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Managing exercise-induced asthma

The symptoms of exercise-induced asthma (EIA) are identical to those produced by any asthma trigger in susceptible individuals - wheezing, breathlessness, chest tightness and coughing. They result from airway narrowing in response to an inflammatory trigger. Acute airway narrowing occurs via a complex cascade of events starting with the release of inflammatory mediators and culminating in the contraction of smooth muscle around the airways.(1)

The resulting airway narrowing is called broncho-constriction. Exercise is the most common trigger of bronchoconstriction, with around 90% of people with allergic asthma experiencing bronchoconstriction in response to moderate to heavy exercise.

What causes EIA?
Most people with asthma find the severity of EIA is greater in cold weather, and for many years it was believed that airway cooling was the provocative trigger associated with exercise. However, this effect of cold air is no longer ascribed to cold per se, but rather to the fact that cold air is drier than warm air. Research suggests that the true trigger is airway drying; in fact, there is a dose-response relationship between water loss from the airways and the severity of EIA.(2) Therefore, dry air, whether warm or cold, is a more potent stimulus to EIA than humid air.
Furthermore, bronchoconstriction is attenuated, or even abolished, if the inspired air is made warm and humid.(3)
The current consensus regarding the aetiology of EIA centres around one major trigger - airway drying(.1) The increased ventilatory flow rates associated with exercise are thought to induce a process that begins with water loss from the airway surface liquid and a consequential change in the osmotic potential of the airway-lining cells. When exercise stops, the rate of water loss from the airway returns to normal and there is a restoration of normal osmolarity within the airway-lining cells.
However, this re-equilibration is accompanied by the release of inflammatory mediators from the affected cells, which trigger contraction of airway smooth muscle and bronchoconstriction. The degree of underlying airway inflammation appears to influence the severity of exercise-induced bronchoconstriction.(4)
These underlying cellular events help to explain the timing of symptoms, as well as why the severity of EIA is so variable both between and within individuals. Typically, symptoms and spirometric evidence of airway narrowing (a >10% fall in the forced expiratory volume in one second [FEV1]) peak around 10 minutes after stopping exercise.(1)
The bronchoconstriction is accompanied by cough, airway inflammation and mucus production. The timing of the response is an important aspect of accurate diagnosis, since bronchoconstriction and symptoms during continuous exercise are very rare; however, there is some evidence that individuals with EIA may develop some airway narrowing during prolonged exercise (>20-30 minutes duration), so symptoms during exercise should not be a reason to exclude EIA as a diagnosis.(5)

Are some types of exercise more provocative than others?
The type of exercise and timing of the EIA response have implications for both management and diagnosis. For people who typically take part in moderate intensity, continuous exercise, symptoms are unlikely to occur until they cease activity (when airway water content recovers). In contrast, people taking part in activities that require repeated sprints (most team sports) are likely to experience symptoms during the activity.

What about environmental factors?
The setting for the exercise also needs to be considered, as this may have implications for the severity of EIA. Dry atmospheres, whether hot or cold, are the most provocative, but in the UK it is generally cold weather that results in air with the lowest moisture content. Therefore, EIA tends to be more severe and prevalent for outdoor exercisers during the winter months. In addition, there may also be some influence of both indoor and outdoor air pollution on symptoms. Outdoor air pollution derives from vehicle exhaust gases, while indoor pollution may arise from certain types of machinery, such as vehicle exhaust gases (pace motorcycles in velodromes), chlorine (swimming pools) and ice-resurfacing machine pollutants (ice rinks).(6)
However, any links between air pollution and either the prevalence or severity of asthma are still largely circumstantial and further research is needed. Notwithstanding the preliminary nature of current evidence, a cautious commonsense approach dictates that the advice to people with EIA should be to avoid exercising outdoors in cold weather or during times when air quality is poor.
It may also be helpful for patients to keep a record of the circumstances under which symptoms arise and their severity, in order to identify conditions that are particularly provocative, or unprovocative.

Is it really asthma?
At this point, it is worth mentioning an asthma-like condition, known as "inspiratory stridor", that is sometimes misdiagnosed as EIA.(7) The symptoms are very similar to asthma, but there is no evidence of postexercise bronchoconstriction, despite severe breathlessness and inspiratory "wheeze".
The dysfunction appears to be related to abnormal vocal cord function. During inspiration, the vocal cords are supposed to abduct (move apart) in order to facilitate unimpeded inflow of air. In people with vocal cord dysfunction (VCD) there is paradoxical movement of the vocal cords, which, instead of moving apart, close over the airway, severely reducing the size of the glottis and creating a huge increase in the flow resistance and work of breathing. The obstruction results in extreme breathlessness and a characteristic wheezing sound (stridor).
However, the sound associated with VCD is subtly different from that observed in people with EIA. In asthma the wheeze is primarily expiratory, has a smooth, slightly lower pitch and is dominated by sounds from the chest. In contrast, people with VCD experience a strong, high-pitched, "sawing" wheeze that emanates from the neck. The timing of the symptoms is also different between EIA and VCD; in EIA, symptoms occur five to 15 minutes after exercise, while in VCD symptoms occur during exercise and resolve rapidly once exercise has stopped.

Pharmacological management
Pharmacological management of EIA is described as part of the British Thoracic Society's British Guideline on the Management of Asthma (see Resources). The reader is referred to this source for specific guidance; however, in summary, the most commonly used pharmacological agents are:

Bronchodilators (β2-agonists)
Frequently known as "reliever" medication, β2-agonists relax the muscles around the airways, dilating them and reducing their resistance to airflow. Short-acting β2-agonists can be used up to four times daily and are most effective when taken prophylactically immediately before exercise or in response to the development of acute EIA. If EIA is mild and infrequent, this may be the only pharmacological treatment required. However, if it is not, then it may be necessary to supplement with inhaled corticosteroids.

Corticosteroids
Known as "preventer" medication, corticosteroids suppress the chronic inflammation that is associated with asthma or frequent bouts of EIA. Reducing inflammation will improve pre-exercise lung function, as well as reducing the sensitivity of the airways to EIA. For patients with mild EIA, a once-daily dose of inhaled corticosteroid may be the only medication required to manage EIA effectively.

Nonpharmacological management
Patients are increasingly turning to nonpharmacological methods of managing chronic conditions such as asthma.
Furthermore, incorporation of nonpharmacological management tools within a traditional pharmacological treatment regimen may enhance disease control and improve the overall quality of patient care. Accordingly, it is relevant to consider the range of nonpharmacological treatment options that exist for asthma and EIA.

Warm-up
About half of people with asthma experience what is known as a "refractory period" following a 10-15- minute bout of moderate-intensity exercise (50-60% maximum heart rate), or "warm-up". For up to two hours after the warm-up, asthmatics can exercise (even intensely) and not experience EIA.(8) The
precise mechanisms for refractoriness remain unknown, but it can be used to good effect in those who show refractoriness.

Dietary modification
The relationship between diet and asthma, as well as the role of diet in modifying the severity of EIA, has only recently been the subject of systematic research, and the results to date appear promising. For example, a study published earlier this year concluded that: "Symptomatic asthma in adults is associated with a low dietary intake of fruit, the antioxidant nutrients vitamin C and manganese, and low plasma vitamin C levels." This goes on to suggest that diet may be "a potentially modifiable risk factor for the development of asthma".(9)
One of the earliest dietary components to be linked to exacerbation of asthma was dietary salt. A high- sodium diet has been found to worsen postexercise falls in FEV1. In contrast, recent evidence suggests that restricting salt intake reduces the severity of postexercise bronchoconstriction by about two-thirds, after as little as one week of restriction.(10) The effective range of sodium intake for EIA attenuation is 1,000-1,800mg/day. This is considerably lower than the recommended daily allowance for reducing hypertension (2,400mg/day), but it is nonetheless readily achievable.
Consumption of fish oils also appears to alleviate EIA. Fish oils are rich sources of omega-3 polyunsaturated fatty acids (PUFAs), which have been implicated in the reduction of inflammatory responses. The link between fish oils and asthma was made by the observation that the prevalence of asthma is very low in Eskimo populations who have high intakes of fish oils.
A recent study has demonstrated a positive effect of three weeks of supplementation with fish oil capsules on the severity of EIA in elite athletes. The double-blind, randomised, crossover study found that fish oil supplementation reduced the postexercise fall in FEV1 from 17% on the normal diet to just 3% on the supplemented diet.(11)
Asthma is an inflammatory disease, and inflammatory cells produce oxidants; therefore, the role of antioxidants in EIA has been investigated. The main antioxidant vitamins studied are C and E, and some studies have demonstrated beneficial effects of both on EIA. Preliminary data suggest that a three-week supplementation with a combination of vitamin C (500mg/day) and vitamin E (33IU/day) reduced the postexercise fall in FEV1 by 10%.(12) An earlier placebo-controlled study examined the effect of vitamin C alone, and with a much shorter supplementation period - just 90 minutes. The postexercise fall in FEV1 was halved from 20% to 10% after the acute supplementation with 500mg of vitamin C.(13)
Therefore, at the very least, patients with asthma and EIA should be encouraged to minimise their salt intake and to maintain a healthy balanced diet, as it may benefit their asthma as well as their general health.

Inspiratory muscle training (IMT)
The principal symptom of bronchoconstriction is an increased sense of respiratory effort, or breathlessness. There is a strong relationship between the strength of the inspiratory muscles and the sense of respiratory effort, and this has been demonstrated directly for people with asthma.(14)
To date, three studies have demonstrated impressive reductions in both consumption of β2-agonists and breathlessness after IMT.(14) No studies have yet examined the influence of IMT on the severity of EIA per se. However, it appears that IMT ameliorates the principal symptom of bronchoconstriction, breathlessness, and this does appear to be beneficial in terms of patients' consumption of medication. The potential role of IMT in the management of breathlessness was reviewed in a previous article in Nursing in Practice.(15) Since publication, an inspiratory muscle trainer has been approved for prescription and is listed within part IX of the Drug Tariff, making it accessible to all patients with breathlessness.
The mainstay of asthma management continues to be pharmacological. However, for patients with mild symptoms, or for those wishing to optimise management using all means available, the nonpharmacological approaches described here offer evidence-based additions to traditional pharmacological management.

Conclusion
The symptoms of EIA are identical to those elicited by other asthma triggers, and typically arise during the five to 15-minute period postexercise. The underlying cause of EIA is water loss from the airway-lining cells.
EIA is common and debilitating, but it need not be a reason for patients with asthma to avoid exercise. The condition is amenable to treatment and can be managed using a combination of pharmacological and nonpharmacological approaches, the combination of which may result in better overall control.

References

  1. Rundell KW, Jenkinson DM. Exercise-induced bronchospasm in the elite athlete. Sports Med 2002;32:583-600.
  2. Eschenbacher WL, Moore TB, Lorenzen TJ, Weg JG, Gross KB. Pulmonary responses of asthmatic and normal subjects to different temperature and humidity conditions in an environmental chamber. Lung  1992;170:51-62.
  3. Anderson SD, Daviskas E, Schoeffel RE, Unger SF. Prevention of severe exercise-induced asthma with hot humid air. Lancet 1979;2(8143):629.
  4. Rouhos A, Ekroos H, Karjalainen J, Sarna S, Sovijarvi AR. Exhaled nitric oxide and exercise-induced bronchoconstriction in young male conscripts: association only in atopics. Allergy 2005;60:1493-8.
  5. Gotshall RW. Airway response during exercise and hyperpnoea in non-asthmatic and asthmatic individuals. Sports Med 2006;36:513-27.
  6. Rundell KW. Pulmonary function decay in women ice hockey players: is there a relationship to ice rink air
  7. quality? Inhal Toxicol 2004;16:117-23.
  8. Rundell KW, Spiering BA. Inspiratory stridor in elite athletes. Chest 2003;123:468-74.
  9. McKenzie DC, McLuckie SL, Stirling DR. The protective effects of continuous and interval exercise in athletes with exercise-induced asthma. Med Sci Sports Exerc 1994;26:951-6.
  10. Patel BD, Welch AA, Bingham SA, et al. Dietary antioxidants and asthma in adults. Thorax 2006;61:388-93.
  11. Mickleborough TD, Gotshall RW. Dietary salt intake as a potential modifier of airway responsiveness in bronchial asthma. J Altern Complement Med 2004;10:633-42.
  12. Mickleborough TD, Murray RL, Ionescu AA, Lindley MR. Fish oil supplementation reduces severity of exercise-induced bronchoconstriction in elite athletes. Am J Respir Crit Care Med 2003;168:1181-9.
  13. Murphy JD, Ferguson CS, Brown KR, Harms CA. The effect of dietary antioxidants on lung function in exercise-induced asthmatics [abstract]. Med Sci Sports Exerc 2003;34:S115.
  14. Schachter EN, Schlesinger A. The attenuation of exercise-induced bronchospasm by ascorbic acid. Ann Allergy 1982;49:146-51.
  15. Weiner P, Magadle R, Beckerman M, Berar-Yanay N. The relationship among inspiratory muscle strength, the perception of dyspnea and inhaled beta2-agonist use in patients with asthma. Can Respir J 2002;9:307-12.
  16. McConnell AK. Inspiratory muscle training for managing breathlessness. NiP 2005;20:60-3.

Resources
Asthma UK
W:www.asthma.org.uk

British Lung Foundation
W:www.lunguk.org

British Thoracic Society
W:www.brit-thoracic.org.uk

Best Treatments
W:www.besttreatments.co.uk

British Guideline on the Management of Asthma
W:www.brit-thoracic.org.uk/page235.html