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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of inducing inspiratory muscle fatigue on the subsequent breathing pattern were examined during resting unstimulated breathing and during CO2 rebreathing. In addition, we examined whether induction of inspiratory muscle fatigue alters CO2 responsiveness. 2. Global inspiratory muscle fatigue and diaphragmatic fatigue were achieved by having subjects breathe against an inspiratory resistive load while generating a predetermined fraction of either their maximal mouth pressure or maximal transdiaphragmatic pressure until they were unable to generate the target pressure. 3. Induction of inspiratory muscle fatigue had no effect on the subsequent breathing pattern during either unstimulated breathing or during CO2 rebreathing. 4. Following induction of inspiratory muscle fatigue, the slope of the ventilatory response to CO2 was significantly decreased from 18.8 +/- 3.3 during control to 13.8 +/- 2.1 l min-1 (% end-tidal CO2 concentration)-1 with fatigue (P < 0.02).
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PMID:The effect of inspiratory muscle fatigue on breathing pattern and ventilatory response to CO2. 148 52

1. The performance of skeletal muscle during repetitive stimulation may be limited by the development of an intracellular acidosis due to lactic acid accumulation. To study this, we have measured the intracellular pH (pHi) with the fluorescent indicator BCECF (2',7'-bis(carboxyethyl)-5(6)- carboxyfluorescein) during fatigue produced by repeated, short tetani in intact, single fibres isolated from the mouse flexor brevis muscle. 2. The pHi at rest was 7.33 +/- 0.02 (mean +/- S.E.M., n = 29, 22 degrees C). During fatiguing stimulation pHi initially went alkaline by about 0.03 units (maximum alkalinization after about ten tetani). Thereafter pHi declined slowly and at the end of fatiguing stimulation (tetanic tension reduced to 30% of the original; 0.3Po), pHi was only 0.063 +/- 0.011 units (n = 14) more acid than in control. 3. We considered three possible causes of acidosis being so small in fatigue: (i) a high oxidative capacity so that fatigue occurs without marked production of lactic acid; (ii) an effective transport of H+ or H+ equivalents out of the fibres; a high intracellular buffer power. 4. The oxidative metabolism was inhibited by 2 mM-cyanide in three fibres. After being exposed to cyanide for 5 min without stimulation, the tetanic tension was reduced to about 0.9 Po and pHi was alkaline by about 0.1 units. The fibres fatigued faster in cyanide and the pHi decline in fatigue was more than twice as large as that under control conditions. 5. Inhibition of Na(+)-H+ exchange with amiloride resulted in a slow acidification of rested fibres; resting pHi was not affected by either inhibition of HCO3(-)-Cl- exchange with DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid) or inhibition of the lactate transporter with cinnamate. 6. Fibres fatigued in cinnamate displayed a markedly larger acidification (approximately 0.4 pH units) and tension fell more rapidly than under control conditions; inhibition of Na(+)-H+ and HCO3(-)-Cl- exchange did not have any significant effect on fatigue. 7. The intracellular buffer power, assessed by exposing fibres to the weak base trimethylamine, was about 15 mM (pH unit)-1 in a HEPES-buffered solution (non-CO2 or intrinsic buffer power) and about 33 mM (pH unit)-1 in a bicarbonate-buffered solution. Somewhat higher values of the intrinsic buffer power was obtained from changes of the partial pressure of CO2 (PCO2) of the bath solution. Application of lactate or butyrate frequently gave an infinite buffer power, which indicates that powerful pH-regulating mechanisms operate in these cases.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes of intracellular pH due to repetitive stimulation of single fibres from mouse skeletal muscle. 152 20

Endurance muscle performance is highly dependent on ATP production from mitochondrial oxidative phosphorylation. To study the role of the mitochondrial oxidative enzymes in muscle fatigue, we analyzed the relationship between the concentrations of substrates associated with ATP synthesis and the muscle performance of electrically stimulated rabbit muscle under CO2-induced acidosis. Two different conditions of pacing-induced muscle performance were produced in the gastrocnemius and soleus muscle groups in anesthetized rabbits by stimulating the sciatic nerve submaximally at two frequencies. Phosphorus nuclear magnetic resonance was used to measure ATP, phosphocreatine, and Pi and to provide data for a calculation of intracellular pH and free ADP. To induce acidosis, the animal was ventilated with 20% CO2. The administration of CO2 effectively reduced the intracellular pH from 6.9 to 6.7 and reduced the isometric tension-time integral (TTI) to below half the value measured in normocapnia at the low pacing frequency. A twofold increase in the pacing frequency resulted in a doubling of the TTI in normocapnia and a tripling of TTI in hypercapnia. The increases in TTI corresponded with increases in free ADP and Pi concentrations. Under the various conditions, all free ADP values were near the in vitro Michaelis-Menten constant (Km) of ADP. The Michaelis-Menten relationship of the oxidative phosphorylative enzymes was applied to the change in substrate concentrations with respect to TTI. From this relationship we observed that the in vivo Km of free ADP was 26 microM, which is close to the in nitro Km, and that Km and maximal reaction velocity did not change under hypercapnia and increased pacing frequency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substrate regulation of mitochondrial oxidative phosphorylation in hypercapnic rabbit muscle. 155 27

The French incidence study has registered all new cases of Type 1 diabetic children under 20 years of age, from a population of 2.32 million, in an exhaustive and prospective manner. Three hundred and forty cases were identified between 1 January 1988 and 31 December 1989, yielding a mean annual incidence rate 7.3 per 10(5). The lowest rate was observed in the youngest age group (0-4 yr: 4.1 per 10(5)) and the highest around pubertal development (10-14 yr: 11.5 per 10(5)). Details of the previous personal and family history, and the clinical and biological pictures of the disease at diagnosis were recorded. Almost 8 per cent of the children had a first-degree relative with Type 1 diabetes. Polyuria, weight loss, fatigue and abdominal pain were the most frequently reported symptoms, which were of median duration 4.4 months. Mean weight loss before diagnosis was 9.4 +/- 6.8 (+/- SD)% of body weight and was not significantly related to age. Ketonuria was detected in 83.8 per cent and acidosis (total CO2 less than or equal to 18 mmol l-1, if measured) in 48 per cent of the cases. Ketonuria and acidosis were significantly more frequent in the younger age group than in the rest of the group (p less than 0.001).
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PMID:Clinical and laboratory features of type 1 diabetic children at the time of diagnosis. 157 13

A previous optimal chemical-mechanical model (C.-S. Poon. J. Appl. Physiol. 62: 2447-2459, 1987) suggested that the normal ventilatory responses to CO2 and exercise inputs and mechanical loading can be predicted by the minimization of a controller objective function consisting of the total chemical and mechanical costs of breathing. In this study the model was generalized to include a description of the inspiratory neuromuscular drive as the control output. With a mechanical work rate index for both inspiration and expiration, the general optimization model accurately reproduced the observed responses in the waveshape of inspiratory drive, breathing pattern, and total ventilation under differing conditions of CO2 inhalation, exercise, and inspiratory/expiratory mechanical loads. The simulation results are in general agreement with a wide range of respiratory phenomena, including exercise hyperpnea, CO2 chemoreflex, and post-inspiratory (postinflow) inspiratory activity, as well as respiratory neural compensations for mechanical loading, respiratory muscle fatigue, and muscle weakness.
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PMID:Optimization character of inspiratory neural drive. 160 12

Respiratory training of premature infants was performed to determine whether improved respiratory muscle strength and/or endurance would result. Twenty-two premature infants were randomized into control and training groups for 2 wk, using inspiratory flow-resistive loads for training (75 cm H2O.L-1.s in wk 1 and 90 cm H2O.L-1.s in wk 2). Respiratory endurance was assessed by the time interval required for the development of a 5-torr rise in transcutaneous CO2 tension during the hypoventilation induced by loaded breathing, using a moderately severe resistive load (250 cm H2O.L-1.s at 1 L.min-1). Respiratory strength was assessed by the maximum negative airway pressure generated during occluded breaths, a pressure-time integral, and an effort index. Results revealed that respiratory muscle endurance, which was not initially different between control and trained groups, increased significantly after 2 wk in the trained group by 137% (median value, p less than 0.05), whereas it remained unchanged in the control group (-24%). The trained group of infants also showed a significant decrease in baseline breathing frequency between the initial and final measurements taken 2 wk apart when compared with controls (p less than 0.05) and a lesser increase in inspiratory time with loading in the final measurement as compared with the initial value (p less than 0.05). There was no significant difference between the control and trained groups in initial or subsequent measures of respiratory muscle strength. Inspiratory flow-resistive load training appears to improve the respiratory endurance of premature infants in whom respiratory muscle fatigue has been described to play a role in the development of respiratory failure.
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PMID:The effects of respiratory training with inspiratory flow resistive loads in premature infants. 163 24

Controversy exists as to whether plasma volume (PV) expansion has the potential to increase maximal oxygen uptake (VO2max). In the present study, VO2max and exercise time to fatigue were measured in nine untrained men when plasma volume (PV) was normal and then again on the next day following two levels of PV expansion. Resting PV was expanded (via intravenous infusion of a 6% dextran solution) by 282 +/- 16 ml (i.e., PVX-1) and then by 624 +/- 26 ml (i.e., PVX-2). PVX-1 increased stroke volume (CO2 rebreathing) during submaximal exercise by 15% (P less than 0.05) above normal levels. VO2max following PVX-1 was increased 4% (P less than 0.05; 3.78 to 3.92 l/min) despite a 4% reduction in hemoglobin concentration. Exercise time to fatigue was also increased (P less than 0.05). PVX-2 resulted in an 11% (P less than 0.05) reduction in hemoglobin concentration during maximal exercise and a return of VO2max and exercise time to normal levels. In summary, we have observed in untrained men that 200-300 ml of PV expansion increases SV, measured during submaximal exercise, yet causes only a small amount of hemodilution. As a result, VO2max is increased slightly and performance is improved. Further PV expansion to levels 500-600 ml above normal results in an excessive hemodilution and a subsequent decline in VO2max and performance to normal levels. There is an optimal PV for eliciting VO2max in untrained men which appears to be approximately 200-300 ml above their normal levels.
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PMID:Maximal oxygen uptake relative to plasma volume expansion. 169 70

The improvement in arterial blood gas tensions following assisted ventilation in chronic obstructive pulmonary disease (COPD) has usually been attributed to the relief of incipient or established respiratory muscle fatigue. The contribution of changes in the load placed upon and the drive to the respiratory muscle pump have not been evaluated. We have investigated the contribution of changes in respiratory muscle strength, the ventilatory response to CO2 and ventilatory function to changes in arterial blood gas tensions in eight patients with severe COPD completing six months domiciliary nasal intermittent positive pressure ventilation. Six patients showed a reduction and two an increase in arterial carbon dioxide tension (PaCO2), median (range) for eight patients, -0.9 kPa (-1.5 to +0.4) (p less than 0.05) and seven showed an improvement in arterial oxygen tension (PaO2), +0.7 kPa (-0.4 to +1.7) (p less than 0.05) during daytime spontaneous breathing. The reduction in PaCO2 was not related to increased inspiratory muscle strength but was correlated with a decrease in gas trapping (Spearman rank correlation coefficient (r(S)) 0.85, p less than 0.05) and in the residual volume (r(s) 0.78, p less than 0.05), suggesting reduced small airway obstruction and, therefore, a reduction in load. The change in PaCO2 also correlated with the increase in ventilation at an end-tidal CO2 of 8 kPa during rebreathing (r(s) -0.76, p less than 0.05) suggesting improved chemosensitivity to CO2. Our data do not support the hypothesis that improvements were due to the relief of muscle fatigue. We suggest that the contribution of changes in load and central drive warrant further investigation.
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PMID:Domiciliary nocturnal nasal intermittent positive pressure ventilation in COPD: mechanisms underlying changes in arterial blood gas tensions. 175 37

Rates of performing work that engender a sustained lactic acidosis evidence a slow component of pulmonary O2 uptake (VO2) kinetics. This slow component delays or obviates the attainment of a stable VO2 and elevates VO2 above that predicted from considerations of work rate. The mechanistic basis for this slow component is obscure. Competing hypotheses depend on its origin within either the exercising limbs or the rest of the body. To resolve this question, six healthy males performed light nonfatiguing [approximately 50% maximal O2 uptake (VO2max)] and severe fatiguing cycle ergometry, and simultaneous measurements were made of pulmonary VO2 and leg blood flow by thermodilution. Blood was sampled 1) from the femoral vein for O2 and CO2 pressures and O2 content, lactate, pH, epinephrine, norepinephrine, and potassium concentrations, and temperature and 2) from the radial artery for O2 and CO2 pressures, O2 content, lactate concentration, and pH. Two-leg VO2 was thus calculated as the product of 2 X blood flow and arteriovenous O2 difference. Blood pressure was measured in the radial artery and femoral vein. During light exercise, both pulmonary and leg VO2 remained stable from minute 3 to the end of exercise (26 min). In contrast, during severe exercise [295 +/- 10 (SE) W], pulmonary VO2 increased 19.8 +/- 2.4% (P less than 0.05) from minute 3 to fatigue (occurring on average at 20.8 min). Over the same period, leg VO2 increased by 24.2 +/- 5.2% (P less than 0.05). Increases of leg and pulmonary VO2 were highly correlated (r = 0.911), and augmented leg VO2 could account for 86% of the rise in pulmonary VO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of exercising legs to the slow component of oxygen uptake kinetics in humans. 175 46

We have conducted a retrospective survey of 79 children out of a total hospital asthmatic patient population of 2,412, admitted over a 32 month period to the ICU for the management of severe status asthmaticus. All patients were in severe respiratory distress with CO2 retention; 19 required mechanical ventilation due to increasing fatigue and worsening bronchospasm, having failed to respond to either inhaled or IV bronchodilator therapy. All patients were ventilated at slow rates (less than 12 min) and their airway pressure (Paw) was deliberately kept below 45 cmH2O, while accepting a PaCO2 in the 45-60 mmHg range, as long as the pH was compensated. Although two patients developed pneumothoraces while on positive pressure ventilation, these were resolved without incidents. Five patients who had mediastinal or subcutaneous air leaks prior to intubation did not develop pneumothoraces. Following the initiation of mechanical ventilation, IV beta-agonist therapy was increased in order to reverse the bronchospasm and reduce the duration of mechanical ventilation. Mean duration of intubation was 42 hours. Fourteen of the 19 patients were weaned and extubated within 48 hours. All patients survived without sequelae. We conclude that a degree of controlled "hypoventilation" by deliberately choosing Paw less than 45 cmH2O can be successfully used to ventilate children with severe status asthmaticus with a reduced rate of pressure-related complications.
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PMID:Efficacy, results, and complications of mechanical ventilation in children with status asthmaticus. 175 29


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