RT Journal Article
SR Electronic
T1 Difference in the physiological response to exercise in patients with distinct severity of COPD pathology
JF Respiratory Care
FD American Association for Respiratory Care
SP respcare.02201
DO 10.4187/respcare.02201
A1 Ryoji Maekura
A1 Toru Hiraga
A1 Keisuke Miki
A1 Seigo Kitada
A1 Kenji Yosimura
A1 Mari Miki
A1 Yositaka Tateishi
YR 2013
UL http://rc.rcjournal.com/content/early/2013/07/02/respcare.02201.abstract
AB 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.