Rie Skovly Thomsen, Iben Elmerdahl Rasmussen, Stine Buus Nymand, Anna Agnes Lytzen, Jacob Peter Hartmann, Milan Mohammad, Malte Lund Adamsen, Birgitte Hanel, Jann Mortensen, Ronan M G Berg
Exertional dyspnoea is a debilitating symptom in chronic obstructive pulmonary disease (COPD) and often persists after the cessation of exercise. The underlying mechanisms are not fully understood, and a potential contributing factor that has not previously been investigated is alveolar-capillary membrane breaching with extravasation of fluid into the lungs. Sixteen individuals with COPD and 16 age- and sex-matched healthy controls were included. Alveolar-capillary membrane permeability was quantified using the pulmonary clearance index (PCI), calculated from scintigraphically determined alveolar clearance of 99mTc-labelled diethylenetriaminepentaacetic acid at rest and following an acute exercise bout performed at maximal exertion, as determined by a prior cardiopulmonary exercise test. In addition, lung tissue mass (LTM) was assessed using low-dose computed tomography, with rest-to-post-exercise changes interpreted as reflecting alterations in interstitial fluid accumulation. The mean change in PCI from rest-to-post-exercise was -0.01 [95% CI: -0.09, 0.06]%/min in the COPD group and -0.05 [95% CI: -0.12, 0.02]%/min in the healthy control group (Group × Time interaction, P = 0.446). The mean change in LTM from rest-to-post-exercise was 16.5 [95% CI: -7.0, 40.0]g/1.73 m2 in the COPD group and 35.2 [95% CI: 11.7, 58.7]g/1.73 m2 in the healthy control group (Group × Time interaction, P = 0.258). In conclusion, the present study found no evidence of alveolar-capillary membrane breaching following maximal exercise, neither in individuals with COPD nor in healthy matched controls.