Asthma is characterized by chronic endobronchial inflammation and the deposition of collagen below the epithelial basement membrane. The functional significance of collagen deposition is unknown, but it can lead to loss of airway distensibility and hence to eventual loss of bronchodilator response. In this study we examined the volume of airway dead space by a single-breath, nitrogen-plateau method at a range of lung volumes during inspiration. Participants were 10 asthmatics and 10 control subjects who were matched for lung volumes and age. The asthmatics increased their dead space by 27.0 ml/L compared with 37.3 ml/L in the control subjects (p = 0.014). The dead-space volumes at 50% TLC were no different (29.3 ml/L lung volume in asthma versus 26.9 ml/L in control subjects, p = 0.25). Loss of airway distensibility did not correlate, however, with loss of bronchodilator responsiveness, implying that factors other than mechanical airway distensibility may act to determine pharmacologic reversibility of airflow obstruction.