Understanding of what constitutes a training load adequate to induce training effects in patients with chronic obstructive pulmonary disease (COPD) is still evolving. The present study investigated whether interval training (IT) is effective in terms of inducing measurable improvements in physiological response and compared its effects on exercise tolerance (ET) and quality of life to those of continuous training (CT).Thirty-six COPD patients, with a forced expiratory volume in one second of 45±4% of the predicted value (mean±sem), were randomly assigned to CT (exercise at 50% of baseline peak work-rate) or IT (work for 30 s at 100% of peak work-rate alternating with 30‐s rest intervals) groups that cycled 40 min·day−1and 2 days·week−1for 12 weeks.After training, both groups showed significantly improved ET (IT, 57±6 to 71±8 W; CT, 57±5 to 70±6 W) and total quality-of-life score of the Chronic Respiratory Disease Questionnaire (IT, 77±3 to 88±2; CT, 78±3 to 93±2). At identical levels of exercise, minute ventilation was significantly reduced (IT, 35.8±2.5 to 31.7±2.5 L·min−1; CT, 36.4±2.7 to 32.5±2.7 L·min−1). The magnitude of improvement in these variables was not significantly different among groups.The present data expand on the principles of exercise prescription for chronic obstructive pulmonary disease patients by demonstrating that interval training elicits substantial training effects, which are similar in magnitude to those produced by continuous training at half the exercise intensity but double the exercise time.

Influence of atopy on exhaled nitric oxide in patients with stable asthma and rhinitis. Ch. Gratziou, M. Lignos, M. Dassiou, Ch. Roussos. #ERS Journals Ltd 1999. ABSTRACT: The level of exhaled NO is increased in patients with allergic asthma and seasonal rhinitis. The aim of this study was to investigate the significance of atopy on NO production in the lower airways.Measurements of exhaled NO were performed in 131 stable asthmatic patients with chronic mild asthma (95 atopics and 36 nonatopics), 72 patients with perennial rhinitis (57 atopics and 15 nonatopics) and 100 healthy controls (20 atopics and 80 nonatopics).Patients with either asthma or rhinitis had higher exhaled NO values (13.3& 1.2 parts per billion (ppb) and 11.7 1.1 ppb) than control subjects (4.8 0.3 ppb, p<0.01). Exhaled NO levels were significantly higher in atopic asthmatics (19 3.6 ppb) compared with nonatopic patients (5.6 0.8 ppb, p<0.001). Similar findings were observed in patients with rhinitis (13.3 1.3 ppb in atopics and 5.8 1.2 ppb in nonatopics, p<0.001). No difference was found in NO levels between atopic and nonatopic control subjects (4.8 0.8 ppb, and 4.5 0.3 ppb).In summary, this study has shown that increased exhaled NO levels are detected only in atopic patients with asthma and/or rhinitis and not in nonatopic patients. These findings may suggest that it is rather the allergic nature of airways inflammation, which is mainly responsible for the higher NO production in the lower airways. Eur Respir J 1999; 14: 897±901.

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The effect of endotoxic shock on the respiratory muscle performance was studied in spontaneously breathing dogs given Escherichia coli endotoxin (Difco Laboratories, 10 mg/kg). Diaphragmatic (Edi) and parasternal intercostal (Eic) electromyograms were recorded using fishhook electrodes. The recorded signals were then rectified and electrically integrated. Pleural, abdominal, and transdiaphragmatic (Pdi) pressures were recorded by a balloon-catheter system. After a short control period, the endotoxin was administered slowly intravenously (within 5 min). Death was secondary to respiratory arrest in all animals. All animals died within 150-270 min after the onset of endotoxic shock. Within 45-80 min of the endotoxin administration, mean blood pressure and cardiac output dropped to 42.1 +/- 4.1 and 40.1 +/- 6.0% (mean +/- SE) of control values, respectively, with little change afterward. Mean inspiratory flow rate and Pdi increased from control values of 0.27 +/- 0.03 l X s-1 and 5.75 +/- 0.7 cmH2O to mean values of 0.44 +/- 0.3 l X s-1 and 8.70 +/- 1.05 cmH2O and then decreased to 0.17 +/- 0.03 l X s-1 and 3.90 +/- 0.30 cmH2O before the death of the animals. There were no major changes in the mechanics of the respiratory system. Edi and Eic increased progressively to mean values of 360 +/- 21 and 263 +/- 22% of control, respectively, before the death of the animals. None of the dogs were hypoxic. Arterial PCO2 decreased from a control value of 42.9 +/- 1.7 Torr to a mean value of 29.9 +/- 2.8 Torr and then increased to 51 +/- 4.3 Torr before the death of the animals.(ABSTRACT TRUNCATED AT 250 WORDS)

R Re es sp pi ir ra at to or ry y m mu us sc cl le es s a an nd d w we ea an ni in ng g f fa ai il lu ur re e ABSTRACT: Weaning failure is, unfortunately, a rather common phenomenon for mechanically-ventilated patients (especially those with chronic obstructive pulmonary disease (COPD)), and the respiratory muscles play a pivotal role in its development.Weaning fails whenever an imbalance exists between the ventilatory needs and the neurocardiorespiratory capacity. This can happen if there is an increase in the energy demands of the respiratory muscles, a decrease in the energy available, a decrease in neuromuscular competence, or if the respiratory muscles pose an impediment to the heart and blood flow.The imbalance created will lead to weaning failure through the development of respiratory muscle fatigue, hypercapnia, dyspnoea, anxiety and organ dysfunction.