Exercise-Induced Bronchospasm
Definitions: Exercise-induced bronchospasm (EIB) is defined as a decline in forced expiratory volume in 1 second (FEV 1 ) or peak expiratory flow rate shortly after the onset or cessation of exercise. The terms exercise-induced asthma (EIA) and EIB are often used interchangeably; however, EIA should be reserved for athletes who have a known diagnosis of asthma or asthma symptoms at rest; EIB should refer to athletes who experience symptoms only while exercising. The rationale for the differentiation between the two terms is the difference in treatment with the mainstay of treatment for asthma and EIA being inhaled corticosteroids, which have little to no benefit in EIB. EIB treatment is aimed more at reducing symptoms while the athlete is exercising.
Pulmonary function criteria: Table 37.1 lists the different testing procedures approved by the World Anti-Doping Agency (WADA) and the resulting decrease in FEV 1 that can be used to diagnose EIB. Maximal decrease in FEV 1 usually occurs after 5–8 minutes of vigorous exercise. Pulmonary function tests (PFTs) usually return to baseline 60 minutes after exercise.
TABLE 37.1
Bronchial Provocation Test
Decrease in FEV 1 for Position Test Results
Eucapnic Voluntary Hyperpnea
>10%
Methacholine Aerosol Challenge
>20%
Mannitol Inhalation
>15%
Hypertonic Saline Aerosol Challenge
>15%
Exercise Challenge (field or laboratory)
>10%
Histamine Challenge
>20%
Epidemiology: Approximately 12% of the total population experiences EIB. EIB can be detected in approximately 41% of people with a history of allergic rhinitis; 40%–90% of asthmatics have EIA. EIB and EIA occur equally between both genders and can develop at any age. The rate of EIB is highest among cold weather athletes (skiing) and indoor sports athletes (ice hockey and swimming); increased prevalence in endurance athletes as well
Risk factors: A history of asthma is the biggest risk factor for EIA. For EIB, risk factors include a family history of asthma, allergic rhinitis, personal or family history of atopy, cold weather sports, and sports that require a high ventilation rate (e.g., Nordic skiing, soccer, and distance running).
Mechanism: At present, the exact mechanism of EIB remains unknown, but current understanding of the pathophysiology is that hyperventilation during exercise causes loss of heat and drying of the airways, leading to dehydration of airway cells and increased intracellular osmolarity. This creates an osmotic gradient that stimulates the release of inflammatory mediators including histamines, leukotrienes, and cytokines. These mediators, along with airway drying, cause an exaggerated response that results in EIB. After the completion of exercise, airway cooling reverses as smaller bronchial vessels warm, creating reactive hyperemia; this warming establishes another osmotic gradient that releases more mediators, causing bronchospasm and airway edema, further contributing to EIB.
Triggers: Oral breathing (unlike nasal breathing, which warms the air, oral breathing does not and is more likely to cause cooling of the airways and trigger EIB), dry air, cold air (essentially, colder, drier air will cause more severe symptoms), pollution, and allergens in the air; intense exercise is more likely to trigger EIB (e.g., cross-country skiing, basketball, and running); chemicals such as chlorine in pools and insecticides, pesticides, herbicides, and fertilizers used to maintain fields can trigger EIB.
Clinical signs and symptoms: Can include wheezing, shortness of breath, coughing (usually after exercise), chest tightness, chest pain (usually reported in children), poor athletic performance, and early fatigue compared with peers; symptoms are similar to those that occur in an acute asthma attack. They often resolve when the activity is discontinued. There can be a late-phase response that occurs 4–8 hours after exercise.
Physical examination: May include the following on examination:
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Lungs—wheezing (particularly expiratory phase); may hear rales or rhonchi; wheezing at rest should raise concerns for true asthma
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Skin—signs of atopic disease such as eczema
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Nose—enlarged and boggy turbinates
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Throat—cobblestoning and enlarged tonsils
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Sinus—tenderness on pressure
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Testing: EIB used to be a disease classically diagnosed and treated by self-reported symptoms. Recent studies have shown a lack of specificity and sensitivity based on symptoms, emphasizing the need for objective testing. Following are the different diagnostic tests that are commonly used to diagnose EIB.
Types of testing:
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PFT can be performed using exercise challenge tests or bronchial provocation testing (where the patient inhales a substance designed to induce bronchoconstriction). Spirometry should initially be performed at rest and then immediately after exercise to establish baselines and compare results. Testing should be ideally performed for at least 8 minutes, allowing the athlete to reach >90% of peak heart rate by 2 minutes and maintaining the same for another 6 minutes.
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The International Olympic Committee (IOC) recommends that FEV 1 be measured at least 3 minutes after the challenge and accepts a 10% decline in FEV 1 as an indication for use of a beta-2 agonist. At present, the IOC requires prior notification for the use of a beta-2 agonist; the notification must be accompanied by objective evidence that justifies the need for medication. The IOC accepts the following tests and the associated decrease in FEV 1 for diagnosing EIB and allowing an athlete to use a beta-2 agonist: eucapnic voluntary hyperpnea (EVH) test (10%), exercise challenge test (10%), or hyperosmolar aerosis test (15%). EVH testing is performed using dry air containing 5% carbon dioxide. Hyperosmolar aerosis can be performed using either hypertonic saline or inhaled powdered mannitol (not available in the United States).
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Sport-specific field testing (e.g., having a hockey player skate on ice till symptoms develop) is ideal when resources are allow. Following are examples of clinical/laboratory testing that can replace field testing:
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Free running
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The patient runs either indoors or outdoors. This can also be performed in a stairwell if space is limited.
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Advantages—Most likely to induce symptoms, requires minimal cardiovascular (CV) monitoring
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Disadvantages—Depending on the season, difficult to control environmental factors such as temperature and humidity and may not trigger EIB in all patients
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Treadmill
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Advantages—CV and pulmonary monitoring can be performed during the workout. Workload can be standardized.
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Disadvantages—Expensive equipment needed; less likely to induce EIB because it is indoors and factors such as temperature, humidity, and pollutants are more controlled.
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Bicycle ergometer
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Advantages—Workload can be easily maintained. CV monitoring is the easiest.
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Disadvantages—Least likely to produce EIB symptoms; need for expensive equipment
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Bronchial provocation testing
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The patient inhales a substance designed to induce bronchoconstriction. It may be used as primary diagnostic test or when exercise challenge is equivocal. See Table 37.1 for types of testing and criteria for positive test.
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Other testing
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Skin testing—probably the most useful because there is a strong correlation between allergies and EIB/EIA
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Computed tomography (CT) of sinuses if there is a concern for chronic sinusitis causing the symptoms
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Chest radiograph—may show signs of underlying lung disease
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Echocardiogram—if a CV abnormality is a possible cause of the symptoms
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Medications and testing: When performing PFT, certain medications must be avoided or stopped so as to not confound the testing and produce false-negative results.
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Inhalers—Albuterol and other beta-agonists should not be used 24 hours before testing.
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Inhaled steroids—stop 1 week before testing
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Theophylline—stop 24 hours before testing
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Leukotriene receptor antagonist—stop 24 hours before testing
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Cromolyn sodium/nedocromil sodium—stop 24 hours before testing
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Antihistamines—do not need to be stopped for PFT but need to be stopped 72 hours before skin testing
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Differential diagnosis:
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Vocal cord dysfunction (VCD)
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VCD can produce respiratory symptoms when the ventilatory rate rises; usually have inspiratory wheezing and/or stridor as opposed to EIB and asthma, which primarily produces expiratory wheezing. The stridor in VCD occurs because of paradoxical closure of the vocal cords. Patients complain of difficulty “getting air in” and difficulty in breathing. VCD is frequently misdiagnosed as asthma and warrants special consideration in the diagnosis of EIB.
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The diagnosis of VCD is often made based on clinical presentation. Flow-volume loop is performed while the patient is symptomatic; flattening of the inspiratory loop can be seen. Laryngoscopy, which allows visualization of vocal cord adduction on inspiration (classically seen as adduction of the anterior two thirds of the vocal cords with a posterior diamond-shaped chink remaining open), is considered to be the gold standard of diagnostic testing for VCD. Treatment is reassurance, education, and speech therapy.
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Gastroesophageal Reflux Disease (GERD)
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May present with atypical symptoms such as chronic cough and wheezing
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Consider in athletes who have symptoms of GERD or worsening symptoms of EIB associated with regurgitation, large meals, or alcohol
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Swimming-Induced Pulmonary Edema (SIPE)
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SIPE presents with shortness of breath and cough during or immediately after swimming with associated evidence of pulmonary edema. Spirometry reveals an acute restrictive pattern, with changes lasting up to 1 week.
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Other
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General deconditioning
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Chronic lung disease including asthma
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CV disorders
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Prevention and treatment:
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Pharmacologic
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Inhaled beta-adrenergic agonists: Prevention and treatment can be achieved by using a short acting beta-2 agonist (e.g., albuterol) inspired approximately 15–30 minutes before exercise; this can often prevent or reduce the symptoms of EIB. Should ideally be performed using a spacer with the inhaler to maximize the concentration of the medicine; only albuterol in an aerosolized form has been shown to be effective in EIB and asthma ( Fig. 37.1 ).
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