Exertional dyspnea in COPD: the dominant role of increased diaphragmatic activation

Abstract

Background: Dyspnea intensity rises in COPD during exercise in tandem with inspiratory neural drive (IND), measured by diaphragm activation. We postulated that selective manipulation of central chemical and inspiratory muscle afferent inputs (by oxygen/opiates and bronchodilator, respectively) would not alter the fundamental relationship between dyspnea and IND during a standardized exercise task.

Methods: This double-blind crossover study compared combined supplemental O₂ (Fi­O₂=0.6) and nebulized fentanyl (100mcg) with nebulized bronchodilator (0.5mg ipratropium bromide+2.5mg salbutamol). We examined dyspnea intensity, IND (EMGdi/EMGdi,max), ventilation, and operating lung volumes, during randomized 4 min constant work rate exercise tests (75% peak work rate) in patients with severe COPD (n=13).

Results: Bronchodilators decreased resting FRC by 0.44 L. Dyspnea:EMGdi/EMGdi,max slopes were similar with both interventions (r=0.698 vs 0.571, p<0.001). At standardized 3 min exercise time, dyspnea and IND were similar despite significant differences in operating lung volumes and breathing pattern between interventions (Table,*p<0.05).

Conclusion: The strong relationship between dyspnea intensity and diaphragm activation during exercise in COPD was not altered by selective therapeutic manipulation of central medullary or cortical motor centers which introduced significant differences in ventilation, and resting and dynamic respiratory mechanics.