The pathogenesis of exercise-induced asthma is closely connected with the fluxes in heat and water that develop inside the tracheobronchial tree during the conditioning of large volumes of air. The proceeding events are linked to the process of respiratory heat exchange. There has been some controversy, the bulk of recent evidence shows there is a fall in airway temperature during rapid breathing, followed by rapid reheating when ventilation decreases. High ventilation, in combination with a low temperature of moved air pushes the conditioning process from the upper to the lower airway. Much movement of heat and water from the mucosa is needed to bring the inspired air to full saturation at body temperature (Eur Respir J 1991). The larger the quantity of thermal energy that is transferred, the cooler the airways will become, the more rapidly they re-warm, and the more the bronchi are narrowed (Eur Respir J 1991). On the other hand, low ventilation or the inhalation of air with high humidity decreases these exchanges, so limiting the thermal changes that lead to the development of airway obstruction. The bronchial narrowing will change severely, if any component of the cooling-rewarming cycle is increased or enlarged (J Clin Invest 1992). The same intrathoracic thermal profile and airflow limitation are both produced by exercise and hyperventilation. It is not fully clear how intra-airway thermal fluxes produce bronchial narrowing. Rapid breathing may cause the evaporation of mucosal surface water and an increase in osmolarity, resulting in post-cell degranulation and constriction of airway smooth muscles (Rev Respir Dis 1985). Still, there is not any evidence that airway dries up. Another theory states that exercise-induced asthma results from hyperemia of the microcirculation in the airway wall with the formation of edema and may not involve constriction of the bronchial smooth muscle. The airways in patients that suffer with asthma have a hyperplasic capillary bed (J Clin Pathol 1960) that is more permeable than in normal people. The constriction and dilatation of the vessels causes the cooling and heating of each airway, with changes in the pulmonary function (J Clin Invest 1992).