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Exercise-induced bronchoconstriction
AUTHOR: Paul M O'Byrne, MB, FRCP(C), FRSC
SECTION EDITORS: Peter J Barnes, DM, DSc, FRCP, FRS, Robert A Wood, MD
DEPUTY EDITOR: Paul Dieffenbach, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Aug 2023.

This topic last updated: May 08, 2023.

INTRODUCTION

Exercise-induced bronchoconstriction describes the acute onset of bronchoconstriction

occurring during or, more frequently, minutes after exercise. The term "exercise-induced
asthma" is often used to describe episodic bronchoconstriction following exercise, but this
wording is potentially misleading, since exercise is not an independent risk factor for
asthma, but rather a trigger of bronchoconstriction in patients with underlying asthma [1].
In fact, there is some speculation that decreased physical activity is a risk factor for asthma,
and that exercise may be helpful in preventing the onset of asthma in children [2]. Thus, the
term exercise-induced bronchoconstriction (EIB) is a more accurate reflection of the
underlying pathophysiology and is generally preferred.

The clinical manifestations, diagnosis, and management of exercise-induced

bronchoconstriction will be discussed here. The clinical manifestations, evaluation, and
management of asthma are reviewed separately. (See "Asthma in children younger than 12
years: Initial evaluation and diagnosis" and "Asthma in adolescents and adults: Evaluation
and diagnosis" and "Pulmonary function testing in asthma" and "Wheezing phenotypes and
prediction of asthma in young children" and "An overview of asthma management" and
"Asthma in children younger than 12 years: Overview of initiating therapy and monitoring
control".)

EPIDEMIOLOGY

The estimated prevalence of exercise-induced bronchoconstriction (EIB) varies from

approximately 5 to 20 percent in the general population [3-6]. In comparison, up to 90
percent of patients with symptomatic asthma have some degree of EIB [7]. The magnitude of
EIB is most strongly correlated with the underlying degree of airway hyperresponsiveness
and the presence of airway inflammation, as measured by the number of airway eosinophils
[8,9]. Thus, many patients with mild, episodic asthma characterized by minimally increased
airway responsiveness and mild airway inflammation do not experience clinically significant
bronchoconstriction even with strenuous exercise.

The prevalence of EIB appears to be higher among elite athletes and has been evaluated in a
number of studies [6,10-13]. As an example, in a study of athletes participating in the
summer Beijing and Athens Olympic Games, the sports most commonly associated with a
Therapeutic Use Exemption for asthma were swimming, cycling, triathlon, pentathlon, and
rowing, with prevalences of approximately 18, 16, 12, 13, 7 percent, respectively [10]. In
contrast, the prevalence of asthma among athletes in disciplines without endurance
demands, such as gymnastics, fencing, and sailing, was less than 5 percent. In a separate
study, positive eucapnic hyperventilation was noted in 39 percent of swimmers and 24
percent of winter sport athletes [13].

PATHOGENESIS

Minute ventilation, the volume of air inhaled or exhaled from a person's lungs per minute,
rises with exercise. EIB probably results from changes in airway physiology triggered by the
large volume of relatively cool, dry air inhaled during vigorous activity [14,15]. This is
supported by the finding that EIB is attenuated when the inspired gas is more fully
humidified and closer to body temperature [16,17]. The effect of large-volume dry air
inhalation on airway surface osmolality may be the primary stimulus responsible for
bronchoconstriction [18]. Other relevant observations regarding EIB include the following:

● Levels of bronchoconstrictive and inflammatory mediators are increased, particularly

leukotrienes LTC4 and LTD4 [19], histamine [20], and interleukin (IL)-8 [21]. (See
"Antileukotriene agents in the management of asthma".)

● Peripheral Th2-type lymphocytes are activated, with an increase in T cells expressing

CD25 (IL-2R), and B cells expressing CD23 [22]. These changes favor production of IgE
and activation of eosinophils. (See "Normal B and T lymphocyte development", section
on 'Th2 cells' and "The biology of IgE", section on 'Regulation of synthesis'.)

● Eosinophil influx and activation, measured using eosinophilic cationic protein levels,
sputum eosinophils, or peripheral eosinophil counts, have been noted in some [23,24],
but not all [17,25], studies of experimental EIB.
 ● In contrast, the fraction of exhaled nitric oxide (FENO) levels, which generally reflect
airway inflammation, do not appear to correlate well with the development or severity
of EIB [26-28]. (See "Exhaled nitric oxide analysis and applications".)

CLINICAL MANIFESTATIONS

Patients with exercise-induced bronchoconstriction (EIB) typically have initial bronchodilation

during the first six to eight minutes of exercise [29,30]. The initial bronchodilation is followed
by bronchoconstriction, which begins by three minutes after exercise, generally peaks
within 10 to 15 minutes, and resolves by 60 minutes ( figure 1). Typical symptoms are
shortness of breath, chest tightness, and cough. Associated hoarseness or stridor is
uncommon and should raise the possibility of paradoxical vocal fold motion. (See "Inducible
laryngeal obstruction (paradoxical vocal fold motion)".)

In most patients with EIB, bronchoconstriction is followed by a refractory period, during

which repeated exertion causes less bronchoconstriction [31]. This refractory period is
generally less than four hours. Inhibitory prostaglandins (particularly prostaglandin E2)
released during the refractory period probably protect against repeated episodes of EIB
( figure 2) [32].

Acute bronchoconstriction was previously believed to be followed by late phase

bronchoconstriction in some patients [33]. Findings in subsequent studies have been
variable [34,35]; however, it does appear that the risk and severity of late phase
bronchoconstriction due to EIB is substantially less than that associated with allergen-
induced asthma [36,37].

Among atopic asthma patients with sensitization to inhalant allergens, EIB may be more
likely to occur when the exercise includes exposure to the relevant allergen. As an example,
runners are more likely to report exercise-related asthma symptoms during their pollen or
mold allergy season [38,39].

DIAGNOSIS

The diagnosis of exercise-induced bronchoconstriction (EIB) is based on the combination of

compatible clinical symptoms (eg, exercise-related symptoms of dyspnea, cough, or wheeze)
and demonstration of reversible airflow limitation in response to exercise or a surrogate
challenge [6,30,40]. In patients with well-documented asthma and typical asthma symptoms
following exercise, formal exercise testing may not be needed unless symptoms do not
resolve with, or are not prevented by, pretreatment with inhaled beta agonists.
In patients without documented asthma, further assessment is helpful to ensure that
alternative causes of dyspnea are not overlooked and that unnecessary therapy is not
prescribed. This is particularly true when an adult develops new onset exercise related
symptoms. Formal testing is also helpful in evaluating highly trained athletes, as exercise
related respiratory symptoms are poor predictors of EIB in this setting [6,41-43]. (See
"Asthma in adolescents and adults: Evaluation and diagnosis", section on 'Diagnosis'.)

● Exercise challenge – An exercise challenge test is the most direct and preferred way to
establish a diagnosis of EIB [30]. This usually involves 6 to 10 minutes of ergometer or
treadmill exercise, sufficient to raise the heart rate to 80 to 90 percent of the predicted
maximum. A test is generally considered positive if the forced expiratory volume in one
second (FEV1) decreases by 10 percent or more, although a fall of 15 percent is more
diagnostic [6,30]. (See "Bronchoprovocation testing", section on 'Exercise challenge'.)

● Surrogate provocation tests – Alternatively, surrogate tests to assess bronchial

hyperresponsiveness (eg, eucapnic voluntary hyperventilation, methacholine,
histamine, or mannitol inhalation challenge) may be performed in specialized
laboratories [44,45]. Depending on the available facilities, a surrogate test can be used
instead of an exercise challenge test. Or, if the direct test is negative, an indirect test
may identify patients with EIB who have a false negative exercise test [46]. Among the
surrogate tests, eucapnic voluntary hyperventilation appears to have the greatest
sensitivity for EIB [47,48]. (See "Bronchoprovocation testing", section on 'Eucapnic
voluntary hyperpnea' and "Bronchoprovocation testing", section on 'Pharmacologic
challenge'.)

● Diagnosis in elite athletes – The International Olympic Committee and the World Anti-
Doping Agency require an objective test to confirm the diagnosis of asthma, such as
spirometry demonstrating airflow limitation with reversibility following inhaled
bronchodilator OR a positive bronchoprovocation test, as described above [40,46]. (See
'World Anti-Doping Agency' below.)

Measurement of peak expiratory flow rates before and after exercise frequently leads to
inaccurate results, but portable devices that record forced expiratory volume in one second
(FEV1) are more accurate [30]. After a baseline value has been established, FEV1 can be
measured before and 2.5, 5, 10, 15, and 30 minutes after exercise and correlated with
symptoms.

DIFFERENTIAL DIAGNOSIS

Other causes of exercise-induced dyspnea must be considered in the differential diagnosis of

exercise-induced bronchoconstriction (EIB), particularly in patients who have no other
manifestations of asthma, have normal baseline spirometry, and derive no benefit from
pretreatment with bronchodilators. Central airway obstruction, paradoxical vocal fold motion
(PVFM), laryngomalacia, exercise-induced anaphylaxis, interstitial lung disease,
gastroesophageal reflux, poor cardiovascular conditioning, coronary heart disease, and
exercise-induced dysrhythmias should be considered in adults who present with atypical
exercise-induced dyspnea. A general approach to the diagnosis of dyspnea and wheezing
illnesses are provided separately. (See "Evaluation of wheezing illnesses other than asthma
in adults" and "Inducible laryngeal obstruction (paradoxical vocal fold motion)", section on
'Evaluation'.)

The following exercise-associated airway processes may be missed on routine pulmonary

function testing. Diagnosis may require direct visualization or a high index of suspicion:

● Central airway obstruction – Features that suggest central airway obstruction include
a lack of response to inhaled bronchodilator, associated hemoptysis, and risk factors
for lung cancer or metastasis to the airway. (See "Clinical presentation, diagnostic
evaluation, and management of malignant central airway obstruction in adults".)

● Exercise-induced laryngeal obstruction (EILO) – The hallmark of EILO (previously

known as paradoxical vocal fold motion and vocal cord dysfunction) is inspiratory
stridor accompanied by respiratory distress that occurs during exercise. However, a
portion of patients have expiratory stridor due to expiratory adduction of the vocal
folds. (See "Inducible laryngeal obstruction (paradoxical vocal fold motion)" and
"Exercise-induced laryngeal obstruction".)

● Exercise-induced laryngomalacia – Exercise-induced laryngomalacia is associated

with inspiratory stridor during exercise caused by abnormal movement of the
aryepiglottic folds into the endolarynx, resulting in subtotal glottic obstruction [49-52].
It is distinct from tracheomalacia. The diagnosis is made by flexible laryngoscopy
during exercise. Exercise-induced laryngomalacia is a form of exercise-induced
laryngeal obstruction. (See "Inducible laryngeal obstruction (paradoxical vocal fold
motion)", section on 'Differential diagnosis'.)

● Exercise-induced anaphylaxis – Exercise-induced anaphylaxis is characterized by the

abrupt onset of signs and symptoms of anaphylaxis during exercise. Prodromal
symptoms may include generalized pruritus, warmth, urticaria, and fatigue. A food co-
factor may be implicated. Some patients develop laryngeal angioedema as a
component, although hypotension and/or cardiovascular collapse are more common.
(See "Exercise-induced anaphylaxis: Clinical manifestations, epidemiology,
pathogenesis, and diagnosis", section on 'Clinical manifestations'.)
 ● Exercise-associated reflux – Laryngopharyngeal reflux during exercise can mimic mild
symptoms of EIB and exercise-induced anaphylaxis, including flushing, throat
discomfort, dysphonia, and chest tightness/cough. However, it is not associated with
severe dyspnea, pruritus, or urticaria. (See "Laryngopharyngeal reflux in adults:
Evaluation, diagnosis, and management".)

● Dysfunctional breathing – Dysfunctional breathing (eg, hyperventilation, deep

sighing, thoracic-dominant breathing, mouth breathing, accessory muscle use at rest,
and thoraco-abdominal asynchrony) can contribute to persistent dyspnea during
exercise and may be present in association with exercise-induced bronchoconstriction
or as an independent diagnosis [53-57]. Physical therapy may help by improving muscle
balance, posture, and diaphragmatic function [57].

The differential diagnosis of EIB is similar among children. In one retrospective review,
treadmill exercise testing was performed in 142 children referred to a pediatric allergy and
pulmonology clinic with exercise-induced dyspnea who had no other signs of asthma or in
whom treatment with beta-2-agonists had failed [58]. Symptoms of exercise-induced
dyspnea were reproduced in 82 percent. Among these 117 children, only 11 (9 percent) had
EIB (defined by reproduction of symptoms and ≥15 percent decrease in FEV1 from baseline).
Other diagnoses included normal physiologic exercise limitation (63 percent), restrictive
abnormalities (13 percent), vocal cord dysfunction (11 percent); laryngomalacia (2 percent),
and hyperventilation and supraventricular tachycardia, each in one patient.

MANAGEMENT

The combination of general measures and pharmacologic intervention can prevent exercise-
induced bronchoconstriction (EIB) in almost all patients. A major goal is to ensure that
exercise is not avoided by patients with EIB. Asthmatics should exercise as much as desired
and should be encouraged by the fact that athletes have won Olympic medals and played
professional sports despite symptomatic asthma.

Monitoring — Response to therapy can be assessed subjectively in terms of symptom

control and exercise tolerance. Peak expiratory flow (PEF) measurement before and after
exercise may be helpful, although measurements of forced expiratory volume in one second
(FEV1) are more reliable [30]. If objective measurement of a patient's response to therapy is
required, a formal exercise test, rather than the more widely available methacholine
challenge, should be considered [59,60]. (See "Bronchoprovocation testing".)

While monitoring of PEF at home or during athletic practice lacks documented benefits in
prevention of EIB, sports medicine clinicians and athletic programs have utilized PEF
monitoring to help detect athletes with subclinical or unrecognized
bronchoconstriction. These athletes may be given a slower warm up, modified workout, and
suggestions for improved compliance or better technique in inhaler use. Should the athlete
continue to experience a reduction in PEF or frequent EIB, a medical evaluation for
medication adjustment would likely be indicated. (See "Peak expiratory flow monitoring in
asthma".)

Nonpharmacologic measures to reduce EIB — Improved understanding of the

pathophysiology of EIB has resulted in general recommendations that can help reduce its
severity. These measures are based upon observed relationships between the severity of
bronchoconstriction and the following factors:

● The magnitude of minute ventilation

● The temperature and humidity of the inspired air

Improving a patient's cardiovascular fitness reduces the minute ventilation required for a
given level of exercise, thereby decreasing the stimulus for bronchoconstriction. Similarly,
bronchoconstriction is lessened when the inspired gas is warmer and more humid. Patients
should be instructed to breathe through a loosely fitting scarf or mask when exercising in
cold, dry conditions [61,62].

The role of a pre-exercise warm-up is unclear. Some studies suggest that high intensity and
variable intensity warm-up routines attenuate the fall in forced expiratory volume in one
second (FEV1), but data are conflicting [46,63,64]. Finally, ensuring that patients know when
and how to use a metered dose or dry powder inhaler correctly can greatly enhance the
efficacy of pharmacologic measures.

The role of controlling adverse environments in reducing symptoms of EIB has not been
formally studied, although it seems reasonable to reduce chloramines in indoor pool
environments, use a heat-exchanger or other face mask during cold weather endurance
exercise, and, for urban athletes, schedule outdoor training around low-traffic hours [30,65].

Selection of pharmacologic therapy — Treatment of EIB has been studied primarily in

patients with both EIB and underlying asthma [30]. Therapeutic options for patients with EIB
as the only manifestation of airway hyperresponsiveness are less well researched. In
general, if EIB occurs frequently in patients with poorly controlled asthma, the most
important strategy is to improve overall asthma control [30,66]. Inhaled glucocorticoids and
leukotriene-modifying agents are often useful in this regard. Prophylactic treatment of EIB
prior to exercise, using an inhaled short-acting beta-2 agonist, should be considered in all
patients with EIB, even if EIB is the sole manifestation of airway hyperresponsiveness. The
following sections describe the pharmacologic management of various patient presentations
( table 1).
 Pre-exercise treatments for EIB

General approach — Short-acting beta-agonists (SABAs; albuterol [salbutamol],

levalbuterol) are the most effective therapy for quick relief of EIB. All patients who report
exercise-related symptoms should have access to a SABA for quick relief and be instructed
on correct technique. Two inhalations (eg, albuterol 90 mcg/inhalation) are generally
sufficient; occasionally four inhalations are needed.

Ipratropium is generally not used for quick relief as bronchodilation is delayed (onset at 15
minutes and peak at one to two hours) compared with SABAs.

Patients who have well-controlled asthma, but frequently have asthma symptoms with
exercise, should be instructed to use prophylactic treatment approximately 5 to 20 minutes
before exercise, usually with two inhalations of a SABA (eg, albuterol, levalbuterol) [30,67]. An
alternative is to use a combination budesonide-formoterol (160 mcg/4.5 mcg) inhaler, 1
inhalation 5 to 20 minutes prior to exercise [66,68]. (See "Treatment of intermittent and mild
persistent asthma in adolescents and adults", section on 'Combination inhaled
glucocorticoid plus formoterol as needed'.)

Equipotent doses of formoterol, salmeterol, and terbutaline appear to be equally effective in

providing short-term control of EIB, although the onset of action is slower with salmeterol
than with the other agents ( table 2) [69]. However, frequent use of inhaled beta-agonists
may lead to tolerance and decreased efficacy, and long-acting beta-agonists (eg, salmeterol,
formoterol) should never be used as monotherapy in asthma [70]. Thus, it is preferable for
athletes who exercise regularly to aim for sufficient control of their asthma that beta-agonist
pretreatment is not routinely needed [46]. (See "Beta agonists in asthma: Acute
administration and prophylactic use".)

Children often present a difficult clinical situation by exercising vigorously and intermittently
throughout the day making pretreatment prior to exercise difficult. In this setting, it might
be tempting to add a long-acting inhaled beta-2 agonist (LABA; such as salmeterol and
formoterol) to provide protection against EIB for 12 or more hours [71,72]. However, LABAs
are not recommended for monotherapy in asthma and should be prescribed in combination
with inhaled glucocorticoid. Alternative strategies, such as use of leukotriene receptor
antagonists, are described below. (See 'Prolonged or recurrent exercise' below.)

Approach in patients with intolerance of short-acting beta-agonists — Some

patients are intolerant of the adverse effects of SABAs, such as jitteriness and increased
heart rate. Several strategies can be used in these patients, including adjusting type or dose
of SABAs or trials of alternative agents for EIB control.
 ● Altering SABA type, dose, or technique – For some patients, switching to an alternate
SABA such as levalbuterol, using a chamber device (spacer) to reduce oral deposition,
or using one inhalation instead of two allows improved tolerance of SABA
pretreatment. Levalbuterol is an isomer of albuterol, R-albuterol. The use of
levalbuterol and chamber devices are discussed separately. (See "The use of inhaler
devices in adults", section on 'Spacers and holding chambers' and "The use of inhaler
devices in children", section on 'Spacers and holding chambers' and "Beta agonists in
asthma: Acute administration and prophylactic use", section on 'Levalbuterol'.)

● Leukotriene receptor antagonists – LTRAs reduce EIB in most patients and improve
recovery to baseline ( table 3) based upon a review of 11 randomized trials in the
American Thoracic Society guideline [30]. Protection from EIB is apparent by two hours
after a single dose of montelukast, and postexercise recovery is accelerated [73,74]. The
long half-life of montelukast allows once-daily dosing with durable protection from EIB
for up to 12 hours [75,76]. However, LTRAs are not effective in all patients [77]. While
LTRAs can be used to prevent EIB, patients will need to keep a SABA on hand for quick
relief of any breakthrough symptoms. (See "Antileukotriene agents in the management
of asthma".)

● Ipratropium – When used to prevent EIB, the inhaled muscarinic antagonist

(anticholinergic agent), ipratropium, reduces the decrease in FEV1 relative to placebo,
but is less effective than SABAs [30,78,79]. For patients who are intolerant of SABAs,
pretreatment with ipratropium will likely provide partial protection against EIB.

Prolonged or recurrent exercise — Patients who exercise for more than three hours or
more than once a day represent a challenge in that use of a SABA multiple times a day is
likely to lead to tachyphylaxis. One might imagine that an inhaled LABA might be useful in
this situation. However, in concert with current guidelines, we do not recommend regular
use of LABAs (ie, once or twice daily) as monotherapy for EIB, because of concerns about a
loss of bronchoprotective effect over time [30,79,80]. Thus, for patients who would require
regular, daily dosing of a SABA or LABA to control EIB, we suggest concomitant use of
inhaled glucocorticoid or a leukotriene receptor antagonist (LTRA; montelukast, zafirlukast).
(See "Beta agonists in asthma: Acute administration and prophylactic use", section on
'Tolerance'.)

LTRAs must be taken at least two hours prior to exercise to have a maximal protective effect,
but the effect lasts 12 (zafirlukast) to 24 (montelukast) hours [30]. While not effective in all
patients, LTRAs appear superior to LABAs when treating asthmatics with EIB. In one
multicenter trial, asthmatics with EIB were randomly assigned to either montelukast or
salmeterol for eight weeks [81]. Therapy was protective within three days for both groups;
however, tolerance to salmeterol developed, and by eight weeks, the bronchoprotective
effect of montelukast was significantly better ( figure 3).

As mentioned above, children with EIB can pose a therapeutic challenge, because they tend
to exercise intermittently throughout the day and often neglect to premedicate with an
inhaled SABA. LTRAs are an effective option in this setting. In a randomized trial of EIB in
children, montelukast and montelukast with budesonide were superior to budesonide and
budesonide with formoterol [82].

Improving asthma control to the point that specific pretreatment is not necessary before
exercise is an additional strategy. This goal can often be accomplished with use of inhaled
glucocorticoids according to current guidelines [30,66]. (See 'Persistent EIB symptoms
despite premedication' below and "An overview of asthma management".)

Persistent EIB symptoms despite premedication — When EIB is refractory to

premedication with a SABA, poor asthma control is often the cause. The most effective
method of achieving asthma control involves appropriate step-up therapies including the
use of inhaled glucocorticoids ( table 4A-C). Other agents frequently involved in asthma
control of these patients include inhaled glucocorticoid-LABA combination therapies, or
leukotriene receptor antagonists (LTRA). (See "An overview of asthma management", section
on 'Initiating pharmacologic treatment' and "Asthma in children younger than 12 years:
Overview of initiating therapy and monitoring control".)

Although inhaled glucocorticoids do not have an immediate protective effect on EIB, they do
improve airway hyperresponsiveness and, over weeks to months, decrease the magnitude of
bronchoconstriction that occurs with a given workload [82-85]. Some studies have noted that
inhaled glucocorticoids do not decrease EIB in a dose-related manner [59,60]. In contrast, a
decrease in methacholine sensitivity (as determined by methacholine challenge) is generally
well-correlated with the inhaled glucocorticoid dose. These findings suggest both a
mechanism for EIB distinct from methacholine, and considerable variability in response to
inhaled glucocorticoid therapy. This variability is partially explained by a greater magnitude
of benefit from inhaled glucocorticoids in patients with higher sputum eosinophilia [9].

Inhaled glucocorticoids do not require a therapeutic use exception (TUE) from the World
Anti-Doping Agency [86], although oral and intravenous glucocorticoids do require a TUE.
(See 'World Anti-Doping Agency' below.)

Refractory EIB due to extreme conditions — Data are limited in terms of strategies to
prevent EIB in high performance athletes and patients exercising in extreme conditions (eg,
very cold, dry air). Therapies that may be useful when added to pretreatment with a SABA
include regular use of an LTRA (eg, montelukast, zafirlukast) or pretreatment with
ipratropium [87]. Nonpharmacologic measures may also be helpful. (See "Antileukotriene
agents in the management of asthma", section on 'Clinical use of leukotriene-modifying
drugs in asthma' and 'Nonpharmacologic measures to reduce EIB' above.)

● Leukotriene receptor antagonists – LTRAs, when added to pretreatment with a SABA

may provide better protection in extreme conditions than either agent alone, based on
clinical experience [88], although the response is variable [87,89]. LTRAs do not require
a TUE from the World Anti-Doping Agency (WADA). (See 'World Anti-Doping Agency'
below.)

● Ipratropium – Among elite cross-country skiers, inhaled ipratropium was associated

with greater improvement in FEV1 than inhaled albuterol (salbutamol) [90]. In addition,
the improvement in FEV1 correlated with greater airways hyperresponsiveness to
methacholine challenge. Whether this response to ipratropium translates into better
protection against EIB during high intensity cold air exercise has not been determined.

Dietary modification — Data are inconclusive about whether dietary interventions are
useful in the management of EIB. Diets rich in anti-inflammatory omega-3 fatty acids have
not been conclusively demonstrated to be helpful in the general population of patients with
asthma [91]. Despite early data suggesting benefit of increased dietary omega-3 fatty acids
in EIB, subsequent data do not support a benefit [30,92,93]. In a randomized trial of 23
patients treated for three weeks with either fish oil supplements (containing omega-3 fatty
acids) or placebo, the group on fish oil was not different from control in sputum eosinophils,
FEV1 percent predicted, symptom score, or response to mannitol challenge (a surrogate for
EIB) [93].

Systematic reviews have reached different opinions about the effect of vitamin C in reducing
EIB possibly due to the small number of subjects and differing choices of outcome
measurements [94,95]. Overall, the data appear inconclusive. Lycopene supplements have
not been shown to reduce EIB [30].

Other therapies — Other types of asthma therapy are not very effective in protecting
against EIB. As an example, oral beta-2 agonists and methylxanthines are marginally
effective or ineffective in almost all patients [96,97].

Oral antihistamines appear to provide modest protection against EIB in patients with
inhalant allergies, but not in nonatopic patients [30].

Several other drugs have been tested as possible prophylactic agents against EIB. Inhaled
medications, such as furosemide [98], prostaglandin E2 [99], indomethacin [100], and
heparin [101], may protect against EIB. However, long-term clinical use of these compounds
has not been directly compared with the prophylactic use of inhaled beta-2 agonists. For this
reason, their role in clinical practice is unclear.
WORLD ANTI-DOPING AGENCY

The World Anti-Doping Agency (WADA), which governs medication use by athletes in
international competition, has published guidelines for the diagnosis and management of
asthma in athletes [102] and a list of medications that require a Therapeutic Use Exemption
(TUE) [86].

The WADA lists beta-agonists on its prohibited medication list due to concerns about
performance enhancement [53,86]. However, inhaled albuterol (salbutamol), maximum dose
1600 mcg/24 hours and 800 mcg/12 hours, inhaled formoterol, maximum delivered dose 54
mcg/24 hours, and inhaled salmeterol, maximum dose 200 mcg/24 hours, are acceptable
and do not need a Therapeutic Use Exception [86]. Nebulized beta-agonists may reach levels
above those permitted. Urinary levels of albuterol over 1000 ng/mL or formoterol over 40
ng/mL are considered to be in excess of therapeutic use to prevent EIB.

In terms of potential effects on performance, a study of 16 athletes found that high-dose

salbutamol (albuterol) 1600 mcg/day for six weeks did not increase strength, power, or
endurance relative to placebo [103].

Inhaled glucocorticoids are permitted by the WADA and do not need a Therapeutic Use
Exception [86]. Systemic glucocorticoids are prohibited in competition, and a Therapeutic
Use Exception may need to be filed for use outside of competition [86,104]. Leukotriene
receptor antagonists (montelukast, zafirlukast) and omalizumab are permitted agents.

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Exercise-induced
bronchoconstriction".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, “The Basics” and “Beyond the
Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th
grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to
print or e-mail these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

● Basics topic (see "Patient education: Exercise-induced asthma (The Basics)")

● Beyond the Basics topics (see "Patient education: Exercise-induced asthma (Beyond the
Basics)")

SUMMARY AND RECOMMENDATIONS

● Definition – Exercise-induced bronchoconstriction (EIB) refers to the episodic

bronchoconstriction that follows exercise in many asthmatic patients. The term EIB
reflects the view that exercise is a trigger of bronchoconstriction in patients with
underlying asthma. (See 'Introduction' above.)

● Avoidance measures – Improving a patient's cardiovascular fitness reduces the minute

ventilation required for a given level of exercise, thereby decreasing the stimulus for
bronchoconstriction. Avoiding exercise in cold, dry air can also reduce the stimulus for
exercise-induced bronchoconstriction. (See 'Nonpharmacologic measures to reduce
EIB' above.)

● Pharmacologic therapy – Therapy for EIB varies somewhat with the clinical setting
( table 1). All patients with EIB should have access to a short-acting beta-agonist
(SABA) available when exercising for relief of asthma symptoms. (See 'General
approach' above.)

• Pre-exercise treatments for EIB – For patients who have otherwise well-controlled
asthma, but who frequently have asthma symptoms with exercise, we recommend
prophylactic use of a SABA (eg, albuterol 90 mcg/inhalation, 2 inhalations) or
combination inhaled glucocorticoid and formoterol (eg, budesonide-formoterol 160
mcg/4.5 mcg, 1 inhalation), approximately 5 to 20 minutes prior to exercise rather
than observation alone (Grade 1B). (See 'Pre-exercise treatments for EIB' above.)

Alternatives for prophylaxis in patients who prefer not to use or cannot tolerate a
SABA include leukotriene receptor antagonists (LTRA) or inhaled ipratropium.
However, neither of these alternatives reverse bronchoconstriction as rapidly as a
SABA or formoterol, so the patient will still need to keep a SABA- or formoterol-
containing inhaler on hand for break-through symptoms. (See 'Approach in patients
with intolerance of short-acting beta-agonists' above.)
 • Prolonged or recurrent exercise – For patients who require daily therapy for EIB
due to prolonged or recurrent exercise, we suggest regular use of an LTRA or an
inhaled glucocorticoid in addition to a short-acting beta-agonist, rather than regular
daily use of a beta-agonist alone (Grade 2B). The use of an LTRA may be particularly
attractive in children, in whom exercise may be unpredictable or repeated
throughout the day, and who may not use their inhalers as directed. (See 'Prolonged
or recurrent exercise' above and 'Pre-exercise treatments for EIB' above.)

• Persistent EIB symptoms despite pretreatment – Most patients with persistent

EIB symptoms despite use of exercise pretreatment therapies have undiagnosed
poorly controlled asthma. For these patients, asthma control should be prioritized
with step-up therapy including an inhaled glucocorticoid, inhaled glucocorticoid-
LABA combination, or LTRA. (See 'Persistent EIB symptoms despite premedication'
above and "An overview of asthma management".)

● Ineffective treatments – Antihistamines, theophylline and oral beta agonists are

minimally effective or ineffective for EIB. (See 'Other therapies' above.)

Use of UpToDate is subject to the Terms of Use.

Topic 533 Version 33.0

GRAPHICS

Exercise-induced bronchoconstriction

The time course of exercise-induced bronchoconstriction in an asthmatic

patient in whom the FEV1 fell by more than 20 percent after cycling.

FEV1: forced expiratory volume in one second.

Graphic 64910 Version 2.0

Refractoriness to repeated exercise-induced
bronchoconstriction

Exercise-induced bronchoconstriction (as measured by a fall in FEV1) is

attenuated when a second exercise challenge is performed one hour after
an initial challenge.

FEV1: forced expiratory volume in one second.

Graphic 78975 Version 2.0

Management of exercise-induced bronchoconstriction (EIB)

Clinical
Intervention Comments
problem

All patients with Educate about features of exercise

EIB that are likely to provoke EIB (eg,
effect of temperature, dry air,
intensity of exertion, allergens,
pollution) and measures for
mitigation

Educate about use of SABA to treat

EIB symptoms (eg, albuterol two
puffs)

Educate about use of SABA or other

agent to prevent EIB

Advise caution about vigorous

exercise when asthma is poorly-
controlled

Patients Try one puff of albuterol instead of May not provide adequate prevention
intolerant of two of EIB symptoms.
SABA
Review inhaler technique and
consider use of spacer/chamber

Improve general control of asthma If asthma not well-controlled (based

(eg, with inhaled glucocorticoid) to
reduce need for prophylaxis
on frequency/severity of symptoms
or need for rescue inhaler, low peak
flow or FEV1), add inhaled
glucocorticoid. If asthma is otherwise
well-controlled, try alternate
preventive agents.

Try alternate SABA (eg, levalbuterol)* Try levalbuterol if above interventions

are unsuccessful and levalbuterol is
available. Levalbuterol can also be
used for breakthrough symptoms.
May not completely eliminate
adverse effects of SABA.

Try regular use of LTRA* ¶ Δ LTRA may be more effective in

children than adults.

Try ipratropium two puffs, 20 to 30

minutes prior to exercise* Δ

Substitute cromolyn or nedocromil

(where available) for SABA for
prophylaxis* Δ
 EIB refractory to Add regular use of LTRA
SABA
Improve general control of asthma
(eg, with inhaled glucocorticoid)

Use cromoglycate with SABA as

prophylaxis (where available)

Reassess diagnosis

Patients who Avoid LABA monotherapy or daily use Tachyphylaxis may occur with daily
exercise for more of SABA SABA or LABA.
than three hours
Try LTRA May be more effective for prevention
or more than
of EIB in children than adults.
once per day
Improve general control of asthma
(eg, with inhaled glucocorticoid)

Patients who Try methods for mitigation (eg,

exercise in warm-up, scarf or face mask),
extreme depending on setting
conditions (eg,
Empiric trial of combination
high intensity or
albuterol-ipratropium 20 to 30
in dry cold air)
minutes prior to exercise

SABA: short-acting beta-agonist; FEV1: forced expiratory volume in one second; LTRA:
leukotriene-receptor antagonist; LABA: long-acting beta-agonist.

​ Choice between levalbuterol, LTRA, ipratropium, and cromoglycate is based on drug availability
*
and patient/clinician preference.

¶ LTRA must be taken at least two hours prior to exercise if used episodically.

Δ Patient will still need to have a SABA inhaler available for treatment of breakthrough
symptoms.

Graphic 105874 Version 2.0

Usual doses of short-acting bronchodilators for asthma in adolescents
and adults*

Drug name(s) Preparation(s) ¶ Dose

Albuterol MDI Δ MDI: 90 Usual dose: 2 inhalations every 4 to 6 hours

mcg/inhalation as needed
(United States) Acute exacerbation at home: 2 to 4
MDI: 100 inhalations, can be repeated every 20
mcg/inhalation minutes for a total of 3 doses, then as
(Canada) directed ◊
Acute care setting: 4 to 8 inhalations every
20 minutes for 3 doses § , then taper
depending on response to therapy

Albuterol DPI DPI Δ : 90 Usual dose: 2 inhalations every 4 to 6 hours,

mcg/actuation (United as needed
States) Acute exacerbation at home: 2 to 4
inhalations, can be repeated every 20
minutes for a total of 3 doses, then as
directed ◊
Acute care setting: 4 to 8 inhalations every
20 minutes for 3 doses § , then taper
depending on response to therapy

Albuterol DPI DPI: 200 Usual dose: 1 inhalation every 4 to 6 hours,

(Canada) mcg/actuation as needed
(Canada) Exercise-induced bronchoconstriction: 1
inhalation 15 minutes prior to exercise

Albuterol solution for Nebulizer solutions:
nebulization
Usual dose: 2.5 mg every 4 to 6 hours, as
0.083% (2.5 mg/3 needed
mL) Acute exacerbation at home: Administer 2.5
0.5% (2.5 mg/0.5 mg, can repeat every 20 minutes for total of
mL) concentrate; 3 doses, then decrease frequency to every 1
must be diluted to 4 hours, as tolerated ¥
in 2.5 mL saline Acute care setting: Administer 2.5 to 5 mg,
can repeat every 20 minutes for total of 3
doses, then decrease frequency to every 1 to
4 hours, as tolerated
Acute care setting (critically ill): Continuous
nebulizer treatment: Use a large volume
nebulizer, 10 to 15 mg/hour in monitored
setting

Albuterol-budesonide MDI: Albuterol 90 mcg Usual dose: 2 inhalations every 4 to 6 hours

MDI and budesonide 80 as needed
 mcg/actuation (United Acute exacerbation at home: 2 inhalations,
States) can be repeated every 20 minutes for a total
of 3 doses, then as directed ¥

Levalbuterol MDI Δ 45 mcg/inhalation Usual dose: 2 inhalations every 4 to 6 hours,

(United States) as needed
Acute exacerbation at home: 2 to 4
inhalations; can be repeated every 20
minutes for a total of 3 doses, then as
directed ◊
Acute care setting: 4 to 8 inhalations every
20 minutes for 3 doses, then taper
depending on response to therapy §

Levalbuterol solution Nebulizer solution: Usual dose: Administer 0.63 to 1.25 mg

for nebulization
0.63 mg/3 mL (equivalent to 1.25 to 2.5 mg albuterol) every
1.25 mg/3 mL 6 to 8 hours, as needed (up to 3 doses per
1.25 mg/0.5 mL 24 hours)
concentrate; Acute exacerbation at home: Administer
must be diluted 1.25 mg; can be repeated every 20 minutes
in 2.5 mL saline for a total of 3 doses, then decrease
frequency to every 1 to 4 hours, as
tolerated ¥
Acute care setting: Administer 1.25 mg to
2.5 mg (equivalent to 2.5 to 5 mg of
albuterol); can repeat every 20 minutes for
total of 3 doses, then decrease frequency to
every 1 to 4 hours, as tolerated

Terbutaline DPI DPI: 0.5 mg/actuation Usual dose: 1 inhalation every 4 hours, as
(Canada) needed
If no effect after 5 minutes, can repeat dose

Ipratropium-albuterol SMI: Ipratropium 20 Usual dose (off-label): 2 inhalations every 6

SMI mcg and albuterol 100 hours, as needed
mcg/inhalation Acute exacerbation (off-label): 4 to 8
(United States) inhalations every 20 minutes for 3 doses,
and then as needed for up to 3 hours

Ipratropium-albuterol Nebulizer solution: Usual dose (off-label): Administer 1 vial (3

solution for Ipratropium 0.5 mg mL) every 4 to 6 hours, as needed
nebulization and albuterol 2.5 mg Acute exacerbation (off-label): Administer 1
per 3 mL/vial ‡ vial (3 mL), every 20 minutes for 3 doses,
and then as needed for up to 3 hours ¥

MDI: metered-dose inhaler; DPI: dry-powder inhaler; SMI: soft mist inhaler.

* Oral formulations of albuterol and terbutaline are less effective than inhaled formulations and
are not recommended in asthma. Inhaled epinephrine (MDI or nebulized) is not recommended
for routine use.
¶ Doses shown and strengths (ie, mcg per puff or inhalation) are based upon product
descriptions approved in the United States and Canada as noted, which may differ from how
strengths are described for products available in other countries. Consult local product
information before use.

Δ Agent can also be used to prevent exercise-induced bronchoconstriction, 2 inhalations 5 to 20

minutes prior to exercise.

◊ Typically, two puffs are used for mild-to-moderate symptoms and four puffs for more severe
symptoms; over the course of the first hour, the patient can determine (based on action plan or
clinician guidance) whether to continue self-care at home or seek additional medical attention.

§ The number of inhalations is based on the severity of respiratory impairment, number of

inhalations the patient has already used, and availability of monitoring. When administering an
albuterol MDI for acute asthma exacerbation in an office or acute care setting, use of a valved
holding chamber and careful attention to technique are recommended.

¥ Over the course of the first hour, the patient can determine (based on action plan or clinician
guidance) whether to continue self-care at home or seek additional medical attention.

‡ Nebulizer solution in Canada is ipratropium 0.5 mg and albuterol 2.5 mg per 2.5 mL.

Graphic 72467 Version 27.0

Usual doses of antileukotriene agents in the management of persistent
asthma

Infant and Adolescent

Medication Preparations Pediatric
small child and adult

Montelukast Granules: 4 mg 12 months* to 5 6 to 14 years: 5 ≥15 years and

per packet years: 4 mg mg chewable adult: 10 mg
granules or tablet once daily tablet once daily
Chewable
chewable tablet in evening in evening
tablets: 4 mg, 5
once daily in
mg
evening
Tablet: 10 mg

Zafirlukast ¶ Tablets: 10 mg, (Not studied) 5 to 11 years: 10 ≥12 years and

20 mg mg twice per day adult: 20 mg
twice per day

Zileuton ¶ Immediate- (Not studied) (Not studied) ≥12 years and

release tablet: adult:
600 mg Immediate
Extended-release release: 600
tablet: 600 mg mg four
times per
day
Extended
release:
1200 mg
twice per
day

Pranlukast Δ Capsules: 112.5 24 months to 5 6 to 11 years: 7 ≥12 years and

mg, 225 mg years: 7 to 10 to 10 mg/kg per adult: 225 mg
mg/kg granules day granules in twice per day
Granules: 50 mg,
per day in two two divided
70 mg, 100 mg
divided doses doses (maximum
per packet
225 mg twice per
day)

* Approved for use in infants ≥6 months in some countries other than United States.

¶ Elevated transaminases and severe hepatoxicity have been reported.

Δ Not available in United States. Available in Japan, Mexico, Venezuela, Turkey, and Korea.

Data from:

1. US Food & Drug Administration approved prescribing information. Available

at https://dailymed.nlm.nih.gov/dailymed/ (Accessed September 20, 2020).
2. Bisgaard H, et al. Pediatric Pulmonol 2009; 44:568.
3. Keam SJ, et al. Drugs 2003; 63:991.
Graphic 77367 Version 6.0
The FEV1 after exercise in patients who received
montelukast (A) and salmeterol (B)

The mean response curves are shown for percentage change in FEV1
from prechallenge FEV1 at baseline (closed circles), days 1 to 3
(closed squares), week 4 (open squares), and week 8 (open circles)
after study treatment.

FEV1: forced expiratory volume in one second.

Data from Edelman, et al. Ann Intern Med, 2000; 132:100.

Graphic 69196 Version 3.0

Classifying asthma severity and initiating treatment in youths greater
than or equal to 12 years of age and adults

Classification of asthma severity (≥12 years of age)

Components of severity Persistent

Intermittent
Mild Moderate Severe

Impairment Symptoms ≤2 days/week >2 Daily Throughout

days/week the day
Normal
but not daily
FEV1/FVC:
Nighttime ≤2x/month 3 to >1x/week Often
8 to 19
awakenings 4x/month but not 7x/week
years 85%
nightly
20 to 39
years 80% Short-acting ≤2 days/week >2 Daily Several
beta2-agonist days/week times per
40 to 59
use for but not daily, day
years 75%
symptom and not
60 to 80 control (not more than
years 70% prevention of 1x on any
EIB) day

Interference None Minor Some Extremely

with normal limitation limitation limited
activity

Lung function Normal FEV1 FEV1 FEV1 ≥60 FEV1

between ≥80% but <80% <60%
exacerbations predicted predicted predicted
FEV1 ≥80% FEV1/FVC FEV1/FVC FEV1/FVC
predicted normal reduced reduced
FEV1/FVC 5% >5%
normal

Risk Exacerbations 0 to 1/year (see ≥2/year (see footnote)

requiring oral footnote)
systemic
Consider severity and interval since last exacerbation
glucocorticoids
Frequency and severity may fluctuate over time for patients
in any severity category

Relative annual risk of exacerbations may be related to FEV1

Recommended step for Step 1 Step 2 Step 3 Step 4 or 5

initiating treatment
And consider short course of
oral systemic glucocorticoids

In two to six weeks, evaluate level of asthma control that is

achieved and adjust therapy accordingly.
Assessing severity and initiating treatment for patients who are not currently taking long-
term control medications. The stepwise approach is meant to assist, not replace, the clinical
decision-making required to meet individual patient needs. Level of severity is determined by
assessment of both impairment and risk. Assess impairment domain by patient's/caregiver's
recall of previous two to four weeks and spirometry. Assign severity to the most severe category
in which any feature occurs. At present, data are inadequate to correlate frequencies of
exacerbations with different levels of asthma severity. In general, more frequent and intense
exacerbations (eg, requiring urgent, unscheduled care, hospitalization, or ICU admission)
indicate greater underlying disease severity. For treatment purposes, patients who had ≥2
exacerbations requiring oral systemic glucocorticoids in the past year may be considered the
same as patients who have persistent asthma, even in the absence of impairment levels
consistent with persistent asthma.

FEV1: forced expiratory volume in one second; FVC: forced vital capacity; ICU: intensive care unit.

Reproduced from: National Heart, Blood, and Lung Institute Expert Panel Report 3 (EPR 3): Guidelines for the Diagnosis
and Management of Asthma. NIH Publication no. 08-4051, 2007.

Graphic 58247 Version 5.0

Classifying asthma severity and initiating treatment in children 5 to 11
years of age

Classification of asthma severity (5 to 11 years of age)

Components of severity Persistent

Intermittent
Mild Moderate Severe

Impairment Symptoms ≤2 days/week >2 Daily Throughout

days/week the day
but not daily

Nighttime ≤2 times/month 3 to 4 >1 time/week Often 7

awakenings times/month but not nightly times/week

Short-acting ≤2 days/week >2 Daily Several times

beta2 agonist days/week per day
use for but not daily
symptom
control (not
prevention of
EIB)

Interference None Minor Some Extremely

with normal limitation limitation limited
activity

Lung function Normal FEV1 FEV1 FEV1 = 60 to FEV1 <60%

between ≥80% 80% predicted
exacerbations predicted predicted FEV1/FVC
FEV1 >80% FEV1/FVC FEV1/FVC = <75%
predicted >80% 75 to 80%
FEV1/FVC
>85%

Risk Exacerbations 0 to 1/year (see ≥2/year (see footnote)

requiring oral footnote)
systemic
Consider severity and interval since last exacerbation
glucocorticoids
Frequency and severity may fluctuate over time for patients in
any severity category

Relative annual risk of exacerbations may be related to FEV1

Recommended step for Step 1 Step 2 Step 3, Step 3,

initiating treatment medium dose- medium dose-
inhaled inhaled
glucocorticoids glucocorticoids
option option, or Step
4
 And consider short course of
oral systemic glucocorticoids

In 2 to 6 weeks, evaluate level of asthma control that is achieved and

adjust therapy accordingly

Assessing severity and initiating therapy in children who are not currently taking long-
term control medication. The stepwise approach is meant to assist, not replace, the clinical
decision-making required to meet individual patient needs. Level of severity is determined by
both impairment and risk. Assess impairment domain by patient's/caregiver's recall of the
previous 2 to 4 weeks and spirometry. Assign severity to the most severe category in which any
feature occurs. At present, data are inadequate to correlate frequencies of exacerbations with
different levels of asthma severity. In general, more frequent and intense exacerbations (eg,
requiring urgent, unscheduled care, hospitalization, or ICU admission) indicate greater
underlying disease severity. For treatment purposes, patients who had ≥2 exacerbations
requiring oral systemic glucocorticoids in the past year may be considered the same as patients
who have persistent asthma, even in the absence of impairment levels consistent with persistent
asthma.

EIB: exercise-induced bronchospasm; FEV1: forced expiratory volume in one second; FVC: forced
vital capacity; ICU: intensive care unit.

Reproduced from: National Heart, Blood, and Lung Institute Expert Panel Report 3 (EPR 3): Guidelines for the Diagnosis
and Management of Asthma. NIH Publication no. 08-4051, 2007.

Graphic 71181 Version 12.0

Classifying asthma severity and initiating treatment in children 0 to 4
years of age

Classification of asthma severity (0 to 4 years of age)

Components of severity Persistent

Intermittent
Mild Moderate Severe

Impairment Symptoms ≤2 days/week >2 days/week Daily Throughout

but not daily the day

Nighttime 0 1 to 2 3 to 4 >1 time/week

awakenings times/month times/month

Short-acting ≤2 days/week >2 days/week Daily Several times

beta2 agonist but not daily per day
use for
symptom
control (not
prevention of
EIB)

Interference None Minor Some Extremely

with normal limitation limitation limited
activity

Risk Exacerbations 0 to 1/year ≥2 exacerbations in 6 months requiring oral

requiring oral systemic glucocorticoids, or ≥4 wheezing
systemic episodes/one year lasting >1 day AND risk
glucocorticoids factors for persistent asthma

Consider severity and interval since last exacerbation

Frequency and severity may fluctuate over time

Exacerbations of any severity may occur in patients in any

severity category

Recommended step for Step 1 Step 2 Step 3 and consider short

initiating treatment course of oral systemic
glucocorticoids

In 2 to 6 weeks, depending on severity, evaluate level of asthma

control that is achieved. If no clear benefit is observed in 4 to 6
weeks, consider adjusting therapy or alternative diagnoses.

Assessing severity and initiating therapy in children who are not currently taking long-
term control medication. The stepwise approach is meant to assist, not replace, the clinical
decision-making required to meet individual patient needs. Level of severity is determined by
both impairment and risk. Assess impairment domain by patient's/caregiver's recall of previous 2
to 4 weeks. Symptom assessment for longer periods should reflect a global assessment, such as
inquiring whether the patient's asthma is better or worse since the last visit. Assign severity to
the most severe category in which any feature occurs. At present, data are inadequate to
correlate frequencies of exacerbations with different levels of asthma severity. For treatment
purposes, patients who had ≥2 exacerbations requiring oral systemic glucocorticoids in the
past 6 months, or ≥4 wheezing episodes in the past year, and who have risk factors for persistent
asthma may be considered the same as patients who have persistent asthma, even in the
absence of impairment levels consistent with persistent asthma.

EIB: exercise-induced bronchospasm.

Reproduced from: National Heart, Blood, and Lung Institute Expert Panel Report 3 (EPR 3): Guidelines for the Diagnosis
and Management of Asthma. NIH Publication no. 08-4051, 2007.

Graphic 80908 Version 11.0