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

Although healthy and diseased bovine respiratory tracts have been intensively studied during the last years, to the authors' knowledge, there have been no attempts to objectively examine the inspiratory drive from the brain to the nerves and muscles and its transformation in pressure. Such technique would be useful in assessing the possibility of altered ventilatory drive or inspiratory muscle fatigue in the context of an animal with ventilatory failure. The relation among ventilation, airway opening occlusion pressure generated 100 milliseconds after onset of inspiration (Pawo100ms) and 6 indexes describing diaphragmatic electromyographic activity (EMGdi) recorded via implanted fishhooks was evaluated during free and impeded CO2 rebreathing in 6 young bulls. The best significant linear correlations (r > 0.8) with inspiratory center afferent stimulation, as judged by end-tidal CO2 concentration in expired air, were found for Pawo100ms, peak moving time average or variance EMGdi, and mean integrated EMGdi, whatever had been the respiratory impedance. However, with an inspiratory load, Pawo100ms responses systematically had greater increase for a given change in the driving EMGdi, implying dependence of the former not only on neural input, but also on configurational factors that determine inspiratory muscle excitation-pressure generation couplings. The reproducibility of EMGdi absolute values and changes was satisfactory up to 10 hours, but could not be repeated from one day to the other. It was concluded that, provided the constancy of the electrical coupling of the recording system to the tissue being studied is ensured, specific EMGdi and Pawo100ms values correlate reliably with amount of CO2 during free and loaded breathing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Airway occlusion pressure and diaphragm global electromyogram analysis for evaluation of inspiratory muscle drive and neuromechanical coupling in cattle. 794 9

Acidosis produced by an increase in CO2 concentration decreases contractility and increases the tendency to fatigue in striated muscle. It is not clear a what levels of CO2 this effect takes place, or in what experimental models it can be observed. In this study we examine the effect of increasing concentrations of CO2 on contractility and fatigue in strips of rat diaphragm in vitro. Six strips of diaphragm from a rat of low-weight were kept in organ bath and supramaximal stimuli of 1, 10, 50 and 100 Hz were applied while CO2 concentration was changed from 5% (29 mmHg), to 10% (48.3 mmHg) to 20% (102 mmHg). To study fatigue we applied 45 series of 50 Hz stimuli per minute for 15 minutes. We obtained these results: a) Contractility. Force of contraction was less with 20% CO2 than with 5% under a stimulus of 1 Hz. No significant differences were found for other concentrations or frequencies. b) Fatigue. Force of contraction decreases as CO2 concentration increased and significant differences were found for all 3 concentrations. The conclusions were: a) an increase in CO2 from 5% to 20% produces a significant decrease in force of contraction under conditions of low-frequency stimuli and b) increases in CO2 concentration from 5% to 10 to 20% increase the muscle's susceptibility to fatigue.
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PMID:[Effects of CO2 on the rat diaphragm in vitro]. 800 Jun 93

1. Intact frog single fibres were investigated under control conditions (1 s tetanus every 2, 3 or 5 min) and during moderate fatigue (interval between tetani 15 or 30 s). 2. Fatigue reduced isometric force (P0) by 25.8 +/- 1.6% (S.E.M.; n = 13) and depressed the maximum velocity of shortening (Vmax) by 10.2 +/- 2.2% (n = 13). The force-velocity relation became less curved, a/P0* (see Methods) being increased by 29.5 +/- 8.8% (n = 13). Thus, power was less affected than isometric force or Vmax. 3. The velocity of unloaded shortening (V0), from slack test measurements, was reduced proportionally more than Vmax during fatigue. Under control conditions V0 was larger than Vmax, but during fatigue their values were not significantly different. 4. Stiffness during shortening was reduced during fatigue indicating fewer attached cross-bridges in fatigue. Force was reduced more than stiffness indicating that, on average, there is less force per attached cross-bridge. 5. The force-lengthening velocity relation showed that the ability to resist forces greater than isometric was well preserved in fatigue. 6. Compared with fatigue, intracellular acidification with CO2 produced a smaller reduction in isometric force. However, reduction in Vmax was not significantly different from that in fatigue. These results are consistent with both inorganic phosphate and H+ increasing in fatigue, but only H+ increasing during acidification, and isometric force being reduced by both, Vmax being sensitive only to H+.
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PMID:Force-velocity relation for frog muscle fibres: effects of moderate fatigue and of intracellular acidification. 800 30

This study investigated the percentage of carbohydrate utilization than can be accounted for by glucose ingested during exercise performed after the ingestion of the potent lipolysis inhibitor Acipimox. Six healthy male volunteers exercised for 3 h on a treadmill at about 45% of their maximal oxygen uptake, 75 min after having ingested 250 mg of Acipimox. After 15-min adaptation to exercise, they ingested either glucose dissolved in water, 50 g at time 0 min and 25 g at time 60 and 120 min (glucose, G) or sweetened water (control, C). Naturally labelled [13C]glucose was used to follow the conversion of the ingested glucose to expired-air CO2. Acipimox inhibited lipolysis in a similar manner in both experimental conditions. This was reflected by an almost complete suppression of the exercise-induced increase in plasma free fatty acid and glycerol and by an almost constant rate of lipid oxidation. Total carbohydrate oxidation evaluated by indirect calorimetry, was similar in both experimental conditions [C, 182, (SEM 21); G, 194 (SEM 16) g.3 h-1], as was lipid oxidation [C, 57 (SEM 6); G, 61 (SEM 3) g.3 h-1]. Exogenous glucose oxidation during exercise G, calculated by the changes in 13C:12C ratio of expired air CO2, averaged 66 (SEM 5) g.3 h-1 (19% of the total energy requirement). Consequently, endogenous carbohydrate utilization was significantly smaller after glucose than after placebo ingestion: 128 (SEM 18) versus 182 (SEM 21) g.3 h-1, respectively (P < 0.05). Symptoms of intense fatigue and leg cramps observed with intake of sweet placebo were absent with glucose ingestion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Availability of glucose ingested during muscle exercise performed under acipimox-induced lipolysis blockade. 807 20

Thirty-six patients underwent assessment of behavioural breathlessness which included monitoring of breathing patterns and end tidal CO2 concentration and completion of questionnaires relating to hyperventilation (HV), anxiety and depression. Twenty-two patients had a positive assessment and underwent breathing retraining. Assessments were repeated immediately after re-training and 2 months later. Ten of the patients (Group A) had behavioural breathlessness either as the primary problem or secondary to an established clinical condition, and twelve (Group B) in association with chronic fatigue. Before re-training, resting end-tidal PCO2 was significantly lower in Group A than Group B (p < 0.05), but there was no significant difference in mean scores for HV-related symptoms, anxiety or depression. Following breathing retraining, both groups showed improvements in breathing patterns, end tidal CO2 levels and scores for HV-related symptoms which were sustained. In Group A the mean score for anxiety decreased (p < 0.01) and the score for depression was significantly lower than in Group B (p < 0.05). Although mean scores for anxiety and depression in Group B did not change significantly, some individuals in the group did show sustained improvement. There was no improvement in symptoms associated with chronic fatigue in Group B. In behavioural breathlessness, breathing retraining is of benefit, not only in restoring more normal patterns of breathing but also in reducing anxiety, particularly in patients without the complication of chronic fatigue.
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PMID:Breathing retraining: effect on anxiety and depression scores in behavioural breathlessness. 812 85

The mechanisms of chronic ventilatory failure in chronic obstructive pulmonary disease are complex. This paper analyses the diverse available information: mechanical factors and gas-exchange, fighter vs. non-fighter, the ventilatory pattern theory and the fatigue threshold theory. Finally we comment on the evidence supporting the new concept that hypercapnia may develop to avoid or prevent fatigue. Indeed, it is very likely that chronic CO2 retention in COPD may develop by mechanical disadvantages of the inspiratory muscles rather than impairment of ventilation-perfusion ratios. This opens a fascinating new research line on the neuromechanical control of breathing. When the respiratory effort is approaching the fatigue level, the respiratory muscles may elicit a negative feedback reflex, the muscle activity is depressed and hypercapnia develops. If this is so, chronic hypercapnia may be an index of imminent fatigue if increases in ventilation or work of breathing are required. Under this condition some degree of central diaphragm fatigue may help to protect the muscle from severe or limiting peripheral fatigue or even muscle injury. Finally, we comment on some therapeutic approaches such as ventilatory stimulants, training, rest and, specially, oxygen administration and the mechanisms involved in the PCO2 increases.
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PMID:[Causes of CO2 retention in patients with chronic obstructive lung disease]. 820 18

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 studied the effect of external high-frequency oscillation using an oscillator (Hayek oscillator [HO]) on 20 patients with severe chronic obstructive pulmonary disease (COPD). Of the 20 patients, 10 were eucapnic and 10 were hypercapnic. The HO generated frequencies from 60 to 140 cycles/min at an amplitude of 36 cm H2O (-26 to +10) and at an inspiratory/expiratory (I/E) ratio of 1:1. The results show that the HO is a powerful ventilator, reducing end-tidal PCO2 (PETCO2) by 6.7 to 9.1 mm Hg in eucapnic patients and by 6.1 to 7.9 mm Hg in hypercapnic patients. The oxygen saturation increased by 2 to 2.87 percent in the eucapnic patients and by 2.6 to 3.7 percent in the hypercapnic group in the various frequencies. The rate of elimination of CO2 and the levels of PETCO2 achieved within a short time were superior to those reported with other external ventilators. We conclude that the HO can be effectively used in severe COPD and respiratory failure for (1) assisting ventilation, thus replacing intubation and conventional mechanical ventilation, and (2) relieving muscle fatigue in short sessions.
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PMID:External high-frequency ventilation in severe chronic obstructive pulmonary disease. 825 45

Two hundred seventy severely hypoxemic (PaO2 < or = 55 mm Hg: mean +/- SD = 48 +/- 6) COPD patients (232 men) were selected for long-term oxygen therapy (LTOT). They were old (mean = 66 +/- 8 years), with severe airflow limitation (FEV1 = 30 +/- 12 percent of predicted), some CO2 retention (PaCO2 = 47 +/- 9 mm Hg), and compensated respiratory acidosis. Eighteen percent of the patients presented some complicating pleuropulmonary diseases (pleural thickening, sequelae of tuberculosis, etc). Overall survival proportion was poor: 70, 50, and 43 percent at 1, 2, and 3 years, respectively. The Cox model showed that the factors which independently reduced survival were lower CO transfer coefficient, smaller intrathoracic gas volume, more severe bronchial obstruction, the fact that oxygen administration did not increase PaO2 above 65 mm Hg, increasing age, and the presence of chest wall abnormalities. When the patients were divided into three groups according to mortality risk, the mean clinical and functional profile of the high-mortality risk group was consistent with the prevalence of emphysematous lesions. Moreover, the best survivors fitted better into the "bronchitic" type; they showed a higher mean PaCO2, suggesting that some degree of hypoventilation could delay muscular fatigue and improve survival. The difference in the proportion of "emphysematous" and "bronchitic" patients is a possible explanation for the variability of the mortality rate reported in literature.
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PMID:Prognosis of severely hypoxemic patients receiving long-term oxygen therapy. 830 23


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