Exercise-Induced Dyspnea
Exercise-Induced Dyspnea
Weiler JM, Bonini S, Coifman R, et al
J Allergy Clin Immunol. 2007;119;1349-1358
Shortness of breath during exercise is an extremely common patient complaint received by both primary care and specialty physicians. The differential diagnosis may include deconditioning, cardiac causes, pulmonary disease, anemia, vocal cord dysfunction, etc. These authors point out that it has been known since biblical times that susceptible individuals may experience increased asthma symptoms with physical exercise. The term "exercise-induced asthma (EIA)" or "exercise-induced bronchospasm (EIB)" became more commonly used to describe this condition during the 1960s and 1970s, especially after the effect of pretreatment with various medications became better known. These authors define EIB as "airway obstruction that occurs in association with exercise without regard to the presence of chronic asthma." They define worsening asthma with exercise as EIA. They note that there is some disagreement among experts in the field regarding the pathophysiology of EIA, in contrast with symptoms of chronic asthma accompanied by increased symptoms with exercise, as there may be different cell types and inflammatory mediators involved in these 2 scenarios. Those fine points are beyond the reach of this summary. Suffice it to say that EIA is most likely triggered by the combination of airway heat and water loss, which may lead to bronchospasm. It is also abundantly clear that symptoms of EIA may be produced by more than simple bronchospasm and inflammatory mediators and cells, and that autonomic nervous system function may play a role in selected patients. The authors also point out the importance of controlling rhinitis symptoms in these patients to improve the conditioning (warming and humidification) of inspired air.
Typically, patients with EIA may experience symptoms of cough, shortness of breath, chest tightness, excess mucus production, and audible wheezing after a burst of strenuous exercise, usually continuous aerobic exercise lasting at least 6-8 minutes. Symptoms may occur either during or immediately after exercise.
The reported incidence of EIA varies between 5% and 20% of the general population. It may occur more commonly in elite athletes, with some studies reporting an incidence as high as 30% to 70% in elite winter athletes. Although some reports vary, most agree that essentially all patients with asthma will experience increased symptoms with physical exercise. Various diagnostic methods exist, but measurement of pulmonary function tests before and after an inhaled short-acting bronchodilator is a first step towards confirming reversible airways obstruction. Reproduction of symptoms following performance of the particular exercise known to produce symptoms is also commonly used (eg, in runners, the patient runs in a manner similar to that producing symptoms, and spirometry is measured before and after exercise). Measurement of peak expiratory flow before and after exercise may be helpful in some patients, but is not adequate in the case of elite athletes needing documentation of EIA for the purposes of using asthma medications in competitive events monitored by the United States Anti-Doping Agency (USADA). In such instances, detailed instructions are given regarding precisely how bronchospasm with exercise needs to be measured to allow approval of these medications in such events.
Eucapnic voluntary hyperventilation and cold, dry air challenges are also done in some centers equipped to perform such challenges. A step-wise approach to the management of EIA is employed, with some patients responding adequately to pretreatment with inhaled short-acting beta agonists (eg, albuterol). However, especially if the individual exercises frequently, such as daily, consideration should be given to the addition of another agent, such as an inhaled corticosteroid, to help with airway inflammation. Leukotriene modifiers such as montelukast may also be helpful in preventing symptoms of EIA if used in advance. Long-acting beta agonists may be helpful as well, but should be used in conjunction with an inhaled corticosteroid.
Exercise-induced dyspnea should be appropriately evaluated with a detailed history, physical examination, and objective measures of lung function (ie, spirometry). I have found in practice that those athletes who fail to adequately respond to preexercise albuterol often need additional asthma therapy. This is especially true in elite athletes who exercise on a daily basis. They may need combination bronchodilators and inhaled steroids, sometimes with additional treatment with a leukotriene antagonist. In most settings, with appropriate therapy, the vast majority of patients with EIA can return to full activity.
Abstract
American Academy of Allergy, Asthma, and Immunology Work Group Report: Exercise-Induced Asthma
Weiler JM, Bonini S, Coifman R, et al
J Allergy Clin Immunol. 2007;119;1349-1358
Shortness of breath during exercise is an extremely common patient complaint received by both primary care and specialty physicians. The differential diagnosis may include deconditioning, cardiac causes, pulmonary disease, anemia, vocal cord dysfunction, etc. These authors point out that it has been known since biblical times that susceptible individuals may experience increased asthma symptoms with physical exercise. The term "exercise-induced asthma (EIA)" or "exercise-induced bronchospasm (EIB)" became more commonly used to describe this condition during the 1960s and 1970s, especially after the effect of pretreatment with various medications became better known. These authors define EIB as "airway obstruction that occurs in association with exercise without regard to the presence of chronic asthma." They define worsening asthma with exercise as EIA. They note that there is some disagreement among experts in the field regarding the pathophysiology of EIA, in contrast with symptoms of chronic asthma accompanied by increased symptoms with exercise, as there may be different cell types and inflammatory mediators involved in these 2 scenarios. Those fine points are beyond the reach of this summary. Suffice it to say that EIA is most likely triggered by the combination of airway heat and water loss, which may lead to bronchospasm. It is also abundantly clear that symptoms of EIA may be produced by more than simple bronchospasm and inflammatory mediators and cells, and that autonomic nervous system function may play a role in selected patients. The authors also point out the importance of controlling rhinitis symptoms in these patients to improve the conditioning (warming and humidification) of inspired air.
Typically, patients with EIA may experience symptoms of cough, shortness of breath, chest tightness, excess mucus production, and audible wheezing after a burst of strenuous exercise, usually continuous aerobic exercise lasting at least 6-8 minutes. Symptoms may occur either during or immediately after exercise.
The reported incidence of EIA varies between 5% and 20% of the general population. It may occur more commonly in elite athletes, with some studies reporting an incidence as high as 30% to 70% in elite winter athletes. Although some reports vary, most agree that essentially all patients with asthma will experience increased symptoms with physical exercise. Various diagnostic methods exist, but measurement of pulmonary function tests before and after an inhaled short-acting bronchodilator is a first step towards confirming reversible airways obstruction. Reproduction of symptoms following performance of the particular exercise known to produce symptoms is also commonly used (eg, in runners, the patient runs in a manner similar to that producing symptoms, and spirometry is measured before and after exercise). Measurement of peak expiratory flow before and after exercise may be helpful in some patients, but is not adequate in the case of elite athletes needing documentation of EIA for the purposes of using asthma medications in competitive events monitored by the United States Anti-Doping Agency (USADA). In such instances, detailed instructions are given regarding precisely how bronchospasm with exercise needs to be measured to allow approval of these medications in such events.
Eucapnic voluntary hyperventilation and cold, dry air challenges are also done in some centers equipped to perform such challenges. A step-wise approach to the management of EIA is employed, with some patients responding adequately to pretreatment with inhaled short-acting beta agonists (eg, albuterol). However, especially if the individual exercises frequently, such as daily, consideration should be given to the addition of another agent, such as an inhaled corticosteroid, to help with airway inflammation. Leukotriene modifiers such as montelukast may also be helpful in preventing symptoms of EIA if used in advance. Long-acting beta agonists may be helpful as well, but should be used in conjunction with an inhaled corticosteroid.
Viewpoint
Exercise-induced dyspnea should be appropriately evaluated with a detailed history, physical examination, and objective measures of lung function (ie, spirometry). I have found in practice that those athletes who fail to adequately respond to preexercise albuterol often need additional asthma therapy. This is especially true in elite athletes who exercise on a daily basis. They may need combination bronchodilators and inhaled steroids, sometimes with additional treatment with a leukotriene antagonist. In most settings, with appropriate therapy, the vast majority of patients with EIA can return to full activity.
Abstract
