Published ahead of print on November 15, 2007, doi:10.1164/rccm.200707-1064OC
Am. J. Respir. Crit. Care Med., Volume 177, Number 6, March 2008, 622-629
A more recent version of this article appeared on March 15, 2008
Submitted on July 19, 2007
Accepted on November 15, 2007
Mechanisms of Dyspnea During Cycle Exercise in Symptomatic Patients with GOLD Stage I COPD
Dror Ofir1, Pierantonio Laveneziana1, Katherine A Webb1, Yuk-Miu Lam2, and Denis E O'Donnell1*
1 Respiratory Investigation Unit, Department of Medicine, Queen's University, Kingston, Ontario, Canada,
2 Department of Community Health and Epidemiology, Queen's University, Kingston, Ontario, Canada
* To whom correspondence should be addressed. E-mail: odonnell{at}queensu.ca.
Rationale: Smokers with a relatively preserved forced expiratory volume in one second (FEV1) may experience dyspnea and activity limitation but little is known about underlying mechanisms.
Objectives: To examine ventilatory constraints during exercise in symptomatic smokers with GOLD stage I COPD so as to uncover potential mechanisms of dyspnea and exercise curtailment.
Methods: We compared resting pulmonary function and ventilatory responses (breathing pattern, operating lung volumes, pulmonary gas exchange) to incremental cycle exercise as well as Borg scale ratings of dyspnea intensity in 21 patients (post-bronchodilator FEV1 91±7%predicted and FEV1/FVC 60±6%; mean±SD) with significant breathlessness and 21 healthy age- and gender-matched control subjects with normal spirometry.
Results: In COPD compared with control, peak oxygen consumption and power output were significantly reduced by more than 20% and dyspnea ratings were higher for a given work rate and ventilation (p<0.05). Compared with the control group, the COPD group had evidence of extensive small airway dysfunction with increased ventilatory requirements during exercise, likely on the basis of greater ventilation-perfusion abnormalities. Changes in end-expiratory lung volume during exercise were greater in COPD than in health (0.54±0.34 vs 0.06±0.32 L, respectively; p<0.05) and breathing pattern was correspondingly more shallow and rapid. Across groups, dyspnea intensity increased as ventilation expressed as a percentage of capacity increased (p<0.0005) and as inspiratory reserve volume decreased (p<0.0005).
Conclusion: Exertional dyspnea in symptomatic patients with mild COPD is associated with the combined deleterious effects of higher ventilatory demand and abnormal dynamic ventilatory mechanics, both of which are potentially amenable to treatment.
Key words: mild COPD, respiratory mechanics, ventilation, dynamic hyperinflation
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