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

Four normal subjects and 5 patients with chronic obstructive pulmonary disease (COPD) (mean FEV1, 1.03 L) had frequency:force curves of their sternomastoid muscle measured before and 5 min after a 12-min walk on a flat treadmill, a progressive exercise test (normal subjects only), and a 10-min period of sustained maximal voluntary ventilation (SMVV). Before each test, all subjects had a normal frequency:force curve, and the ratio of the force response at 20 Hz to that at 50 Hz was normal. After SMVV, all the normal subjects and 4 of the 5 patients developed a greater than 15% fall in 20:50 ratio, and this was taken to indicate the presence of low frequency fatigue (LFF). During SMVV, all the subjects achieved minute ventilation greater than 70% of predicted maximal breathing capacity (MBC). During the 12-min walk, all the patients exceeded 70% MBC, and 4 developed LFF. The normal subjects performing progressive exercise also exceeded 70% MBC, and all showed LFF. The 12-min walk did not cause LFF in the normal subjects, but no subject reached 70% of MBC. Despite the presence of LFF in the sternomastoid muscle, the patients were all able to walk the same distance during a second 12-min walk. In both the normal and patient groups, the ventilatory response to CO2 was not changed by the presence of LFF. There were no changes in maximal inspiratory and expiratory mouth pressures or spirometry with LFF. High, sustained levels of minute ventilation cause sternomastoid LFF, but the clinical significance of this phenomenon is not yet certain.
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PMID:Sternomastoid muscle function and fatigue in normal subjects and in patients with chronic obstructive pulmonary disease. 642 15

When the ventilatory muscles are unable to develop the required force as it occurs during fatigue, hypercapnic respiratory failure ensues. We present evidence that when the respiratory muscles work in a fatiguing load domain the central controllers respond at an early stage with tachypnea, while when the muscles fail bradypnea ensues which is followed by apnea. Although bradypnea and apnea in addition to muscle inability to develop force may reduce alveolar ventilation by virtue of reducing the total minute ventilation, tachypnea may also be followed by hypercapnia at constant total minute ventilation by virtue of a reduction in tidal volume (VT). Such a strategy will increase the ratio of dead space (VD) to tidal volume (VD/VT) and PCO2 will rise. It is argued that this mechanism could satisfactorily explain the high levels of CO2 in patients with chronic obstructive lung disease, as well as the CO2 retention at an early stage in acute cases of fatigue during, for example, the weaning period of a patient from the respirator. Bradypnea and apnea contribute to CO2 retention at a later stage, when the muscles are exhausted and total ventilation decreases. This sequence in frequency of breathing is explained as an advantageous strategy adopted for the respiratory muscles, because it allows the muscles to operate at an optimal length. It is also hypothesized that muscle afferents, probably via the small fibers III and IV and/or Golgi and tendon organs, are responsible for this interaction of CNS and respiratory muscles.
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PMID:Ventilatory muscle fatigue governs breathing frequency. 650 21

This article reviews factors that may limit exercise performance in patients with COPD. These factors include alteration in pulmonary mechanics, respiratory muscle fatigue, impairment in pulmonary gas exchange, abnormal perception of breathlessness and ventilatory control, cor pulmonale, and poor nutritional status. The clinical application of exercise testing in patients with COPD and the role of various therapeutic modalities in altering exercise performance in COPD are discussed.
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PMID:Exercise impairment in chronic obstructive pulmonary disease. 672 35

A single derived index of the power spectrum of the diaphragm electromyogram (EMG) has been used in detecting fatigue. Additional information in the EMG could be used to study diaphragm function in other respiratory conditions. Diaphragm EMGs and calculated power spectra at 12 frequencies were measured in normal subjects and patients with severe chronic obstructive pulmonary disease during several respiratory maneuvers both before and after treadmill exercise to dyspnea. The power spectra were characterized by the first five moments. Changes in the EMG were similar when assessed by multivariate analysis of variance of the spectral estimates or of the moments. Factor analysis provided two latent variables that correlated with the first and second moment respectively. The first moment was found to be the most sensitive single discriminant of fatigue and is only slightly improved by adding other information. It is concluded that the first and second moments of the EMG power spectra provide a concise, parsimonious description of the changes in the EMG.
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PMID:Multivariate analysis of diaphragm EMG power spectral moments. 672 71

We studied the effects of theophylline on diaphragmatic strength and fatigue in 15 patients with severe chronic obstructive pulmonary disease. Diaphragmatic strength was assessed by measurement of the transdiaphragmatic pressure generated at functional residual capacity during a maximal inspiratory effort against closed airways. Diaphragmatic fatigue was induced by resistive loaded breathing. The electrical activity of the diaphragm was recorded with an esophageal electrode during the fatigue runs, and the high-low ratio of the electrical signal was analyzed to assess diaphragmatic fatigue. Studies were performed before and after 7 and 30 days of theophylline administration (mean plasma level, 13 +/- 2 mg per liter). A control group received a placebo instead of theophylline. Theophylline increased maximal transdiaphragmatic pressure by 16 per cent after 7 days of administration (P less than 0.01), and this increase persisted after 30 days. No significant change in maximal transdiaphragmatic pressure was observed in the group given the placebo. Theophylline also suppressed diaphragmatic fatigue in all patients who received it. We conclude that theophylline has a potent and long-lasting effect on diaphragmatic strength and fatigue in patients with fixed airway obstruction.
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PMID:Effects of theophylline on diaphragmatic strength and fatigue in patients with chronic obstructive pulmonary disease. 673 52

The use by West et al. of gases with different solubilities and of appropriate models has indicated that impairment of gas exchange in patients with chronic obstructive pulmonary disease and respiratory failure resulted essentially from altered ventilation/perfusion ratios. To understand why some patients do not appear to be capable of compensating this impairment and become hypercapnic, it is necessary to examine the other components of the respiratory system (control of ventilation, respiratory muscles) and their interactions. The measurement of occlusion pressure and of average inspiratory flow, and analysis of the timing of the respiratory cycle provides interesting information on the output of the control system and the efficiency of respiratory muscles. Electromyography of respiratory muscles also affords useful information on the degree of fatigue of these muscles. The use of this data should help to clarify the problem that has remained unanswered for many years: is the patient with hypercapnia someone who does not want to, or cannot, increase his ventilation? Other studies in the same group of patients during sleep have supplied evidence for the presence of numerous episodes of arterial oxygen desaturation with marked effects on the cardiovascular system. Pathophysiology should also consider this aspect of respiratory failure which occurs in the third of our lifetime devoted to sleep.
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PMID:[Physiopathology of chronic respiratory insufficiency]. 678 66

1. Normal respiratory muscles have a large functional reserve. 2. Muscles have a tremendous capacity for adaptation. Adaptation is task-specific (eg, muscles use similar motor units for the same tasks). 3. Muscular fatigue results when motor units are required to perform an unaccustomed task. Continued effort in the face of fatigue, especially high-tension low-repetition effort, may produce a reversible "use atrophy" (eg, fiber damage, splitting, and regeneration). 4. Exercising damaged or regenerating muscle may produce irreversible damage. 5. Exercising the respiratory muscles of some patients may make them more susceptible to fatigue or, at least, produce no further improvement in function. Alternating rest and exercise improves pulmonary function tests in some patients. 6. Retraining a weak or damaged muscle requires that it first be "shut down" and rested before attempting retraining. 7. Training a rested muscle to different tasks--before these tasks are needed--may be the critical step in successful rehabilitation. 8. Resistance breathing probably improves both respiratory muscle strength and respiratory muscle endurance. 9. There are at least three immediate tasks for clinicians to define: Where in the present natural history of COPD should respiratory muscles be rested? How long should they be rested? How best can they be retrained?
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PMID:When should respiratory muscles be exercised? 686 48

We studied the power spectrum of the diaphragm electromyogram (EMG) at frequencies between 31 and 246 Hz in four young normal subjects and five patients with chronic obstructive lung disease (COPD). Diaphragm EMGs were analyzed during spontaneous breathing and maximum inspiratory efforts to determine the effect of signal-to-noise ratio on the power spectrum and if treadmill exercise to dyspnea was associated with diaphragm fatigue. We found that the centroid frequencies of the power spectra (fc) were strongly correlated (r = 0.93) with ratios of power at high frequencies to power at low frequencies (H/L) for all subjects. Of the two indices, H/L had the largest standard deviation expressed as a percentage of the mean. The mean values of both of these decreased significantly after exercise, fc from 100.2 to 97.3 and H/L from 1.07 to 0.97. Signal-to-noise ratios were higher in maximal inspiratory efforts and after exercise in normal subjects and higher in COPD patients. The signal-to-noise ratio was correlated negatively with fc and H/L, indicating that these indices of the shape of the power spectrum are influenced by signal strength and noise levels as well as muscle function. We conclude that the fc and H/L index similar qualities of the power spectrum, that they are partially determined by the signal-to-noise ratio, and that, in some cases, exercise to dyspnea is associated with apparently mild diaphragm fatigue.
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PMID:Power spectral analysis of the diaphragm electromyogram. 687 80

Transdiaphragmatic pressure (Pdi) was measured at functional residual capacity (FRC) in four normal seated subjects during supramaximal, supraclavicular transcutaneous stimulation of one phrenic nerve (10, 20, 50, and 100 Hz--0.1 ms duration) before and after diaphragmatic fatigue, produced by breathing through a high alinear inspiratory resistance. Constancy of chest wall configuration was achieved by placing a cast around the abdomen and the lower one-fourth of the rib cage. Pdi increased with frequency of stimulation, so that at 10, 20, and 50 Hz, the Pdi generated was 32 +/- 4 (SE), 70 +/- 3, and 98 +/- 2% of Pdi at 100 Hz, respectively. After diaphragmatic fatigue, Pdi was less than control at all frequencies of stimulation. Recovery for high stimulation frequencies was complete at 10 min, but at low stimulation frequencies recovery was slow: after 30 min of recovery, Pdi at 20 Hz was 31 +/- 7% of the control value. It is concluded that diaphragmatic fatigue can be detected in man by transcutaneous stimulation of the phrenic nerve and that diaphragmatic strength after fatigue recovers faster at high than at low frequencies of stimulation. Furthermore, it is suggested that this long-lasting element of fatigue might occur in patients with chronic obstructive lung disease, predisposing them to respiratory failure.
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PMID:Detection of diaphragmatic fatigue in man by phrenic stimulation. 725 45

Chronic obstructive pulmonary disease (COPD) have several pathophysiological characteristics in common, the main one being an increased airways resistance (raw). It is the result of bronchial abnormalities and reduced parenchymal elasticity, and is influenced by lung volume. Raw decreases with increasing lung volume, and increases with decreasing lung volume. Such expiratory events are generally compensated on the inspiratory side. Inspiration is shortened to prolong expiration, and breathing takes place at higher lung volume to take benefit of the higher lung recoil. This inspiratory load is associated to an increased inspiratory drive, and contributes to put inspiratory muscles at disadvantage. However, with time, adaptative changes take place that restore their force at a shorter length. Chronic fatigue, often suspected in this setting, is therefore not currently demonstrated. Bronchial and parenchymal abnormalities lead to ventilation-perfusion mismatch, that contribute to hypoxemia and hypercapnia through deadspace and shunt effects. Hypercapnia can also correspond in part to protective mechanisms, if the energy requirements for its maintenance are too high.
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PMID:[Physiopathology of COPD (steady-state)]. 765 65


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