Asthma medication use prior to cycling while breathing diesel exhaust did not affect vasculature.

Abstract

Background The combined effects of physical activity and air pollution exposure on vascular function are insufficiently understood, particularly after the inhalation of a β 2 -agonist, a vasodilating agent.

Objective To assess the micro- and macrovascular response to physical activity after β 2 -agonist use while breathing diesel exhaust (DE) in individuals with exercise-induced bronchoconstriction.

Methods On four exposure visits, eighteen adults inhaled either 400 μg of the β 2 -agonist salbutamol or placebo before resting for 60 min, followed by a 30-min cycling bout. During rest and cycling, participants inhaled filtered air (FA) or DE (300 μg/m3 of PM 2.5 ). Microvascular (central retinal arteriolar and venular equivalents, CRAE and CRVE, respectively) and macrovascular parameters (blood pressure (BP)) and heart rate (HR)) were assessed at baseline (T 1 ), 10 min (T 2 ) and 70 min (T 3 ) after cycling.

Results The cycling bout increased CRAE (T 2 -T 1 difference (95th % confidence interval): 4.88 μm (4.73, 5.00 μm), p < 0.001; T 3 -T 1 difference: 2.10 μm (1.62, 2.58 μm), p = 0.031) and CRVE (T 2 -T 1 difference: 3.78 μm (3.63, 3.92 μm), p < 0.001; T 3 -T 1 difference: 3.73 μm (3.63, 3.92 μm), p < 0.001). The exposure to DE had no effect on CRAE (FA-DE difference at T 2 : 0.46 μm (−0.02, 0.92 μm); p = 0.790; FA-DE difference at T 3 : 1.76 μm (1.36, 2.16 μm), p = 0.213) and CRVE (FA-DE difference at T 2 : 0.26 μm (−0.35, 0.88 μm), p = 0.906; FA-DE difference at T 3 : 0.55 μm (0.05, 1.06 μm), p = 0.750). Compared to T 1 , systolic BP was decreased at T 2 by 2.5 mmHg (2.8, 2.3 mmHg, p = 0.047), independent of inhaled exposure. Heart rate at T 2 was significantly increased by 3 bpm (2, 3 bpm, p = 0.025) after the DE-exposure when compared to FA.