Exercise-induced asthma: why is it so frequent in Olympic athletes?

In 2008, the PRACTALL initiative, endorsed by the European Academy of Allergy and Clinical Immunology and the American Academy of Allergy, Asthma and Immunology, defined exercise-induced asthma (EIA) as lower airway obstruction and symptoms of cough, wheezing or dyspnea induced by exercise in patients with underlying asthma [1]. The same clinical presentation in individuals without asthma was defined as exercise-induced bronchoconstriction (EIB). However, these definitions are limited by the heterogeneity in asthma expression. In fact, multiple asthma phenotypes exhibiting differences in clinical response to treatment exist and assessment should be multidimensional, including variability in clinical, physiologic and pathologic parameters. Two different clinical phenotypes of asthma in athletes, reflecting different underlying mechanisms, have been recently suggested by Haahtela et al.: the pattern of ‘classical’ asthma, characterized by early onset childhood asthma, methacholine responsiveness, atopy and signs of eosinophilic airway inflammation; and another distinct phenotype with onset of symptoms during sports career, bronchial responsiveness to eucapnic hyperventilation test and a variable association with atopic markers and eosinophilic airway inflammation [2]. A consistent body of evidence has shown that Olympic-level athletes have an increased risk for asthma and allergy, especially those who take part in endurance sports, such as swimming or running, and in winter sports [3]. Data from the first panEuropean study on allergy and asthma in Olympic athletes – the GA2LEN Olympic study – revealed that one in four of the European athletes participating in the Beijing Olympic Games reported chest tightness and wheeze and one out of three reported exercise-induced shortness of breath [GA2LEN Olympic Study Coordinating Centre, Oslo, Norway, Data on File]. Classical postulated mechanisms behind EIA include the osmotic, or airway-drying, hypothesis [4]. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell shrinkage and release of inflammatory mediators that cause airway smooth muscle contraction. However, a proof of concept of this hypothesis would require that all athletes would develop bronchoconstriction at a certain point. This does not happen, suggesting the EIB explanatory model in athletes will probably include the interplay between environmental training factors, including allergens and ambient conditions such as temperature, humidity and air quality, and an athlete’s personal risk factors such as genetic and neuroimmunoendocrine determinants. Genetic susceptibility to EIB has been linked with the gene for the aqueous water channel aquaporin 5. Airway hydration during exercise is mainly dependent on the water movement, following the osmotic force generated by sodium and chloride, through aquaporin channels expressed