Fitness Exercise Science · Supplementary · from Fitness Exercise Science

Case 2: Exercise-Induced Bronchoconstriction

Patient Presentation

Demographics: 16-year-old female high school cross-country runner

Chief Complaint: "I can't breathe during my races and my times are getting slower."

History of Present Illness: Sophia is a competitive cross-country runner who has noticed increasing difficulty breathing during the last mile of her 5K races over the past cross-country season (September through November). She describes a sensation of "chest tightness and wheezing" that begins approximately 8-10 minutes into sustained hard running and peaks about 5 minutes after she finishes racing. The symptoms resolve spontaneously within 30-45 minutes of stopping exercise.

She reports that the symptoms are significantly worse on cold, dry days and during early morning practices. She denies symptoms at rest, during warm-up, or during low-intensity training runs. She does not experience nocturnal cough, symptoms with allergen exposure, or any other triggers besides exercise. Her coach has noted audible wheezing at the finish line.

Her race times have declined by approximately 90 seconds over the season, and she has become anxious about competition. She has tried "breathing through her nose" and other self-directed strategies without improvement. She has no prior diagnosis of asthma and takes no medications. She has been otherwise healthy.

Past Medical History:

• Allergic rhinitis (seasonal, mild; spring pollen)
• Eczema in childhood (resolved by age 8)
• No prior asthma diagnosis
• No hospitalizations

Medications:

• Cetirizine 10 mg daily during spring allergy season
• No inhalers or asthma medications

Social History:

• 11th grade high school student
• Competitive cross-country runner (3 years)
• No tobacco, alcohol, or drug use
• No pets at home
• Lives in a northern climate with cold, dry autumn weather

Family History:

• Mother: Asthma (mild, well-controlled)
• Father: Healthy
• Brother: Eczema

Physical Examination

• Vital Signs: BP 108/64 mmHg, HR 56 bpm, RR 14, Temp 98.4°F, SpO2 99%, BMI 20.1 kg/m²
• General: Fit, athletic female in no distress (examined at rest)
• HEENT: Mild inferior turbinate edema bilaterally; pale, boggy nasal mucosa; Dennie-Morgan lines under eyes; no nasal polyps
• Cardiovascular: Bradycardia (athletic); regular rhythm; no murmurs
• Respiratory (at rest): Clear to auscultation bilaterally; no wheezing; good air movement; normal inspiratory-to-expiratory ratio
• Chest: No accessory muscle use; no pectus deformity
• Skin: Mild xerosis antecubital fossae bilaterally; no active eczema

Workup and Results

Laboratory Studies:

Eucapnic Voluntary Hyperventilation (EVH) Challenge:

Imaging/Additional Studies:

• Chest X-ray: Normal; no hyperinflation or infiltrates
• FeNO (fractional exhaled nitric oxide): 38 ppb (elevated; > 25 ppb suggestive of eosinophilic airway inflammation)
• Exercise field test: Audible wheezing at 10 minutes of continuous running in cold air; SpO2 maintained at 96%

Clinical Image

Pathophysiology of exercise-induced bronchoconstriction (EIB) demonstrating the osmotic theory: increased ventilation during exercise causes airway surface liquid evaporation, raising mucosal osmolarity, which triggers mast cell degranulation and release of bronchoconstricting mediators (histamine, leukotrienes, prostaglandins), leading to bronchial smooth muscle contraction. Source: Educational illustration.

Diagnosis

Exercise-Induced Bronchoconstriction (EIB) with Atopic Diathesis (ICD-10: J45.990)

Key Diagnostic Criteria:

• ≥ 10% fall in FEV1 from baseline following EVH challenge (patient: 21% fall — diagnostic and moderate severity)
• Symptoms isolated to sustained vigorous exercise (> 6-8 minutes)
• Complete reversibility with bronchodilator
• Atopic background (allergic rhinitis, childhood eczema, elevated IgE, eosinophilia, elevated FeNO) suggesting underlying airway inflammation
• Normal baseline spirometry (characteristic of EIB)

Treatment Plan

1. Pre-exercise Short-Acting Beta-Agonist (SABA): Albuterol MDI 2 puffs 15-20 minutes before exercise; demonstrate proper inhaler technique with spacer; effective for 2-4 hours
2. Daily Controller Therapy: Given elevated FeNO and atopic markers suggesting underlying eosinophilic inflammation, initiate low-dose inhaled corticosteroid (fluticasone 44 mcg 2 puffs BID) for 4-6 weeks, then reassess
3. Warm-Up Protocol: Prescribe structured high-intensity interval warm-up (7-8 brief sprints over 20-30 minutes before competition) to induce refractory period — evidence-based strategy that reduces EIB severity by 40-50%
4. Environmental Strategies: Wear a heat-exchange mask or buff during cold-weather training to warm and humidify inspired air; when possible, schedule intense efforts during warmer parts of the day
5. Consider Leukotriene Receptor Antagonist: Montelukast 10 mg daily as adjunctive therapy if ICS + SABA insufficient; particularly useful given her leukotriene-mediated pathophysiology
6. Nasal Treatment: Treat allergic rhinitis with intranasal corticosteroid (fluticasone nasal spray) — nasal inflammation worsens lower airway responsiveness through the unified airway model
7. Anti-Doping Compliance: Educate patient and family that albuterol (inhaled, up to 1600 mcg/24 hours) and ICS are permitted by WADA/USADA without a TUE; document diagnosis in medical record
8. Follow-up: Repeat EVH challenge or spirometry with exercise challenge in 6-8 weeks; monitor FeNO as a marker of controller therapy response

Key Learning Points

• Exercise-induced bronchoconstriction (EIB) affects 10-50% of elite athletes (highest prevalence in winter sport and endurance athletes) and is underdiagnosed because baseline spirometry is typically normal
• The eucapnic voluntary hyperventilation (EVH) test is the gold standard for EIB diagnosis, recommended by the IOC; a ≥ 10% fall in FEV1 is diagnostic — exercise testing in the clinic often lacks sufficient ventilatory demand to provoke EIB
• The osmotic theory of EIB posits that water loss from the airway surface during hyperventilation creates a hyperosmolar environment that triggers mast cell mediator release — this explains why cold, dry air exacerbates symptoms
• The refractory period phenomenon (reduced EIB severity for 1-3 hours after an initial bronchoconstrictive episode) can be therapeutically exploited through structured high-intensity interval warm-ups
• EIB with underlying atopic inflammation (elevated FeNO, eosinophilia) responds better to inhaled corticosteroids than EIB without atopy, making FeNO measurement clinically useful for guiding controller therapy decisions

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