Is improved pulmonary vasodilation why endurance trained individuals have elevated diffusing capacity compared to untrained individuals?

Abstract

Contrary to our traditional understanding, the pulmonary vasculature may adapt to endurance training. Improved pulmonary vasodilation may be the principal mediator for trained individuals who exhibit greater diffusing capacity (DLCO), capillary blood volume (VC; representing recruitment and distension) and membrane diffusing capacity (DM; representing recruitment) at rest and during exercise as compared to untrained. Potential functional differences may be investigated using pulmonary vasodilators ( e.g., oral sildenafil). The purpose of this study was to examine the effects of sildenafil on DLCO, VC, and DM, in trained and untrained participants. We hypothesized that sildenafil would increase rest and exercise DLCO, VC, and DM, with a lesser relative response in trained due to improved baseline pulmonary vascular function. In this randomized, double-blind, placebo-controlled cross-over design (NCT: 04985929), DLCO was measured at rest (supine and seated) and during cycle ergometry (60 Watts, 30%, 60%, and 90% of V̇O2peak). DLCO was conducted using the modified Roughton-Forster multiple FiO2 breath-hold technique over 6 visits, where participants were given either oral placebo or sildenafil (50 mg, single dose, 30 min wash-in). To date, 18 participants (6 female) (56% target sample size) have been recruited into two groups: trained (T) and untrained (UT) (Mean V̇O2peak = 66.6 ± 7.2 mL.kg−1.min−1 and 37.8 ± 3.2 mL.kg−1.min−1, respectively). Estimated PASP was reduced between placebo and sildenafil across all participants at rest (mean Δ = -2.7 mmHg; p<0.01), indicating effective pulmonary vasodilation. Under placebo, T had higher DLCO at rest (supine), 30%, 60%, and 90% of V̇O2peak (p<0.05), consistent with previous literature. There was no effect of sildenafil on DLCO, VC, or DM (all p>0.200) or drug by workload interactions (all p>0.189) in either group. These preliminary results suggest that pharmacological augmentation of the nitric oxide vasodilatory pathway does not increase DLCO regardless of training status. We speculate that this pathway may not be the primary driver responsible for the elevated DLCO observed in endurance trained participants. Natural Sciences and Engineering Research Council of Canada. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.