Vascular effects of physical activity are not modified by short-term inhaled diesel exhaust: Results of a controlled human exposure study

Abstract

BackgroundThe combined effects of physical activity and air pollution exposure on vascular function are insufficiently understood, particularly after the inhalation of a β2-agonist, a vasodilating agent. ObjectiveTo assess the micro- and macrovascular response to physical activity after β2-agonist use while breathing diesel exhaust (DE) in individuals with exercise-induced bronchoconstriction. MethodsOn four exposure visits, eighteen adults inhaled either 400 μg of the β2-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 PM2.5). 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 (T1), 10 min (T2) and 70 min (T3) after cycling. ResultsThe cycling bout increased CRAE (T2-T1 difference (95th % confidence interval): 4.88 μm (4.73, 5.00 μm), p < 0.001; T3-T1 difference: 2.10 μm (1.62, 2.58 μm), p = 0.031) and CRVE (T2-T1 difference: 3.78 μm (3.63, 3.92 μm), p < 0.001; T3-T1 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 T2: 0.46 μm (−0.02, 0.92 μm); p = 0.790; FA-DE difference at T3: 1.76 μm (1.36, 2.16 μm), p = 0.213) and CRVE (FA-DE difference at T2: 0.26 μm (−0.35, 0.88 μm), p = 0.906; FA-DE difference at T3: 0.55 μm (0.05, 1.06 μm), p = 0.750). Compared to T1, systolic BP was decreased at T2 by 2.5 mmHg (2.8, 2.3 mmHg, p = 0.047), independent of inhaled exposure. Heart rate at T2 was significantly increased by 3 bpm (2, 3 bpm, p = 0.025) after the DE-exposure when compared to FA. DiscussionAcute physical activity induces a vasodilatory response in the micro- and macrovasculature in healthy adults by increasing CRAE and CRVE, and by reducing systolic BP post exercise, despite breathing DE. The DE-associated increase in HR might be indicative of an increased sympathetic response to physical activity while breathing DE.