Exercise-induced bronchoconstriction (EIB), previously known as exercise-induced asthma, is a condition characterized by the transient narrowing of the airways in the lungs that occurs during or shortly after physical exercise, leading to symptoms such as wheezing, shortness of breath, cough, chest tightness, decreased exercise tolerance, and fatigue.[1][2] This airway constriction is triggered primarily by rapid breathing of dry, cool air during exercise, which causes dehydration and cooling of the airway surfaces.[1][3] EIB can affect individuals with underlying asthma as well as those without it, and it is distinct from chronic asthma in that symptoms typically resolve within 10 to 90 minutes after exercise cessation if untreated.[1][2]EIB impacts 40% to 90% of people with asthma, up to 20% of the general population without diagnosed asthma, and 30% to 70% of elite athletes as of 2025, particularly in endurance or winter sports.[1][4] In children and adolescents, it may lead to avoidance of physical activity and reduced quality of life, while in athletes, it can impair performance.[1][3] With appropriate management, most individuals can participate in exercise without significant limitations.[1]
Overview
Definition
Exercise-induced bronchoconstriction (EIB) is defined as a transient and reversible narrowing of the airways that leads to airflow obstruction, occurring during or shortly after physical exercise in individuals with or without underlying asthma.[1][5] This condition manifests as acute bronchoconstriction triggered by the physiological demands of exercise, such as increased respiratory rate and airway dehydration, resulting in measurable reductions in lung function, typically assessed by a ≥10% decrease in forced expiratory volume in one second (FEV1).[1][6]Historically, the condition was termed "exercise-induced asthma" to describe exercise-related respiratory symptoms primarily in asthmatic patients, but this nomenclature evolved to "exercise-induced bronchoconstriction" around 2013, as recommended by expert panels including the American Thoracic Society, to encompass cases occurring in non-asthmatic individuals and to avoid implying an asthma diagnosis.[3][4] This shift reflects a broader understanding that EIB represents a physiological response rather than a subset of asthma exclusively.[4]Physiologically, EIB symptoms typically emerge after 5-10 minutes of sustained moderate-to-high intensity exercise, reach peak severity 5-10 minutes after cessation, and resolve spontaneously within 30-60 minutes in the absence of intervention.[7][8] This temporal pattern distinguishes the acute, self-limited nature of the response from other respiratory events.[1]Unlike chronic asthma, which involves persistent airway inflammation and symptoms triggered by multiple factors beyond exercise, EIB is characteristically episodic and confined to exercise provocation, often resolving without ongoing treatment in non-asthmatic individuals.[9][10] While up to 90% of people with asthma may experience EIB, the condition can occur independently, highlighting its distinct clinical boundaries.[11]
Signs and Symptoms
Exercise-induced bronchoconstriction (EIB) manifests primarily through respiratory symptoms that arise during or shortly after physical exertion. The most common symptoms include shortness of breath, wheezing, chest tightness or pain, and coughing, which typically begin within a few minutes of starting intense exercise and may peak 5 to 15 minutes after cessation.[2][12] These symptoms often resolve within 30 to 60 minutes with rest, though in some cases, a late-phase response can recur up to 12 hours later and persist for a day.[12][1]The severity of EIB is graded based on the percentage decrease in forced expiratory volume in one second (FEV1) from pre-exercise levels, providing a clinical measure of airflow obstruction. Mild EIB involves a 10% to less than 25% fall in FEV1, often resulting in reduced athletic performance without significant discomfort.[1] Moderate EIB features a 25% to 50% decline, leading to noticeable shortness of breath and chest discomfort that interferes with activity.[1] Severe cases, with more than a 50% drop in FEV1, are rare but can cause gasping for air, profound fatigue, and an inability to continue exercise, potentially requiring medical intervention.[1]Associated objective signs include a measurable reduction in peak expiratory flow (PEF) by at least 10% post-exercise, alongside prolonged symptom recovery in moderate to severe instances, which may last beyond an hour without treatment.[1] These signs, while supportive of diagnosis through pulmonary function tests, highlight the acute nature of airway narrowing.[1]EIB significantly affects daily life by inducing fatigue and diminished exercise tolerance, often leading individuals to avoid physical activities due to fear of symptom onset.[2][1] This avoidance can foster anxiety around exertion, contribute to social isolation, and increase risks of obesity and overall poor health from reduced fitness levels.[1] In affected children and athletes, it may manifest as poorer-than-expected performance or reluctance to participate in sports, further impacting quality of life.[2]
Pathophysiology
Underlying Mechanisms
Exercise-induced bronchoconstriction (EIB) primarily arises from hyperventilation during physical activity, which leads to the inhalation of large volumes of air that must be humidified and warmed by the airways. This process causes evaporative water loss from the airway surface liquid lining the epithelium, resulting in dehydration and cooling of the airways. The resultant osmotic imbalance triggers the release of inflammatory mediators from mast cells and other cells within the airway mucosa.[13][4]The core osmotic mechanism involves an increase in the osmolarity of the periciliary fluid due to water evaporation, which stimulates sensory nerves and degranulates mast cells. This degranulation releases key mediators such as histamine, leukotrienes (e.g., cysteinyl leukotrienes), and prostaglandins (e.g., prostaglandin D2), which promote smooth muscle contraction, increased vascular permeability, mucus secretion, and epithelial inflammation. These pathways collectively narrow the airways, with the severity correlating to the extent of hyperventilation and water loss. In individuals without atopy, particularly athletes, EIB may involve greater epithelial damage and impaired airway chloride secretion, leading to prolonged inflammation independent of mast cell mediators.[13][4][14]Environmental factors significantly modulate these processes, with cold, dry air exacerbating EIB by increasing the water content deficit and thus the evaporative demand on the airways. In contrast, humid or warm air reduces this deficit, mitigating dehydration and subsequent mediator release. Additionally, the thermal hypothesis posits that rapid rewarming of the cooled airways after exercise cessation induces hyperemia, vascular engorgement, and edema, further contributing to post-exercise bronchoconstriction.[13][4]
Risk Factors
Exercise-induced bronchoconstriction (EIB) is more prevalent among females than males, particularly after puberty, due to hormonal influences and differences in airway responsiveness.[15] Children and adolescents also face elevated risk, as rapid growth and high activity levels can exacerbate airway sensitivity during physical exertion.[16] A family history of asthma or atopy further increases susceptibility, suggesting a genetic predisposition to airway hyperreactivity.[1]Individuals with underlying medical conditions such as atopy or allergic rhinitis are at greater risk for EIB, as these promote chronic inflammation in the airways.[5] Comorbidities like vocal cord dysfunction can mimic or compound EIB symptoms, complicating diagnosis and management.[1] Obesity serves as another key risk factor, particularly in adolescents, by contributing to mechanical strain on the respiratory system and systemic inflammation.[17]Environmental exposures play a significant role in heightening EIB risk, with cold and dry air causing rapid airway cooling and dehydration during exercise.[2] High levels of air pollution, including ozone and particulate matter, irritate the bronchial mucosa and provoke bronchoconstriction.[1] Indoor allergens, such as chlorine byproducts in swimming pools or chemical fumes in gyms, similarly trigger symptoms in susceptible individuals.[2]Lifestyle factors, including participation in high-intensity endurance sports like running, swimming, or cycling, substantially elevate EIB risk due to prolonged hyperventilation and exposure to triggering conditions.[1] In contrast, regular aerobic training in non-asthmatic individuals may offer protective effects by enhancing airway tolerance and reducing symptom severity over time.[5]
Epidemiology
General Prevalence
Exercise-induced bronchoconstriction (EIB) affects 5% to 20% of the general population without asthma and up to 90% of individuals with asthma.[5][1] This wide range reflects variations in diagnostic criteria and study populations, with higher rates often observed in pediatric and adolescent groups.[18]Prevalence peaks during adolescence, with estimates of 10% to 17% among schoolchildren aged 7 to 17 years.[19] In children and adolescents, rates can reach 3% to 35%, influenced by factors such as atopy and environmental exposures.[13]Gender trends show higher incidence in males before puberty, shifting to slightly elevated rates in females afterward, potentially due to hormonal influences on airway responsiveness.[20]Geographic variations contribute to prevalence differences, with higher rates reported in regions featuring cold, dry air, such as northern latitudes, where environmental triggers exacerbate symptoms.[1] Underdiagnosis is common, as many cases present asymptomatically or mildly, leading to underreporting in non-athletic populations and reduced physical activity.[21] As of 2025, overall prevalence remains stable at 5% to 20% in the general population.[19][22]
Prevalence in Athletes
Exercise-induced bronchoconstriction (EIB) is notably prevalent among elite athletes, with rates ranging from 20% to 50%, particularly in those engaged in high-intensity endurance sports.[23] This elevated incidence surpasses that in the general population and is attributed to the physiological demands of prolonged, intense exercise that challenge airway patency.[5]Sports-specific variations highlight environmental and training factors as key influencers. In elite endurance athletes, such as cross-country skiers, prevalence can reach up to 50%, driven by exposure to cold, dry air during winter training.[24] Swimmers, exposed to chlorinated indoor pools, exhibit rates of 30% to 70%, with one study reporting 68% in elite competitors.[25] In contrast, winter sports like ice hockey show higher rates around 30%, compared to lower figures of 15% to 25% in indoor summer sports such as cycling, where warmer, humid conditions predominate.[26][27]Underreporting is a significant issue in professional athletes, with up to 66% of cases undiagnosed due to performance pressures and symptom attribution to training fatigue.[28] Prevalence has remained relatively stable since the 2010s, but recent 2020s studies indicate a potential rise among urban athletes, linked to increased air pollution exposure during outdoor sessions.[29] As of 2025, rates in elite athletes continue to range from 20% to 50%.[23] EIB episodes can impair performance by contributing to a 10% to 15% reduction in maximal oxygen uptake (VO2 max) through exercise-induced hypoxemia and limited aerobic capacity.[30]
Diagnosis
Clinical Evaluation
The clinical evaluation of exercise-induced bronchoconstriction (EIB) begins with a detailed patient history to identify patterns suggestive of the condition. Key components include assessing the patient's exercise history, such as the type, intensity, duration, and frequency of activities that provoke symptoms, as these often correlate with bronchoconstriction in susceptible individuals.[31] Symptom timing and patterns are crucial, with typical features encompassing shortness of breath, wheezing, cough, or chest tightness that onset during or shortly after exercise, peak within 5-20 minutes post-exertion, and resolve within 30-90 minutes.[1] Family and medical history should probe for atopy, asthma, allergies, or other respiratory conditions, as these increase susceptibility to EIB.[4] Environmental exposures, including cold or dry air, high pollen levels, pollutants, or chlorinated environments, must also be explored as potential triggers that exacerbate symptoms.[31]A focused physical examination follows to assess for supportive findings and exclude alternative causes. Auscultation of the lungs is essential, listening for expiratory wheezing or abnormal breath sounds that may indicate airway narrowing, though the exam is often unremarkable outside of acute episodes.[1]Baseline lung sounds should be evaluated for diminished air entry or crackles, while cardiac assessment, including checking for murmurs or irregular rhythms, helps rule out cardiovascular contributions to exertional dyspnea.[31] Signs of atopy, such as eczematous skin or nasal polyps, may also be noted during the exam.[4]Patients are often advised to maintain symptom diaries over 1-2 weeks to track exercise intensity, duration, environmental conditions, and associated symptoms, providing valuable data on triggers and patterns that inform the evaluation.[31] This self-monitoring aids in correlating subjective experiences with potential EIB episodes.Differential diagnosis is integral to the clinical evaluation, distinguishing EIB from conditions with overlapping exertional symptoms. Exercise-induced anaphylaxis is differentiated by systemic features like urticaria, pruritus, or hypotension accompanying respiratory distress.[1] Cardiac conditions, such as arrhythmias or coronary artery disease, are considered when dyspnea occurs with chest pain or palpitations, necessitating targeted cardiovascular evaluation.[31]Vocal cord dysfunction (or inducible laryngeal obstruction) presents with inspiratory stridor and poor response to asthma therapies, often requiring laryngoscopy for confirmation.[4]Red flags during evaluation include persistent symptoms at rest, which may signal underlying uncontrolled asthma rather than isolated EIB, prompting immediate referral to a pulmonologist or allergist.[31] Other concerning features, such as hemoptysis, fever, or significant hypoxemia, warrant urgent specialist consultation to exclude serious pathologies.[1] If the history and exam suggest EIB but require confirmation, objective pulmonary function tests may be pursued.[4]
Pulmonary Function Tests
Pulmonary function tests (PFTs) play a central role in diagnosing exercise-induced bronchoconstriction (EIB) by providing objective measurements of lung function before and after exercise provocation. These tests help identify airflow limitation that may not be evident at rest, distinguishing EIB from other causes of exercise-related symptoms. Spirometry, the cornerstone of PFTs for EIB, involves standardized maneuvers to assess key parameters of respiratory mechanics.[32][1]Spirometry measures forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC), typically performed immediately before exercise and repeatedly afterward to detect transient airway narrowing. The test requires patients to inhale fully and exhale forcefully into a device, with FEV1 representing the volume exhaled in the first second, which is particularly sensitive to obstructive changes in EIB. FVC assesses total lung capacity but is less emphasized due to potential fatigue from repeated efforts. Baseline spirometry establishes normal resting function in most EIB cases, necessitating post-exercise assessment for diagnosis.[32][33]Diagnosis of EIB is confirmed by a ≥10% decrease in FEV1 from baseline, measured at intervals of 5, 10, 15, and 30 minutes post-exercise, with the maximum fall determining severity (mild: 10–25%; moderate: 25–50%; severe: >50%). Some protocols use a ≥15% threshold for greater specificity, particularly in athletic populations. This criterion reflects the acute, transient nature of EIB, where airway obstruction peaks within 5–30 minutes after cessation of activity.[32][1]Following the post-exercise measurement, a bronchodilator such as albuterol (200–400 mcg) is administered to evaluate reversibility, with an improvement in FEV1 of ≥12% and ≥200 mL from the post-exercise nadir suggesting an underlying asthmatic component. This response indicates variable airflow limitation typical of asthma-related EIB, guiding therapeutic decisions. Spontaneous recovery often occurs within 30–90 minutes, but bronchodilator testing enhances diagnostic confidence.[34][32]Limitations of PFTs include the potential for normal baseline spirometry in many EIB patients, which does not exclude the condition and requires provocative testing for confirmation. Standardized protocols are essential, incorporating environmental controls (e.g., dry air, temperature 20–25°C) and exercise intensity achieving 80–90% of maximum heart rate to ensure reproducibility, as variability can reach 20–30% between tests.[32][1]For ongoing monitoring, portable peak expiratory flow (PEF) meters enable home-based assessment, tracking ≥15% variability or post-exercise decline as an indicator of EIB control. Although less precise than spirometry due to lower repeatability, PEF monitoring is valuable for athletes and patients in resource-limited settings, correlating with FEV1 changes but requiring validation against lab tests.[32][34]
Provocative Challenge Tests
Provocative challenge tests are essential for confirming exercise-induced bronchoconstriction (EIB) by deliberately inducing airway narrowing under controlled conditions, allowing measurement of the response through serial spirometry, typically assessing the percentage fall in forced expiratory volume in one second (FEV1) from baseline. These tests are particularly valuable when clinical history and resting pulmonary function are inconclusive, as they simulate the physiological stressors of exercise to provoke symptoms and quantify hyperresponsiveness. A positive test is generally defined as a ≥10% drop in FEV1 from baseline, with greater declines indicating more severe EIB. Baselinespirometry is performed prior to the challenge to establish normal lung function.The exercise challenge test remains the cornerstone for diagnosing EIB, involving sustained aerobic exercise on a treadmill or cycle ergometer to achieve 80-90% of the individual's maximum heart rate for 6-8 minutes under standardized environmental conditions, such as temperature (20-25°C) and humidity (<50%). Post-exercise FEV1 is measured at intervals (e.g., 5, 10, 15, and 30 minutes) to detect the maximum decline, which correlates directly with the hyperpnea and thermal stress of real-world activity. This method is recommended by the American Thoracic Society (ATS) as the preferred diagnostic approach when facilities allow, offering high specificity for EIB in both athletes and non-athletes.Eucapnic voluntary hyperventilation (EVH) serves as a non-exercise alternative that closely mimics the respiratory demands of intense activity, requiring the subject to breathe a dry, compressed gas mixture (5% CO2, 21% O2, balance N2) at a target ventilation rate of 30 times their baseline FEV1 in liters per minute for 6 minutes. This protocol induces airway desiccation and cooling similar to exercise hyperpnea, with FEV1 monitored for up to 20 minutes afterward; it is considered the gold standard for elite athletes by the International Olympic Committee due to its sensitivity in detecting mild EIB. EVH is especially useful in settings where exercise equipment is unavailable or when standardizing workload is challenging.Inhaled agents like mannitol and methacholine provide surrogate assessments of airway hyperresponsiveness when direct exercise provocation is impractical, acting as indirect and direct challenges, respectively. Mannitol, an osmotic agent delivered as a dry powder in escalating doses (e.g., 0, 5, 10, 20, 40, 80, 160, 160, 160 mg), provokes bronchoconstriction by releasing mediators from airway cells, with a positive response indicated by a ≥15% FEV1 fall; it shows high sensitivity (up to 96%) for identifying EIB compared to EVH as a reference. Methacholine, administered via nebulizer in doubling concentrations (0.031 to 16 mg/mL), directly stimulates smooth muscle contraction, with a positive test at a provocative concentration causing a 20% FEV1 drop (PC20 ≤8 mg/mL often suggesting EIB); it is widely used per European Respiratory Society (ERS) guidelines but may overestimate responsiveness in non-asthmatic individuals.Field-based tests offer a practical, sport-specific option for provocation, such as running on a track or performing interval sprints to replicate competitive demands, with pre- and post-exercise FEV1 measurements showing strong correlations (r=0.7-0.9) to laboratory exercise challenges. These tests are particularly effective for athletes, as they incorporate real-world variables like terrain and weather, though they require portable spirometry and controlled timing to ensure reliability.Safety protocols are critical for all provocative challenges to minimize risks, including pre-test screening for contraindications such as recent respiratory infection, uncontrolled asthma (FEV1 <70% predicted), or cardiovascular instability, and withholding bronchodilators (e.g., short-acting β-agonists for 4-6 hours, long-acting for 24-48 hours). Emergency equipment, including inhaled short-acting bronchodilators and oxygen, must be immediately available, with testing aborted if FEV1 falls >30% or severe symptoms occur; severe asthma is a relative contraindication per ATS/ERS standards.
Management
Non-Pharmacological Approaches
Non-pharmacological approaches to managing exercise-induced bronchoconstriction (EIB) emphasize lifestyle modifications, environmental adaptations, and behavioral strategies to minimize airway narrowing during or after physical activity. These methods aim to precondition the airways, reduce exposure to triggers, and enhance overall respiratory resilience without relying on medications. Evidence from clinical guidelines supports their use as first-line interventions, particularly for mild cases or in combination with other strategies, to improve exercise tolerance and quality of life.[4]Warm-up routines are a cornerstone of non-pharmacological prevention, involving 10-15 minutes of low- to moderate-intensity exercise prior to vigorous activity to induce a refractory period in the airways. This preconditioning reduces the release of inflammatory mediators and attenuates the severity of EIB in up to 50% of affected individuals by limiting subsequent bronchoconstriction for 1-2 hours. High-intensity interval warm-ups, such as alternating short bursts of intense effort with recovery periods, have shown the most consistent benefits, reducing the maximum percent fall in forced expiratory volume in one second (FEV1) by approximately 10-11% compared to no warm-up.[4][35][36]Environmental controls play a critical role in mitigating triggers like cold, dry air, which can exacerbate airway dehydration and cooling. Individuals with EIB are advised to exercise in warm, humid conditions when possible or use accessories such as scarves, masks, or heat and moisture exchangers to prewarm and humidify inhaled air, particularly during cold-weather activities. These measures can reduce the FEV1 fall by about 15%, as they help maintain airway moisture and prevent osmotic changes that provoke bronchoconstriction. Additionally, avoiding high-pollution or allergen-heavy environments, such as during peak pollen seasons or in chlorinated pools without proper ventilation, further lowers risk.[4][1][5]Breathing techniques, including pursed-lip and diaphragmatic breathing, offer practical ways to control hyperventilation and optimize airflow during exercise. Pursed-lip breathing involves inhaling slowly through the nose and exhaling through slightly pursed lips to prolong expiration, which helps reduce air trapping and maintains positive airway pressure. Diaphragmatic breathing, focusing on deep abdominal expansion, strengthens respiratory muscles and may decrease EIB symptoms by improving ventilation efficiency, though evidence is primarily from broader asthma management studies. These techniques are simple to integrate into routines and can be particularly useful for athletes to minimize rapid breathing rates that dry the airways.[1][37]Dietary advice centers on avoiding triggers and supporting airway health through targeted choices. Individuals sensitive to aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) should refrain from these agents before exercise, as they can worsen EIB in those with underlying aspirin-exacerbated respiratory disease by inhibiting protective prostaglandins. Maintaining adequate hydration is essential to preserve airway surface liquid and reduce dehydration-induced narrowing, with studies indicating that proper fluid intake before and during activity can attenuate EIB severity. A low-sodium diet may also benefit some by decreasing airway hyperresponsiveness, while supplements like ascorbic acid (vitamin C) have been suggested to halve EIB severity in select cases, though results vary.[1][38][4]Training adjustments involve gradual progression and selection of suitable activities to build tolerance without overwhelming the airways. Starting with lower intensities and incorporating cross-training—such as switching between running and swimming in controlled environments—allows for aerobic fitness improvements that reduce minute ventilation demands and EIB frequency. Low-risk sports, including short-duration efforts like sprinting, tennis, or gymnastics, are preferable over prolonged endurance activities in cold air, as they limit exposure time to triggers and enhance overall conditioning. These adaptations not only prevent episodes but also promote long-term adherence to physical activity.[1][5]
Pharmacological Treatments
Pharmacological treatments for exercise-induced bronchoconstriction (EIB) primarily target acute symptom relief and long-term control of airway inflammation and hyperresponsiveness. These therapies are evidence-based and follow guidelines from organizations such as the American Thoracic Society (ATS), emphasizing stepwise management based on symptom frequency and response. Short-acting beta-agonists (SABAs) serve as first-line agents for prevention, while additional classes like inhaled corticosteroids (ICS), leukotriene modifiers, and mast cell stabilizers are used for persistent or refractory cases. A 2025 systematic review and network meta-analysis of randomized controlled trials confirmed the efficacy of ICS-based regimens (daily low-dose ICS or as-needed ICS-formoterol) for mild EIB and addition of montelukast or long-acting beta-agonists (LABAs) for severe cases, while reducing reliance on SABAs alone.[4][1][39]Short-acting beta-agonists, such as inhaled albuterol, are recommended as the initial treatment for EIB, administered 15-30 minutes before exercise to relax airway smooth muscle and inhibit mast celldegranulation. This approach attenuates EIB in 80-95% of patients with asthma, providing protection for 2-4 hours. The typical dose is 2-4 puffs (180-360 mcg), with guidelines advising use no more than twice weekly to avoid tolerance or indicate need for escalation; frequent reliance suggests underlying asthma requiring controller therapy.[4][40][1]For patients with persistent symptoms or suboptimal SABA response, daily low-dose inhaled corticosteroids like budesonide address underlying airway inflammation. Administered via inhaler (e.g., 200 mcg daily), ICS can reduce the magnitude of EIB by 50% or more after 2-4 weeks of consistent use, though they are not effective as pre-exercise rescue. If EIB remains frequent, combination therapy with long-acting beta-agonists (LABA) may be added, but ICS alone or in combo is prioritized for inflammation control over 15-20% of cases needing step-up.[4][41][1]Leukotriene modifiers, such as oral montelukast (10 mg once daily), are an alternative for SABA non-responders, blocking cysteinyl leukotriene-mediated bronchoconstriction for up to 24 hours without developing tolerance. This class is particularly useful in targeting inflammatory mediators in patients with allergic components, showing moderate efficacy in reducing FEV1 fall by approximately 11% compared to placebo. Montelukast is well-tolerated and suitable for children as young as 6 years, though individual responsiveness varies, with some non-responders identified by baseline hyperresponsiveness.[4][42][43]Mast cell stabilizers, including cromolyn sodium (20 mg inhaled pre-exercise), offer adjunctive protection by inhibiting mediator release from mast cells, attenuating EIB by about 50% for 1-2 hours. However, their shorter duration of action and lesser potency compared to SABAs make them less commonly used. These agents are typically reserved for combination with SABAs in select cases rather than monotherapy.[4][44][45]Overall dosing guidelines emphasize minimizing SABA use to twice weekly or less; if exceeded, escalate to daily ICS or leukotriene modifiers, with monitoring for adherence and side effects like oral thrush from ICS. Therapy selection considers athlete status, given anti-doping implications for beta-agonists.[4][46][1]
Monitoring and Follow-Up
Ongoing monitoring and follow-up for exercise-induced bronchoconstriction (EIB) are essential to evaluate treatmentefficacy, ensure symptom control, and adjust management strategies based on individual responses and environmental factors. Regular assessments help track airway function stability and detect any progression or complications early, particularly in athletes or active individuals where exercise intensity may vary.[31][1]Spirometry is a cornerstone of follow-up, recommended every 3-6 months to monitor forced expiratory volume in one second (FEV1) stability and response to therapy. Pre- and post-exercise spirometry, measuring FEV1 at intervals such as 5, 10, 15, and 30 minutes after exertion, can quantify any reduction (≥10% from baseline indicates ongoing EIB) and assess protective effects, with a goal of limiting post-exercise decline to less than 10%. This objective testing complements initial diagnostic evaluations and provides quantifiable data on airway hyperresponsiveness over time.[47][31][1]Symptom scoring using validated scales, such as a 0-10 severity rating for dyspnea, wheezing, or chest tightness, alongside exercise logs, aids in recognizing patterns and correlating subjective experiences with objective measures. Patients are encouraged to record symptom frequency, triggers, and duration during physical activity to facilitate pattern identification during clinic visits, ensuring that self-reported data informs but does not solely guide adjustments.[48][47]Adherence to management plans is verified through patient education on proper inhaler technique, demonstrated during visits, and tracking medication refills or usage patterns to confirm consistent application. Non-adherence can undermine efficacy, so follow-up includes reviewing barriers and reinforcing education to promote long-term compliance.[1][48]Complications such as overuse of short-acting β2-agonists (SABAs) are closely watched, with use exceeding twice per week signaling inadequate control and potential tachyphylaxis, which diminishes bronchodilator responsiveness and prolongs recovery. Monitoring SABA frequency helps prevent tolerance development and prompts escalation of preventive measures.[31][1]Persistent symptoms despite optimized management trigger referrals to specialists, such as allergists or pulmonologists, for comprehensive evaluation including potential allergy testing or advanced provocation challenges to rule out alternative diagnoses.[48][47]
Research Directions
Current Studies
Recent research has focused on biomarkers for predicting exercise-induced bronchoconstriction (EIB), with elevated fractional exhaled nitric oxide (FeNO) emerging as a key indicator of underlying airway inflammation. A 2023 multicenter study demonstrated that FeNO levels ≥40 ppb provide good specificity for diagnosing EIB in athletes, serving as a reliable non-invasive biomarker for assessing severity and guiding management in athletes and non-athletes alike.[49] Additionally, investigations into genetic factors have linked variants in the ADRB2 gene, which encodes the beta-2 adrenergic receptor, to increased susceptibility to EIB, influencing response to beta-agonist therapies.[50]The impact of COVID-19 on EIB has been a prominent area of study from 2022 to 2024, revealing heightened risks in affected individuals. A 2022 review in athletic populations showed that post-infection residual inflammation contributes to prolonged symptoms like breathlessness and cough, affecting return to sport.[51] In judokas, a 2025 midterm follow-up study indicated correlations between severe acute COVID-19 and worsened respiratory function in those with EIB, with persistent declines in metrics like maximal inspiratory pressure (MIP) and FEV1 for up to 90 days, underscoring the need for respiratory monitoring in recovered athletes.[52]Diagnostic advancements include the development of wearable sensors for real-time monitoring of peak expiratory flow (PEF) and respiratory parameters during exercise. A 2024 validation study in elite soccer athletes confirmed the accuracy of a new chest strap sensor for estimating respiratory frequency, achieving reliability comparable to traditional spirometry and supporting early EIB detection in dynamic settings.[53] Similarly, wearable respiratory systems introduced in 2024 have enabled continuous tracking of breathing patterns, with applications for identifying ventilatory thresholds in athletes prone to EIB.[54]Updated prevalence data from a 2025 systematic review highlights the role of declining air quality in exacerbating EIB among urban youth. The meta-analysis of global trends found that chronic exposure to air pollutants, such as particulate matter and nitrogen dioxide, is associated with reduced lung function and higher EIB risk in children and adolescents aged 5-18 years, particularly in urban environments with poor air quality.[55] This evidence points to environmental factors as a modifiable contributor to rising EIB cases in this demographic.[56]Treatment trials have emphasized the efficacy of combination therapies over short-acting beta-agonists (SABA) alone. A 2024 review of randomized controlled trials showed that inhaled corticosteroid (ICS)-formoterol as reliever therapy significantly reduces severe asthma exacerbations, including EIB episodes, compared to SABA monotherapy, with odds ratios indicating approximately 55% lower risk (OR 0.45, 95% CI 0.34-0.60).[57] Studies confirm that as-needed ICS-formoterol prolongs time to first severe event and improves overall control in EIB-prone patients.[58]
Future Therapies
Emerging biologics targeting eosinophilic inflammation show promise for managing exercise-induced bronchoconstriction (EIB) in patients with severe asthma. Anti-IL-5 therapies, such as mepolizumab, have demonstrated potential in improving physical activity levels and exercise tolerance by reducing airway hyperresponsiveness, a key contributor to EIB symptoms. Ongoing clinical trials, including a multicenter study evaluating mepolizumab's effects on physical activity in severe asthma, hypothesize that 6 months of treatment could enhance exercise capacity in patients experiencing EIB-related limitations, with preliminary real-world data indicating sustained reductions in exacerbations and improved lung function over 2 years.[59][60]Gene therapy approaches targeting beta-2 adrenergic receptor (ADRB2) polymorphisms represent an early investigational frontier for EIB, particularly in individuals with genetic variants that impair bronchodilator responses. A 2025 preclinical study explored isoprenaline-modified polyethyleneimine vectors for efficient gene delivery to ADRB2-expressing cells in murine asthma models, achieving targeted expression in bronchoalveolar lavage fluid and lung tissues to reduce inflammation and airway hyperresponsiveness. These efforts build on established associations between ADRB2 variants and variable EIB severity, aiming to personalize interventions by correcting polymorphisms that reduce beta-agonist efficacy.[61][62]Inhaled anti-inflammatory nanoparticles offer a novel delivery mechanism for leukotriene inhibitors, enhancing targeted action in the airways while minimizing systemic side effects associated with oral formulations like montelukast. A 2014 study developed montelukast-loaded nanostructured lipid carriers for pulmonary deposition, demonstrating sustained drug release and reduced inflammation in experimental asthma models with limited systemic distribution. Recent reviews discuss ongoing advancements in nanotechnology for airway diseases, including potential for improved bioavailability and tolerability in EIB prevention.[63][64]Allergen-specific immunotherapy (AIT) is being evaluated as a vaccine-like approach for atopic EIB, particularly in pediatric populations where environmental allergens exacerbate exercise triggers. A 2023 prospective cohort study in children aged 5-16 years with allergic rhinoconjunctivitis (74% with asthma) demonstrated that 3 years of subcutaneous pollen AIT led to significant reductions in symptom scores (from 19.9 to 10.3) and improved health-related quality of life, with sustained effects observed. This immunomodulatory strategy may protect against atopic-driven EIB by altering immune responses to allergens, offering long-term disease modification beyond symptomatic relief.[65][66]Personalized medicine initiatives incorporating genotype-guided treatment have shown reductions in asthma exacerbations in children through meta-analysis of RCTs, integrating genetic factors like ADRB2 polymorphisms. These approaches support precision interventions for EIB susceptibility, with potential for athlete-specific strategies based on individual genotypes.[67]