Etiology of exercise-induced asthma: physical stress-induced transcription

Abstract

Exercise-induced asthma (EIA) occurs with a high prevalence in both asthmatic and nonasthmatic individuals. Although understanding of the functional genomics (proteomics) in sports medicine remains limited, this review focuses on immunologic changes as reflected in transcriptional regulation in respect to EIA. Studies demonstrated that leukotrienes play a significant role in EIA. Exercise increases the distribution of leukotrienes and influences the leukotriene transcription pathway; it could be shown that the genes ALOX5 and ALOX5AP encoding for 5-lipooxygenase (5-LO) and 5-lipoxygenase-activating protein (FLAP) as well as activators for 5-LO, p38 -mitogen-activated protein kinase (MAPK), and others, are enhanced after exercise in healthy subjects. Possibly EIA is triggered via leukotriene release if a predisposition or other conditions (eg, epithelial injury and repair) are present. Furthermore, exercise influences transcription factors such as nuclear factor-kappa B (NF-jB), activator protein-1 (AP1), cytokines, and chemokines and promotes cellular responses linked to EIA, which are possibly able to modify further the incidence or the severity of EIA.