Supplemental oxygen improves exercise tolerance of normoxemic and hypoxemic chronic obstructive pulmonary disease (COPD) patients. We determined whether nonhypoxemic COPD patients undergoing exercise training while breathing supplemental oxygen achieve higher intensity and therefore improve exercise capacity more than patients breathing air. A double-blinded trial was performed involving 29 nonhypoxemic patients (67 years, exercise SaO2 > 88%) with COPD (FEV1 = 36% predicted). All exercised on cycle ergometers for 45 minutes, 3 times per week for 7 weeks at high-intensity targets. During exercise, they received oxygen (3 L/minute) (n = 14) or compressed air (3 L/minute) (n = 15). Both groups had a higher exercise tolerance after training and when breathing oxygen. However, the oxygen-trained group increased the training work rate more rapidly than the air-trained group. The mean +/- SD work rate during the last week was 62 +/- 19 W (oxygen-trained group) and 52 +/- 22 W (air-trained group) (p < 0.01). After training, endurance in constant work rate tests increased more in the oxygen-trained group (14.5 minutes) than in the air-trained group (10.5 minutes) (p < 0.05). At isotime, the breathing rate decreased four breaths per minute in the oxygen-trained group and one breath per minute in the air-trained group (p = 0.001). We conclude that supplemental oxygen provided during high-intensity training yields higher training intensity and evidence of gains in exercise tolerance in laboratory testing.
The recommended method to measure exhaled nitric oxide (NO) cannot reveal the source of NO production. We applied a model based on the classical Fick's first law of diffusion to partition NO in the lungs. The aim was to develop a simple and robust solution algorithm with a data quality control feature, and apply it to patients with known alterations in exhaled NO. Subjects with allergic rhinitis, allergic asthma, chronic obstructive pulmonary disease (COPD) smokers and controls were investigated. NO was measured at three expiratory flow rates. An iteration method was developed to partition NO. The airway tissue content of NO was increased in asthma, 144 +/- 80 ppb (P = 0.04) and decreased in smokers, 56 +/- 36 ppb (P = 0.02). There was no difference between subjects with rhinitis, 98 +/- 40 ppb and controls, 98 +/- 44 ppb. The airway transfer rate was increased in allergic asthma and allergic rhinitis, 12 +/- 4 vs. 12 +/- 5 ml sec(-1), compared to controls, 8 +/- 2 ml sec(-1) (P < 0.001). The alveolar levels were no different from controls, 2 +/- 1 ppb. In COPD the alveolar levels were increased, 4 +/- 2 ppb (P < 0.001). Extended NO analysis reveals from where in the respiratory system NO is generated. Hence, this new test can be added to the tools the physician has for the diagnosis and treatment of patients with respiratory disorders.
Only a third of Swedish patients with COPD had their diagnosis confirmed with spirometry. Our data indicate that female gender, current smoking, higher BMI and short exhalation time increase the risk of being diagnosed with COPD without fulfilling the spirometric criteria for the disease.
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