Exercise-induced bronchodilation (EIBD) is primarily driven by parasympathetic withdrawal; however, the role of sympathetic activity via beta-adrenergic receptors (β-AR) remains unclear. We sought to determine the contribution of β-AR to EIBD in healthy males and females following fatiguing single-leg knee extension exercise. Fourteen healthy young adults (7 males, 7 females) completed two randomized exercise visits with or without systemic β-AR blockade (propranolol). Participants performed forced vital capacity (FVC) maneuvers before and immediately after exercise to quantify EIBD. Spirometric outcomes included forced expiratory volume in one second (FEV₁), FEV₁/FVC, peak expiratory flow (PEF), and flows at 25%, 50%, and 75% of FVC. Mean slope ratio (SR) of the maximal expiratory flow-volume (MEFV) was also quantified from the effort-independent portion of the MEFV. EIBD was confirmed by increases in FEV₁ (Δ4 ± 3% and Δ5 ± 3%) and FEV 1 /FVC (Δ3 ± 1% and Δ3 ± 4%) during the control condition in males and females respectively. Propranolol did not significantly alter these global markers of bronchodilation. Compared to control, propranolol significantly blunted airflow at 25% FVC (Δ0 ± 0.4L·s −1 vs. Δ0.3 ± 0.3L·s −1 ; p = 0.05) and 50% FVC (Δ0.1 ± 0.4L·s −1 vs. Δ0.4 ± 0.4L·s −1 ; p = 0.05). Females (Δ0.08 ± 0.11; p = 0.03) but not males (Δ-0.04 ± 0.07; p = 0.96) exhibited a significant increase in mean SR with propranolol. While β-AR blockade did not affect typical markers of EIBD, it impaired airflow in small airways, especially in females, suggesting sex-specific sympathetic regulation of bronchodilation. These findings highlight a nuanced role for β-AR in modulating EIBD.
Doherty et al. (Fri,) studied this question.