference between Group 1 and 2 in the mean values of VO2 max, maximal respiratory exchange ratio (R max), VEmax, LT, oxygen pulse, and other variables obtained during the maximal exercise tests. Lactate accumulation during the endurance test in Group 2 was larger than in Group 1 (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:What limits endurance in normal children? 833 13

The effect of bicarbonate ingestion on total excess volume of CO2 output (CO2 excess), due to bicarbonate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g.kg-1 body mass) of CaCO3 (control) and NaHCO3 (alkalosis). The resting arterialized venous blood pH (P < 0.05) and bicarbonate concentration ([HCO3-]b; P < 0.01) were significantly higher in acute metabolic alkalosis [AMA; pH, 7.44 (SD 0.03); [HCO3-]b, 29.4 (SD 1.5) mmol.l-1] than in the control [pH, 7.39 (SD 0.03); [HCO3-]b, 25.5 (SD 1.0) mmol.l-1]. The blood lactate concentrations ([la-]b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher [la-]b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol.l-1, P < 0.05] and at 3 min after exercise [14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol.l-1, P < 0.05] were found in AMA compared with the control. The CO2 excess increased significantly from the control [3177 (SD 506) ml] to AMA [3897 (SD 381) ml; P < 0.05]. The CO2 excess per body mass was found to be significantly correlated with both the increase of [la-]b from rest to 3 min after exercise (delta[la-]b; r = 0.926, P < 0.001) and with the decrease of [HCO3-]b from rest to 3 min after exercise (delta [HCO3-]b; r = 0.872, P < 0.001), indicating that CO2 excess per body mass increased linearly with both delta [la-]b and delta [HCO3-]b.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of acute sodium bicarbonate ingestion on excess CO2 output during incremental exercise. 839 8


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