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

Abstract

Background: The combined effects of physical activity and air pollution exposure on vascular function are insufficiently understood, particularly after the inhalation of a beta(2)-agonist, a vasodilating agent. Objective: To assess the micro- and macrovascular response to physical activity after beta(2)-agonist use while breathing diesel exhaust (DE) in individuals with exercise-induced bronchoconstriction. Methods: On four exposure visits, eighteen adults inhaled either 400 mu g of the beta(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 mu g/m(3) 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 (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 mu m (4.73, 5.00 mu m), p < 0.001; T-3-T-1 difference: 2.10 mu m (1.62, 2.58 mu m), p = 0.031) and CRVE (T-2-T-1 difference: 3.78 mu m (3.63, 3.92 mu m), p < 0.001; T-3-T-1 difference: 3.73 mu m (3.63, 3.92 mu m), p < 0.001). The exposure to DE had no effect on CRAE (FA-DE difference at T-2: 0.46 mu m (-0.02, 0.92 mu m); p = 0.790; FA-DE difference at T-3: 1.76 mu m (1.36, 2.16 mu m), p = 0.213) and CRVE (FA-DE difference at T-2: 0.26 mu m (-0.35, 0.88 mu m), p = 0.906; FA-DE difference at T-3: 0.55 mu m (0.05, 1.06 mu m), 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. Discussion: Acute 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.