1. Exercise Induced Bronchoconstriction
Enoch Samraj
KINE 5327 –Pulmonary Physiology
Dr. Paul McDonough
May 6, 2011

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Abstract
This paper looks at the effect of exercise. EIB is of clinical interest because the ability to
exercise without severe limitation is important in maintain fitness and health, and in the
accomplishment of activities of daily living. While exercise does not cause asthma, it is part of
the asthmatic diathesis where exercise is one of man stimuli that induce airflow limitation. Thus
the diagnosis and treatment of EIB is important clinically not just for athletic performance but
also in the early recognition of potential early manifestation of more severe airways disease.

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CHAPTER 1
Introduction
The benefits of exercise cannot be overestimated as physical activity has been shown to
be protective for a variety of chronic illnesses such as hypertension, ischemic heart diseases, type
2 diabetes, osteoporosis, colonic cancer, anxiety, and depression. Low levels of activity are
associated with increased mortality; 12% of deaths in the USA can be attributed to low levels of
physical activity. (Pate et al. 1995). In spite of this many asthma patients are still unwilling to
undertake any exercise due to the fear of precipitating an attack and are, therefore, unfit. The
relationship between asthma and exercise has long been known; it was Aretaeus (120-200AD),
over 1800 years ago, who noted that physical exertion provoked airway obstruction (Adams &
London 1856). Over 300 years ago, Sir John Floyer, who himself being asthmatic, described the
adverse effect of physical activity on his asthma, and also noted that different exercises had a
lesser or greater adverse effect (Floyer 1698).
Exercise induced asthma (EIA) is a common and age-long phenomenon, many health
practioners don not have an adequate understanding of its diagnosis, characteristics, prevention,
and management. While EIA has been a widely used term, exercise induced bronchoconstriction
(EIB) has now become the term used in research literature and is more accurate in describing this
phenomenon (Gotshall 2002).
Asthma: Epidemiology and its pathogenesis
Asthma is a complex and multifactorial disorder that represents a significant public health
problem in many industrialized nations. The clinical manifestations of asthma are typified by
episodes of breathlessness and wheezing in convert with airway hyper-reactivity to a range of
stimuli. Underlying these symptoms is persistent inflammation of the airway wall, coupled with
a multiplicity of structural changes collectively termed as airway remodeling
Asthma is a disorder of the conducting airways, which contract too much and too easily
spontaneously and in response to a wide range of exogenous and endogenous stimuli. This
airway hyper-responsiveness is accompanied by enhanced sensory irritability of the airways and
increased mucus secretion. The different clinical expressions of asthma involve varying
environmental factors that interact with the airways to cause acute and chronic inflammation, and

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the varying contributions of smooth muscle contractions, edema and remodeling of the formed
elements of the airways. (Stephen T.H., 2008).
The prevalence of asthma significantly increased worldwide from 1980 until the late
1990, and perhaps has recently plateaued. (Akinbami et al. 2007). When this change was first
appreciated, the first instincts of most observers were to attribute the increase to improved
recognition and diagnosis. And indeed it has certainly improved. Nonetheless, a number of
carefully done cohort studies have confirmed that the true prevalence has increased. (Bloom
&Cohen 2009). The reasons for the world- wide increase in the prevalence of asthma over recent
decades and the international patterns of asthma prevalence are poorly understood and not
adequately addressed and explained by the current knowledge of the causation of asthma. (Eder
et al. 2006). This has led to the investigation of the role of novel risk factors that may increase
the susceptibility to atopy and the development of asthma.
Airway Inflammation
Airway inflammation in asthma is a multicellular process involving mainly eosinophils,
neutrophils, CD4+ T lymphocytes and mast cells, with eosinophilic infiltration being the most
striking feature (Kay 2005). The inflammatory process is largely restricted to the conducting
airways but as the disease becomes more severe and chronic the inflammatory infiltrate spreads
both proximately and distally to include small airways and in some cases adjacent alveoli (Kraft
et al. 1999). The inflammatory response in the small airways appears to be predominantly
outside the airway smooth muscle, whereas in the large airways inflammation of the submucosa
dominates (Haley et al.1998, cited in Holgate 2008). This Th2 type of inflammation is common
to chronic allergic inflammatory responses at multiple tissue sites and indeed is seen at these
sites in patients with asthma who frequently express comorbidities such as chronic rhinitis,
sinusitis, atopic dermatitis, and food allergy (Kay 2001 cited in Holgate 2008).
A fundamental feature of asthma associated with allergic sensitization is the ability of the
airway to recognize common environmental allergens and to generate a Th2 cytokine response to
them. Allergen sensitization is the uptake and processing of inhaled allergens by dendritic cells
situated in the airway epithelium and submucosa and which extend their processes to the airway
surface. (Garnier et al. 2005). The uptake of allergen is enhanced by IgE bound to high affinity

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receptors on dendritic cells that facilitate allergen internalization (Kitamura et al. 2007). Once
inside the dendritic cell, processing of allergens by cathepsin S and the subsequent selection of
peptited loaded onto and presented by HLA molecules (MHC class II) is fundamental to the
ability of these cells to serve as antigen-presenting cells to T lymphocytes (Riese & Chapman
2000). Once the dendritic cell has engaged allergen, it receives signals to migrate to local
lymphoid collections where antigen presentation takes place. Its specific chemokine receptors,
including CCR7 and its ligands CCL19 and CCL21 and to a lesser extent CXCR4 and its ligand
CXCL12, are involved in this chemotactic migration to enable contact with naive T-cells
(Humrich et al. 2006). Presentation of a selected antigen peptide to the T-cell receptor initiates
sensitization and the subsequent immune response to the specific allergen (Smit & Lukacs
2006).
The capacity of dendritic cells to generate interleukin (IL)-12 determines the balance
between Th1 and Th2 responses, IL-12 polarizing T-cell differentiation in favor of a Th1 response
(Kuipers et al. 2004). However, while IL-12 is able to counteract Th2 sensitization, it is also able
to contribute to maximal expression of allergic airway disease post sensitization (Meyts et al.
2006). Once sensitized, T cells not only migrate back to the airways to the site of the antigen
presentation under the influence of the chemokines CCL11, CCL24, CCL26, CCL7, CCL13,
CCL17, and CCL22 (Garcia et al. 2005), but these cells also become potent producers of a range
of cytokines, the majority of which are expressed on the long arm of chromosome 5, namely IL-
3, IL-4, IL-5, IL-6, IL-9, IL-13, and granulocyte-macrophage colony-stimulating factor (Ryu et
al. 2006).
There is now persuasive evidence that at least in mild to moderate asthma Th2-type cells
dominat the T-cell repertoire in the airways (Anderson 2002). Through cytokine production, they
have the capacity to recruit secondary effector cells such as macrophages, basophils and
eosinophils into the inflammatory zone where these cells become primed and subsequently
activated for mediator secretion (Akbari et al. 2006). Overall it is the Th2-type cell bearing the
CCR4 chemokine receptor that is the cell which dominates the allergic immune response and
may be the cell most probably responsible for contributing to the ongoing chronic inflammatory
response.

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Characteristics of Exercise-induced Bronchoconstriction (EIB)
EIB is typically characterized as a reduction in post-exercise pulmonary function. This is
generally expressed as a percent reduction in forced expiratory volume in 1 second (FEV1), pre-
to post exercise. Maximal expression of EIB is generally 3 to 10 minutes post exercise (Brudno
et al. 1994). A refractory period of up to 3 hours after recovery from exercise, during which
repeat exercise causes less bronchospasm, has been observed (Beck et al. 1999). EIB is ‘self-
limiting’ in that the reductions in pulmonary function, although often severe, dissipate over 30
minutes to an hour (Godfrey et al. 1975 cited in Robert 2002). This is in stark contrast with
antigen induced asthma, which more often requires medical intervention to limit or control the
attack (Robert 2002). There is no literature reports of an exercise-related death caused
specifically by EIB, whereas in contrast, antigen-induced asthma can prove to be fatal (Beck et
al. 2001).
Epidemiology of EIB
The prevalence of EIB in the general population is unknown. However, it is generally
considered that 80 to 90% of individuals with asthma, 40% of those with allergic rhinitis, and
about 12 to 15% of the general population experience EIB with moderate exercise (McFadden &
Gilbert 1994). In a screening study of 166 middle and high school athletes, 13% demonstrated
EIB (Kukafka et al. 1998). Interestingly, recently studies have showed that athletes training in
cold, dry climates may have chronic airway inflammation as a result. Karjalainen et al. evaluated
both asthmatic and non-asthmatic cross-country skiers for the presence of airway inflammation
and hyper-responsiveness, or atopy. Therefore it can be concluded that repeated exposure of the
airways to inadequately conditioned air might induce inflammation and remodeling in
competitive skiers.
Mechanism and Stimulus
Inspired air has a temperature of 69-73.4 degree Fahrenheit and a water content of 6-12
mg/l. At 30-60 % relative humiditiy with normal inspiration, inhaled air is conditioned by the
nasal passages to body temperature (37℃ ) and a water content of 44mg/l before the air arrives in
the lower airways. However during exercise with resulting high ventilation of a large volume of

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air, the nasal cavity is bypassed and the humidification and conditioning of the air is shifted to
the lower airways (Schroekenstein & Busse 1988). The exact stimulus for bronchoconstriction
leads to two hypothesis: the thermal hypothesis (cooling of the airways) and the osmotic
hypothesis (Loss of water vapor). The thermal hypothesis suggests that the increased ventilation
causes airway cooling by transferring of thermal energy to the inspired air; which is followed by
rapid rewarming of the airways. The rewarming of the respiratory mucosa induces a reactive
hyperaemia of bronchial microvasculature and oedema of the airways. The larger the quantity of
thermal energy that needs to be transferred, the more rapidly the airways rewarm and the more
bronchi are narrowed (McFadden 1990). This theory is buttressed from the observation that
inhalation of cold, dry air during exercise caused a greater reduction of FEV1 than did inhalation
of ambient or hot dry air (Strauss et al. 1977).
Osmotic theory was developed later and it suggested that it was the increased rate of
respiratory water also caused by hyperpnoea of exertion that induces hyperosmolality of the
epithelium, and that this provides a favorable environment for the release of mediators that cause
airway narrowing (McFadden 1990). The relative role of heat and water loss in pathogenesis is
still being debated; however increasing number of documents show the release of mediators from
inflammatory cells in exercise induced asthma (Awopeju & Erhabor 2011). Mast cell
degranulation has been shown in bronchial biopsies from humans after exercise (Crumi et al.
cited in Awopeju & Erhabor 2011) A significant correlation has been reported between the
severity of EIB and the degree of blood eosinophilia, and eosinophilia in induced sputum of
asthma patients (Otani et al. 2004 cited in Awopeju & Erhabor 2011). Although inflammation is
a critical component of asthma and EIB, the role or significance of inflammation on the
pathogenesis of EIB in subjects without asthma is unclear, further studies are needed to clarify
this (Awopeju & Erhabor 2011).
Most subjects with EIB have classic symptoms of airway obstruction following exercise:
dyspnea, cough, chest tightness that starts 10-15 minutes into exercise and peaks 8-15 minues
after the exertion is completed (Erhabor et al. cited in Awopeju & Erhabor 2011).
(Awopeju & Erhabor 2011) showed that 66.15% of asthma patients with no history of
EIA were found to demonstrate the classic pattern of EIA. The reason for this asynchrony

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between history and exercise challenge is not known; however, poor perception among asthma
sufferers is suggested as one of the causes. Other factors in patient’s history that may suggest the
prevalence of EIA are: symptoms that vary by season or outdoor temperature; decreased, or
altered exercise regimen; complaints of decreased or limited endurance; minimal problems with
swimming or being in a warm humid environment.
While many of the studies have focused on the concept that EIB constitutes a
bronchoconstriction or bronchospasm, there is no direct evidence that bronchiolar smooth muscle
indeed undergoes active contraction resulting in airway obstruction in EIB. While it is likely to
be a major component of the airway obstruction, there is a suggestion that EIB may be vascular
phenomenon. That is, the airway narrowing associated with EIB is due to vascular engorgement
post exercise and mucosal oedema (McFadden 1990). According to (McFadden 1990) this
engorgement of the airways restricts airflow; in addition this engorgement may increase
bronchiolar smooth muscle reactivity to histamine and isocapnic hyperventilation. It is difficult
to distinguish between vascular engorgement and bronchoconstriction in humans. Furthermore,
there is an increased production of mucus in the airways which could contribute to the airway
obstruction, although this has not been extensively studied.
Mediators
In attempting to address possible mediators of airway cooling and water loss, neural and
biochemical factors have been studied. Although human airways are not innervated by
adrenergic supply, circulating catecholamines can stimulate airway β2-adrenoreceptors and cause
bronchodialation and inhibit mast cell mediator release, an important mechanism for
bronchodialation during exercise in healthy volunteers. It has been suggested that an impaired
sypmathoadrenal response to exercise may facilitate bronchoconstriction in individuals with EIB,
either via reduced counter dilation or reduced inhibition of mast cell mediator release, however,
there are no substantive data to indicate that those with EIB have reduced sympathoadrenal
response to exercise (Wilber et al. cited in Awopeju & Erhabor 2011).
In contrast to the neural mediation of EIB, there is much greater data which supports the
biochemical factors as mediators of the EIB response. Mast cells, along with eosinophils,

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neutrophils, basophils, lymphocytes and macrophages, constitute potential sites for synthesis of
inflammatory and bronchoconstricting agents. The role of mediator release in EIB has been
investigated by detecting the mediators in body fluids following exercise challenge, and by
determining the effect of specific antagonists or inhibitors of synthesis on the exercise-induced
airway response.
Histamine release from mast cells has been studied extensively. H1 receptor antagonists
demonstrate 30 to 50% protection in EIB (Finnerty et al. cited in Gotshall 2002). However it has
been difficult to demonstrate increased histamine release in individuals with EIB either in blood
or in broncho-alveolar lavage fluid (Makker et al. cited in Gotshall 2002).
Prostanoids derived from the cyclo-oxygenation of arachindonic acid constitute
prostaglandins and thromboxane A2 (TxA2). Prostaglandin (PG) D2, PGF2α, and TxA2 are potent
bronchoconstrictors, whereas PDE2 and PGI2 are bronchodilators. Thus, a potential imbalance in
release of these agents could contribute to EIB. Uses of cycl-oxygenase inhibitors and
thromboxane synthesis and receptor antagonists have not consistently demonstrated a significant
role for bronchoconstricting prostaglandin or thromboxane in EIB (Byrne & Jones 1986 cited in
Gotshall 2002). The overall results suggest an attenuating effect on EIB of cyclo-oxygenase
inhibition, but not with thromboxane receptor inhibition. However, there is a clear role for PGE2,
a bronchodilator, in the contribution to the refractory period following EIB (Byrne & Jones 1986
cited in Gotshall 2002).
Sulfidopeptide leukotrienes are produced by 5-lipo-oxygenase actions on arachindonic
acid, followed by conjugation with glutathione. Leukotriene (LT) C4 is the initial product
formed, followed by LTD4 and LTE4. Leukotrienes are all bronchoconstrictors in asthma, and are
about 100 to 1000 times more potent than histamine (Drazen 1999 cited in Gotshall 2002). There
have been numerous investigations done on the role of leukotriene synthesis. Results have led to
the acceptance of the central role of leukotrienes in the bronchoconstriction of both allergen-
induced and exercise-induced asthma (Drazen 1999). Mast cells are most likely the predominant
source of leukotrienes release in EIB (Lane & Lee 1996 cited in Gotshall 2002). As seen earlier,
Eosinophils do not appear to play a major role in EIB, in contrast to allergen –induced asthma
(Gauvreau et al. 2000 cited in Gotshall 2002).

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Diagnosis of EIB
Initially there is an important distinction that must be made: determining if the individual
has chronic asthma or solitary EIB. Most individuals with chronic asthma will have EIB.
However those with solitary EIB do not usually have respiratory distress related to a non-
exercise stimulus (Gotshall 2002).
The American Thoracic Society has published guidelines for exercising challenge testing
for EIB (American Thoracic Society 2000 cited in Gotshall 2002). These guidelines contained
extended contraindications and specific exercise criteria. However more recently (Anderson et
al. 2001) published guidelines for exercise testing for EIB using the cycle ergometer
accompanied by breathing cool, dry compressed air. Both of these resources provide a
comprehensive and competent protocol for testing EIB. In general, exercise of about 6-8 minutes
at 85-90 percent of maximal heart rate while orally breathing cool, dry air. This should be
adequate enough to stimulate EIB in those who are susceptible (Gotshall 2002). FEV1 is the
primary outcome variable. Peak expiratory flow rate (PEFR) can also be used, although it is
more effort dependent. Pulmonary function tests (PFTs) are conducted before the exercise and at
5, 10, 15, 20, and 30 minutes post-exercise. A β2 agonist inhaler may be used if there is
appreciable dyspnea or if the PFTs have not returned to within 10 percent of baseline (Gotshall
2002).
In most cases, post exercise FEV1 is expressed as a percent of a certain pre-exercise
value. A decrease in 10% post exercise is typically considered abnormal. According to the
American Thoracic Society about 15-20 percent reductions is a diagnostic of EIB. However
according to (Anderson 1985) 10 to 25% reduction in FEV1 can be termed as mild EIB; 25 to
35% reduction, moderate EIB; 35 to 50% reduction, moderate to severe asthma; and over 50%
reduction, severe EIB. This schema is consistent with what is commonly reported in literature
(Gotshall 2002).
Another technique used to diagnose the severity of EIB, is to find out the area under the
curve, expressed as (AUC), defined by the percent fall in FEV1 post exercise over time.
Therefore, longer and greater the depression in the FEV1 post exercise, the more severe is the

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EIB. People with upper airway abnormalities such as vocal cord dysfunction or abnormal
movement of the arytenoid region might show similar reductions in FEV1 as indicative of EIB
(Gotshall 2002). A severely deviated septum could also potentially cause a reduction in FEV1.
These can be differentiated by the use of flow volume loops, and examining the different
characteristics.
Since bronchodialation occurs with exercise, there could be some overshadowing of post-
exercise PFT decrements. Therefore it may be beneficial to measure FEV1 during exercise as
well. Thus it has been suggested that an airway liability index, calculated as the maximum
increase in FEV1 during exercise minus the maximal post exercise fall in FEV1 expressed as a
percent of the pre-exercise value. This value might be useful to uncover EIB in those individuals
with depressed PFT at rest (Gelb et al. 1985).
Prevention & Treatment
The effects of climatic condition on EIB have been well documented; breathing in cold,
dry air is the most potent stimulus for EIB. Therefore the characteristics of the inspired air have a
significant impact on post exercise pulmonary function test in the individuals with EIB (Bar-Or
1977). Thus exercising in warmer, more humid conditions can attenuate the severity of EIB.
According to (Bar-Yishay 1982) swimming typically lowers the prevalence of EIB, although
there are numerous swimmers with asthma.
The Intensity of the exercise is an important factor when considering preventing or
attenuating symptoms of EIB. In general, the greater the intensity and duration of the exercise,
the more severe is the EIB (Silverman & Anderson 1972). Therefore when considering EIB,
concepts of exercise load, intensity, and duration need to be accounted for. The minimum
requirements for eliciting reproducible EIB appear to be exercise at 60 to 90 % of maximal heart
rate while running for 4 to 8 minutes (Gotshall 2002).
Individuals with EIB typically demonstrate a refractory period after the initial post-
exercise reductions in pulmonary function, while returning to full susceptibility in 2 to 3 hours
(Godfrey et al. 1975). This refractory period can be used as a technique to reduce the EIB
response to exercise by conducting an exercise warm up period at intensity below 60% of

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maximal heart rate. Therefore a continuous exercise warm up of 15 minutes appears to be
effective in reducing the EIB symptoms of subsequent exercise (Gotshall 2002). This could be
potentially beneficial for athletes with EIB who wish to exercise at high levels.
Diet can play a potential role attenuating EIB, according to (Bara & Barley 2001) several
studies using caffeine in individuals with asthma, had a modest effect on improving airway
function for about 4 hours. This would suggest that caffeine might reduce the severity of EIB
however this needs to be further studied.
The potential role of antioxidant status in influencing the symptoms of EIB has been
investigated. (Nueman et al. 2000) supplemented the diet with lycopene 30 mg/day for 1 week to
increase antioxidant status. The results showed 55% of the participants with EIB were protected
with this dose. In another study, 2g of ascorbic acid was supplemented 1 hour before exercise in
individuals with EIB. Nine of the 20 participants demonstrated a protective mechanism to EIB
(Cohen et al. 2000 cited in Gotshall 2002). These data suggests that an increase in antioxidant
status could potentially relieve some of the severity of EIB.
According to (Gotshall 2002) the dietary supplement most reviewed, with regard to
altering severity of EIB is dietary sodium chloride. In another study (Mickelborough et al. 2001)
performed a series of experiments to discover the role of dietary salt as a modifier of the severity
of EIB. The results showed elevation of dietary salt intake over 2 weeks exacerbated the
decrements in FEV1 measured post exercise, while dietary salt restriction over 2 weeks
significantly ameliorated EIB.
Individuals with asthma require control of their asthma before exercise. Therefore they
may need specific treatment for asthma. Individuals without asthma typically require treatment
specifically for exercise induced bronchoconstriction. β2-adrenergic agonists are considered the
first line therapy for preventing or treating EIB. Most athletes depend on short-acting β2-
agonists in haled 5 to 15 minutes before a period of exercise and also to alleviate symptoms post
exercise. According to (Anderson 1993) 90% of those with EIB will have reduction in EIB with
the use of inhaled β2-agonist. Long lasting β2-agonists such as salmeterol when inhaled for 30 to
60 minutes before exercise can have protection lasting up to 12 hours (Kemp et al. 1993). An

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alternative to β2-agonist therapy includes sodium cromoglycate and nedocromil. Inhaled sodium
cromoglycate and nedocromil are generally successful in modifying EIB mainly via prevention
of mast cell mediator release (Lee et al. 1982).
If the above therapies are not successful, oral theophylline or inhaled anticholinergic
therapy may also be considered. These are fall in the category of bronchodilators. Rapid-release
theophylline can be taken 1 to 2 hours before exercise, while sustained release theophylline can
be taken daily for prophylaxis. Inhaled anticholinergics need to be taken at least 30 minutes
before exercise to have any benefit. For a more complete protection, theophylline may be used in
combination with β2-agonist (Gotshall 2002).
Certain diuretics, when inhaled, have shown effectiveness in EIB. Furosemide has been
effective in several studies. According to (Munyard et al. 1995) furosemide reduced the post
exercise decrease in FEV1 in children with EIB to only 5 %, compared with the decrease with
placebo of 14.4%. Furosemide may be used with other drugs for more complete protection and
effectiveness (Novembre et al. 1994). Novembre et al. compared the effectiveness of furosemide
to nedocromil alone and in combination. In children with EIB, post-exercise decreases in FEV1
were 29, 15 and 11%, respectively, with placebo, nedocromil and furosemide. However, in
combination the post exercise decrease in FEV1 was only 5.75 %.
Anti-inflammatories
Anti-inflammatory treatment has been a proven treatment for asthma and for EIB. Both
oral anti-inflammatory and inhaled require proper planning in regard to exercise, as both require
a considerable amount of time to be effective. Thus corticosteroid treatment typically is used
regularly as a maintenance/prophylaxis drugs. Corticosteroids typically, enhance the
effectiveness of the β2-agonists (Sears 1998). Corticosteroids are effective in attenuating the post
exercise fall in FEV1. According to (Hofstra et al. 2000) fluticasone propionate reduced the post
exercise fall in FEV1 from 34% to approximately 8% in children with EIB. However, some
individuals are more resistant to corticosteroid therapy; thus requiring combination therapy with
the addition of other drugs, such as β2-agonists, to effectively control EIB.

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Antileukotriene agents are currently recommended for long term asthma therapy but have
been shown to block the bronchial constriction in exercise challenge studies (Makker et al.
1993). Heparin, a widely used anticoagulant, when inhaled, has been shown to be more effective
than sodium cromoglycate in preventing EIB. The exact mechanism is not clear, but is thought to
be due to inhibition of mast cell mediator release (Garrigo et al. 1996).
In a multicenter trial of comparative effectiveness of montelukast, an oral leukotriene
antagonist, and the long lasting β2-agonist, salmeterol (Edelman et al. 2000) found that the EIB
broncho-protective effect of montelukast was maintained through the 8 weeks of study.
However, a significant loss of broncho-protection at weeks 4 and 8 were seen with salmeterol.

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Conclusion
Exercise-induced asthma is a significant problem in adults and children, especially in
children. Symptoms that are not addressed can lead patients to avoid sport and physical activity
unnecessarily. Therefore exercise tailored to the patients EIB severity has both physical and
emotional benefits. Early recognition and accurate diagnosis are the primary steps towards
appropriate management.
Prevention is the main approach to EIB management. There are a few measures that can
be taken to diminish EIB. Inhaled β2-antagonist and sodium cromoglycate are two effective
prophylactic medications. The use of non-pharmacological interventions can be effective to
alleviate EIB. Appropriate warm up and climatic conditions can attenuate EIB.
Education of patients, coaches and parents on the nature of EIB can significantly
influence individuals with EIB to maintain a healthy and active lifestyle and consequently reach
their peak physical potential. It should be noted that individuals with EIB are potentially capable
of very high athletic performance despite their condition. This fact is clearly seen in elite
Olympic level athletes who have EIB. Many pharmacological agents that are effective in the
treatment of asthma and EIB are banned. However, when treating an athlete, the potential use of
a banned substance should be considered in treating the EIB.

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18. Exercise induced bronchoconstriction
18