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Am Fam Physician. 2004;69(4):808-809

to the editor: I enjoyed reading the article1 in American Family Physician on exercise-induced bronchospasm (EIB). It is apparent that more knowledge and patient education are needed about this prevalent and under-diagnosed condition. I would like to clarify the difference between EIB and exercise-induced asthma (EIA). Although the difference between them has not been fully elucidated, EIB is a bronchospastic disorder, and EIA is an inflammatory condition. As the authors state, “80 to 90 percent of patients with asthma also have EIB.”1 In addition, 5 to 10 percent of patients with EIB have no concomitant respiratory or allergic disease.

Studies on EIB are lacking. Two studies2,3 examined subjects after exercise and were unable to document increased inflammation on bronchoalveolar lavage or in blood histamine levels. This evidence suggests that EIB may not have an inflammatory base.

Other researchers have included patients with chronic asthma in studies determining the efficacy of treatment of EIB. This erroneous inclusion has led to the assumption that anti-inflammatories, such as inhaled steroids, help patients with EIB, when, in actuality, they help patients with EIA.

Although this sounds like semantics, I think it is important to properly define the terms. Diagnosing patients with asthma and initiating anti-inflammatory therapy still can be associated with stigmas, inability to enter military professions, and changes of insurance premiums. It also can be confusing for patients to hear they have “exercise-induced asthma” (a chronic disease) when in truth they only have “exercise-induced bronchospasm” (a transient problem). As more research is done to elucidate the relationship between EIA and EIB, we can better define the terms and appropriate treatments.

IN REPLY: We thank Dr. Hermansen for raising the issue of the differences between exercise-induced asthma (EIA) and exercise-induced bronchospasm (EIB). The terms EIA and EIB often are used interchangeably in the literature. In our review of the literature we were unable to discover a consensus regarding the pathophysiology of EIA, EIB, and the relationship, if any, between the two terms. Therefore, we have chosen to follow the National Asthma Education and Prevention Program (NAEPP) guidelines,1 in which the expert panel has preferred the term EIB and has used the functional definition of EIB rather than a pathophysiologic one. Currently, there are several theories that attempt to explain the mechanism of EIB. The two with the most consensus are the thermal and osmolarity theories.

The thermal theory is based on the assumption that hyperventilation during exercise causes loss of heat and drying of the airways that in turn causes a transient bronchoconstrictive response.2 The osmolarity theory3 suggests that it is the heat lost during exercise and the rapid rewarming of the airways after exercise that causes a reactive hyperemia of the microvasculature and edema of the airways that sets up an osmotic gradient, which stimulates the release of proinflammatory substances from mast cell and other inflammatory cells. This therapy could possibly explain why steroids and other anti-inflammatory agents46 have been shown to improve symptoms in patients with EIB.

As Dr. Hermansen has noted, more research is needed to elucidate the pathophysiology of EIB. Because our article was in the series “Practical Therapeutics,” we stayed away from too many details regarding pathophysiology.

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This series is coordinated by Kenny Lin, MD, MPH, deputy editor.

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