Bronchodilators accelerate the dynamics of muscle O2 delivery and utilisation during exercise in COPD.

Abstract

Expiratory flow limitation and lung hyperinflation promote cardiocirculatory perturbations that might impair O(2) delivery to locomotor muscles in patients with chronic obstructive pulmonary disease (COPD). The hypothesis that decreases in lung hyperinflation after the inhalation of bronchodilators would improve skeletal muscle oxygenation during exercise was tested. Twelve non- or mildly hypoxaemic males (forced expiratory volume in 1 s (FEV(1))=38.5+/-12.9% predicted; Pao(2)>60 mm Hg) underwent constant work rate cycle ergometer exercise tests (70-80% peak) to the limit of tolerance (Tlim) after inhaled bronchodilators (salbutamol plus ipratropium) or placebo. Muscle (de)oxygenation (approximately fractional O(2) extraction) was determined in the vastus lateralis by changes (Delta) in the deoxyhaemoglobin/myoglobin signal ([HHb]) from near-infrared spectroscopy, and cardiac output (QT) was monitored by impedance cardiography. Bronchodilators reduced lung hyperinflation and increased Tlim compared with placebo (454+/-131 s vs 321+/-140 s, respectively; p<0.05). On-exercise kinetics of QT and pulmonary O(2) uptake V(o(2))were accelerated with active treatment; Delta[HHb] dynamics, however, were delayed by approximately 78% and the signal amplitude diminished by approximately 21% (p<0.01). Consequently, the ratio between V(o(2)) and Delta[HHb] dynamics decreased, suggesting improved microvascular O(2) delivery (tau-V(o(2))/MRT-Delta[HHb]=4.48+/-1.57 s vs 2.08+/-1.15 s, p<0.05). Of note, reductions in lung hyperinflation were related to faster QT kinetics and larger decrements in tau-V(o(2))/MRT-Delta[HHb] (p<0.01). Decreases in operating lung volumes after the inhalation of bronchodilators are associated with faster 'central' cardiovascular adjustments to high-intensity exercise with beneficial consequences on muscle oxygenation in patients with moderate to severe COPD.