Several studies in mild COPD have shown higher than normal ventilatory equivalent for carbon dioxide (VE/VCO2) during exercise. Our objective was to examine pulmonary gas exchange abnormalities and the mechanisms of high VE/VCO2 in mild COPD and its impact on dyspnea and exercise intolerance.

METHODS: Twenty-two subjects (11 GOLD grade-1B COPD patients, 11 age-matched healthy controls) undertook physiological testing and a symptom-limited incremental cycle exercise test with arterial blood gas collection.

RESULTS: Patients (post-bronchodilator FEV1: 94±10 %predicted; mean±SD) had evidence of peripheral airway dysfunction and reduced peak oxygen uptake compared to controls (80±18 versus 113±24 %predicted; p<0.05). Arterial blood gases were within the normal range and effective alveolar ventilation was not significantly different from controls throughout exercise. The alveolar-arterial O2 gradient was elevated at rest and throughout exercise in COPD (p<0.05). VE/VCO2, dead space-to-tidal volume ratio (VD/VT), and arterial-to-end tidal CO2 difference were all higher (p<0.05) in COPD than controls during exercise. In COPD versus controls, there was significant dynamic hyperinflation and greater tidal volume constraints (p<0.05). Standardized dyspnea intensity ratings were also higher (p<0.05) in COPD versus controls in association with higher ventilatory requirements. Within all subjects, VD/VT correlated with the VE/VCO2 ratio during submaximal exercise (r=0.780, p<0.001).

CONCLUSION: High VD/VT was the most consistent gas exchange abnormality in smokers with only mild spirometric abnormalities. Compensatory increases in minute ventilation during exercise maintained alveolar ventilation and arterial blood gas homeostasis but at the expense of earlier dynamic mechanical constraints, greater dyspnea and exercise intolerance in mild COPD.