Abstract Exercise in healthy subjects is usually associated with progressive bronchodilatation. Though the decrease in vagal tone is deemed to be the main underlying mechanism, activation of bronchial β2-receptors may constitute an additional cause. To examine the contribution of β2-adrenergic receptors to bronchodilatation during exercise in healthy humans, we studied 15 healthy male volunteers during maximum exercise test at control conditions and after a non-selective β-adrenergic blocker (carvedilol 12.5mg twice a day until heart rate decreased at least by 10beats/min) and inhaled β2-agonist (albuterol 400μg). Airway caliber was estimated from the partial flow at 40% of control forced vital capacity (V˙part40) and its changes during exercise from the slope of linear regression analysis of V˙part40 values against the corresponding minute ventilation during maximal exercise until exhaustion. At control, V˙part40 increased progressively and significantly with exercise. After albuterol, resting V˙part40 was significantly larger than at control increased but did not further increase during exercise. After carvedilol, V˙part40 was similar to control but its increase with exercise was significantly attenuated. These findings suggest that β2-adrenergic system plays a major role in exercise-induced bronchodilation in healthy subjects.