NATA Ashtma Position Statement

224 Volume 40

•

Number 3

•

September 2005

Journal of Athletic Training 2005;40(3):224–245

q by the National Athletic Trainers’ Association, Inc

www.journalofathletictraining.org

National Athletic Trainers’ Association

Position Statement: Management of Asthma

in Athletes

Michael G. Miller*; John M. Weiler†; Robert Baker‡; James Collins§;

Gilbert D’Alonzo\

*Western Michigan University, Kalamazoo, MI; †University of Iowa and CompleWare, Iowa City, IA; ‡Michigan

State University Kalamazoo Center for Medical Studies, Kalamazoo, MI; §San Diego Chargers, San Diego, CA;

\Temple University School of Medicine, Philadelphia, PA

Michael G. Miller, EdD, ATC, CSCS; John M. Weiler, MD; Robert Baker, MD, PhD, ATC; James Collins, ATC; and Gilbert

D’Alonzo, DO, contributed to conception and design; acquisition and analysis and interpretation of the data; and drafting,

critical revision, and ﬁnal approval of the article.

Address correspondence to National Athletic Trainers’ Association, Communications Department, 2952 Stemmons Freeway,

Dallas, TX 75247.

Objective:

To present guidelines for the recognition, prophy-

laxis, and management of asthma that lead to improvement in

the quality of care certiﬁed athletic trainers and other heath care

providers can offer to athletes with asthma, especially exercise-

induced asthma.

Background:

Many athletes have difﬁculty breathing during

or after athletic events and practices. Although a wide variety

of conditions can predispose an athlete to breathing difﬁculties,

the most common cause is undiagnosed or uncontrolled asth-

ma. At least 15% to 25% of athletes may have signs and symp-

toms suggestive of asthma, including exercise-induced asthma.

Athletic trainers are in a unique position to recognize breathing

difﬁculties caused by undiagnosed or uncontrolled asthma, par-

ticularly when asthma follows exercise. Once the diagnosis of

asthma is made, the athletic trainer should play a pivotal role

in supervising therapies to prevent and control asthma symp-

toms. It is also important for the athletic trainer to recognize

when asthma is not the underlying cause for respiratory difﬁ-

culties, so that the athlete can be evaluated and treated prop-

erly.

Recommendations:

The recommendations contained in this

position statement describe a structured approach for the di-

agnosis and management of asthma in an exercising popula-

tion. Athletic trainers should be educated to recognize asthma

symptoms in order to identify patients who might beneﬁt from

better management and should understand the management of

asthma, especially exercise-induced asthma, to participate as

active members of the asthma care team.

Key Words:

airway hyperresponsiveness, airway obstruc-

tion, exercise-induced asthma, exercise-induced broncho-

spasm, pulmonary function tests, certiﬁed athletic trainer

INTRODUCTION

sthma is deﬁned as a chronic inﬂammatory disorder

of the airways characterized by variable airway ob-

struction and bronchial hyperresponsiveness.

Airway

obstruction can lead to recurrent episodes of wheezing, breath-

lessness, chest tightness, and coughing, particularly at night or

in the early morning.

Asthma can be triggered by many stim-

uli, including allergens (eg, pollen, dust mites, animal dander),

pollutants (eg, carbon dioxide, smoke, ozone), respiratory in-

fections, aspirin, nonsteroidal anti-inﬂammatory drugs

(NSAIDs), inhaled irritants (eg, cigarette smoke, household

cleaning fumes, chlorine in a swimming pool), particulate ex-

posure (eg, ambient air pollutants, ice rink pollution), and ex-

posure to cold and exercise.

1–5

Airﬂow limitation is often re-

versible, but as asthma symptoms continue, patients may

develop ‘‘airway remodeling’’ that leads to chronic irreversible

airway obstruction.

6,7

Severe attacks of asthma can also cause

irreversible airﬂow obstruction that can lead to death.

4,8

The National Heart, Lung, and Blood Institute of the Na-

tional Institutes of Health launched the National Asthma Ed-

ucation and Prevention Program (NAEPP) in March 1989 to

address the increasing prevalence of asthma in the United

States and its economic costs to the society; the program was

updated in 1997 (as NAEPPII).

An updated expert panel re-

port from the NAEPP is expected to be released in 2006. The

Global Initiative for Asthma (GINA) was also developed to

provide worldwide guidelines for asthma awareness and man-

agement.

These guidelines are extremely comprehensive and

have been regularly updated to reﬂect advances in the diag-

nosis and management of asthma. Nevertheless, the guidelines

do not describe the role of certiﬁed athletic trainers or other

allied health care professionals in recognizing and managing

asthma in an athletic population.

PURPOSE

The purpose of this position statement is to provide athletic

trainers and other allied health care professionals who care for

athletes with information to:

1. Identify the characteristics and diagnostic criteria of asth-

Journal of Athletic Training 225

ma, especially exercise-induced asthma (EIA) or exercise-

induced bronchospasm (EIB).

2. Provide guidelines for referral so that patients with asthma

and those in whom asthma is suspected can receive a thor-

ough evaluation.

3. Describe management plans to prevent attacks and to con-

trol asthma exacerbations when they occur.

4. Educate certiﬁed athletic trainers and athletes about phar-

macologic and nonpharmacologic therapies and techniques

to help control asthma.

RECOMMENDATIONS

Based on current research and literature, the National Ath-

letic Trainers’ Association provides the following guidelines

for the identiﬁcation, examination, management, and prophy-

laxis of asthma, including EIA, and the education of athletes,

parents, coaches, and health care personnel about asthma. Not

all individuals who suffer from asthma present in the same

manner, nor do they all respond to the same management or

treatment plan. Therefore, these recommendations are intended

to provide the certiﬁed athletic trainer and other health care

professionals with an overall guide for a better understanding

of the asthmatic condition.

Asthma Identiﬁcation and Diagnosis

1. All athletes must receive preparticipation screening eval-

uations sufﬁcient to identify the possible presence of asth-

ma.

9–12

In most situations, this evaluation includes only

obtaining a thorough history from the athlete. However,

in special circumstances, additional screening evaluations

(eg, spirometry testing or the challenge testing described

below) should also be performed because the history

alone is not reliable.

2. Athletic trainers should be aware of the major signs and

symptoms suggesting asthma, as well as the following as-

sociated conditions

5,13,14

a. Chest tightness (or chest pain in children)

b. Coughing (especially at night)

c. Prolonged shortness of breath (dyspnea)

d. Difﬁculty sleeping

e. Wheezing (especially after exercise)

f. Inability to catch one’s breath

g. Physical activities affected by breathing difﬁculty

h. Use of accessory muscles to breathe

i. Breathing difﬁculty upon awakening in the morning

j. Breathing difﬁculty when exposed to certain allergens

or irritants

k. Exercise-induced symptoms, such as coughing or

wheezing

l. An athlete who is well conditioned but does not seem

to be able to perform at a level comparable with other

athletes who do not have asthma

m. Family history of asthma

n. Personal history of atopy, including atopic dermatitis/

eczema or hay fever (allergic rhinitis)

Note: Although there is a correlation between the presence

of symptoms and EIA, the diagnosis should not be based

on history alone.

Rather, these symptoms should serve to

suggest that an athlete may have asthma.

3. The following types of screening questions can be asked

to seek evidence of asthma

a. Does the patient have breathing attacks consisting of

coughing, wheezing, chest tightness, or shortness of

breath (dyspnea)?

b. Does the patient have coughing, wheezing, chest tight-

ness, or shortness of breath (dyspnea) at night?

c. Does the patient have coughing, wheezing, or chest

tightness after exercise?

d. Does the patient have coughing, wheezing, chest tight-

ness, or shortness of breath (dyspnea) after exposure to

allergens or pollutants?

e. Which pharmacologic treatments for asthma or allergic

rhinitis, if any, were given in the past, and were they

successful?

4. Patients with atypical symptoms, symptoms despite proper

therapy, or other complications that can exacerbate asthma

(such as sinusitis, nasal polyps, severe rhinitis, gastro-

esophageal reﬂux disease, or vocal cord dysfunction)

should be referred to a physician with expertise in sports

medicine (eg, allergist; ear, nose, and throat physician;

cardiologist; or pulmonologist with training in providing

care for athletes).

Testing might include a stress electro-

cardiogram, upper airway laryngoscopy or rhinoscopy,

echocardiogram, or upper endoscopy.

Pulmonary Function Testing

5. Athletes with a history of asthma or of taking a medica-

tion used to treat asthma and those suspected of having

asthma should consult a physician for proper medical

evaluation and to obtain a classiﬁcation of asthma severity

(Table 1). This evaluation should include pulmonary func-

tion testing.

16–18

6. An exercise challenge test is recommended for athletes

who have symptoms suggestive of EIA to conﬁrm the

diagnosis.

7. If the diagnosis of asthma remains unclear after the above

tests have been performed, then additional testing should

be performed to assist in making a diagnosis.

15,20,21

Phy-

sicians should be encouraged, when possible, to test the

athlete using a sport-speciﬁc and environment-speciﬁc ex-

ercise-challenge protocol, in which the athlete participates

in his or her venue to replicate the activity or activities

and the environment that may serve to trigger airway hy-

perresponsiveness.

20,21

In some cases, athletes should also

be tested for metabolic gas exchange during strenuous ex-

ercise to determine ﬁtness (eg, to assess anaerobic thresh-

old and V

max), especially to rule out the diagnosis of

asthma or to rule in another diagnosis (eg, pulmonary ﬁ-

brosis) for a patient with an unclear diagnosis.

Asthma Management

8. Athletic trainers should incorporate into the existing emer-

gency action plan an asthma action plan for managing and

urgently referring all patients who may experience signif-

icant or life-threatening attacks of breathing difﬁculties

(Figure 1).

1,2

Immediate access to emergency facilities

during practices and game situations should be available.

For example, athletic trainers should be familiar with ap-

propriate community resources and must have a fully

functional telephone (mobile or cellular) available, pre-

programmed with emergency medical care access num-

bers. A telephone might be the single most important de-

226 Volume 40

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Table 1. National Asthma Education and Prevention Program II: Classiﬁcation of Asthma Severity*

Clinical Features Before Treatment†

Symptoms‡

Nighttime

Symptoms Lung Function

Step 4

Severe persistent

● Continual symptoms

● Limited physical activity

● Frequent exacerbations

Frequent ● FEV

or PEF #60% predicted

● PEF variability .30%

Step 3

Moderate persistent

● Daily symptoms

● Daily use of inhaled short-acting beta

agonist

● Exacerbations affect activity

● Exacerbations $2 times/wk; may last

days

.1 time/wk ● FEV

or PEF .60%–,80% predicted

● PEF variability $30%

Step 2

Mild persistent

● Symptoms .2 times/wk but ,1 time/d

● Exacerbations may affect activity

.2 times/mo ● FEV

or PEF $80% predicted

● PEF variability 20–30%

Step 1

Mild intermittent

● Symptoms #2 times/wk

● Asymptomatic and normal PEF be-

tween exacerbations

● Exacerbations brief (from a few hours to

a few days); intensity may vary

#2 times/mo ● FEV

or PEF $80% predicted

● PEF variability ,20%

*FEV

indicates forced expiratory volume in 1 s; PEF, peak expiratory ﬂow.

†The presence of one of the features of severity is sufﬁcient to place a patient in that category. An individual should be assigned to the most

severe grade in which any feature occurs. The characteristics noted in this ﬁgure are general and may overlap because asthma is highly variable.

Furthermore, an individual’s classiﬁcation may change over time.

‡Patients at any level of severity can have mild, moderate, or severe exacerbations. Some patients with intermittent asthma experience severe

and life-threatening exacerbations separated by long periods of normal lung function and no symptoms.

vice to have on the practice ﬁeld for a patient who is

experiencing an asthma exacerbation. In addition, athletic

trainers should have pulmonary function measuring de-

vices (such as peak expiratory ﬂow meters [PFMs] or por-

table spirometers) at all athletic venues for athletes for

whom such devices have been prescribed and should be

familiar with how to use these devices.

9. Patients who are experiencing any degree of respiratory

distress (including a signiﬁcant increase in wheezing or

chest tightness, a respiratory rate greater than 25 breaths

per minute, inability to speak in full sentences, uncon-

trolled cough, signiﬁcantly prolonged expiration phase of

breathing, nasal ﬂaring, or paradoxic abdominal move-

ment) should be referred rapidly to an emergency depart-

ment or to their personal physicians for further evaluation

and treatment. Referral to an emergency room or equiv-

alent facility should be sought urgently if the patient is

exhibiting signs of impending respiratory failure (eg,

weak respiratory efforts, weak breath sounds, uncon-

sciousness, or hypoxic seizures).

10. All patients with asthma should have a rescue inhaler

available during games and practices, and the certiﬁed ath-

letic trainer should have an extra rescue inhaler for each

athlete for administration during emergencies. In case of

emergencies, a nebulizer should also be available. With a

metered dose inhaler (MDI), athletes should be encour-

aged to use a spacer to help ensure the best delivery of

inhaled therapy to the lungs.

11. Athletic trainers and coaches should consider providing

alternative practice sites for athletes with asthma triggered

by airborne allergens when practical. Indoor practice fa-

cilities that offer good ventilation and air conditioning

should be considered for at least part of the practice if this

can be accomplished, although in most cases it will not

be practical. For example, indoor and outdoor allergens or

irritants, tobacco smoke, and air pollutants might trigger

asthma, and attempts should be made to limit exposure to

these triggers when possible. Another option is to sched-

ule practices when pollen counts are lowest (eg, in the

evening during the ragweed pollen season). Pollen count

information can be accessed from the National Allergy

Bureau at http://www.aaaai.org/nab.

12. Patients with asthma should have follow-up examinations

at regular intervals, as determined by the patient’s primary

care physician or specialist, to monitor and alter therapy.

In general, these evaluations should be scheduled at least

every 6 to 12 months, but they may be more frequent if

symptoms are not well controlled.

Asthma Pharmacologic Treatment

13. Athletic trainers should understand the various types of

pharmacologic strategies used for short- and long-term

asthma control and should be able to differentiate controller

from rescue or reliever medications (Figure 2).

24–30

14. Patients with EIA may beneﬁt from the use of short- and

long-acting b

-agonists. Rapid-acting agents can be used

for prophylaxis during practice and game participation.

When the goal is to prevent EIA, a short-acting b

-ago-

nist, such as albuterol, should be inhaled 10 to 15 minutes

before exercise. The excessive need (3–4 times per day)

for short-acting b

-agonist therapy during practice or an

athletic event should cause concern, and a physician

should evaluate the patient before return to participation.

Long-acting b

-agonists should, in general, only be used

for asthma prophylaxis and control and are usually com-

bined with an inhaled corticosteroid. Athletic trainers

should understand the use, misuse, and abuse of short-

acting b

-agonists.

15. Patients with asthma may also beneﬁt from the use of

Journal of Athletic Training 227

Figure 1. Sample asthma action plan. Extracted from

Managing Asthma: A Guide for Schools.

National Heart, Lung, and Blood Institute.

Available at: http://www.nhlbi.nih.gov/health/prof/lung/asthma/asthpsch.htm. Accessed June 7, 2005.

leukotriene modiﬁers, inhaled or parenteral corticoste-

roids, and cromones (such as cromolyn sodium).

16. Pharmacotherapy should be customized for each asthma

patient, and a specialist (an allergist or pulmonologist with

expertise in sports medicine) should be consulted to max-

imize therapy when symptoms break through despite ap-

parently optimal therapy.

17. Patients with past allergic reactions or intolerance to as-

pirin or NSAIDs should be identiﬁed and provided with

alternative medicines, such as acetaminophen, as needed.

Asthma Nonpharmacologic Treatment

18. Health care providers should identify and consider non-

pharmacologic strategies to control asthma, including nose

breathing, limiting exposure to allergens or pollutants, and

air ﬁltration systems.

31–33

However, these therapies should

be expected to provide only limited protection from asth-

ma in most circumstances.

19. Proper warm-up before exercise may lead to a refractory

period of as long as 2 hours, which may result in de-

228 Volume 40

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September 2005

Figure 1. Continued.

creased reliance on medications by some patients with

asthma.

20. Patients who have been diagnosed previously as having

asthma or suspected of having asthma should follow the

recommendations of NAEPPII and GINA for evaluation

and everyday management and control.

1,2

Asthma Education

21. Athletes should be properly educated about asthma, es-

pecially EIA, by health care professionals who are knowl-

edgeable about asthma.

35–52

Athletes should be educated

about the following:

a. Recognizing the signs and symptoms of uncontrolled

asthma.

b. Using spirometry recording devices to monitor lung

function away from the clinic or athletic training room.

c. Methods of limiting exposure to primary and second-

ary smoke and to other recognized or suspicious asth-

ma triggers (eg, pollens, animal allergens, fungi, house

dust, and other asthma sensitizers and triggers). Pa-

tients with asthma who smoke should be provided with

Journal of Athletic Training 229

Figure 1. Continued.

information about smoking cessation and encouraged

to participate in classes to change socialization patterns.

d. The need for increased asthma rescue medication (eg,

short-acting b

-agonists) as a signal for asthma ﬂare-

up. Increased use of short-acting b

-agonists signals a

need for enhanced treatment with asthma controller

therapy.

e. The proper techniques for using MDIs, dry powder in-

halers, nebulizers, and spacers to control asthma symp-

toms and to treat exacerbations. Health care profes-

sionals should periodically check the patient’s

medication administration techniques and should ex-

amine medication compliance.

f. Asthma and EIA among competitive athletes. These

conditions are common, and athletic performance need

not be hindered if the patient takes an active role in

controlling the disease and follows good practice and

control measures.

22. The athletic trainer should also be familiar with vocal cord

dysfunction and other upper airway diseases, which can

sometimes be confused with asthma.

15,53,54

Vocal cord

dysfunction may be associated with dyspnea, chest tight-

230 Volume 40

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Figure 2. Asthma pharmacologic management.

PEF indicates peak expiratory ﬂow.

ness, coughing, wheezing, and inspiratory stridor. In many

cases, the condition is triggered with exercise. Visual in-

spection of the vocal cords by a physician experienced in

examining the upper airway during exercise to differen-

tiate vocal cord dysfunction from asthma is recommended.

23. Patients with asthma should be encouraged to engage in

exercise as a means to strengthen muscles, improve re-

spiratory health, enhance endurance, and otherwise im-

prove overall well-being.

24. The athletic trainer should differentiate among restricted,

banned, and permitted asthma medications. Athletic train-

ers should be familiar with the guidelines of the Interna-

tional Olympic Committee Medical Commission, the

United States Anti-Doping Agency, the World Anti-Dop-

ing Agency, and the doping committees of the various

federations.

25. The athletic trainer should be aware of the various Web

sites that provide general information and frequently asked

questions on asthma and EIA. These sites include the

American Academy of Allergy, Asthma and Immunology

(www.aaaai.org); the American Thoracic Society (www.

thoracic.org); the Asthma and Allergy Foundation of Amer-

Journal of Athletic Training 231

ica (www.aafa.org); the American College of Allergy,

Asthma, & Immunology (www.acaai.org); and USA Swim-

ming (http://www.usaswimming.org/USASWeb/pRainbow/

Documents/6c812467-b717-4c16-a32c-a1d9bcc9f444/

Asthma-%20Comprehensive%20Guide%2004%20Nov%

2029.pdf).

BACKGROUND AND LITERATURE REVIEW

Deﬁnition and Pathophysiology of Asthma

Asthma is a common condition that has been recognized for

more than 2000 years.

Asthma is usually deﬁned operation-

ally as a chronic inﬂammatory disorder of the airways.

1,2,4,56

In many patients, this chronic inﬂammation causes an increase

in airway hyperresponsiveness, leading to recurrent episodes

of wheezing, breathlessness, chest tightness (or chest pain in

children), and coughing, particularly at night or in the early

morning and after exercise, especially in cold, dry environ-

ments. These episodes are associated with widespread but var-

iable airﬂow obstruction that is often reversible, either spon-

taneously or with treatment.

1,2,4

This deﬁnition implies that

asthma has multiple causes, and indeed, it is a complex dis-

order.

The chronic inﬂammatory process causes excess mucus pro-

duction and bronchial smooth muscle constriction,

57–61

which

result from a release of inﬂammatory mediators that include

histamine, tryptase, prostaglandin, and leukotrienes from mast

cells.

62–66

Airways may also accumulate thick, viscous secre-

tions produced by goblet cells and submucosal glands; more-

over, there is leakage of plasma proteins and accumulated cel-

lular debris.

57–61,67

Although airway narrowing affects the

tracheobronchial tree, small bronchi (2–5 mm in diameter) are

most affected.

68–70

Maximal expiratory ﬂow rate is reduced

and residual lung volumes are increased as air is trapped be-

hind the blocked airways.

As a result, during an asthma at-

tack, the respiratory rate increases to compensate for the in-

creased obstruction of the airways and the inability of the

usually elastic lung to recoil (dynamic hyperinﬂation). The pa-

tient must work harder to breathe as the thorax becomes over-

inﬂated. With progression of the attack, the diaphragm and

intercostal muscles must compensate and contribute more en-

ergy during respiration.

In a severe attack, muscle efﬁciency

is eventually lost, and the increased breathing rate leads to

respiratory muscle fatigue and physical distress that may result

in death. Indeed, as many as 4200 to 5000 people die from

asthma each year in the United States.

Environmental Factors

Environmental factors, such as allergens, air pollution, oc-

cupational sensitizers, and tobacco smoke, may cause or ex-

acerbate asthma.

74–79

These factors are important triggers that

should be considered when evaluating a patient with asth-

ma.

79–83

Recently, concern about indoor air pollution has been

heightened.

79,80,82–84

Indoor ambient air can contain allergens

and pollution that can cause or exacerbate asthma and other

respiratory ailments when susceptible individuals are exposed

to these environments.

Many factors should be considered

indoors, such as adequacy of ventilation, humidity level, pres-

ence of allergens, presence of wall-to-wall carpeting and up-

holstered furniture, and types of building materials.

85–87

In-

door animal allergens (such as from cats, dogs, and other pets)

are an important trigger of symptoms in many people.

Cock-

roach allergens are commonly seen indoors (such as in swim-

ming pool locker rooms), and the cockroach allergenic mate-

rials can remain for a long period of time, even after

extermination.

89–92

Indoor mold and fungal spores, house dust

mites, and particulate matter, such as aerosols or smoke from

cigarettes, wood, or fossil fuels, also can trigger asthma symp-

toms.

93–107

Tobacco smoke is a risk factor for the development

of asthma, and smoking tobacco appears to increase asthma

severity.

108–110

Other indoor air irritants, such as chlorine, can exacerbate

asthma and cause eye and lung irritation.

111,112

School-age

children who frequently visit chlorinated pools may have an

increased risk of developing asthma, especially if they have

other risk factors for asthma.

113

Even individuals who do not

usually enter the water but who are exposed to indoor chlo-

rinated pools (eg, lifeguards, coaches) may have respiratory

irritation on exposure to chlorine.

114,115

Many actions can be taken to limit indoor allergen exposure,

including prohibiting smoking indoors, using air cleaners

equipped with a high-efﬁciency particulate air cleaner (HEPA)

ﬁlter, washing walls, vacuuming carpets, and cleaning mattress

covers weekly.

116–119

Additional measures include removing

carpets and installing linoleum or wood ﬂooring, washing pets

(dogs and cats) and their bedding twice a week, keeping pets

out of the bedroom or living room at all times to reduce ex-

posure, covering mattresses and pillows, and controlling hu-

midity to help manage dust mites and mold.

81,82,120

Some of

these measures, such as the removal of a family pet from the

home, can be very difﬁcult, so it is necessary to discuss the

effect of these exposures with the asthma patient. Although

air ﬁlters might help, the house should be cleaned thoroughly

before their use and regularly thereafter.

When inhaled, outdoor air pollution, caused by sulfur diox-

ide, carbon monoxide, nitrogen dioxide, ozone, and particulate

matter, can cause pulmonary function decrements, increased re-

liance on medications, bronchial hyperresponsiveness, and in-

creased asthma symptoms.

121–125

Many pollens (trees, grasses,

and weeds) are inhaled into the bronchi and cause allergen-

induced asthma.

126,127

Tree pollens predominate in the spring,

grass pollens in the late spring or early summer (and fall), and

weed pollens in the late summer and fall in the United States,

depending on geographic location, but may be present at other

times of the year in locations outside of the United

States.

128,129

Information about the pollen seasons in the Unit-

ed States can be accessed from the National Allergy Bureau

Web site.

Although it is virtually impossible to avoid all outdoor pol-

lution and allergens, some practical precautions can be imple-

mented: move indoors and close all windows, close car win-

dows when traveling, limit exposure when pollen is at its

highest levels, monitor local weather stations for allergy re-

ports, and practice indoors if possible when pollen counts are

high.

Diagnosis and Classiﬁcation of Asthma

Asthma can be difﬁcult to diagnose and classify (see Table

1). Some individuals, especially elite athletes, do not display

consistent signs or symptoms of asthma.

9,10,130

Asthma symp-

toms may be present only during certain times (seasons) of

232 Volume 40

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the year or only after exercise and may be highly variable,

depending upon the athlete, the environment, and the activi-

ty.

The ﬁrst step in determining whether asthma is present is

to obtain a detailed medical history. Questions regarding past

experiences, symptoms, smoking history, and family history

can help to rule out other respiratory disorders such as chronic

bronchitis, emphysema, bronchiectasis, allergic rhinitis, upper

respiratory infection, congestive heart failure, disorders of the

upper airway (eg, vocal cord dysfunction), and nonrespiratory

conditions such as anxiety. Most importantly, the athletic train-

er should ask general questions as listed in Recommendation

3 to assist in making a proper diagnosis.

If a patient appears

to have one or more symptoms suggestive of asthma, then lung

function testing should be performed (see Table 1).

However,

it is important to recognize that the history and baseline phys-

ical examination will fail to identify many patients with

EIA.

9,10,12

Lung function tests are essential to assess asthma severity

and airﬂow limitation and to determine whether the obstruc-

tion is fully reversible with treatment.

16–18,131–133

The most

common measures of airway function are the forced expiratory

volume in 1 second (FEV

), the forced vital capacity (FVC),

and the peak expiratory ﬂow rate (PEFR). These tests can be

performed while the patient is at rest or after a challenge. The

FEV

measures the volume of air in liters forcefully exhaled

out of the airway in 1 second after a full inspiration. The FVC

measures the total volume of air in liters forcefully exhaled

out of the airway when the breath continues (usually for a

period of 6 or more seconds). The FVC procedure is effort

dependent and requires the patient to fully understand that he

or she needs to inhale a deep breath and then ‘‘blast’’ the air

out of the lungs into the measurement device. The FVC testing

also requires considerable expertise by the technician and the

ability to communicate with the patient. The PEFR measures

the maximal ﬂow rate of air (in L/s or L/min) out of the air-

ways and is easier to perform than an FEV

or FVC maneuver,

although PEFR testing is also effort dependent. A ﬂow volume

curve (ﬂow loop) provides a graphic depiction of the breathing

effort in which ﬂow rate is plotted against volume (in L/s) of

air exhaled and inhaled (in L), as shown in Figure 3. A vol-

ume-time curve (called a spirogram) is another way to plot

the breath, in which the volume of air exhaled (in L) is plotted

against time (in seconds). The FEV

/FVC ratio is also exam-

ined, along with a variety of measures of ﬂow, such as the

ﬂow between 25% and 75% of the FVC (called the FEF

25–75

Asthma is an example of an obstructive lung disease in

which the airways obstruct the outﬂow of air. In contrast, pul-

monary ﬁbrosis is an example of a restrictive lung disease in

which the functional size of the lungs decreases. In obstructive

lung diseases, the FEV

decreases, whereas the FVC remains

relatively normal, so the FEV

/FVC ratio decreases (until late

in the disease or with severe exacerbations, when the FVC

may also decrease).

131

In restrictive lung disease, both the

FEV

and the FVC decrease proportionally (so that the FEV

FVC ratio is normal). Nomograms exist to provide guidance

as to normal ranges for FEV

and FVC based on age, size and

race.

134,135

It is important to recognize racial differences in the

normal values for these tests. Generally, levels should be at

least 80% of the predicted values to be considered ‘‘normal.’’

The FEV

/FVC ratio should also be above 80%. An increase

of 12% or more in FEV

after an inhaled bronchodilator (eg,

a b

-agonist such as albuterol) suggests reversible airway dis-

ease and may be used as a diagnostic criterion of asthma.

131

A decrease in FEV

after a challenge (such as after inhalation

of methacholine or running on a treadmill) suggests that the

airways are reactive to the stimulus.

It is important to de-

termine a patient’s personal best FEV

, FVC, and PEFR,

which are identiﬁed by plotting these values over time. These

values can also demonstrate variability between morning and

evening and over time, which may reﬂect airway hyperreac-

tivity.

Spirometers are used in the clinic or training room to de-

termine these pulmonary function values.

136

Patients may also

be given a PFM to measure PEFR away from the clinic or

athletic training room (Tables 2 and 3). The PFM is a small,

handheld device that measures maximal ﬂow rate during

forced exhalation.

137–140

Maximal ﬂow rate usually occurs

within the ﬁrst 120 to 150 milliseconds of a forced exhala-

tion.

140

When used properly, a PFM can be somewhat helpful

in following the course of asthma and might even be useful

in suggesting the presence of asthma. The PFM can also be

used to identify asthma triggers and to monitor medication

changes, and it may help to reduce asthma morbidity.

141–147

The device allows the asthmatic patient to measure lung var-

iability over time to assist in determining when to seek med-

ical attention. The PFM should be used at least daily (in the

morning after awakening) and preferably also in the late af-

ternoon or evening.

1,2,148

At least 2 or 3 trials should be per-

formed at each speciﬁed time and the highest value recorded.

The device should be used before taking any medications and

at least 4, but preferably 8, hours after inhalation of a bron-

chodilator, if possible. The device should be used for at least

a 2- to 3-week monitoring period. Some devices record the

PEFR electronically, which can assist the patient in keeping

the data secure and available. Over time, the patient’s personal

best value will be determined. Subsequently, if the PEFR value

is less than 80% of the personal best or if daily variability is

greater than 20% of the morning value, then the patient should

be reevaluated in an attempt to ﬁnd better control measures.

If the PEFR value is less than 50% of the personal best, the

individual should seek immediate attention (see Table 2).

Spi-

rometry, including the use of PFMs, may be especially useful

in patients who do not perceive the severity of their symp-

toms.

149,150

The PFM should be used regularly, even if asthma symp-

toms appear to be well controlled.

132,151–153

Patients who have

good PFM technique (see Table 3) adhere to their treatment

plan and control their symptoms better than those who have

poor technique. The PFM should be available in all athletic

training facilities and on the ﬁeld in medical kits.

Unfortunately, some reports suggest that PFM recordings

are not always reliable indicators of airﬂow obstruction.

154–159

In certain cases, elite or well-trained athletes may possess large

lung capacities, which may exceed the measuring capacity of

the PFM. In addition, it appears that PFM values are not con-

sistent from one to another PFM from the same manufacturer,

across different PFM devices, when men and women use

PFMs, with different techniques while using a single PFM,

and at high altitudes.

159–164

The most accurate spirometry test-

ing is performed with ofﬁce-based spirometry testing equip-

ment.

140

However, as noted above, spirometry testing requires

training

22,165

and may be impractical for everyday asthma

management, especially in primary care settings in which most

patients are not being seen for asthma.

140

If baseline lung function tests are within normal values and

Journal of Athletic Training 233

Figure 3. Flow volume loop and volume time curve.

Table 2. Peak Flow Zones for Asthma Management*

Green zone

● PEF values are between 80% and 100% of personal best

● No asthma management changes are necessary at this time

Yellow zone

● PEF values are between 50% and 80% of personal best

● Caution is warranted; use of medications is required

Red zone

● PEF values are less than 50% of personal best

● Danger: emergency action is needed, including medications or

hospital visit

*Adapted with permission from Li JTC.

140

PEF indicates peak expiratory

ﬂow.

Table 3. General Instructions for Using a Mechanical Peak Flow

Meter*

1. The movable indicator is placed at the beginning of the numbered

scale.

2. The patient stands or sits tall and straight.

3. The patient then inhales maximally.

4. The patient places his or her lips tightly around the mouthpiece.

5. The patient is told to ‘‘blast’’ the air out of his or her lungs and into

the device. The patient then forcefully exhales as fast and hard as

possible.

6. The value is recorded.

7. Steps 1–6 are repeated 2 more times.

8. The highest number is marked as the value for that time period.

*For example, a Mini-Wright peak ﬂow meter (Clement Clarke Interna-

tional Ltd, Essex, UK). Adapted with permission from Li JTC.

140

234 Volume 40

•

Number 3

•

September 2005

Table 4. National Asthma Education and Prevention Program II: Usual Dosages for Long-Term Control Medications*

Medication Dosage Form Adult Dose Child Dose

Inhaled corticosteroids

Systemic corticosteroids

Methylprednisolone

Prednisolone

Prednisone

2, 4, 8, 16, 32 mg tablets

5 mg tablets

5 mg/5 cc

15 mg/5 cc

1, 2.5, 5, 10, 20, 50 mg tablets:

5 mg/cc, 5 mg/5cc

● 7.5–60 mg daily in a single dose

or qod as needed for con-

trol

● Short-course ‘‘burst’’ to achieve

control; 40–60 mg/d as single

or 2 divided doses for 3–10 d

● 0.25–2 mg/kg daily in single dose

or qod as needed for con-

trol

● Short-course ‘‘burst’’: 1–2 mg/kg/

d, maximum 60 mg/day for 3–

10 days

Long-acting inhaled beta

-agonists (Should not be used for symptom relief or for exacerbations. Use with inhaled corticosteroids.)

Salmeterol

Formoterol

MDI 21 mcg/puff

DPI 50 mcg/blister

DPI 12 mcg/single-use capsule

2 puffs q12h

1 blister q12h

1 capsule q12 h

1–2 puffs q12h

1 blister q12h

1 capsule q12h

Combined medication

Fluticasone/salmeterol DPI 100, 250, or 500 mcg/50 mcg 1 inhalation bid; dose depends on

severity of asthma

1 inhalation bid; dose depends on

severity of asthma

Cromolyn and nedocromil

Cromolyn

Nedocromil

MDI 1 mg/puff

Nebulizer 20 mg/ampule

MDI 1.75 mg/puff

2–4 puffs tid–qid

1 ampule tid–qid

2–4 puffs bid–qid

1–2 puffs tid–qid

1 ampule tid–qid

1–2 puffs bid-qid

Leukotriene modiﬁers

Montelukast 4 or 5 mg chewable tablet

10 mg tablet

10 mg qhs 4 mg qhs (2–5 yrs)

5 mg qhs (6–14 yrs)

10 mg qhs (.14 yrs)

Zaﬁrlukast

Zileuton

10 or 20 mg tablet

300 or 600 mg tablet

40 mg daily (20 mg tablet bid)

2,400 mg daily (give tablets qid)

20 mg daily (7–11 yrs) (10 mg tablet

bid)

Methylxanthines (Serum monitoring is important [serum concentration of 5–15 mcg/mL at steady state])

Theophylline Liquids, sustained-release tablets,

and capsules

Starting dose 10 mg/kg/d up to 300

mg max; usual max 800 mg/d

Starting dose 10 mg/kg/d; usual

max:

● ,1 year of age: 0.2 (age in wk)

15 5 mg/kg/d

● $1 year of age: 16 mg/kg/d

*qod indicates every other day; bid, twice a day; tid, 3 times a day; qid, 4 times a day; qhs, at bedtime; MDI, metered dose inhaler; DPI, dry

powder inhaler.

the reversibility test with a b

-agonist is equivocal, then a

challenge test (eg, with methacholine) may be performed to

test for bronchial hyperresponsiveness.

During these tests,

progressively increasing concentrations of the aerosolized drug

are administered during a multistage procedure.

After each

stage, spirometry testing is performed to determine whether a

20% reduction in FEV

from baseline is obtained. If the re-

duction is less than 20% after all stages have been performed,

then the test is considered negative, and the patient is deter-

mined not to have bronchial hyperresponsiveness. It is impor-

tant to note, however, that these tests alone are not diagnostic

of asthma. A positive test must be interpreted in the context

of other information to make the deﬁnitive diagnosis of asth-

ma.

Exercise challenge and other surrogate challenges (such as

eucapnic hyperventilation) are described in the EIA section of

this statement.

19,21

Pharmacotherapy for Asthma

It is important to ascertain the correct diagnosis before med-

ications are prescribed and for the health care professional to

know the types of medications that are prescribed.

1,2,24–30,166,167

Only a small percentage of asthmatic patients take their med-

ications precisely as prescribed by their physician; the most

common cause of treatment failure is failure to use the pre-

scribed treatment.

167

Regardless, asthma can be managed

through various medications to prevent or control symptoms;

for an updated medication list, refer to the NAEPPII and

GINA guidelines.

1,2

The medications used to treat asthma are

classiﬁed as either controller or rescue (reliever) medications.

Controller Medications. Controller medications are daily,

long-term interventions used prophylactically to manage the

symptoms of mild, moderate, and severe asthma and gener-

ally should not be used to manage acute asthmatic symp-

toms.

1,2,25–28

Examples include inhaled corticosteroids, sys-

temic corticosteroids, cromones (sodium cromolyn and

nedocromil sodium), long-acting inhaled b

-agonists, theoph-

ylline, and leukotriene modiﬁers (Table 4 provides sample

agents).

Inhaled corticosteroids are effective controller medications

for treating persistent mild, moderate, and severe asthma.

1,2

They act by decreasing airway inﬂammation, mucus produc-

tion, and bronchial hyperresponsiveness.

168–173

Proper use of

inhaled corticosteroids can lead to a decrease in the number

and severity of asthma exacerbations, improve lung function,

lessen bronchial hyperresponsiveness, and reduce the need for

symptom relief with short-acting b

-agonists.

174–180

Inhaled

corticosteroids should not be used to treat acute asthmatic at-

tacks.

Their adverse effects include hoarseness, coughing,

Journal of Athletic Training 235

and occasionally thrush or oral candidiasis.

177,181

However,

rinsing the mouth after inhalation and using a spacer generally

help to prevent oral candidiasis.

Systemic corticosteroids are administered orally or paren-

terally for individuals who have severe persistent asthma that

remains poorly responsive to inhaler therapy.

182

Systemic ther-

apy has the same mechanisms of action as inhaled corticoste-

roids. However, long-term use of systemic agents can cause

more signiﬁcant systemic adverse events than inhaled corti-

costeroids, including osteoporosis, glucose intolerance, glau-

coma, weight gain, skin thinning, bruising, ﬂuid and electro-

lyte abnormalities, growth suppression, and muscle

weakness.

1,2,183

To minimize these adverse events, oral corti-

costeroids are often taken daily in the morning or every other

day, and patients should be monitored closely by a physi-

cian.

183

Oral corticosteroids are used much less frequently to-

day than in the past since the advent of high-potency inhaled

corticosteroids such as ﬂuticasone and budesonide.

1,2

The cromones, cromolyn sodium and nedocromil sodium,

are inhaled asthma medications used to control mild persistent

asthma and are considered less effective anti-inﬂammatory

agents than inhaled corticosteroids.

25,26,184

Although the exact

mechanisms of action are poorly understood, they are thought

to inhibit IgE-mediated mediator release from mast cells and,

thus, to inhibit acute airﬂow limitations induced by exercise,

cold air, and allergens. The cromones are generally used to

treat mild persistent asthma and to prevent EIA.

1,2

Cromones

should be used as second-line drug therapy alternatives for

treating mild persistent asthma, perhaps combined with an in-

haled b

-agonist; however, several doses each day are usually

needed to control asthma.

1,2

Only minimal adverse events are

seen with these agents, including occasional coughing and an

unpleasant taste, particularly with nedocromil sodium.

Long-acting inhaled b

-agonists (eg, salmeterol and for-

moterol) have the same mechanisms of action as short-acting

-agonists but a 12-hour duration of action, compared with

4 to 6 hours for the short-acting agents.

185–190

A single dose

of formoterol or salmeterol before exercise can protect the ath-

lete from asthma symptoms associated with exercise for up to

12 hours.

191–193

Formoterol has a shorter onset of action than

salmeterol, approximately 5 minutes as compared with 15 to

30 minutes.

192,194

All b

-agonists, including formoterol and

salmeterol, are restricted asthma medications according to the

International Olympic Committee, World Anti-Doping Agen-

cy, and United States Anti-Doping Agency; elite athletes tak-

ing these medications, their physicians, and their athletic train-

ers should review the guidelines posted by these agencies.

Patients using long-acting b

-agonists regularly may display

a decrease in the duration of action.

195–197

In one study, for-

moterol had a shortened duration of action by day 14 of reg-

ular daily use.

198

Thus, patients should not expect these drugs

to remain effective over the 12-hour dosing interval after reg-

ular, daily, extended use. Studies also show that the use of

long-acting b

-agonists does not affect persistent airway in-

ﬂammation.

199

These agents should only be used in combi-

nation with inhaled corticosteroids, which may be more ben-

eﬁcial than ingesting each drug separately.

200–202

Combination

therapy (an inhaled, long-acting b

-agonist and an inhaled cor-

ticosteroid) has been shown to decrease the need for short-

acting b

-agonists, decrease nocturnal asthma, improve lung

function, decrease asthma exacerbations, and prevent

EIA.

200,202–205

Leukotriene modiﬁers, taken orally, block leukotriene syn-

thesis or block leukotriene receptors.

206–208

Leukotriene mod-

iﬁers can be used to control allergen-, aspirin-, and exercise-

induced bronchoconstriction; improve lung function; and de-

crease asthma exacerbations.

209–215

Used primarily as second-

line therapy, leukotriene modiﬁers can reduce the dose of an

inhaled corticosteroid required to treat mild persistent asthma

and may improve asthma control.

214–217

Adverse events are

usually minimal, with reports of headaches and gastrointestinal

discomfort. However, zileuton (Zyﬂo, Abbott Laboratories,

Abbott Park, IL) may be associated with liver toxicity; there-

fore, liver function should be monitored regularly when using

this medication.

218

Unlike b

-agonists, the duration of action

of the leukotriene modiﬁers does not diminish over time.

215

In the past, theophylline has been used alone as a controller

agent, but now it is usually used in combination with another

agent, such as an inhaled corticosteroid.

219

Finally, some patients who have allergic asthma may beneﬁt

over the long term from the administration of various forms

of allergy immunotherapy.

220–222

The decision to initiate such

therapy must be made by the patient and physician after a

careful evaluation. Even in the most successful cases, addi-

tional medical therapy is often required in conjunction with

immunotherapy.

Rescue (Reliever) Medications. Rescue medications act

rapidly to treat acute bronchoconstriction and associated symp-

toms of coughing, wheezing, shortness of breath (dyspnea),

and chest tightness.

1,2,25–28

Several classes of drugs act in this

manner, including rapid-acting inhaled b

-agonists, inhaled an-

ticholinergics, and short-acting theophylline.

Rapid-acting inhaled b

-agonists are the most commonly

used reliever therapy for chronic asthma. These b

-agonists

act quickly to cause bronchodilation by relaxing airway

smooth muscle, decreasing vascular permeability, and modi-

fying mediator release from mast cells.

185

Rapid-acting in-

haled b

-agonists are also the most frequently used agents to

prevent EIA and to treat its symptoms.

223

These medications

can be used as ‘‘rescue therapy’’ at times of an acute attack.

However, because of their relatively short duration of action

(2–4 hours), repeat treatments may be necessary for EIA.

Some authors

224,225

suggest that repeated use of short-acting

-agonists can lead to tolerance and less effectiveness over

time. Furthermore, the chronic use of long-acting inhaled b

agonists can decrease the effectiveness of the short-acting in-

haled b

-agonists.

189,225

Inhaled anticholinergic agents (eg, ipratropium) may be

used as bronchodilators.

226

These agents block acetylcholine

release from cholinergic innervation in airway smooth muscle

but have no anti-inﬂammatory action.

Short-acting theophylline is a bronchodilator that has been

used for many years to relieve asthma exacerbations.

29,227

Theophylline’s onset of action is delayed when compared with

that of b

-agonists, and so it is not currently used as ﬁrst-line

rescue therapy.

1,2

Theophylline is a controversial drug because

its beneﬁts might be outweighed by potential adverse events

such as seizures.

228

Adverse events can be serious and severe

if dosing is not closely monitored. Short-acting theophylline

should not be administered to patients who are already receiv-

ing chronic therapy with sustained-release theophylline thera-

py.

Short-acting oral b

-agonists, although rarely used, function

primarily by relaxing airway smooth muscle within a few min-

utes after administration and for a period of up to 4 hours;

however, they have no anti-inﬂammatory actions.

24,29

Adverse

236 Volume 40

•

Number 3

•

September 2005

Table 5. Sample Nonsteroidal Anti-Inﬂammatory Drugs

Generic

Name

Brand

Name(s) Manufacturer

Diclofenac, miso-

prostol

Arthrotec GD Searle LLC, Chicago, IL

Celecoxib Celebrex GD Searle LLC

Diclofenac Voltaren Novartis Pharmaceuticals Corp,

East Hanover, NJ

Diclofenac Cataﬂam Novartis Pharmaceuticals Corp

Diﬂunisal Dolobid Merck & Co, Inc, West Point, PA

Etodolac Lodine Wyeth-Ayerst International Inc,

Madison, NJ

Flurbiprofen Ansaid Pharmacia & Upjohn Co, Kalama-

zoo, MI

Ibuprofen Motrin McNeil-PPC, Fort Washington, PA

Advil Wyeth, Madison, NJ

Indomethacin Indocin Merck & Co, Inc

Ketoprofen Orudis Rhoˆne-Poulenc Rorer New Zealand

Ltd, Auckland, New Zealand

Ketorolac Toradol Roche Pharmaceuticals, Nutley, NJ

Nabumetone Relafen GlaxoSmithKline, Research Trian-

gle Park, NC

Naproxen Naprosyn Roche Pharmaceuticals

Aleve Bayer, Morristown, NJ

Oxaprozin Daypro GD Searle LLC

Piroxicam Feldene Pﬁzer Inc, New York, NY

Rofecoxib Vioxx Merck & Co, Inc

Salsalate Disalcid 3M Pharmaceuticals, Northridge,

Sulindac Clinoril Merck & Co, Inc

events include tachycardia, hypertension, and decreased ap-

petite. If used chronically, increasing doses of short-acting oral

-agonists might indicate loss of control of asthma.

1,2

All

athletes using short-acting oral b

-agonists should be advised

that many sporting organizations restrict or prohibit the use of

these agents.

Finally, systemic glucocorticosteriods are administered oral-

ly or parenterally for individuals who have acute asthma ex-

acerbations. The mechanisms of action are similar to those for

corticosteroids used to treat chronic severe asthma.

1,2

Asthma Medication Delivery Techniques

Many of the newer asthma medications are delivered to the

lungs by inhalation devices.

The most common types of in-

halers are MDIs and dry powder inhaler devices. The MDIs

release a speciﬁc amount of a drug from a pressurized canister

to propel medication into the lungs when the patient takes a

breath. When using MDIs, patients must exhale ﬁrst, then

place the inhaler at or slightly in front of the lips, and slowly

inhale at the same time that they are activating the inhaler to

release the drug. Patients hold their breath for a few seconds

(approximately 10) before exhaling. Patients who have difﬁ-

culty coordinating MDI activation with breathing generally

beneﬁt from the use of a spacer.

229–231

A spacer is attached to

the MDI device to reduce side effects of inhaled corticoste-

roids in the mouth and for patients who have difﬁculty coor-

dinating the activation of an MDI and breathing. Dry powder

inhalers are often easier to use than MDIs, and they do not

permit use of a spacer.

Aspirin, Nonsteroidal Anti-Inﬂammatory Drugs, and

Asthma

Aspirin-sensitive athletes may manifest nasal congestion;

itchy, watery, or swollen eyes; coughing; difﬁculty breathing;

wheezing; urticaria; and possible shock when they ingest as-

pirin or other NSAIDs.

232–236

This is not a true allergy because

it is not caused by IgE, but it is treated in the same manner

as an allergic reaction. Athletic trainers should also be aware

of triad syndrome: athletes with asthma, nasal polyps, and as-

pirin sensitivity may have a severe asthma attack when they

take an NSAID.

237

Although only a small percentage of the population has as-

pirin-sensitive asthma,

238–240

this condition is particularly con-

cerning in an athletic population because many athletes who

have asthma use anti-inﬂammatory drugs to treat injuries.

Therefore, athletic trainers must understand that some patients

who have asthma could suffer fatal consequences if they take

aspirin or NSAIDs.

Aspirin-sensitive athletes should also avoid COX-2 inhibi-

tors, but acetaminophen in moderate doses can usually be tak-

en without difﬁculty.

241

Salsalate, choline magnesium trisali-

cylate, and dextropropoxyphene may be used as substitute

medication in patients with aspirin sensitivity if tolerat-

ed.

240,242

Athletic trainers should be familiar with the many

prescription and over-the-counter products that contain aspirin

and other NSAIDs, including ibuprofen (eg, Motrin, McNeil-

PPC, Fort Washington, PA; Advil, Wyeth, Madison, NJ) and

naproxen (eg, Aleve, Bayer, Morristown, NJ). Health care pro-

fessionals should supply as much information to the patient as

possible, including a list of products to avoid (Table 5).

Nonpharmacologic Treatment for Asthma

Athletes with asthma need to keep their asthma under op-

timal control to prevent exercise-induced breathing symp-

toms.

31,32,243,244

Masks and nose breathing help to warm and

moisturize inhaled air before it reaches the smaller airways.

This may decrease the inﬂammatory reaction in the airways

and thus decrease the frequency and intensity of EIA. These

maneuvers are effective for some but not all athletes.

224

Nose

breathing is not effective at high ventilation rates. Limiting

environmental exposures (eg, to cold air and pollen) may de-

crease symptoms in susceptible athletes; however, this may not

be practical in some sports.

Theoretically, exercise training might decrease symptoms by

conditioning the body to exercise, but research has not sup-

ported this theory.

245,246

Nevertheless, an asthmatic individual

should participate in exercise programs tailored to his or her

capacity to perform.

A refractory period can occur after exercise, when the air-

way response to exercise is inhibited for up to 2 to 3 hours.

Some athletes have taken advantage of this phenomenon to

help control EIA.

31,32,34,247–251

However, there are no speciﬁc

guidelines to follow, and each athlete must experiment to de-

termine the best individual protocol.

Because hyperosmolarity plays a role in mediating EIA,

limiting sodium in the diet has received some attention. Re-

stricting dietary salt may cause a relative decrease in airway

obstruction.

252,253

Both sodium and chloride appear to play

roles, but this remains an area of active investigation, and no

speciﬁc guidelines are available.

254

A diet supplemented with

n-3 polyunsaturated fatty acid in ﬁsh oil has shown favorable

results in elite athletes with EIA.

255

Journal of Athletic Training 237

Exercise-Induced Asthma or Bronchospasm

Most asthmatic individuals have a ﬂare of their asthma after

exercise.

256,257

Some individuals only have asthma signs and

symptoms associated with exercise.

By deﬁnition, a tempo-

rary narrowing of the airways (bronchospasm) induced by

strenuous exercise in which the patient has no symptoms is

known as EIB.

When symptoms are present, EIB is de-

scribed as EIA.

This section reviews the incidence of EIA

and EIB in the athletic population and considers special di-

agnostic or therapeutic measures that should be taken in an

athletic population.

Exercise-induced asthma is commonly seen in athletes in all

levels of athletic competition.

5,9,10,31,243,244,258–269

In most pa-

tients who have chronic asthma (at least 80%), exercise is a

trigger for bronchoconstriction.

13,243

Exercise-induced asthma

can also occur in patients who do not otherwise have asthma,

such as in about 40% of patients who suffer from allergic

rhinitis in season.

243,270,271

The incidence of EIA in the gen-

eral population has been estimated to be between 12% and

15%.

13,271

Rates as high as 23% have been reported in school-

age children, and the incidence in athletes may also be this

high.

258,262,263,265

Exercise-induced asthma may be more com-

mon in urban environments than in rural areas.

261

Other fac-

tors, such as high ozone levels, might also account for in-

creased EIA rates.

272

Exercise-induced asthma can be a signiﬁcant disability for

the athlete, especially in endurance sports.

262,263,273

For ex-

ample, EIA is relatively common in cross-country skiers, and

some studies suggest that the cold air athletes breathe while

cross-country skiing may provoke inﬂammation.

274,275

Simi-

larly, athletes who participate in swimming and long-distance

running have a high incidence of asthma.

262

Among Olympic

athletes, asthma appears to be more common in those who

participate in winter sports than in those who participate in

summer sports.

262,263

At least 1 in 5 United States athletes who

participated in the 1998 Winter Olympics had the condition,

compared with 1 in 6 at the 1996 Summer Olympic

Games.

262,263

Wilber et al

265

found a 23% overall incidence

of EIA among athletes in the 7 winter sports tested. In addi-

tion, more females than males participating in the Winter

Games reported an asthma condition or medication

use.

262,263,265

Of the winter sports athletes tested, females had

an incidence of 26%, compared with 18% in males.

265

Although EIA impairs performance, it can be overcome.

Amy Van Dyken, an athlete who suffered from relatively se-

vere asthma, won 4 gold medals in swimming in the 1996

Olympic Games.

273

Other well-known elite athletes have also

been able to excel when their asthma was under good con-

trol.

273

Pathophysiology of Exercise-Induced Asthma

Two major theories exist to explain EIA: the cooling/warm-

ing hypothesis and the drying hypothesis.

31,256,257,260,276–287

As ventilation increases, airways progressively cool, which re-

sults in bronchoconstriction. This theory is supported by the

higher incidence of EIA in athletes participating in cold en-

vironments.

263

In addition to cooling, the increased ventilation

can lead to airway dehydration as inhaled air is humidiﬁed.

The main effect of inhaling cold air is actually attributable to

the fact that cold air carries less moisture. As with chronic

asthma, inﬂammatory cells and mediators may increase in the

lung in response to exercise in patients with EIA.

248,279,288–290

Environmental allergens may enhance the likelihood of bron-

choconstriction, and irritants such as sulfur dioxide, nitrogen

dioxide, ozone, and chlorine have been implicated as causing

patients to have exercise-induced symptoms.

31,243,291

Exercise-Induced Asthma Diagnosis

Two requirements are needed to diagnose EIA: symptoms

and obstructed airways, both associated with exercise.

13,269

First, the patient has any of a constellation of symptoms

associated with exercise, including shortness of breath (dys-

pnea), coughing, chest tightness (or chest pain in children),

wheezing, and decreased exercise tolerance.

13,262,263

Symp-

toms generally occur 5 to 8 minutes after sufﬁciently intense

exercise starts. The EIA may be associated with speciﬁc sports

as well as speciﬁc environments.

262–267

Where allergens are

present, outdoor activities and cold air exposure may be more

likely to foster the appearance of EIA, which would not occur

in other environments.

Second, the patient should have objective evidence of air-

way obstruction associated with exercise.

224

Generally, a drop

from baseline of at least 10% to 15% in FEV

after a challenge

test supports the diagnosis of EIA.

19,292

Pulmonary function

should be monitored 5, 10, 15, and 30 minutes after the chal-

lenge.

The exercise needs to last for 6 to 8 minutes at an

intensity level high enough to raise the athlete’s heart rate to

at least 80% of maximum

and ventilation to approximately

40% to 60% of maximum.

Exercise challenges can be per-

formed in a laboratory (using a treadmill, a cycle ergometer,

a rowing machine, or a free running asthma screening test

[FRAST]).

293

Alternatively, an exercise challenge test in the

laboratory can attempt to mimic the conditions and intensity

of the sport.

20,21

Indeed, 78% of cross-country skiers reported

a false-negative test during standard laboratory exercise chal-

lenges, suggesting that the standard tests are not as sensitive

as sport-speciﬁc exercise challenge tests for endurance ath-

letes.

20,21

Cold, dry air and near-maximal exercise intensity

(greater than 90% peak heart rate) are required to provoke a

positive result, especially in the cold-weather athlete. Time of

day can be important: in a group of asthmatics, a greater drop

in pulmonary function (FEV

) to exercise challenge was mea-

sured in the evening than in the morning.

294

Additional challenge tests include eucapnic voluntary hy-

perventilation or inhalation of hypertonic saline.

21,269,295

The

former test requires the athlete to hyperventilate dry air con-

taining 5% carbon dioxide, 21% oxygen, and the balance of

nitrogen at 30 times FEV

for 6 minutes.

It is important to evaluate athletes with atypical EIA symp-

toms because upper airway conditions such as vocal cord dys-

function or abnormal movement of the arytenoids region may

be the cause.

15,53

The signs and symptoms of vocal cord dys-

function can be similar to asthma and can be confused with

EIA.

54,296,297

This laryngeal disorder involves the unintention-

al paradoxic adduction of the vocal cords with breathing and

can be triggered by exercise.

296,297

The patient is often female

and may also have gastroesophageal reﬂux disease or a psy-

chiatric illness. Vocal cord dysfunction often occurs with asth-

ma, making control of EIA difﬁcult. Diagnosis of vocal cord

dysfunction involves the direct visualization of the paradoxic

vocal cord motion, but the condition is often suspected when

voice changes and inspiratory stridor occur during an attack,

as well as when the inspiratory (bottom) portion of the ﬂow

volume loop is truncated.

238 Volume 40

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September 2005

Table 6. National Asthma Education and Prevention Program II:

Treatment of Exercise-Induced Asthma*

One goal of management is to enable patients to participate in any

activity they choose without experiencing asthma symptoms. EIB should

not limit either participation or success in vigorous activities.

Recommended treatments include:

C Beta

-agonists will prevent EIB in more than 80 percent of patients.

● Short-acting inhaled beta

-agonists used shortly before exercise

(or as close to exercise as possible) may be helpful for 2 to 3

hours.

● Salmeterol has been shown to prevent EIB for 10 to 12 hours

(Kemp et al 1994

301

C Cromolyn and nedocromil, taken shortly before exercise, are also

acceptable for preventing EIB.

C A lengthy warmup period before exercise may beneﬁt patients who

can tolerate continuous exercise with minimal symptoms. The

warmup may preclude a need for repeated medications.

C Long-term–control therapy, if appropriate.

● There is evidence that appropriate long-term control of asthma

with anti-inﬂammatory medication will reduce airway responsive-

ness, and this is associated with a reduction in the frequency and

severity of EIB (Vathenen et al, 1991

302

Teachers and coaches need to be notiﬁed that a child has EIB, should

be able to participate in activities, and may need inhaled medication

before activity. Individuals involved in competitive athletics need to be

aware that their medication use should be disclosed and should adhere

to standards set by the U.S. Olympic Committee (Nastasi et al, 1995

303

The U.S. Olympic Committee’s Drug Control Hotline is 1-800-233-0393.

EIB indicates exercise-induced bronchospasm.

Table 7. United States Anti-Doping Agency Regulated Asthma

Medications

Drug class: b

-agonists:

Advair* (GlaxoSmithKline, Research Triangle Park, NC)

albuterol*

bambuterol

bitolterol

Brethaire* (Riker Laboratories, Inc, Northridge, CA)

Combivent* (Boehringer Ingelheim Pharmaceuticals Inc, Ridgeﬁeld

(CT)

fenoterol

Foradil* (Novartis Pharmaceuticals Corp, East Hanover, NJ)

formoterol*

metaproterenol

orciprenaline

pirbuterol

Proventil* (Schering-Plough Corp, Kenilworth, NJ)

reproterol

salbutamol*

salmeterol*

Serevent* (GlaxoSmithKline)

terbutaline*

Ventolin* (GlaxoSmithKline)

Xopenex* (Sepracor, Marlborough, MA)

Available at: http://www.usantidoping.org. Accessed June 6, 2005.

*Allowed by inhaler or nebulizer only to prevent or treat asthma or ex-

ercise-induced asthma. Abbreviated Therapeutic Use Exemption (TUE)

must be on ﬁle with United States Anti-Doping Agency or international

federations, as appropriate. A salbutamol (albuterol) level greater than

1000 ng/mL is prohibited even with abbreviated TUE.

Exercise-Induced Asthma Treatment

Most of the drugs described for the treatment of chronic

asthma are used to prevent EIA attacks.

1,2,269,298–300

Table 6

contains recommendations from the NAEPPII for the treat-

ment of EIA.

The key feature is that a b

-agonist can be used

both to prevent attacks and to treat them when they occur.

Once an asthmatic individual meets the requirements for stage

1 through 4 asthma, the NAEPPII treatment guidelines should

be followed.

Asthma Education

Throughout this position statement, information has been

presented to inform and educate the athletic trainer and allied

health personnel about asthma and asthma management. Of

particular importance is a properly prepared asthma manage-

ment plan. Educating athletes about asthma and having a writ-

ten management plan will help control their disease.

1,2,304

Sev-

eral groups

35–44,48–51

have shown that an effectively written

management plan can reduce medication errors, asthma ex-

acerbations, and hospital visits. Without a written asthma ac-

tion plan, many patients have a difﬁcult time controlling their

asthma symptoms.

45–47,305

It is also imperative that an acces-

sible line of communication between the patient and health

care professional be identiﬁed.

An effective management plan should include a written doc-

ument that addresses the following: (1) goals of the patient,

(2) proper use and frequency of PEFR monitoring, (3) guide-

lines for altering medications based upon readings from PFMs

or asthma symptoms, (4) contact numbers for all health care

professionals, including emergency numbers, and (5) environ-

mental factors to avoid or monitor. The health care profes-

sionals developing the asthma management plan should dis-

cuss all goals or expectations with the athlete. This education

empowers the athlete and promotes better compliance.

Athletic trainers working with elite or Olympic athletes

must be familiar with International Olympic Committee,

World Anti-Doping Agency, and United States Anti-Doping

Agency medication guidelines (Table 7). Certain asthma med-

ications may be banned, restricted, or permitted, depending on

the organization and the medication. A banned medication is

one the athlete cannot take. In some cases, a prohibited sub-

stance is prohibited at all times or only prohibited in compe-

tition, meaning the athlete must allow sufﬁcient time for the

substance to clear the system before competition. Restricted

medications must have prior physician approval and comple-

tion of forms (such as the Therapeutic Use Exemption, or

TUE) before the athlete can compete. For example, the United

States Anti-Doping Agency lists salbutamol/albuterol, salme-

terol, terbutaline, and formoterol as restricted b

-agonists that

require a TUE before competition.

Additional information about the diagnosis and management

of asthma can be obtained at the National Asthma Education

and Prevention Program Web site (http://www.nhlbi.nih.gov/

health/prof/lung/index.htm or http://www.nhlbi.nih.gov/about/

naepp/) and the GINA Web site (www.ginasthma.com).

CONCLUSIONS

Asthma can affect individuals regardless of age, sex, or so-

cioeconomic status. This National Athletic Trainers’ Associa-

tion asthma position statement is designed to present guide-

lines for the recognition, prophylaxis, and management of

asthma. The information should lead to improvements in the

quality of care certiﬁed athletic trainers and other heath care

providers can offer to patients with asthma, particularly ath-

letes and especially those with EIA. In the end, these guide-

Journal of Athletic Training 239

lines should reduce the incidence of asthma complications and

improve the quality of life for patients with asthma, especially

those in whom exercise is an important trigger.

DISCLAIMER

The NATA publishes its position statements as a service to

promote the awareness of certain issues to its members. The

information contained in the position statement is neither ex-

haustive not exclusive to all circumstances or individuals. Var-

iables such as institutional human resource guidelines, state or

federal statutes, rules, or regulations, as well as regional en-

vironmental conditions, may impact the relevance and imple-

mentation of these recommendations. The NATA advises its

members and others to carefully and independently consider

each of the recommendations (including the applicability of

same to any particular circumstance or individual). The posi-

tion statement should not be relied upon as an independent

basis for care but rather as a resource available to NATA mem-

bers or others. Moreover, no opinion is expressed herein re-

garding the quality of care that adheres to or differs from

NATA’s position statements. The NATA reserves the right to

rescind or modify its position statements at any time.

ACKNOWLEDGMENTS

We gratefully acknowledge the efforts of Michael C. Koester, MD,

ATC; James L. Moeller, MD, FACSM; Kenneth W. Rundell, PhD;

Chad Starkey, PhD, ATC; Randall L. Wilber, PhD; and the Pro-

nouncements Committee in the preparation of this document.

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