We examined the feasibility of home-based walking training to maintain the benefits of a short-term exercise training in patients with severe chronic obstructive pulmonary disease (COPD). After initial recovery from an exacerbation, 46 patients were randomized into a training and a control group, and 30 patients completed the programme (mean +/- SD FEV1, 36 +/- 7% predicted). The training group performed a 10-day walking training programme in the hospital, followed by a 6-month programme of supervised walking training at home, integrated into daily activities. The control group did not have exercise training in the hospital or at home. Until 6 months after discharge, lung function, exercise performance and symptom scores were assessed. Six-minute walking distance in the training group improved from day 1 to day 10 (P<0.001) and this effect was maintained over 6 months (P<0.001). On average, daily walking distance at home was 2308 m and walking was reported on 157 days. Quality of life (QoL) scores changed significantly over 6 months (P<0.001). The control group showed no significant changes in exercise performance or QoL scores throughout the whole study period. Therefore, (i) significant improvements in exercise performance and Chronic Respiratory Disease Questionnaire (CRQ) scores could be achieved after recovery from an exacerbation and (ii) these improvements were maintained after discharge, when supported by a home-based walking training.
Clinical experience suggests that exercise is beneficial for recovery after an acute exacerbation in patients with severe chronic obstructive pulmonary disease (COPD). The aim of this study was to quantify the clinical benefit of exercise in these patients. Twenty-nine inpatients were randomly assigned to a training group (n = 15, FEV1 34% pred) or a control group (n = 14, FEV1 38% pred). On ten consecutive days, patients in the training group performed a 6-min treadmill walking test and, in addition, five walking sessions per day at > or = 75% of the respective treadmill walking distance. Patients in the control group performed only treadmill walking tests on days 1, 5, and 10. To directly compare the possible benefit of exercise training all patients had an exercise test on day 11 at the same work load as on day 1. In the training group, 6-min walking distance increased from 237 to 420 m, in the control group from 230 to 255 m over the 10 day period which was significantly different (P < 0.0001). Minute ventilation and oxygen uptake increased significantly (P < 0.05) in the training but not in the control group. When comparing exercise tests on days 1 and 11, minute ventilation, oxygen uptake, PaCO2, lactic acid concentration, and Borg scale were significantly reduced to achieve the same work load (P < 0.01) only in the training group. Intrathoracic gas volume and residual volume decreased, and FEV1 and vital capacity increased in the training (P < 0.05) but not in the control group. Our data demonstrate that exercise training significantly improves the exercise capacity in patients with severe COPD after an acute exacerbation of their disease.
F Fa ac ct to or r a an na al ly ys si is s o of f e ex xe er rc ci is se e c ca ap pa ac ci it ty y, , d dy ys sp pn no oe ea a r ra at ti in ng gs s a an nd d l lu un ng g f fu un nc ct ti io on n i in n p pa at ti ie en nt ts s w wi it th h s se ev ve er re e C CO OP PD D ) <65% of predicted were investigated. Before the study, therapy was optimized, including inhaled bronchodilators, theophylline and steroids. Exercise capacity was determined from the best 6 min walking distance achieved in five self-paced treadmill walks performed on consecutive days. Lung function testing comprised spirometry and body plethysmography. Four different tools were chosen to rate dyspnoea and quality of life: the Baseline Dyspnoea Index (BDI), the Oxygen Cost Diagram (OCD), a modified Medical Research Council (MRC) Scale, and the Chronic Respiratory Disease Questionnaire (CRQ).Principal component factor analysis revealed that the data could be reduced to three hypothetical underlying variables (factors), which accounted for 79% of the total variance. BDI, MRC, OCD, CRQ and walking distance were attributed to the first factor, forced expiratory volume in one second and airway resistance to the second factor, and lung volumes to the third factor. Thus, our data suggest that the pathophysiological condition of severe COPD is characterized by three statistically independent entities: 1) exercise capacity, dyspnoea and quality of life ratings; 2) airway obstruction; and 3) pulmonary hyperinflation. These findings suggest that, as a physically measurable variable, the performance in a standardized walking test corresponds well to clinical ratings of dyspnoea and quality of life, whereas lung function parameters do not.
Hydrogen peroxide (H 2 O 2 ) is known to be detectable in exhaled air. The present study aimed to determine whether the concentration of exhaled H 2 O 2 depends on expiratory flow rate in order to make inferences on the site of its production within the lung.Breath condensate was collected in cooled Teflon tubes, at three different expiratory flow rates, in 15 healthy or mild asthmatic subjects. Tests were repeated 2±5 times to assess reproducibility.Mean SEM concentrations of H 2 O 2 at flow rates of 140, 69 and 48 mL . s -1 were 0.12 0.02, 0.19 0.02 and 0.32 0.03 mM, respectively. These values differed significantly from each other (p<0.001). For comparison, average coefficients of variability within repeated measurements at each of the three flow rates were 68, 62 and 82%, respectively.These data demonstrate that the concentration of exhaled hydrogen peroxide depends on expiratory flow rate. Since flow dependence is an indicator of production within the airways, this result suggests that, to a large extent, the exhaled hydrogen peroxide originates within the airways. However, even under strictly controlled conditions, a high degree of variability persists, which may limit the usefulness of exhaled hydrogen peroxide as a marker of airway inflammation.
Systemic corticosteroids have been recommended as a therapeutic option in patients with moderate to severe COPD. In an early stage of the disease, i.e. chronic bronchitis with mild or no airflow obstruction, a trial with inhaled steroids could reveal potential benefits, particularly in terms of a modulation of airway inflammation. We therefore investigated the effect of inhaled fluticasone (1000 microg day(-1)) on markers of airway inflammation in 19 patients with chronic bronchitis (mean+/-SEM FEV1, 83.4+/-3.0% predicted; FEV1/VC, 67.5+/-2.4%) in a double-blind, cross-over, placebo-controlled manner. Visits were performed before and after two 4-week treatment periods. separated by a 4-week washout period. Lung function, the concentration of exhaled nitric oxide, differential cell counts in induced sputum and the number of cells positive for iNOS, as well as the levels of LDH, ECP, neutrophil elastase and IL-8 in sputum supernatants were determined. Although the total cell number decreased significantly after fluticasone (geometric mean 12.3 vs. 7.7 x 10(6)/ml; P<0.05) it was not significantly different from the change observed after placebo (14.2 vs. 10.6 x 10(6)/ml; n.s.). None of the other parameters showed statistically significant changes after fluticasone or placebo and the results did not depend on the presence of airway hyperresponsiveness. We conclude that in patients with chronic bronchitis short-term treatment with inhaled corticosterids did not improve lung function or inflammatory parameters to an extent which was statistically significant as compared to spontaneous variability.
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