We tested the hypothesis that the decrease in dyspnea in patients with COPD with inhaled albuterol is in part due to increased diaphragmatic contractility. Eleven patients with COPD inhaled albuterol or placebo in a double-blind randomized manner. Subsequently, dyspnea was measured while patients breathed through inspiratory resistors, and diaphragmatic contractility was quantified during maximal inspiratory efforts and after twitch stimulation of the phrenic nerves. Albuterol produced a decrease in dyspnea (5 +/- 2 to 4 +/- 2 [SD] Borg units, p < 0.01), and increases in maximal transdiaphragmatic pressure (92.4 +/- 37.2 to 102.8 +/- 37.2 cm H(2)O, p < 0.03) and potentiated twitch transdiaphragmatic pressures (21.6 +/- 7.1 to 25.2 +/- 7.6 cm H(2)O, p < 0.02). The decrease in dyspnea correlated with the increases in maximal and twitch transdiaphragmatic pressures: r = -0.64 (p = 0. 04) and r = -0.65 (p = 0.04), respectively. Compared with placebo, albuterol produced an increase in inspiratory capacity (1.87 +/- 0. 71 to 2.26 +/- 0.74 L, p = 0.002), which accounted for the increases in maximal and twitch transdiaphragmatic pressures. The decrease in dyspnea correlated with the increase in inspiratory capacity (r = -0. 62, p = 0.04), but not with the increase in FEV(1) (r = -0.13, p = 0. 72). In conclusion, albuterol relieves dyspnea and enhances respiratory muscle output in patients with COPD primarily by improving the length-tension relationship of the diaphragm rather than by improving its contractility.