Mechanisms of dyspnea during cycle exercise in symptomatic patients with GOLD stage I chronic obstructive pulmonary disease

15 Mar 2008
Respiratory conditions
  • COPD
Respiratory topics
  • Risk factor: physical activity
Type of resource
Peer-reviewed article
Ofir D, Laveneziana P, Webb KA, Lam YM, O'Donnell DE


Smokers with a relatively preserved FEV(1) may experience dyspnea and activity limitation but little is known about underlying mechanisms.


To examine ventilatory constraints during exercise in symptomatic smokers with GOLD (Global Initiative for Chronic Obstructive Lung Disease) stage I chronic obstructive lung disease (COPD) so as to uncover potential mechanisms of dyspnea and exercise curtailment.


We compared resting pulmonary function and ventilatory responses (breathing pattern, operating lung volumes, pulmonary gas exchange) with incremental cycle exercise as well as Borg scale ratings of dyspnea intensity in 21 patients (post-bronchodilator FEV(1), 91 +/- 7% predicted, and FEV(1)/FVC, 60 +/- 6%; mean +/- SD) with significant breathlessness and 21 healthy age- and sex-matched control subjects with normal spirometry.


In patients with COPD compared with control subjects, 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).


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.