Assessment of EIB: What You Need to Know to Optimize Test Results

In the general population, particularly in individuals with asthma, cough is a common symptom, often reported after exertion, although regular exercise may be associated with a reduction in the prevalence of cough. In athletes, exercise-induced cough is also a particularly frequent symptom. The main etiologies of cough in athletes are somewhat similar to non-athletes, including asthma/airway hyperresponsiveness, upper airways disorders such as allergic or non-allergic rhinitis, and exercise-induced laryngeal obstruction, although these conditions are more frequently observed in athletes. In these last, this symptom can also be related to the high ventilation and heat exchange experienced during exercise, particularly during exposure to cold/dry air or pollutants. However, gastroesophageal reflux, a common cause of cough in the general population, despite being highly prevalent in athletes, has not been reported as a main cause of cough in athletes. Cough may impair quality of life, sleep and exercise performance in the general population and probably also in athletes, although there are few data on this. The causes of cough should be documented through a systematic evaluation, the treatment adapted according to identified or most probable cough etiology and pattern of presentation, while respecting sports anti-doping regulations. More research is needed on exercise-induced persistent cough in the athlete to determine its pathophysiology, optimal management and consequences.

Diagnosing Airway hyper-responsiveness (AHR) requires bronchial provocation tests that are performed at rest and after exercise or hyperventilation in either a lab or field setting. Presently, it is unclear whether the proposed AHR field test for swimming induces sufficient provocation due to lack of intensity. Thus we aimed to examine how the 8 minute field swim test compared to all out racing and a lower intensity practice exposure affected AHR. We hypothesized that the race would affect AHR the most thereby highlighting the importance of maximal effort in swim AHR.

10 female and 15 male swimmers completed three conditions (sanctioned race of different distances, 8 min field swim challenge and swim practice). Forced vital capacity (FVC), forced expired volume in 1 second (FEV₁) and forced expiratory flow (FEF_25-75) were measured at rest and after each exercise condition (at 6 and 10 min) in accordance with standard protocols. AHR was defined as a decrease in FEV₁ of ≥10% post exercise.

A significant increase in FEV₁ and FEF_25-75 was observed for both post swim field test and post-race. The practice condition reduced FEV₁ in 44% of swimmers although the magnitude of change was small. There was a wide variability in the individual responses to the 3 conditions and AHR was diagnosed in one swimmer (race condition).

All conditions have poor sensitivity to diagnose EIB and total accumulated ventilation (distance swum) did not influence AHR. These results also indicate that elite swimmers, despite many risk factors, are not limited by respiratory function in race conditions. It is proposed that the swim field test not be used for AHR assessment in swimmers due to too high relative humidity.

The first practice parameter on exercise-induced bronchoconstriction (EIB) was published in 2010. This updated practice parameter was prepared 5 years later. In the ensuing years, there has been increased understanding of the pathogenesis of EIB and improved diagnosis of this disorder by using objective testing. At the time of this publication, observations included the following: dry powder mannitol for inhalation as a bronchial provocation test is FDA approved however not currently available in the United States; if baseline pulmonary function test results are normal to near normal (before and after bronchodilator) in a person with suspected EIB, then further testing should be performed by using standardized exercise challenge or eucapnic voluntary hyperpnea (EVH); and the efficacy of nonpharmaceutical interventions (omega-3 fatty acids) has been challenged. The workgroup preparing this practice parameter updated contemporary practice guidelines based on a current systematic literature review. The group obtained supplementary literature and consensus expert opinions when the published literature was insufficient. A search of the medical literature on PubMed was conducted, and search terms included pathogenesis, diagnosis, differential diagnosis, and therapy (both pharmaceutical and nonpharmaceutical) of exercise-induced bronchoconstriction or exercise-induced asthma (which is no longer a preferred term); asthma; and exercise and asthma. References assessed as relevant to the topic were evaluated to search for additional relevant references. Published clinical studies were appraised by category of evidence and used to document the strength of the recommendation. The parameter was then evaluated by Joint Task Force reviewers and then by reviewers assigned by the parent organizations, as well as the general membership. Based on this process, the parameter can be characterized as an evidence- and consensus-based document.

Exercise-induced bronchoconstriction (EIB) occurs in patients with asthma, children, and otherwise healthy athletes. Poor diagnostic accuracy of respiratory symptoms during exercise requires objective assessment of EIB. The standardized tests currently available are based on the assumption that the provoking stimulus to EIB is dehydration of the airway surface fluid due to conditioning large volumes of inhaled air. “Indirect” bronchial provocation tests that use stimuli to cause endogenous release of bronchoconstricting mediators from airway inflammatory cells include dry air hyperpnea (eg, exercise and eucapnic voluntary hyperpnea) and osmotic aerosols (eg, inhaled mannitol). The airway response to different indirect tests is generally similar in patients with asthma and healthy athletes with EIB. Furthermore, the airway sensitivity to these tests is modified by the same pharmacotherapy used to treat asthma. In contrast, pharmacological agents such as methacholine, given by inhalation, act directly on smooth muscle to cause contraction. These “direct” tests have been used traditionally to identify airway hyperresponsiveness in clinical asthma but are less useful to diagnose EIB. The mechanistic differences between indirect and direct tests have helped to elucidate the events leading to airway narrowing in patients with asthma and elite athletes, while improving the clinical utility of these tests to diagnose and manage EIB.

Asthma or asthmalike conditions can limit the ability of athletes to perform. This article reviews the diagnosis and treatment of asthma and exercise-induced bronchoconstriction in athletes.

Regular exercise is one of the most effective means to maintain good health. A substantial proportion of the general population engages in competitive sports, including many people with asthma; when controlled, asthma does not restrict exercise performance. Indeed, exercise training can improve asthma symptoms, quality of life, exercise capacity, and pulmonary function, as well as reduce airway responsiveness.¹

Intense exercise imposes demands on the cardiorespiratory system. Cardiac output increases, as does minute ventilation, which can reach 200 liters per minute in high-level athletes.² At high minute ventilations, the airways are the site of intense respiratory heat and water exchange as . . .