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KEY POINTS
■ Exercise-induced bronchospasm is common among athletes and asthmatic patients but underrecognized by both patients and clinicians.
■ Although probably multifactorial in cause, IB results from airway drying, hyperosmolar cellular changes, and mediator-induced bronchoconstriction.
■ Clinicians should distinguish between patients with isolated IB and patients with persistent asthma in whom exercise is just one trigger.
■ Although a preliminary diagnosis can be made in patient with bronchoconstrictive symptoms after exercise, exercise bronchoprovocative testing helps to verify diagnosis.
■ Nonpharmacologic treatment includes proper warm-up and cooldown, wearing a face mask, and short-burst exercise. Short-acting beta2-agonists and leukotriene antagonists are most effective in reducing bronchospasm. Patients with persistent asthma should receive inhaled corticosteroids.
Exercise-induced bronchospasm (EIB) is defined as acute, transient airway narrowing that occurs during and most often after exercise.1 The bronchospasms peak 5 to 10 minutes after stopping exercise and usually resolve in another 20 to 30 minutes.2 EIB is objectively defined as a greater than 10% decline in forced expiratory volume in the first second of expiration (FEV1) after exercise provocation.1 The National Asthma Education and Prevention Program Expert Panel Report 3 (EPR3) describes a 15% decrease in peak expiratory flow or FEV1 from pre-exercise baseline as compatible with EIB.2
Although the terms exercise-induced bronchospasm and
exercise-induced asthma (EIA) are sometimes used interchangeably, some authors suggest a distinction. EIB may focus primarily on the acute bronchospastic component, whereas EIA may incorporate the inflammatory component and patient signs and symptoms (dyspnea, wheezing, chest tightness, and cough).3 Patients may experience either isolated exercise-induced bronchospasm or chronic asthma in which exercise is one of many triggers. Clinicians need to distinguish patients in whom symptoms are triggered only by exercise (EIB) from patients with chronic asthma in whom EIB is also present.4
Exercise-induced bronchospasm is a treatable disorder but may be underrecognized by patients and clinicians. The prevalence of EIB and EIA in athletes ranges from 10% in male track and field athletes to 55% in competitive figure skaters. Variability in prevalence data may be a result of varying definitions and the use of different diagnostic techniques.5
PATHOPHYSIOLOGY
The pathogenesis of EIB is multifactorial and not completely understood. During exercise, large volumes of air are exchanged that are cooler and dryer than lung tissue. This overwhelms the ability of the upper airway to warm air effectively, so air that is cool and dry (relative to the body) reaches the distal airways.1
Several mechanisms have been proposed as to how this cool, dry air may provoke EIB. Initially, researchers hypothesized that airway cooling may stimulate receptors in the airways, causing bronchial constriction through a reflex pathway.5 The thermal hypothesis proposed that airway cooling is followed by rapid rewarming, which leads to a reactive hyperemia of the bronchial microvasculature together with edema of the airway wall, causing airway narrowing.6
However, neither airway cooling nor airway rewarming appears to be necessary for EIB to occur. Some studies have shown that severe EIB can occur under conditions of inspiring hot dry air, leading some researchers to question the role of cold air in the pathogenesis.6
The osmotic hypothesis suggests that water loss from airways is a better predictor of EIB than heat loss and that mucosal dehydration is the essential pathophysiologic event for EIB. This theory suggests that as water evaporates from the airways, their surfaces become hyperosmolar, providing an osmotic stimulus for water to move from airway cells that results in cell volume loss. After cell shrinkage, regulatory cellular volume increase may lead to the release of inflammatory mediators from mast cells (including prostaglandin F2 and histamine). These inflammatory mediators cause the smooth muscles of the airways to contract, producing bronchospasm.6
PRESENTATION AND INITIAL EVALUATION
Common signs and symptoms in the patient with EIB include dyspnea, wheezing, cough, and chest tightness associated with exercise. More subtle symptoms include fatigue and poor performance for conditioning level (complaint of being "out of shape" and deconditioned.)1 Symptoms are provoked by 6 to 15 minutes of continuous exercise of at least 80% maximum workload.7
The evaluation of EIB begins with a thorough history and physical examination. A history of cough, shortness of breath, chest tightness, wheezing, or endurance problems during exercise in a patient with normal physical findings at rest suggests EIB. Resting peak expiratory flow or office spirometry results will be normal if the patient has isolated EIB.
Diagnosing EIB from the patient's self-report of symptoms may not be completely reliable.8 Some patients who do not report symptoms test positive on exercise provocation, and some patients who do report symptoms test negative on exercise provocation. Use of history alone has been shown both to underdiagnose and to overdiagnose the problem. An exercise challenge test can be used to help establish the diagnosis.2
When to test depends on several factors, including certainty of preliminary diagnosis and burden of testing on the patient. If EIB is strongly suspected and the patient has comorbid disease or financial reasons why testing would be burdensome, a bronchodilator trial based on clinical grounds alone may be indicated. Improvement in exercise-related symptoms with bronchodilator trial may help confirm the diagnosis. However, if the diagnosis of EIB is uncertain and the patient has no medical or financial reasons to limit testing, clinicians should use formal testing for confirmation.