Exercise-induced asthma: is there space for late-phase reactions?

Abstract

EDITORIALExercise challenge provokes bronchoconstriction in the majority of asthmatics. The reaction is particularly frequent in childhood, with an estimated prevalence of 70-90% in asthmatic children, because of the high level of physical activity in this age group [1,2]. Bronchoconstriction is maximal 5-10 min after the challenge and tends to a complete recovery within 30-90 min, depending on the degree of the initial response. Although the topic has been extensively published, there are still diverse opinions about the existence of an exercise-induced late asthmatic response. Mechanisms of exercise-induced asthmaThe mechanisms of exercise-induced asthma (EIA) are not completely clear, and there are controversies about the precise nature of the stimuli responsible for inducing bronchoconstriction [3]. This contributes to maintaining the debate on the occurrence of late-phase reactions (LPR). The determinants of the bronchoconstrictor response are most likely the temperature and the water content of the inspired air and the minute ventilation during exercise; the inflammation of the airways and the underlying degree of airway responsiveness play a further contributory role.MCFADDEN and co-workers [4] have provided evidence that the respiratory heat loss during exercise, which causes airway cooling followed by rapid rewarming, may act as the appropriate stimulus for EIA. The rapid resupply of heat to the airways may cause asthma by means of an exaggerated hyperaemia and bronchial oedema [4]. There are many studies supporting the respiratory heat loss theory and the consequent thermal changes in the airways as the stimulus for EIA [3]. DEAL et al. [5] and MCFADDEN and co-workers [6] measured the temperature at different points of the tracheobronchial tree using thermocouples and clearly demonstrated that the fall in the airway temperature is directly related to the minute ventilation and inversely related to the inspired air temperature and water content. These variations are present both in normal and asthmatic subjects. Some subjects may develop EIA because of an increased sensitivity of their airways due to the previous degree of inflammation or to the difference in postexertional thermal events, since asthmatic airways rewarm twice as rapidly as those of controls [7]. However, at the present time, there is a lack of evidence of direct changes in the airway blood flow due to airway temperature variations.The second major hypothesis concerning the mechanisms of EIA was proposed by ANDERSON and co-workers [8]. They suggested that the respiratory water loss during exercise can lead to a hypertonicity of the airway lining fluid, and that the osmotic and not the cooling effect of exercise due to evaporated water is the more important factor in determining EIA. This theory is supported by other data [3]. Furthermore, in a recent study, ARGYROS et al. [9] found that the EIA is correlated to the loss of mucosal water and that it can be achieved without significant heat loss or airway cooling. ANDERSON and co-workers ...

Bronchial hyperresponsiveness, atopy, airway inflammation, and asthma

“…There are different receptor and cell targets for histamine, metacholine, cold air, etc., and each is blocked to a greater or lesser extent by different antagonists. Exercise responses are partly mediated by mast cell activation and may be followed by a late response (9), though this is disputed by some (10). The challenges now considered to be more discerning are rather different from the standard histamine and metacholine inhalations which held sway in previous decades.…”

Exercise induced asthma in children and adolescents and the relationship to sports

“…However, difficulties in reproducing the late reaction to exercise have cast doubt on the existence of a true late asthmatic reaction to exercise (30)(31)(32). It has been recommended that studies of late asthmatic reactions should be compared with control days without exercise, as late asthmatic reactions after exercise might be confused with spontaneous variation in lung function (32). Sano, et al, in the present issue of Pediatric Allergy and Immunology report that 28.1 per cent of a group of 32 children with EIA also had a late response to exercise (within eight hours of the exercise test) (29).…”

The Role of Endothelium-Derived Mediators in Exercise-Induced Bronchoconstriction

“…The findings related to the participation of inflammatory mediators in either the maintenance or induction of bronchoconstriction provoked by exercise are conflicting [5]. There is no information concerning the late consequences of many years of respiratory tract stimulation by EIB.…”