Warm-up Exercise and Exercise-induced Bronchoconstriction
Warm-up Exercise and Exercise-induced Bronchoconstriction
Potential physiological mechanisms have been proposed as to why exercise would cause a refractory period of EIB. Exercise is believed to result in dehydration of the airway surface, which increases airway osmolarity, releasing inflammatory mediators (prostaglandins, leukotrienes, and histamine) from the mast cell, and it is the release of these mediators that causes bronchoconstriction. Of note, the pathophysiology of EIB in a patient with asthma may be different from bronchoconstriction in an the athlete after exercise. The cause of this refractory period is not fully understood but may be due to depletion of catecholamines, increased circulation of prostaglandin, or degranulation of mast cell mediators. Depletion of mast cell mediator stores is a popular theory to explain refractory period after exercise. It has been hypothesized that warm-up causes a gradual discharge of mast cell mediators, and a time would be required for replenishment. If exercise is resumed within this period, then mediator stores would not be replenished, and therefore, EIB would not occur. McKenzie et al. have suggested that if depletion of mast cell mediators explains the refractory period, then the duration of the warm-up would seem to be most critical. As the most consistent response was observed after high-intensity interval exercise, it would seem that duration of warm-up exercise is not most critical at attenuating EIB.
Physiological Mechanism for Refractory Period
Potential physiological mechanisms have been proposed as to why exercise would cause a refractory period of EIB. Exercise is believed to result in dehydration of the airway surface, which increases airway osmolarity, releasing inflammatory mediators (prostaglandins, leukotrienes, and histamine) from the mast cell, and it is the release of these mediators that causes bronchoconstriction. Of note, the pathophysiology of EIB in a patient with asthma may be different from bronchoconstriction in an the athlete after exercise. The cause of this refractory period is not fully understood but may be due to depletion of catecholamines, increased circulation of prostaglandin, or degranulation of mast cell mediators. Depletion of mast cell mediator stores is a popular theory to explain refractory period after exercise. It has been hypothesized that warm-up causes a gradual discharge of mast cell mediators, and a time would be required for replenishment. If exercise is resumed within this period, then mediator stores would not be replenished, and therefore, EIB would not occur. McKenzie et al. have suggested that if depletion of mast cell mediators explains the refractory period, then the duration of the warm-up would seem to be most critical. As the most consistent response was observed after high-intensity interval exercise, it would seem that duration of warm-up exercise is not most critical at attenuating EIB.
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