Bronchodilator therapy in COPD is deemed successful if it improves ventilatory mechanics to a degree where effective symptom alleviation and increased exercise capacity are achieved. A greater understanding of the pathophysiologic mechanisms of dyspnea and exercise intolerance in COPD has prompted a reevaluation of the manner in which we currently assess therapeutic efficacy. The traditional reliance on an improved postbronchodilator FEV(1) as indicative of a positive clinical response has recognized limitations. To the extent that pharmacologic volume reduction is a desirable therapeutic goal with favorable implications for dyspnea relief and increased exercise tolerance, the potential value of bronchodilator-induced changes in lung volume measurements is currently being studied. It is unlikely, however, given the multifactorial nature of dyspnea and exercise limitation in COPD, that resting spirometric measurements of maximal flows and volumes alone will be sufficiently sensitive to adequately predict a positive clinical response to bronchodilator therapy. Thus, additional direct measurements of exercise dynamic hyperinflation and exercise endurance together with reliable subjective measurements of dyspnea and quality of life are recommended in the setting of a suitable placebo-controlled design.