Differences in Physiological Response to Exercise in Patients With Different COPD Severity

Abstract

BACKGROUND: Patients with 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 subjects (82 males, 9 females, average age 69.7 ؎ 6.8 y) consecutively underwent incremental cardiopulmonary exercise testing using a cycle ergometer. Arterial blood gases, lactate, and catecholamines were measured during cardiopulmonary exercise testing. RESULTS: The pathophysiology of the COPD differed among the 4 subject groups. Subjects with the most severely reduced exercise capacity (peak oxygen uptake < 623 mL/min) were characterized by exercise-induced steep decrease in P aO 2 slope (؊78 ؎ 70 mm Hg/L/min), rapid progression of respiratory acidosis, little change in lactic acidosis, and sympathetic activation at low-intensity work load (plasma norepinephrine 1.41 ؎ 0.94 ng/mL at 20 watts work load), in addition to the limitation of increase in ventilation and impaired gas exchange. CONCLUSIONS: The mechanisms of exercise intolerance in COPD patients significantly differed among subjects with different exercise capacities. Subjects 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 lifethreatening pathophysiological conditions could be improved by medication and/or pulmonary rehabilitation.

Exertional dyspnoea and cortical oxygenation in patients with COPD

“…Therefore, we cannot rule out the effect of skeletal muscle afferent activity on cortical activation. MAEKURA et al [34] found that the arterial pH decreased rapidly in COPD patients with severely reduced exercise capacity, and that their acidaemia was a result of both lactic acidosis and respiratory acidosis. We did not measure arterial lactic acid in this study, but increases in arterial lactic acid levels might have been different in the different groups of patients and might have resulted in different effects on cerebral metabolism or oxygen uptake [14].…”

Personalized pulmonary rehabilitation and occupational therapy based on cardiopulmonary exercise testing for patients with advanced chronic obstructive pulmonary disease

“…The aim of the PPR-OT program is for patients with advanced COPD to be able to safely live at home for a longer time without feeling breathlessness with their remaining cardiopulmonary capacity, which has been improved to the greatest extent possible by medication and PPR, including exercise training. As pathophysiological responses to exercise vary widely among patients with COPD, 10 we determined the safe range of activity for each patient, based on their CPET parameters. The criteria for a safe range were 1) PaO 2 >60 mmHg and 2) Borg scale score of <2 and/or lower than the norepinephrine (NE) threshold as there is a strong linear positive correlation between the NE threshold and the onset of dyspnea during incremental exercise.…”

“…The criteria for a safe range were 1) PaO 2 >60 mmHg and 2) Borg scale score of <2 and/or lower than the norepinephrine (NE) threshold as there is a strong linear positive correlation between the NE threshold and the onset of dyspnea during incremental exercise. 10 The safe range was identified by oxygen uptake (mL/min), which was determined according to each patient’s pulse oximeter O 2 saturation (SpO 2 ) (%) reading and pulse rate (beats/min) using a watch-type pulse oximeter, in addition to the Borg scale ( Figures 2 , S1 ). We designed this pulse oximeter in collaboration with Minolta Co Ltd (Hachioji City, Tokyo, Japan).…”

“…The three pathophysiological life-threatening conditions included the following: 1) Exercise-induced hypoxemia ([PaO 2 slope ≤−55 mmHg·L −1 ·min −1 ] = decrease in ·[difference in at rest and during peak exercise]); 2) sympathetic overactivity ; and 3) progressive respiratory acidosis at low-intensity exercise). 10 , 11 …”

“… 8 , 9 Using symptom-limited cardiopulmonary exercise testing (CPET), we previously identified three life-threatening pathophysiological conditions that are related to a poor prognosis (ie, exercise-induced hypoxemia, sympathetic overactivity, and progressive respiratory acidosis during low-intensity exercise). 10 , 11 These three conditions have cumulative negative effects on survival of patients with COPD.…”