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

Exercise performance data, circulatory function and respiratory and leg muscle quality, expressed as muscle fiber composition, are reviewed and together with our own data discussed as possible limiting factors for physical performance in chronic obstructive pulmonary disease (COPD). COPD is regarded as synonymous with reduced physical performance, exaggerated breathlessness or dyspnea, muscle hypotrophy and/or wasting and, frequently, malnutrition. Impaired right ventricular circulatory function seems to be essential. The observed preponderance of fast twitch (FT), 'glycogenolytic' and capillary-poor muscle fiber type in the investigated muscles might reflect endowment, a 'hypoxic vasoconstriction'-related downregulation of the other main fiber type: the slow twitch (ST), capillary-rich, fatigue-resistant fiber, and/or selective muscle trauma to ST fibers. Ischemic heart disease (IHD) patients demonstrate a similar fiber type pattern in leg muscles. Both COPD and IHD patients have low leg muscle and plasma deposits of antioxidants such as coenzyme Q10 (CoQ10) and alpha-tocopherol. This could reflect a depressed resistance to radical induced cell trauma and/or malnutrition. The magnitude of the antioxidant reduction is less pronounced in patients rich in FT fibers indicating a ST fiber-related susceptibility to trauma. Treatment of other muscle disorders including heart muscle with, e.g., CoQ10 improves performance due to a causative enhanced antioxidant potential, reduced catabolism and/or an upregulated muscle anabolism, increased mitochondrial volume/function, etc. Such data are lacking in COPD.
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PMID:Exercise-limiting factors in respiratory distress. 151 68

The purpose of this study was to compare respiratory responses with moderate and slow rates of unsupported arm exercise (UAE) with a newly developed electromechanical device. Twenty-one patients with chronic obstructive pulmonary disease (COPD) were studied. Exercise endurance limits, metabolic, ventilatory and sensation outcomes were determined at rest prior to exercise and at end-exercise endurance limits. Increases from baseline rest for both exercise rates were observed in: oxygen uptake, carbon dioxide production, inspiratory flow, minute ventilation, respiratory rate, dyspnea, respiratory effort, and arm fatigue. Endurance limits were similar for both rates of UAE. These data provide standards against which UAE in COPD can be evaluated.
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PMID:Standardization of a device to measure unsupported arm exercise endurance in chronic obstructive pulmonary disease. 152 10

Impairment of exercise tolerance is a common problem in patients with severe chronic obstructive pulmonary disease. The cause of exercise intolerance in patients with severe chronic obstructive pulmonary disease is multifactorial and includes impaired lung mechanics, fatigue of inspiratory muscles, impaired gas exchange, right ventricular dysfunction, malnutrition, occult cardiac disease, deconditioning, and psychologic problems; however, impaired lung mechanics and gas exchange abnormalities seem to be the major limiting factors. Recently, the approach to management of pulmonary rehabilitation in patients with chronic obstructive pulmonary disease has changed because improvement in exercise tolerance has been demonstrated after pulmonary rehabilitation. Other adjunctive measures that have been shown to contribute to the observed improvement in exercise tolerance include administration of oxygen, nutritional support, cessation of smoking, and psychosocial support. The roles of ventilatory muscle endurance training, respiratory muscle rest therapy, nasally administered continuous positive airway pressure, and training of the muscles of the upper extremities are less clearly defined.
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PMID:Exercise limitation and pulmonary rehabilitation in chronic obstructive pulmonary disease. 154 79

To evaluate the frequency of the causes of exercise limitation in patients with chronic pulmonary disease and to assess the relationship between the resting pulmonary functional parameters and the degree of exercise dyspnea, we reviewed the data from 88 consecutive stable patients with chronic lung disease (62 COPD, 16 interstitial lung disease [ILD]). In each patient, the intensity of dyspnea was measured by a Borg scale (BS) during an incremental symptom-limited exercise test. COPD patients stopped exercise due to fatigue (46%), dyspnea (36%), cardiac limitation (12%), and peripheral circulatory limitation (6%). ILD patients stopped exercise due to dyspnea (62%), fatigue (25%), and cardiac limitation (12%). In all patients, dyspnea severity increased linearly with exercise intensity as measured as VO2, VE, and VE/MVV. The severity of dyspnea expressed as the slope of the relationship between BS and VE/MVV (DBS/D[VE/MVV]) showed in COPD a significant inverse correlation with VC, FEV1, MIP, and a positive correlation with PaCO2 and VE/MVV at rest. In ILD, DBS/D(VE/MVV) showed a significant inverse correlation with VC, FEV1, TLC, and PaO2 and a positive correlation with VE/MVV at rest. The predicting power of all equations was very low.
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PMID:Dyspnea on exercise. Pathophysiologic mechanisms. 157 44

Failure of weaning from mechanical ventilation in COPD patients is often related to diaphragmatic fatigue. Whether there is a central respiratory drive fatigue and a reserve of excitability is still debated. The purpose of this study was to analyze the following in 13 COPD patients weaned from mechanical ventilation: (1) ventilatory (VE/PETCO2) and neuromuscular (P0.1/PETCO2) response to hypercapnia; (2) the maximum reserve capacity measured through changes in the VE/PETCO2 and P0.1/PETCO2 slopes after doxapram (DXP) infusion, which, given during the test, allows measurement of the maximum response capacity to overstimulation; and (3) analyze the influence of these changes on the outcome of weaning. The results show a variable P0.1/PETCO2 response and a low VE/PETCO2. DXP infusion does not change the slopes of these relations but increases the end-expiratory volume (delta FRCd); (p less than 0.02). Since there was no change in the VE/PETCO2, P0.1/PETCO2, and delta FRC values with or without DXP, there was no excitability reserve in patients who were successfully weaned. When weaning failed, DXP did not change VE/PETCO2 and P0.1/PETCO2 slope, but delta FRCd was greater the delta FRC (p less than 0.001). The excitability reserve in these patients leads to an increase in end-expiratory volume, probably worsening the diaphragm dysfunction.
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PMID:Effects of doxapram on hypercapnic response during weaning from mechanical ventilation in COPD patients. 160 Jul 86

Data from the present study indicate a change in the pattern of chest wall muscle recruitment and improved ventilation with pursed-lip breathing (PLB) in COPD. Pursed lip breathing led to increased rib cage and accessory muscle recruitment during inspiration and expiration, increased abdominal muscle recruitment during expiration, decreased duty cycle of the inspiratory muscles and respiratory rate, and improved SaO2. In addition, PLB resulted in no change in pressure across the diaphragm and a less fatiguing breathing pattern of the diaphragm. Changes in chest wall muscle recruitment and respiratory temporal parameters concomitant with the increased SaO2 indicate a mechanism of improving ventilation with PLB while protecting the diaphragm from fatigue in COPD. Alterations in the pattern of respiratory muscle recruitment with PLB may be associated also with the amelioration of dyspnea. Further investigation is necessary to explore the relationship between the pattern of respiratory muscle recruitment during PLB and dyspnea.
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PMID:The pattern of respiratory muscle recruitment during pursed-lip breathing. 172 14

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

We have examined the role of the Chronic Respiratory Questionnaire in practice. The questionnaire covers aspects of disability in patients with chronic lung disease in terms of dyspnoea, fatigue, emotional function and mastery. It therefore provides a measure of physical disability and quality of life in patients with lung disease. The questionnaire was validated in older patients with chronic obstructive lung disease and is particularly responsive to changes within an individual. Its major disadvantages include the lack of sensitivity in patients with minor symptoms or possibly those in a younger age group and that it is also not possible to make comparisons between populations with the CRQ. It is, however, particularly good at demonstrating changes in disability in older patients with chronic airways disease.
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PMID:Experience of using the CRQ (Chronic Respiratory Questionnaire). 175 17

The aim of physical exercise retraining in patients with chronic obstructive lung disease undergoing rehabilitation is to increase the anaerobic work capacity with a rise in VO2 max. Exercise programmes must take into account the duration, frequency and intensity of exercise. In these patients, numerous factors limit physical exercise, including (a) decreased ventilatory capacity and respiratory muscles fatigue; (b) decreased efficacy of the pulmonary gas exchanges; (c) altered pulmonary vascular bed with altered cardiovascular response. The most widely used training methods are walking (or running), practising on a conveyor belt and using an ergometric bicycle. The last named seems to be the best method to evaluate the physiological effects of exercise or for experimental studies. Patients who are fit to participate in a retraining programme must be in a stable period and have a stable pharmacological regimen; they must be subjected to a preliminary exercise test in order to evaluate the main physiological parameters and to obtain information on their tolerance to exercise, on the presence of lactic acidosis and on the degree of hypoxaemia and hypercapnia. In the absence of contra-indications, a training programme can be set up with 30 to 45 minutes of exercise per day at least 3 to 5 times a week during 5 to 8 weeks, with a load amounting to 50-60% of VO2 max. Two questions remain to be answered: (a) is oxygen therapy useful during retraining; (b) what effect has training on survival?
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PMID:[Indications and results of exercise rehabilitation in patients with chronic obstructive lung diseases]. 177 75

Ventilatory function tests, ventilatory cycle analysis, mouth occlusion pressure (P0.1) and effective inspiratory impedance (P0.1/Vt/Ti) were measured in 11 healthy subjects and in 26 patients with chronic obstructive pulmonary disease (COPD). In COPD patients these measurements were repeated 20 min after inhalation of 400 micrograms of fenoterol. In patients we observed an increase of mean inspiratory flow (Vt/Ti), and a decrease of inspiratory time (Ti) and inspiratory duty cycle (Ti/Ttot). P0.1 and effective inspiratory impedance were significantly increased. Moreover, we found a direct correlation between forced expiratory volume in 1 s (FEV1) and ventilatory cycle components (Ti/Ttot, Ti) and an indirect correlation between FEV1 and Vt/Ti.P0.1 was directly correlated with Vt/Ti and indirectly correlated with ventilatory cycle components. These observations lead us to speculate on the possible role of two opposite mechanisms acting on the control of breathing of COPD patients. While the 'intensity' component of the ventilatory cycle would be set to maintain the tidal volume at a constant level, the 'timing' component would act in order to prevent inspiratory muscle fatigue. Furthermore, in patients responsive to beta 2-agonist drugs, fenoterol inhalation would act in synergy with the timing component of ventilatory cycle, lowering P0.1 and the effective inspiratory impedance.
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PMID:Control of breathing in chronic obstructive pulmonary disease patients at rest and after beta-2 agonist inhalation. 185 81


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