Does inhaled albuterol improve diaphragmatic contractility in patients with chronic obstructive pulmonary disease?

We tested the hypothesis that the decrease in dyspnea in patients with COPD with inhaled albuterol is in part due to increased diaphragmatic contracti lity. Eleven patients with COPD inhaled albuterol or placebo in a double-bl ind randomized manner. Subsequently, dyspnea was measured while patients br eathed through inspiratory resistors, and diaphragmatic contractility was q uantified during maximal inspiratory efforts and after twitch stimulation o f the phrenic nerves. Albuterol produced a decrease in dyspnea (5 +/- 2 to 4 +/- 2 [SD] Borg units, p < 0.01), and increases in maximal transdiaphragm atic pressure (92.4 +/- 37.2 to 102.8 +/- 37.2 cm H2O, p < 0.03) and potent iated twitch transdiaphragmatic pressures (21.6 +/- 7.1 to 25.2 +/- 7.6 cm H2O, p < 0.02). The decrease in dyspnea correlated with the increases in ma ximal and twitch transdiaphragmatic pressures: r = - 0.64 (p = 0.04) and r = - 0.65 (p = 0.04), respectively. Compared with placebo, albuterol produce d 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 transdiap hragmatic pressures. The decrease in dyspnea correlated with the increase i n inspiratory capacity (r = -0.62, p = 0.04), but not with the increase in FEV1 (r = -0.13, p = 0.72). in conclusion, albuterol relieves dyspnea and e nhances respiratory muscle output in patients with COPD primarily by improv ing the length-tension relationship of the diaphragm rather than by improvi ng its contractility.