Background

Exercise-induced bronchoconstriction (EIB) is a transient narrowing of the lower airways after vigorous exercise.1 Exercise requires increased ventilation, which results in respiratory water loss leading to airway drying and cooling. Evaporative water loss leading to an increase in the osmolarity of the airway surface liquid and consequent release of mediators is thought to be the major stimulus and mechanism for EIB.2 Mast cell mediators include histamine, leukotrienes and prostaglandins, which act on specific receptors on the bronchial smooth muscle causing bronchoconstriction.3 Leukotrienes from eosinophils and neuropeptides from sensory nerves may also be involved in EIB. EIB can occur in people with or without chronic asthma, although it is highly prevalent in people with asthma.1

The intensity and duration of exercise are key determinants of the airway response.2 Guidelines therefore recommend an exercise challenge of 6–8 min at 80–90% of the predicted maximum heart rate.4 However, laboratory exercise may have poor sensitivity to identify EIB if the intensity does not induce enough ventilation to achieve an adequate rate of respiratory water loss. In athletes, field exercise, eucapnic hyperventilation or osmotic challenge may be more appropriate tests.3

A decrease in the forced expiratory volume in 1 s (FEV₁) of 10–15% after exercise is the threshold for the diagnosis of EIB.4 ,5 EIB may be associated with cough, wheeze, chest pain or tightness, dyspnoea or excessive mucus production.6 However, the amount of bronchoconstriction does not always correlate well with the baseline level of lung function or presence or severity of symptoms.7 ,8 Nevertheless, these symptoms or the effect of bronchoconstriction on ventilation could limit athletic performance.

An initial airway response to exercise inducing a …