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Exercise-induced bronchoconstriction results from the alteration of normal lung physiology occurring with evaporative water loss, thermal changes, and irritant exposure induced by a large increase in minute ventilation and demand on the respiratory system to heat and humidify air with exercise-related hyperpnea.[9][10][1] Ventilation increases by 200 L/min, and airway cooling with mucosal dehydration occur.As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium.[9] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation.

Exercise-induced bronchoconstriction results from the alteration of normal lung physiology occurring with evaporative water loss, thermal changes, and irritant exposure induced by a large increase in minute ventilation and demand on the respiratory system to heat and humidify air with exercise-related hyperpnea.[9][10][1] Ventilation increases by 200 L/min, and airway cooling with mucosal dehydration occur. As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium.[9] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation. Bronchial blood flow is increased.[1][10][9][6] Reactive oxygen species are generated with increased lipid peroxidation.[8] Sensory and autonomic nerves are activated.[1] The results are direct and neuronal activation of bronchoconstriction.[1][10]

Also, nasal breathing becomes insufficient, leading to mouth breathing and increased exposure of lung surfaces to pollutants, irritants, and allergens, which result in the generation of reactive oxygen species and a neutrophilic inflammatory response.[3][2][11] Some research shows people genetically unable to counteract oxidative stress with glutathione may have an increased risk of EIB.[11]

Changes in mucus composition and decrease function of mucociliary clearance can lead to mucus plugging and bacterial growth.[9] Intense physical training can independently lead to transient immune suppression with a shift to T2 lymphocyte response and has been linked to increased atopy and viral upper respiratory infection (URI).[2]

Long term exposure can lead to epithelial damage and shedding, with remodeling and inflammation resembling asthma.[3] The process is partially reversible as studies have shown the lung damage and hyperresponsiveness improves over weeks to years when exposure and exercise are stopped.[3][2]