Exercise-induced bronchoconstriction (EIB) occurs when the airways narrow as a result of exercise. This condition has been referred to as exercise-induced asthma (EIA); however, this term is no longer preferred. While exercise does not cause asthma, it is frequently an asthma trigger.

It might be expected that people with EIB would present with shortness of breath, and/or an elevated respiratory rate and wheezing, consistent with an asthma attack. However, many will present with decreased stamina, or difficulty in recovering from exertion compared to team members, or paroxysmal coughing from an irritable airway. Similarly, examination may reveal wheezing and prolonged expiratory phase, or may be quite normal. Consequently, a potential for under-diagnosis exists. Measurement of airflow, such as peak expiratory flow rates, which can be done inexpensively on the track or sideline, may prove helpful. In athletes, symptoms of bronchospasm such as chest discomfort, breathlessness, and fatigue are often falsely attributed to the individual being out of shape, having asthma, or possessing a hyperreactive airway rather than EIB.

While the potential triggering events for EIB are well recognized, the underlying pathogenesis is poorly understood. It usually occurs after at least several minutes of vigorous, aerobic activity, which increases oxygen demand to the point where breathing through the nose (nasal breathing) must be supplemented by mouth breathing. The resultant inhalation of air that has not been warmed and humidified by the nasal passages seems to generate increased blood flow to the linings of the bronchial tree, resulting in edema. Constriction of these small airways then follows, worsening the degree of obstruction to airflow. There is increasing evidence that the smooth muscle that lines the airways becomes progressively more sensitive to changes that occur as a result of injury to the airways from dehydration. The chemical mediators that provoke the muscle spasm appear to arise from mast cells. Mouth breathing as a result of decreased nasal breathing also increases lung surface exposure to irritants, pollutants, and allergens, causing neutrophilic inflammation in response to reactive oxygen species formation; research has found that individuals with genetically hindered glutathione counteraction of this oxidative stress are likely at a higher risk of developing EIB.

Exercise-induced bronchoconstriction can be difficult to diagnose clinically given the lack of specific symptoms and frequent misinterpretation as manifestations of vigorous exercise. There are many mimics that present with similar symptoms, such as vocal cord dysfunction, cardiac arrhythmias, cardiomyopathies, and gastroesophageal reflux disease. It is also important to distinguish those who have asthma with exercise worsening, and who consequently will have abnormal testing at rest, from true exercise-induced bronchoconstriction, where there will be normal baseline results. Because of the wide differential diagnosis of exertional respiratory complaints, the diagnosis of exercise-induced bronchoconstriction based on history and self-reported symptoms alone has been shown to be inaccurate and to result in an incorrect diagnosis more than 50% of the time. An important and often overlooked differential diagnosis is exercise-induced laryngeal obstruction (EILO). The latter can co-exist with EIB and is best differentiated using objective testing and continuous laryngoscopy during exercise (CLE) testing.

Objective testing should begin with spirometry at rest. In true exercise-induced bronchoconstriction, the results should be within normal limits. Should resting values be abnormal, then asthma, or some other chronic lung condition, is present. There is, of course, no reason why asthma and exercise-induced bronchoconstriction should not co-exist but the distinction is important because without successful treatment of underlying asthma, treatment of an exercise component will likely be unsuccessful. If baseline testing is normal, some form of exercise or pharmacologic stress will be required, either on the sideline or practice venue, or in the laboratory.

Treadmill or ergometer-based testing in lung function laboratories are effective methods for diagnosing exercise-induced bronchoconstriction, but may result in false negatives if the exercise stimulus is not intense enough.

Field-exercise challenge tests that involve the athlete performing the sport in which they are normally involved and assessing FEV₁ after exercise are helpful if abnormal but have been shown to be less sensitive than eucapnic voluntary hyperventilation.

The International Olympic Committee recommends the eucapnic voluntary hyperventilation (EVH) challenge as the test to document exercise-induced asthma in Olympic athletes. In the EVH challenge, the patient voluntarily, without exercising, rapidly breathes dry air enriched with 5% CO₂ for six minutes. The presence of the enriched CO₂ compensates for the CO₂ losses in the expired air, not matched by metabolic production, that occurs during hyperventilation, and so maintains CO₂ levels at normal.