Background: It has been known for many years that there are variations between asthmatic patients in terms of their perception of breathlessness during airway obstruction.
Study objective: To investigate the relationship between beta(2)-agonist consumption and the score of perception of dyspnea, in mild asthmatics, and the relationship between the effect of specific inspiratory muscle training (SIMT) on the score of perception of dyspnea and beta(2)-agonist consumption in "high perceivers."
Methods: Daily beta(2)-agonist consumption was assessed during a 4-week run-in period in 82 patients with mild asthma. Patients with a mean beta(2)-agonist consumption of > 1 puff/d ("high consumers") then were randomized into two groups: one group of patients received SIMT for 3 months; the other group of patients was assigned as a control group and received sham training. Inspiratory muscle strength and perception of dyspnea were assessed before patients entered the study, following the 4-week run-in period, and after completing the training period.
Results: Following the 4-week run-in period, 23 high-consumer patients (mean [+/- SEM] beta(2)-agonist consumption, 2.7 +/- 0.4 puffs/d) were detected. The mean Borg score during breathing against resistance was significantly higher (p < 0.05) in the patients with high beta(2)-agonist consumption than in the subjects with low mean beta(2)-agonist consumption. Following SIMT, the mean maximal inspiratory pressure increased significantly from 94.1 +/- 5.1 to 109.7 +/- 5.2 cm H(2)O (p < 0.005) in the training group. The increase in inspiratory muscle strength was associated with a statistically significant decrease in the mean Borg score during breathing against resistance (p < 0.05) as well as in the mean daily beta(2)-agonist consumption.
Conclusions: We have shown that patients with mild asthma, who have a high beta(2)-agonist consumption, have a higher perception of dyspnea than those with normal consumption. In addition, SIMT was associated with a decrease in perception of dyspnea and a decrease in beta(2)-agonist consumption.