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Mini Symposium 5: Allergy and sports

Background: It is well-known that exercise can induce bronchial asthma in predisposed individuals. Mechanisms of exercise-induced asthma (EIA) are less known and the question is much debated. Clark et al. demonstrated that vigorous exercise can induce gastroesophageal reflux (GER) in normal subjects. Therefore, the trigger of EIA could be an abnormality of gastroesofageal tract, as it is demonstrated by our previous studies too. Moreover, patients with EIA reported, besides the asthma symptoms, also other peculiar symptoms, such as heartburn, pyrosis, epigastric pain, and regurgitation, alone or in any combination. These increase after exercise and can induce or worsen the arising of the EIA symptoms. The aim of our study was devoted to evaluate further the role of GER in EIA, and the efficacy of an antacid pretreatment so to prevent the development of asthma symptoms induced by exercise. Methods: Ten patients with EIAwere selected: six males and four females aged between 14 and 36 years. The study design included the upper bowel endoscopy and the lung function evaluated by the peak expiratory flow (PEF). This was measured before and after exercise, with and without the pretreatment with the aluminium hydroxide and magnesium hydroxide. Results: The results of the upper bowel endoscopy showed that all patients had the lower oesophageal sphincter incompetence associated with different gastroesophageal abnormalities. Two patients were positive for Helicobacter pylori. This is to consider adequately too. The PEF values, measured after exercise and without antacid treatment, showed a significant decrease (P< 0.0001) of lung function (84.82 8.90%) when they were compared to the basal values. The PEF measurements, evaluated after exercise and after the administration of antacid drug (97.74 3.85%) did not show any significant difference (P< 0.09) with the basal values. But they were significantly higher (P1⁄4 0.001) than PEF values determined after exercise and without antacid treatment. Conclusions: Ourresults indicatethat themechanisms, underlying exercise-induced asthma can be caused by a GER through a neural reflex triggered by gastric acid in the lower oesophageal tract. This neural reflex induces the release of neurokinins from sensory nerves. These peptides increase or amplify inflammation and cause bronchoconstriction.