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

The interrelationships among blood lactate (La-) and plasma norepinephrine (NE) and epinephrine (Epi) were studied simultaneously with measures of ventilation (VE) and gas exchange during incremental exercise to exhaustion in nine healthy young men. We wanted to observe whether the tight coupling that exists during normoxic exercise between the concentrations of La- ([La-]) and of both NE and Epi would also be found in hypoxia (inspired O2 fraction = 0.14). In addition, we used recently advocated methods of V slope [CO2 output vs. O2 uptake (VO2)] to select the ventilatory threshold (VT) and log-log transformation of [La-] and VO2 to select the lactate threshold (LT). Peak VO2 was reduced from 4,164 +/- 184 ml/min in normoxia to 3,635 +/- 144 ml/min in hypoxia (P < 0.05). The increase in [La-] was linearly related to the increases in both NE and Epi concentrations in the normoxic and hypoxic tests (r = 0.92-0.96). Estimates of VO2 at VT were significantly greater than those at LT in both normoxia and hypoxia, but these estimates were poorly correlated (r = -0.11-0.46). VT and LT were reduced by hypoxia. Visual interpretation of the VT by examination of VE vs. VO2 and VE/VO2 vs. VO2 did not differ from the LT, but they were less than the VTs by the V-slope method (P < 0.05); yet, all were poorly correlated. The tight coupling between the increase in [La-] and the increase in plasma catecholamines might indicate a common mechanism for the increase or a causative link. VT and LT provided estimates of the general trend in the data, but the poor correlation between them questions the utility of attempting to predict one from the other.
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PMID:Gas exchange, blood lactate, and plasma catecholamines during incremental exercise in hypoxia and normoxia. 856 54

We wished to determine if the degree of hypocapnia correlates with increased frequency of absence seizures and if there is a critical pCO2 at which absence seizures are reliably provoked. Twelve untreated children with newly diagnosed absence epilepsy were continuously monitored by EEG and end-expiratory CO2 recording during quiet respiration and hyperventilation (to absence seizure or exhaustion) while breathing four gas mixtures: (a) room air, (b) 100% O2, (c) 4% CO2 in room air, or (d) 4% CO2 + 96% O2). In quiet respiration, a reduction in number of spike and wave bursts and total seconds of spike and wave was noted in children breathing supplemental CO2 (gases c and d vs. gases a and b), p < 0.05. Supplemental O2 had no effect. Eight subjects had absence seizures elicited with each trial of hyperventilation. All subjects had their own critical pCO2, ranging from 19 to 28 mmHg. Three children had no seizures, two despite hypocapnia to pCO2 of 19 and 21 and 1 who achieved a pCO2 of only 25. In 1, absence seizures were provoked in only six of nine hyperventilation trials to pCO2 of 17-23. In 67% of subjects, absence seizures were reliably provoked by hypocapnia. Critical pCO2 varied among children with absence. Determination of whether variation in sensitivity to hypocapnia may be helpful in determining response to antiepileptic drugs (AEDs) or remission of seizures will require further study.
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PMID:Will a critical level of hyperventilation-induced hypocapnia always induce an absence seizure? 861 75

Patients with chronic heart failure have an increased ventilation/carbon dioxide production ratio (VE/VCO2) during exercise. Recently it was discussed whether the cause of this increase was a ventilatory stimulus driven other than by CO2. Dyspnoea during exercise is thought to be related to impaired respiratory function. However, clinical confirmation is scarce. Ninety-two patients (age 51 +/- 9 years) with heart failure due to idiopathic dilated cardiomyopathy exercised on a bicycle ergometer to exhaustion, and measurement of ventilatory gases and Swan-Ganz catheterization were performed. The maximal oxygen consumption corrected for body weight (VO2max. kg-1) was 16.6 +/- 5.5 ml x min-1 x kg-1. The increase in (VE/VCO2) during exercise was related to an increase in respiratory rate (r = 0.43; P < 0.00001) but not to an increase in cardiac index or capillary wedge pressure. Nineteen patients stopped exercising because of dyspnoea. Their maximal tidal volume and VO2max . kg-1 were lower than the 67 patients who stopped exercise because of fatigue (P < 0.001 and P < 0.00001 respectively). Other variables showed no significant difference. In conclusion, the increase in VE/VCO2 during exercise may reflect a non-CO2 driven ventilatory stimulus as it cannot be attributed to increased pulmonary vascular pressures or an insufficient increase in cardiac output leading to a ventilation-perfusion mismatch. Low oxygen uptake is a prominent finding in patients with chronic heart failure who experienced dyspnoea during exercise, and dyspnoea is in part related to impaired respiratory function.
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PMID:Ventilation and dyspnoea during exercise in patients with heart failure. 868 22

1. Seven active subjects (24 +/- 1 years; maximal oxygen uptake (VO2,max), 3.77 +/- 0.2 l min-1; mean +/- S.E.M.) performed constant work rate heavy exercise (CWHE, approximately 80% of maximal incremental work rate) to exhaustion on 2 days, one with (unload) and one without (control) respiratory muscle unloading. 2. With unloading, a special device applied flow-proportional mouth pressure assist (positive with inspiratory (I), negative with expiratory (E) flows) throughout each breath. No pressure assist occurred during control CWHE. To confirm unloading, respiratory muscle pressures (Pmus) were derived (n = 5) from measured pleural pressure and chest wall elastic and resistive pressures. 3. Other than minor differences in early exercise, the temporal course of minute ventilation (VE) was similar in both tests as exercise progressed. The fall in estimated mean alveolar CO2 (PA,CO2) throughout CWHE was identical in both tests. There were no significant differences (ANOVA) in VE, tidal volume, frequency, oxygen consumption rate (VO2), heart rate or PA,CO2, between unload and control CWHE, at matched times (at 50% of control duration and at the end of exercise). Unloading reduced Pmus significantly throughout CWHE; at 50% control duration, peak Pmus,I and Pmus,E fell by 24 and 41%, respectively, with unloading, as did mean Pmus,I and Pmus,E (21 and 44%). 4. The lack of any significant changes in VE, PA,CO2 or breathing pattern, despite a marked reduction in respiratory muscle load throughout CWHE, indicates that the load on the respiratory muscles has only a minor role in the regulation of ventilation during heavy exercise. 5. The absence of improvement in CWHE duration (control, 11.4 +/- 1.2 min; unload, 12.6 +/- 2.1 min, n.s.) with unloading implies that respiratory muscle function does not limit endurance exercise performance during cycling in healthy humans.
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PMID:Lack of importance of respiratory muscle load in ventilatory regulation during heavy exercise in humans. 882 Nov 50

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

The large subunit core of ribulose-bisphosphate carboxylase from Synechococcus PCC 6301 expressed in Escherichia coli in the absence of its small subunits retains a trace of carboxylase activity (about 1% of the kcat of the holoenzyme) (Andrews, T. J (1988) J. Biol. Chem. 263, 12213-12219). During steady-state catalysis at substrate saturation, this residual activity diverted approximately 10% of the reaction flux to 1-deoxy-D-glycero-2,3-pentodiulose-5-phosphate as a result of beta elimination of inorganic phosphate from the first reaction intermediate, the 2,3-enediol form of ribulose bisphosphate. This indicates that the active site's ability to stabilize and/or retain this intermediate is compromised by the absence of small subunits. Epimerization and isomerization of the substrate resulting from misprotonation of the enediol intermediate were not significantly exacerbated by lack of small subunits. The residual carboxylating activity partitioned product between pyruvate and 3-phosphoglycerate in a ratio similar to that of the holoenzyme, indicating that stablization of the penultimate three-carbon aci-acid intermediate is not perturbed by lack of small subunits. The underlying instability of the five-carbon enediol intermediate was revealed, even with the holoenzyme, under conditions designed to lead to exhaustion of substrate CO2 (and O2). When carboxylation (and oxygenation) stalled upon exhaustion of gaseous substrate, both spinach and Synechococcus holoenzymes continued slowly to beta eliminate inorganic phosphate from and to misprotonate the enediol intermediate. With carboxylation and oxygenation blocked, the products of these side reactions of the enediol intermediate accumulated to readily detectable levels, illustrating the difficulties attendant upon ribulose-P2 carboxylase's use of this reactive species as a catalytic intermediate.
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PMID:Side reactions catalyzed by ribulose-bisphosphate carboxylase in the presence and absence of small subunits. 903 45

To investigate the effects of mechanical ventilatory limitation on the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycle ergometry to exhaustion once while breathing room air; once while breathing 3% CO2-21% O2-balance N2; and once while breathing HeO2 (79% He and 21% O2). Minute ventilation (VE) and respiratory mechanics were measured continuously during each 1-min increment in work rate (10 or 20 W). Data were analyzed at rest, at ventilatory threshold (VTh), and at maximal exercise. When the subjects were breathing 3% CO2, there was an increase (P < 0.001) in VE at rest and at VTh but not during maximal exercise. When the subjects were breathing HeO2, VE was increased (P < 0.05) only during maximal exercise (24 +/- 11%). The ventilatory response to exercise below VTh was greater only when the subjects were breathing 3% CO2 (P < 0.05). Above VTh, the ventilatory response when the subjects were breathing HeO2 was greater than when breathing 3% CO2 (P < 0.01). Flow limitation, as percent of tidal volume, during maximal exercise was greater (P < 0.01) when the subjects were breathing CO2 (22 +/- 12%) than when breathing room air (12 +/- 9%) or when breathing HeO2 (10 +/- 7%) (n = 7). End-expiratory lung volume during maximal exercise was lower when the subjects were breathing HeO2 than when breathing room air or when breathing CO2 (P < 0.01). These data indicate that older subjects have little reserve for accommodating an increase in ventilatory demand and suggest that mechanical ventilatory constraints influence both the magnitude of VE during maximal exercise and the regulation of VE and respiratory mechanics during heavy-to-maximal exercise.
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PMID:Ventilatory response to exercise in subjects breathing CO2 or HeO2. 907 58

To determine if ventilation (VE) during maximal exercise would be increased as much by 3% CO2 loading as by resistive unloading of the airways, we studied seven subjects (39 +/- 5 years; mean +/- S.D.) during graded-cycle ergometry to exhaustion while breathing: (1) room air (RA); (2) 3% CO2, 21% O2, and 76% N2; or (3) 79% He and 21% O2). VE and respiratory mechanics were measured during each 1-min increment (20 or 30 W) in work rate. VE during maximal exercise was increased 21 +/- 17% when breathing 3% CO2 and 23 +/- 16% when breathing HeO2 (P < 0.01). Further, the ventilatory response to exercise above ventilatory threshold (VTh) was increased (P < 0.05) when breathing HeO2 (0.89 +/- 0.26 L/min/W) as compared with breathing RA (0.65 +/- 0.12). When breathing HeO2, end-expiratory lung volume (% total lung capacity, TLC) was lower during maximal exercise (46 +/- 7) when compared with RA (53 +/- 6, P < 0.01). In conclusion, VE during maximal exercise can be augmented equally by 3% CO2 loading as by resistive unloading of the airways in younger subjects. This suggests that in younger subjects with normal lung function there are minimal mechanical ventilatory constraints on VE during maximal exercise.
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PMID:Ventilation and respiratory mechanics during exercise in younger subjects breathing CO2 or HeO2. 927 4

A series of untrained, healthy, obese women (body mass index 32.5 +/- 0.9 kg.m-2) were subjected to a protocol of intense exercise on a cycloergometer and compared with lean controls (body mass index 20. 9 +/- 0.5 kg.m-2). Physiological parameters, blood lactate, bicarbonate, plasma metabolites, oxygen consumption and CO2 production were measured. Impedance-derived extracellular water and plasma changes in lactate and bicarbonate were used to determine changes in bicarbonate pools and lactate-displaced CO2. From these and respiratory gases, the respiratory quotient was calculated and thence overall fuel consumption. Anaerobic energy during exercise accounted for about 1.8% of all energy consumed in the lean but only 0.7% in the obese. Obese women fatigued at lower workloads and energy expenditure levels than did the lean, and their lactate buildup was similar when compared on the basis of fat-free mass. The data support the postulation of fatigue being triggered by a combination of factors: stretched cardiovascular work would be the main factor for obese women, in part limiting lactate production. For lean women, the triggering factor for fatigue could be the loss of buffering capacity; but it is the combination of stretching cardiovascular capacity, exhaustion of glycogen and available glucose and increase in lactate/loss of bicarbonate buffer that determines the onset of fatigue.
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PMID:During intense exercise, obese women rely more than lean women on aerobic energy. 944 96

The etiology of exercise hypocapnia is unknown. The contributions of exercise intensity (ExInt), lactic acid, environmental temperature, rectal temperature (Tre), and physical conditioning to the variance in arterial CO2 tension (PaCO2) in the exercising sheep were quantified. We hypothesized that thermal drive contributes to hyperventilation. Four unshorn sheep were exercised at approximately 30, 50, and 70% of maximal O2 consumption for 30 min, or until exhaustion, both before and after 5 wk of physical conditioning. In addition, two of the sheep were shorn and exercised at each intensity in a cold (<15 degrees C) environment. Tre and O2 consumption were measured continuously. Lactic acid and PaCO2 were measured at 5- to 10-min intervals. Data were analyzed by multiple regression on PaCO2. During exercise, Tre rose and PaCO2 fell, except at the lowest ExInt in the cold environment. Tre explained 77% of the variance in PaCO2, and ExInt explained 5%. All other variables were insignificant. We conclude that, in sheep, thermal drive contributes to hyperventilation during exercise.
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PMID:Thermal drive contributes to hyperventilation during exercise in sheep. 965 92


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