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🫁 Exercise-Induced Bronchoconstriction Simulator

A model of exercise-induced bronchoconstriction demonstrating the role of airway cooling and drying, as well as the prophylactic use of beta-agonists.

Asthma & Inhaler Therapy2DModerate60 FPS
exercise-induced-bronchoconstriction-simulator ↗ Open standalone

Warm, Humid Airway at Rest

A resting airway conditions every breath to near body temperature.

  • 6–8: Resting minute ventilation (L/min)
  • ~37°C: Airway mucosal temp (fully conditioned)
  • 100%: Baseline FEV1 (of predicted)
  • 100%: Airway caliber (baseline lumen)

Nasal conditioning of air

Nose warms and humidifies air before it reaches airways.

Periciliary fluid layer

A thin water film keeps mucosa moist and stable.

Relaxed smooth muscle tone

Bronchial smooth muscle sits at resting, unconstricted tone.

Exercise Onset — Rapid Cooling and Drying

High ventilation overwhelms the airway's ability to condition air.

  • 100–150: Peak minute ventilation (L/min in athletes)
  • −3 to −5°C: Airway surface cooling (lower airway temp)
  • Bypasses: Mouth breathing effect (nasal humidification)
  • Rising: Water loss rate (per breath surface flux)

Ventilation exceeds conditioning capacity

Fast deep breaths outpace airway warming and humidifying.

Evaporative cooling of mucosa

Evaporation pulls heat and water from airway lining.

Mouth breathing bypass

Oral breathing skips the nose's conditioning entirely.

Osmotic Mucosal Stress and Mast Cell Degranulation

Water loss concentrates airway surface fluid, triggering mediator release.

  • Rises: Periciliary osmolarity (as water leaves surface)
  • Hyperosmolar: Mast cell trigger (stress signal)
  • Histamine,: Key mediators (leukotrienes, prostaglandins)
  • 3–8 min: Onset window (into exercise)

Osmotic theory of EIB

Dehydrated airway surface fluid becomes hyperosmolar quickly.

Mast cell degranulation

Hyperosmolarity triggers mast cells to release mediators.

Smooth muscle activation

Released mediators bind receptors on bronchial smooth muscle.

Bronchoconstriction Peak — Post-Exercise Airway Narrowing

Airway caliber falls sharply minutes after exercise stops.

  • 10–15%: Typical FEV1 drop (from baseline)
  • >20%: Severe EIB threshold (FEV1 fall)
  • 5–20 min: Peak timing (post-exercise)
  • 30–60 min: Spontaneous recovery (typical window)

Smooth muscle contraction

Airway smooth muscle bands tighten, narrowing the lumen.

Symptom presentation

Wheeze, chest tightness, and dyspnea emerge post-exercise.

Refractory period

A brief window of reduced response can follow.

Pre-Treated with SABA — Blunting the Response

A short-acting beta-agonist taken early prevents most narrowing.

  • 15 min: Dosing window (before exercise)
  • 2–4 h: Protection duration (typical coverage)
  • ~80%: FEV1 drop reduction (with prophylaxis)
  • β2 agonist: Mechanism (smooth muscle relaxation)

Prophylactic timing

Dosing 15 minutes ahead maximizes protective effect.

Receptor-level protection

β2 receptors keep smooth muscle relaxed despite mediators.

Limits of prophylaxis

Daily use can blunt long-term protective effect.

⚙ Under the hood

A model of exercise-induced bronchoconstriction demonstrating the role of airway cooling and drying, as well as the prophylactic use of beta-agonists.

CanvasBiomedicine

2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install

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