Abstract
Background: Patients with chronic obstructive pulmonary disease (COPD) have reduced exercise tolerance associated with dyspnea. This exercise intolerance is primarily due to impaired ventilatory mechanics, but it is also associated with a combination of factors, including inefficient gas exchange, lactic acidosis at a low work rate, and exercise-induced hypoxemia. The survival prognosis of COPD patients with severely reduced exercise capacity is extremely poor, but the pathophysiology of these patients during exercise remains to be accurately established. The present study aimed to characterize life-threatening factors such as hypoxemia, acidosis, and sympathetic activation during exercise in these patients.
Methods: We monitored changes in life-threatening factors and compared these factors among quartile groups, defined according to their peak oxygen uptake status. Ninety-one COPD patients (82 males, 9 females; average age, 69.7 ± 6.8 years) consecutively underwent incremental cardiopulmonary exercise testing (CPET) using a cycle ergometer. Levels of arterial blood gases, lactate, and catecholamines were measured during CPET.
Results: We found that the pathophysiology of the COPD patients differed among patient groups. Patients with the most severely reduced exercise capacity (peak oxygen uptake ≤623 ml·min-1) were characterized by exercise-induced steep decrease in arterial oxygen pressure (PaO2-slope: −78 ± 70 mmHg·L-1·min-1), rapid progression of respiratory acidosis, little change in lactic acidosis, and sympathetic activation at low-intensity workload (plasma norepinephrine level, 1.41 ± 0.94 ng·ml-1 at 20 W), in addition to the limitation of increase in ventilation and impaired gas exchange.
Conclusions: The mechanisms of exercise intolerance in COPD patients significantly varied among patients with different exercise capacities. Patients with the most severely reduced exercise capacity had the characteristics of exercise-induced hypoxemia, sympathetic overactivity, and progressive respiratory acidosis at low-intensity exercise. These life-threatening pathophysiological conditions could be improved by medication and/or pulmonary rehabilitation.
Footnotes
- ↵*Correspondence: Ryoji Maekura, M.D., Department of Respiratory Medicine, National Hospital Organization Toneyama Hospital, 5-1-1 Toneyama, Toyonaka-city, Osaka 560-0045, Japan. Phone: +81-6-6853-2001; Fax: +81-6-6853-1221; E-mail: rmaekura{at}toneyama.go.jp
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Financial Support: This study was supported by funding from the Health and Labour Sciences Research Grants, Clinical Research, H20-translational research-general-002 and the Osaka Tuberculosis Research Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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