Exertional dyspnea in athletes

Exertional dyspnea in active patients can be challenging to diagnose and to treat. While exercise-induced asthma (EIA) is the most common cause of exertional dyspnea in athletes, two less common causes—vocal cord dysfunction and pulmonary embolism—should also be considered. These less common causes of exertional dyspnea require treatments unlike those used for EIA. In addition, they may represent more significant health risks, and should be included in any differential diagnosis of exertional dyspnea.

The shortness of breath experienced by some active individuals does not always have a straightforward pathophysiology.

The most common cause of exertional dyspnea in active patients is exercise-induced asthma (EIA), defined as “an intermittent narrowing of the airways, accompanied by a decrease in some measure of airflow that the individual experiences as wheezing, chest tightness, coughing, and dyspnea that is triggered by exercise.”[1] Up to 90% of chronic asthma patients can experience exercise-induced asthma during the course of their disease.[2] Exercise-induced asthma seems to have an increased prevalence in more athletic populations.[3] The symptoms of EIA include the typical asthma symptoms mentioned above, and may also include poor performance for a given level of conditioning, or performance changes that are season- and climate-related.

Transient airway narrowing during and following exercise causes exercise-induced asthma symptoms. These symptoms may last 1 to 2 hours following the cessation of exercise. High ventilatory rates during exercise lead to evaporative water loss of airway surface liquid. This process leads to cooling and changes in osmolarity of the airway surface liquid that triggers the inflammatory mediators that cause smooth muscle constriction and airway edema.

Diagnosis of EIA

Diagnosis of EIA can often be challenging. History-taking focuses on respiratory symptoms, family history, and environmental and activity triggers. In sport there are some unique precipitating factors worth considering. These include the cold, dry environment of Nordic skiing, chlorine in swimming pools, and pollution from ice resurfacing machines. The physical examination is often normal at rest. If the patient has incompletely treated baseline asthma, the exam may include wheezing, end-inspiratory coughing, and a prolonged expiratory phase. Resting spirometry may also be normal.

Historically, the best test of exercise-induced asthma has been a combination of spirometry and a field challenge.[3] The field challenge should be similar in intensity and environment to the athlete’s typical exercise situation. For example, if a cross-country skier with possible EIA performs treadmill exercise in a warm, humid lab, there may be no changes on spirometry, thus leading to a false-negative result. The combination of field challenge and spirometry can be logistically difficult to undertake, and therefore a number of surrogate tests have been developed in an attempt to diagnose EIA more conveniently.

Provocative tests for EIA include pharmacologic challenge tests, voluntary hyperventilation, and osmotic challenge tests. Chemical challenge tests such as methacholine and histamine challenge are useful in the diagnosis of chronic asthma. When compared with spirometry and field challenge, pharmacologic challenge tests appear to be more sensitive for airway reactivity, but much less specific for exercise-induced asthma.[3] Voluntary hyperventilation tests attempt to mimic the high minute ventilation that occurs during exercise. The eucapnic voluntary hyperpnoea (EVH) test uses mixed gases to maintain isocapnia while the patient ventilates at a level consistent with exercise. Spirometry is performed after the hyperventilation to assess for airflow limitation. When compared with field challenge and spirometry, EVH testing demonstrates improved sensitivity and specificity.[4] Research has recently been done with respect to osmotic challenge tests. Either hypertonic saline or mannitol in an inhaled form is used to provoke an asthmatic response. At present, these tests show some promise as alternative diagnostic tests for EIA, but more research needs to be done. In summary, although a combination of field challenge and spirometry is regarded as the gold standard for EIA, it can be inconvenient or logistically difficult. EVH testing is an alternative that is preferred by the International Olympic Committee.

Treatment of EIA

Treatment can be divided into pharmacologic and nonpharmacologic strategies. The simplest nonpharmacologic treatment is to choose activities and environments that are less asthmogenic. Ideally, a warm humid environment is best. Activities that do not involve high ventilatory rates are best for patients with EIA. These include baseball, football, golf, gymnastics, martial arts, sprinting, swimming, tennis, weightlifting, and water polo.[5,6] Another effective tactic for attenuating EIA attacks is the implementation of an effective warm-up. An appropriate warm-up is 15 minutes of activity prior to the practice or competition. The exercise intensity should be such that it does not induce bronchospasm.

When considering pharmacologic treatment of exercise-induced asthma, it is important to ensure that underlying asthma is treated sufficiently to ensure normal baseline spirometry. Once normal baseline spirometry is established, medications can be administered before exercise to prevent an exercise-induced attack. If treating competitive athletes, the prescribing physician should be aware of the doping regulations for the athlete’s particular sport. Some asthma medications are banned, while others require laboratory documentation of the patient’s condition.[7] Table 1 lists restricted medications.

The most common pharmacologic strategy is to take a short-acting beta-agonist (such as salbutamol) 30 to 60 minutes before exercise. These medications can also be taken as “rescue” medications after exercise to reduce symptoms in the event of an attack. There has been some concern about the long-term frequent use of short-acting beta-agonists leading to diminished effectiveness.[6] For this reason, other medications can be prescribed to decrease the frequency of beta-agonist usage. These include inhaled corticosteroids, long-acting beta-agonists, mast cell stabilizers, and leukotriene antagonists. None of these alternate medications can be used as a rescue medication to abort an attack. Both inhaled corticosteroids and long-acting beta-agonists are effective in attenuating exercise-induced asthma.[6] Inhaled corticosteroids such as fluticasone and budesonide need to be taken for several weeks to be effective. Leukotriene antagonists (montelukast and zafirlukast) are partially effective in attenuating EIA, and last for at least 8 hours, making them an effective adjunct treatment, especially in patients who are exercising more than once a day. Mast cell stabilizers such as necrodomil sodium and cromolyn sodium are less effective than beta-agonists in preventing EIA, but may have a role in patients who are unable to take beta-agonists. In summary, short-acting beta-agonists taken 30 to 60 minutes before activity are the mainstay of pharmacologic treatment of EIA. Other agents such as inhaled corticosteroids, long-acting beta-agonists, and leukotriene antagonists can be used as adjunct treatments to decrease the need for short-acting beta-agonists.

Exercise-induced asthma is a common condition affecting many asthmatics. Clinical findings in the office are often few, and there is no reliable, convenient laboratory test to confirm the diagnosis. Fortunately, there are a number of pharmacologic and nonpharmacologic strategies that can be implemented to reduce the frequency and severity of EIA episodes. In fact, many Olympic medals in highly aerobic sports such as swimming have been won by athletes with severe asthma that has been controlled with the above strategies.[7] Consequently, properly treated EIA does not hinder performance.

Conditions that mimic EIA

The following cases serve to illustrate two less common conditions that occur in high-performance athletes. Both pulmonary embolism and vocal cord dysfunction can mimic EIA, thus it is always useful to consider them in the diagnosis of active patients with exertional dyspnea (Table 2). Unlike exercise-induced asthma, these entities can limit performance, and may represent significant health risks.

Case 1

A 25-year-old elite cross-country skier presented with a 2-week history of increasing shortness of breath on exertion. Her symptoms resembled a previous episode approximately 2 years before that had resolved after a hiatus in training. Three years before, the patient had been given a diagnosis of exercise-induced asthma (EIA), for which she was prescribed salmeterol and fluticasone for exacerbations. Approximately 1 week before presentation, she had restarted her fluticasone and salmeterol, and had introduced loratidine. The patient also had a history of pneumonia approximately 4 years earlier that had been resolved with outpatient antibiotic therapy.

Previously, this athlete had been tested for allergies and had reacted to dogs, feathers, dust mites, trees, and moulds. There was no history of ASA sensitivity. She was a nonsmoker and otherwise healthy. Her only medication was a triphasic estrogen/progestin oral contraceptive.

On examination she was in no visible distress. There was no evidence of clubbing or cyanosis. Pulse was 76 and regular; blood pressure was 120/80. Auscultation of lung fields revealed good air entry and no abnormal breath sounds. Cardiovascular examination revealed normal S1 and S2 with no murmurs or extra heart sounds. The rest of the physical examination was normal. Spirometry and methacholine challenge were performed. Both were within normal limits.

The patient was referred for an exercise study to assess for exercise-induced asthma. The study failed to show any evidence of obstruction. While exercising, her hemoglobin saturation dropped from 99% to 79%. An urgent ventilation/perfusion scan was obtained. The scan demonstrated multiple segmental defects bilaterally affecting approximately 40% of her pulmonary vasculature (Figure). She was immediately admitted to hospital and treated with anticoagulants.

Workup for hypercoagulability, including lab tests for protein S, protein C, and factor V Leiden, demonstrated no abnormalities. The only identified hypercoagulable risk factor was the use of a triphasic oral contraceptive. This medication was subsequently stopped.

After a 3-month period of treatment with oral anticoagulants, the patient returned to activity. She experienced profound dyspnea and fatigue that limited her exercise capacity at first. This improved over the course of 6 months with a return to training and eventually to high-level competition. For contraception, a progestin-only preparation was recommended.

Case 2

A 25-year-old elite track-and-field athlete presented with a 3-year history of exertional dyspnea. While running, she developed tightness in her throat, with some slight chest tightness. She also noticed a stridorous sensation when breathing heavily that resolved on cessation of running. The symptoms seemed to be worst during the autumn, at the same time as she would suffer from some nasal congestion and postnasal drip.

Several asthma medications were tried, including salbutamol, salmeterol, montelukast, and fluticasone. These provided minimal benefit. Formoterol appeared to offer some improvement, but was subsequently banned by the athlete’s regulatory body and was discontinued. A second trial of formoterol at a later date seemed to have little beneficial effect.

The athlete had no previous complaints of allergies until the year before when she developed some perennial rhinitis. There was no concomitant history of either urticaria or atopic dermatitis. Allergy testing revealed skin reactions to alder, maple, and grass. Other than a history of gastroesophageal reflux disease and some visual impairment, the patient had no other medical issues. She was on no medications other than multivitamins, calcium, and vitamins C and E. A lifelong nonsmoker, she did have a significant exposure to passive smoke.

On examination, the patient was in no apparent distress. Her pulse was regular at 54 beats per minute. Blood pressure was 126/92. Respiratory rate was 14. There was no evidence of clubbing, cyanosis, or lymphadenopathy. Nasal mucosa was erythematous and congested. Cardiovascular examination revealed normal S1 and S2, with no extra heart sounds. There was no peripheral edema or jugular venous distension. Auscultation of the lungs revealed good air entry bilaterally with no adventitial sounds. Abdominal, neurological, and endocrine examinations were unremarkable.

Spirometry was within normal limits. A methacholine challenge test was not suggestive of underlying bronchial hyperreactivity. A progressive exercise test was performed, during which the patient developed audible inspiratory stridor that led to a flattening of the inspiratory limb on her flow-volume loop. Exercise was terminated at this point.

The patient was diagnosed with vocal cord dysfunction and started on a nasal corticosteroid to reduce her rhinitis and postnasal drip. This treatment proved to be of little benefit. It was thought that perhaps gastroesophageal reflux was irritating her upper airway and aggravating her symptoms. A 24-hour pH study and esophageal physiology testing were performed. These tests demonstrated both acid reflux and a hypotensive lower esophageal sphincter. The patient is presently undertaking a trial of pantoprazole to reduce her gastric acid secretion and to reduce her upper airway irritation.


Exertional dyspnea, which is common in the young athlete, may not always have a straightforward pathophysiology. The two cases described here illustrate exertional dyspnea not caused by exercise-induced asthma. Both pulmonary embolism and vocal cord dysfunction are uncommon entities, but are important in the differential diagnosis of exertional dyspnea. These entities can be difficult to distinguish in the active patient. They can each present with dyspnea on exertion, chest tightness, and a decline in performance.

Pulmonary embolism

Several cases of pulmonary embolism in young athletes have been reported in the literature.[8-13] Although an uncommon condition in this generally healthy population, pulmonary embolism can have significant consequences, and is an important diagnosis to consider in athletes. In the reported cases in the literature, the patient with pulmonary embolism had usually been treated for a number of other conditions before the correct diagnosis was reached. These conditions included acute bronchitis, pneumonia, and asthma. Early identification of pulmonary embolism would reduce unnecessary investigations, treatments, and morbidity for these patients.

Athletes have some unique possible risk factors for thromboembolism. Some authors have suggested that the illicit use of substances such as anabolic steroids and diuretics may put athletes at higher risk.[9,13,14] In addition, some competitive athletes such as wrestlers and rowers opt to (ill-advisedly) dehydrate themselves routinely to “make weight.” This behavior may lead to an increase in blood viscosity, and hence venous stasis. Similarly, athletes who take erythropoietin to increase the oxygen capacity of their blood may also be increasing their thromboembolic risk.[15]

Although the usual source of thrombosis in pulmonary embolism is the pelvic and proximal thigh veins, athletes may be more at risk for development of thrombus in their upper extremities. Paget-von Schrötter syndrome, or effort-induced thrombosis, denotes the formation of such a thrombus in the upper extremity (usually in the axillary vein) as a result of heavy arm use. This condition typically occurs in throwers.[16] The symptoms of effort-induced thrombosis are those of vascular obstruction in the upper extremity, and include swelling, aching pain, paresthesia, and numbness in the distal arm. If chest symptoms occur, then pulmonary embolism should be considered. The pathophysiology of effort-induced thrombosis is not well understood, but is believed to be related to trauma to the vessel wall, precipitating thrombosis.

The woman in the case described above was investigated for hypercoagulable conditions, but all of her results were normal. Her only identifiable risk factor for thromboembolism was her use of a combined oral contraceptive preparation. The relative risk in oral contraception users of second- and third-generation oral contraceptives compared with non-users is between 3 and 6, although the absolute risk is very low. In a healthy population, the risk of thromboembolism increases with oral contraceptive use from less than 1 per 10 000 woman-years to 3 to 4 per 10 000 woman-years.[17,18] The relative risk of thromboembolism for combined oral contraceptive users is approximately one-half of that in pregnancy.[18] The risk of thromboembolic disease is possibly higher for patients using oral contraceptives with a third-generation progestin (such as desogestrel, gestodene, and norgestimate) than for patients using a second-generation progestin (norgestrel, levonorgestrel, and norgestrienone).[18] A progestin-only preparation such as injectable medroxyprogesterone acetate (DepoProvera) or oral norethindrone (Micronor) would be appropriate substitutions able to provide contraception while mitigating the risk of recurrence.

Vocal cord dysfunction

Vocal cord dysfunction (VCD) refers to the involuntary paradoxical adduction of the vocal cords on inspiration. Other terms for this include paradoxical vocal cord motion, vocal cord dystonia, laryngeal dyskinesis, vocal cord adduction, and Münchausen’s stridor.[19,20] During an episode of VCD, inappropriate vocal cord adduction can lead to inspiratory airflow obstruction. This obstruction can cause a sensation of throat or chest tightness, air hunger, and stridor. Patients may also complain of coughing or hoarseness. Vocal cord dysfunction primarily occurs in younger patients (ages 9 to 43 years).[21] There is also a gender bias, with female patients outnumbering males by approximately two to one. The actual incidence in the general population and the athletic population is unknown. VCD has been reported in skiing, swimming, track, cross-country running, figure skating, boxing, wrestling, soccer, basketball, football, racquetball, and tae kwon do.[21] An athlete with VCD is often misdiagnosed as asthmatic, but subsequently fails asthma therapy before further assessment provides the true diagnosis. As would be expected, asthma therapy does not help this condition; in fact some asthma treatments such as corticosteroids, intubation, and hospitalization may actually harm the patient.

Typically, VCD features an abrupt onset and resolution of symptoms. The pattern of occurrence is generally variable and not easily reproducible. VCD sufferers rarely experience arterial desaturation.[19-21] Exercise-induced asthma (EIA) differs from VCD in that there is no gender bias; symptoms generally start after 6 to 12 minutes of exercise and are most severe 5 to 10 minutes after exercise. In addition, about 50% of subjects are refractory to repeated exercise challenge for a period of 2 hours after an episode of EIA.[22] Typically athletes with EIA respond well to inhaled beta-agonists. Unfortunately, VCD and EIA can coexist in athletes.

VCD can be suspected during pulmonary function testing if there is a restriction of the inspiratory flow while symptomatic during exercise testing. This restriction may present as auditory inspiratory stridor at the time of testing or as a specific pattern on the flow-volume loops, with the inspiratory curve appearing blunted or flattened. This finding can occur in the presence or absence of expiratory flow obstruction. Pulse oximetry is generally normal. Direct fibre-optic laryngoscopy is the definitive investigation of choice. It is important that this be performed while the patient is symptomatic. To induce symptoms, patients should carry out a graded exercise test. Once their symptoms are present, the challenge is stopped and laryngoscopy is performed.

Treatment for vocal cord dysfunction can be difficult. Acute treatment can involve having the patient pant or cough. This action seems to resynchronize the respiratory cycle by activating the vocal cord abductors and widening the glottic aperture.[21] Administration of heliox (a helium-oxygen mixture) can also help by reducing airway turbulence, and therefore improving airflow through the larynx.[20]

Long-term treatment of vocal cord dysfunction focuses on education and speech therapy. The goal is to retrain the patient to breathe appropriately when under stress. Postural correction can help to reduce the rounded-shoulder-neck-forward position, which can aggravate symptoms. There has been some suggestion that jaw thrusting during exercise may also reduce symptoms. VCD can often have a psychological component (such as anxiety secondary to performance expectations), and therefore formal evaluation may be indicated. Strategies aimed at reducing the patient’s level of stress are particularly important. An attempt should also be made to treat any other conditions that may irritate the larynx, such as gastroesophageal reflux disease and allergic rhinitis.[21,23]


Pulmonary embolism and vocal cord dysfunction represent two relatively uncommon entities that cause exertional dyspnea in athletes and may be confused with exercise-induced asthma. As the treatment for all three conditions is vastly different, inclusion of both vocal cord dysfunction and pulmonary embolism in the differential diagnosis of exertional dyspnea will permit earlier diagnosis and more appropriate management of these conditions.

Table 1. Summary of restricted medications in the treatment of asthma.

Banned substances Permitted in certain circumstances
Bambuterol (†Bambec, †Oxeol) *Formoterol (efformoterol, Foradil, Oxeze-Turbuhaler, †Oxis)
Clenbuterol (†Broncoterol, †Spiropent, Ventipulmin [veterinary]) *Salbutamol (Albuterol, Alti-, Nu-, Med-, Dom-Salbutamol, Apo-Salvent, Ventolin, Novo-Salmol, Airomir, Salbu-2, -4, Asmavent, Combivent, Ventidisk, Sabulin)
Fenoterol (Berotec, Duovent UDV) *Salmeterol (Serevent)
Isoproterenol (isoprenaline, Isuprel) *Terbutaline (Bricanyl Turbuhaler, †Brethine)
Orciprenaline (metaproterenol, Apo-, Alti-, Tanta-Orciprenaline) *Glucocorticosteroids administered as an inhaler
Reproterol (†Bronchospamin)  

*Permitted only by inhalation. Athletes must provide written declaration to the relevant medical authority in advance of a doping control test or competition. Written declaration should be made at the time the medication is prescribed. (N.B. Athletes who give notification of the intent to use an inhaled, permitted beta-2 agonist at the 2004 Summer Olympic Games will now be required to submit clinical and laboratory evidence that justifies the treatment and will be assessed by an independent medical panel.)
†Other brand names used outside Canada.
Montelukast, zafirlukast, cromolyn sodium, sodium cromoglycate, nedocromil and ipratropium are all permitted if needed to treat a justifiable medical condition. 

Source: Compiled from data on the Canadian Centre for Ethics in Sport web site at.


Table 2. Clinical findings of exercise-induced asthma, vocal cord dysfunction, and pulmonary embolism.

Clinical finding Exercise-induced
Vocal cord 
Exertional dyspnea + + +
Chest pain +/– +/–
Inspiratory stridor +
Expiratory limitation +
Arterial desaturation +/– +/– ++
Response to b-agonists +
Abnormal spirometry +/– +(during exercise)/–

Competing interests
None declared.


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M. Koehle, MD, D.R. Lloyd-Smith, MD, D.C. McKenzie, MD, PhD

Dr Koehle is a physician at the Allan McGavin Sports Medicine Centre and St. Paul’s Hospital, and a clinical instructor fellow in the Department of Family Practice at the University of British Columbia. Dr Lloyd-Smith is a primary care physician at the Allan McGavin Sports Medicine Centre and a clinical professor in the School of Human Kinetics, UBC. Dr McKenzie is a physician at the Allan McGavin Sports Medicine Centre and a professor of Human Kinetics at the University of British Columbia.

M. Koehle, MD, D.R. Lloyd-Smith, MD, D.C. McKenzie, MD, PhD. Exertional dyspnea in athletes. BCMJ, Vol. 45, No. 10, December, 2003, Page(s) 508-514 - Clinical Articles.

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