During CO2 rebreathing we measured ventilation and the pressure generated during the first 0.1 sec of inspiratory effort against a closed airway (P 0.1) in 12 asthmatics during acute exacerbation, 10 normal subjects, and 10 patients with chronic obstructive pulmonary disease. In normal subjects, the ventilatory responst to CO2 correlated with the P 0.1 response measured as delta In P 0.1. Patients with chronic obstructive pulmonary disease showed depressed responses to CO2 in terms of both ventilation and deltaIn P0.1. However, P 0.1 values in the patients with chronic obstructive pulmonary disease were greater than those of the normal subjects when they were compared at an alveolar PCO2 of 60 mm Hg. Asthmatics' responses to CO2 were similar to those of patients with chronic obstructive pulmonary disease. When measured at an alveolar PCO2 of 60 mm Hg, asthmatics' P 0.1 values were greater than those of both normal subjects and patients with chronic obstructive pulmonary disease. As the asthmatics' airway obstruction decreased so did their P 0.1. The asthmatics, and to a lesser extent the patients with chronic obstructive pulmonary disease, demonstrated increased inspiratory muscle activity that could not be explained on the basis of chemical drive or alterations in functional residual capacity. In the case of the asthmatics it was possible that the increased inspiratory muscle activity was a response to airway obstruction.