The Effects of Acute Ozone Pollution Exposure on Muscle Sympathetic Activity and Cardiac-Autonomic Control

Background: Ground level ozone (O 3 ) is a respiratory irritant well established to cause reductions in lung function. O 3 exposure may also promote progressive autonomic imbalance to the cardiovascular system as previously indicated by reductions in heart rate variability (HRV) and elevated basal blood pressure. However, no studies have directly assessed whether muscle sympathetic activity (MSNA) increases in this context. This study investigated whether short-term O 3 exposure promotes autonomic imbalance (via MSNA and HRV), with O 3 exposure being hypothesized to both decrease HRV and increase MSNA. Our secondary objective was to validate O 3 induced reductions in lung function as shown in previous studies. Methods: Twenty-eight healthy adults (female N. = 12; 23 ± 4 years [mean ± SD]) were randomized to a single 90 minute, double-blinded exposure of either: (i) artificial O 3 (0.75 parts per million [ppm]; N.14) or (ii) room air (RA) (naturally occurring O 3 <0.01 ppm). Spirometry was performed pre/post exposure, while blood pressure (finger photoplethysmography), MSNA (microneurography [N. 25]), and HRV (Lead~II ECG) were measured at several points during exposure. MSNA was quantified as burst frequency (burst/min) and burst incidence (burst/100 heart beats [hb]). HRV was averaged (5-minute bins) and assessed through time-domain (mean and standard deviation RR interval, root squared mean successive differences, percentage of RR interval differences >50ms) and frequency-domain (high frequency [ 0.15-0.4 Hz), low frequency [0.04-0.15 Hz], low/high frequency ratio) indices. Delta MSNA,HRV, and blood pressure were analyzed during exposure using two-way repeated measures ANOVA model. Pre/post exposure spirometry was assessed through students t-test. Results: O 3 and RA groups showed no difference in baseline lung function (forced expiratory volume [FEV 1 ] ~ 4.58 ± 0.98 vs 4.3 ± 0.84 L), heart rate (62 ± 8 vs 61 ± 6 beats/min), arterial pressure (MAP~87 ± 9 vs 81 ± 5 mmHg, p=0.06), burst frequency (16 ± 5 vs 16 ± 5 bursts/min), burst incidence (25 ± 10 vs 25 ± 10 bursts/100hb) and HRV time/frequency domain measures. O 3 group, but not RA, saw a reduced post-exposure FEV 1 (-8 ± 9% p<0.01 vs baseline). MAP response was unchanged between groups during exposure, while O 3 group showed greater time-dependent increases than RA group in burst frequency (+7 ± 4 vs +2 ± 3 bursts/min at 90 minutes exposure, p<0.05) and incidence (+10 ± 7 vs +3 ± 5 bursts/100hb at 90 minutes exposure, p<0.05). No differences were found in HRV time and frequency domain responses between O 3 and RA groups during exposure. Conclusion: These findings provide evidence of short-term O 3 induced sympathetic vasomotor activation that accompanies reductions in lung function. The increase of MSNA demonstrates sympathetic activation is present during initial O 3 exposure, and may partly contribute to early autonomic imbalance in the absence of observable changes to blood pressure and HRV. Supported by the Natural Sciences and Engineering Research Council of Canada (AWS; SAB) and a Killam Laureate Doctoral Scholarship (SAB). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.