Exercise-induced bronchospasm (EIB)

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist, Assistant Professor at NSU

The prevalence of exercise-induced bronchoconstriction (EIB) is 10% in the general population, up to 90% of those with asthma, and 50% of those with allergic rhinitis. Asthma is the most common chronic respiratory disease, affecting up to 10% of adults and 30% of children (JACI, 2011).

Definition

Exercise-induced (EI) asthma and EI bronchospasm are not the same. In 2007, the AAAAI Work Group made a distinction between exercise-induced (EI) asthma and EI bronchospasm:

- EIA: exercise induces symptoms of asthma in patients who have asthma (90% of patients)
- EIB: exercise induces bronchospasm in patients without chronic asthma, for example, an elite athlete

Some old synonyms include exercise-induced airway narrowing, thermally induced asthma and "locker room cough."

The all-encompassing term is exercise-induced (EI) hypersensitivity syndromes which includes EI-asthma, EI-bronchoconstriction, EI-rhinitis, EI-anaphylaxis and EI-urticaria.

Exercise is one of the many stimuli which can produce airway obstruction in patients with asthma. In fact, physical activity is the second leading cause of airway constriction after upper respiratory tract infections.

Exercise-induced bronchospasm is an airway obstruction that occurs 5-15 minutes after physical exertion, thus the name "locker room cough."

EIA symptoms start after exercise, peak 8 to 15 minutes after exercise and spontaneously resolve in 60 minutes. A refractory period of up to 3 hours after recovery, during which repeat exercise causes lessbronchospasm, has been observed.

EIA is diagnosed by a 15% decrease in FEV1.

Exercise-induced urticaria or anaphylaxis are not related to EIA. Exercise-induced urticaria is extremely rare, only 500-1000 cases have been reported.

Exercise-induced bronchospasm (EIB) (click to enlarge the image):



Epidemiology

EIB affects:

90% of asthmatics
40-50% of patients with allergic rhinitis
3-13% of the general population
10-20% of athletes
50% of cold weather athletes
23% of summer sport athletes

90% of patients with asthma and 40 of people with allergic rhinitis have EIB. However, many patients have bronchospasm only during exercise. One study found unrecognized EIB in 29% of athletes.

Aerobic exercise (soccer) is much more prone to induce EIB than anaerobic exercise (weight lifting).

Asthmogenic sports (endurance):
- basketball
- cycling
- running
- soccer
- hockey

Less asthmogenic sports:
- baseball
- football
- swimming
- weight lifting

EIA is most frequently seen in children and young adults because of their high levels of physical activity.

The sequence of events in EIA is characteristic:

1. Airways dilate during exercise (FEV1 increases by 5% in normal people).
2. When the exercise is over, airway obstruction begins and progresses until it reaches a peak in 5-10 minutes
3. Spontaneous resolution occurs in 30 minutes.

The tendency toward spontaneous remission is a hallmark of EIA: one needs only to reverse the acute event and the patient will then remain free of symptoms.

Pathogenesis

In elite athletes with EIA, neutrophils play a more important role than eosinophils (major culprit in non-EI asthma). Both nitric oxide (NO) and leukotrienes have been linked to thermally induced asthma.

There are 2 theories for EIA pathogenesis: thermal and osmotic.

Osmotic theory has been gaining a wider acceptance in recent years.

Thermal hypothesis, there is no role for biochemical mediators. Mnemonic: dry and cool:

1. Dry airway.
Air movement leads to drying of the airway which results in increased perfusion in an attempt to combat the drying, thus leading to airway edema andbronchospasm.

2. Cool airway.
Air movement leads to a decreased temperature of the airway which triggers increased perfusion in an attempt to heat the airway, thus leading tobronchospasm.

Osmotic theory: airway cooling leads to mucosal drying and increased osmolarity which stimulates mast cell degranulation. Mediators play a key role in osmotic theory in contrast to thermal theory. Leukotrienes have a significant effect on the microcirculation. Leukotriene D4 receptor antagonists (montelukast, Singulair) and 5-lipoxygenase synthesis inhibitors prevent EIB.

Dr. Anderson introduced the osmotic theory and has developed a mannitol-based method to test for EIB. Methacholine is more sensitive than mannitol for evaluation of bronchial hyperresponsiveness in children with asthma http://goo.gl/Dh0m

Diagnosis

Exercise-induced asthma can be diagnosed by history only and formal testing is usually required only in competitive athletes.

Points in the patient history:
- Onset during or after exercise
- EIB not affect first 5 minutes of exercise
- Symptoms duration longer than 5 minutes

Testing for EIA
- FRAST: free running asthma screening test
- Treadmill exercise test
- Cycling
- Hyperventilation protocol - most sensitive and specific for elite athletes
- Mannitol protocol (not yet approved in the U.S)

FRAST

A simple screening test in children:
1. Establish a baseline PEF.
2. Have the child run continuously for 7 minutes (same duration as treadmill exercise test). Modified version: have the child run until he/she has symptoms.
3. Check PEF, more than 15% decrease in PEF is diagnostic of EIA.

Treadmill exercise test for EIA

This is the most commonly used test. The setup is similar to the widely used Bruce protocol for exercise cardiac stress test but the maximum heart rate is achieved faster, within 2 minutes. The goal is HR more than 90% of maximum predicted value for age: 220 - age = predicted maximum heart rate. For example, a 40-year-old's predicted maximum heart rate is 220 - 40 = 180 beats/minute.

Before the exercise challenge, the patient's baseline pulmonary function should be obtained, preferably FEV1, or less ideally, PEF.

A baseline FEV1 of less than 60% is an absolute contraindication to a treadmill exercise test for EIA. A baseline FEV1 of less than 70% is a relative contraindication. Consider CAD and 12-lead EKG monitoring in patients older than 40 years of age.

The athlete exercises on a treadmill until heart rate reaches 90% ff the maximum predicted heart rate. This is maintained for 7 minutes (similar duration to RAST).

After the exercise, FEV1 is measured at 5, 10, 15, 20 and 30 minutes and then compared with the baseline measurements.

A decrease of 10% from baseline is abnormal but not diagnostic of EIA. A decrease of 15% from baseline is diagnostic of EIA.

Eucapnic hyperventilation (EHV)

This is the "new" test. It is preferred in competitive athletes but is more difficult to perform.

The US Olympic Committee requires a positive challenge test to be documented for an athlete to qualify for the use of bronchodilators.

Exercise-induced dyspnea differential diagnosis includes exercise-induced vocal cord dysfunction (EIVCD), exercise-induced laryngomalacia (EIL) and more (http://buff.ly/1jzVPHS).

Management

Non-pharmacological treatment:

- warm-up
- cool-down
- breath through the nose

Pharmacological treatment

Mnemonic for drugs used for treatment of EIB - CLIMB:

Cromolyn
Leukotriene receptor antagonist (LTRA), montelukast
Inhaled steroids (ICS)
Mast cell stabilizers other than cromolyn
Beta-2 agonists, albuterol

Adrenergic receptor agonists have been the agent of choice for acute asthma symptoms since the first reported use of “adrenal substance” for acute asthma in 1900 in JAMA.

The usual treatment of mild isolated EIB is a short-acting bronchodilator taken 15-30 minutes before exercise. The medication should be accompanied by warm-up and cool-down and nasal breathing to attenuate the symptoms. Beta 2-agonists are the most effective agents for EIB. Intermittent use is recommended to avoid tolerance or decreased effectiveness with daily regular use. Tolerance to beta 2-agonists is not prevented by concomitant use of inhaled corticosteroid. Leukotriene inhibitors (LTRA) and mast cell stabilizers can be useful in EIB but are less effective than beta 2-agonists.

Controller medication (listed above) are required in EIA.

Do inhaled beta-agonists have a "doping" effect in non-asthmatic competitive athletes?

No. In 17 of 19 randomized placebo-controlled trials in non-asthmatic competitive athletes, performance-enhancing effects of the inhaled beta (2)-agonists formoterol, salbutamol (albuterol), salmeterol and terbutaline could not be proved. In contrast to inhaled beta(2)-agonists, oral administration of salbutamol (albuterol) seems to be able to improve the muscle strength and the endurance performance. There appears to be no justification to prohibit inhaled beta(2)-agonists from the point of view of the ergogenic effects.

In patients with asthma and chronic productive cough, polymorphonuclear (PMN) neutrophil leukocytes in sputum suggest:

(A) infection
(B) GERD
(C) presence of a foreign body
(D) exercise-induced asthma
(E) extrinsic asthma

Correct answers: A, B, C

ATS practice guideline: exercise-induced bronchoconstriction:



References

An official American Thoracic Society clinical practice guideline: exercise-induced bronchoconstriction. Am J Respir Crit Care Med. 2013 May 1;187(9):1016-27. doi: 10.1164/rccm.201303-0437ST.
http://www.ncbi.nlm.nih.gov/pubmed/23634861
Chapter 72 - Exercise-Induced Airway Narrowing. Adkinson: Middleton's Allergy: Principles and Practice, 6th ed.
Recognition and Management of Exercise-Induced Bronchospasm. AFP, 2003.
Exercise-Induced Asthma. eMedicine, 2007.
Exercise-induced asthma. Sports Med. 1998 Jan;25(1):1-6.
Identifying exercise-induced bronchospasm. Postgraduate Medicine, 2004.
Do inhaled beta(2)-agonists have an ergogenic potential in non-asthmatic competitive athletes? Sports Med. 2007;37(2):95-102.
Exercise-induced hypersensitivity syndromes in recreational and competitive athletes: a PRACTALL consensus report (what the general practitioner should know about sports and allergy). Schwartz LB, Delgado L, Craig T, Bonini S, Carlsen KH, Casale TB, Del Giacco S, Drobnic F, van Wijk RG, Ferrer M, Haahtela T, Henderson WR, Israel E, Lötvall J, Moreira A, Papadopoulos NG, Randolph CC, Romano A, Weiler JM. Allergy. 2008 Aug;63(8):953-61.
Solis-Cohen S. The use of adrenal substance in the treatment of asthma. JAMA. 1900;34:1164.
Long-acting β-agonists and exercise. Miles Weinberger. JACI, Volume 122, Issue 2, Pages 251-253 (August 2008).
The elite athlete: Yes, with allergy we can. Sergio Bonini, MD, Timothy Craig, DO. JACI, Volume 122, Issue 2, Pages 249-250 (August 2008).
ACAAI 2008: Exercise-Induced Asthma. Medscape, 01/2009.

Related reading

49-year-old man with childhood asthma who was told he would never be able to do exercise runs a marathon every day for a year. CNN, 2011.
My EIB Journal from ACAAI - exercise-induced bronchoconstriction (EIB)
Exercise-induced bronchoconstriction - Am Fam Physician 2011 review.
New Insights Into Exercise-induced Bronchoconstriction: syndrome caused by increased production of eicosanoids? Medscape, 2012.
Asthma remains the most common health problem among elite athletes. "Regular, moderate exercise can improve your immune system, which can also help avoid asthma attacks". BMJ, 2012.

PowerPoint Presentations

Exercise-induced asthma. Dr Pascale Kippelen.
Exercise-induced Bronchospasm. Wayne R. Lamarre.

Published: 08/02/2008
Updated: 04/20/2012

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