EXERCISE-INDUCED ASTHMA

Authors
Citation
Ra. Tan et Sl. Spector, EXERCISE-INDUCED ASTHMA, Sports medicine, 25(1), 1998, pp. 1-6
Citations number
28
Categorie Soggetti
Sport Sciences
Journal title
ISSN journal
01121642
Volume
25
Issue
1
Year of publication
1998
Pages
1 - 6
Database
ISI
SICI code
0112-1642(1998)25:1<1:>2.0.ZU;2-W
Abstract
Exercise-induced asthma (EIA) is characterised by transient airway obs truction occurring after strenuous exertion. A fall of 10% or more in the FEV1 after exercise is diagnostic. Inhalation of large volumes of dry, cold air during exercise leads to loss of heat and water from the bronchial mucosa and airway cooling and drying. Proposed mechanisms f or bronchoconstriction include: (i) mucosal drying and increased osmol arity stimulating mast cell degranulation; and (ii) rapid airway rewar ming after exercise causing vascular congestion, increased permeabilit y and oedema leading to obstruction. EIA symptoms start after exercise , peak 8 to 15 minutes after exercise and spontaneously resolve in abo ut 60 minutes. A refractory period of up to 3 hours after recovery, du ring which repeat exercise causes less bronchospasm, has been observed . The amount of ventilation and the temperature of inspired air are im portant factors in determining the severity of EIA. Greater ventilatio n and cold, dry air increase the risk for EIA. Education regarding the nature and management of EIA is important not only for asthmatics but also for their families and coaches. With the proper precautions and workout techniques, there is no limit to what individuals with asthma can achieve in sports. Prevention is the main objective in managing EI A. Nonpharmacological measures include warming up before vigorous exer tion, covering the mouth and nose in cold weather, exercising in warm, humidified environments if possible and warming down after exercise. Aerobic fitness and good control of baseline bronchial reactivity also help to diminish the effects of EIA. Inhaled beta-agonists are the me dications of choice in EIA prophylaxis. Inhaled sodium cromoglycate (c romolyn sodium) or nedocromil may also be used. Agents that may be add ed if inhaled beta-agonists or sodium cromoglycate are not adequate in clude anticholinergic agents (such as ipratropium bromide), theophylli ne, calcium channel blockers, alpha-agonists, antihistamines and oral beta-agonists. Newer agents include antileukotriene agents, inhaled he parin and inhaled furosemide (frusemide).