Spring is here again and welcome after a particularly chilly winter. Now is the time when we dust off our running shoes, pull out the decaying swimmers, and take a new lease out on life!
One problem that rears it’s head often at this time of year is that of seasonal allergies, rhinitis, and asthma. One problem particularly troubling to exercisers is that of Exercise Induced Asthma and/or Bronchospasm. This months blog follows this topic- remember management can be difficult and medical advice is wlays recommended. Happy exercising!
Exercise Induced Asthma and Bronchospasm
Exercise Induced Bronchospasm (EIB) is defined as a transitory ↑ in airway resistance that occurs following vigorous exercise. EIB represents a pathology different to that of classic asthma. It represents 6-12% of the general population, and 4-80% of the sporting population. The higher athlete prevalence is thought to be due to the high training loads in combined with the training environment of the athletes.
Exercise Induced Asthma (EIA) specifically refers to the individual with background asthma also triggered by exercise. It includes around 90% of asthmatics. EIA severity is ↓ by inhaled steroid treatment in a dose-dependent fashion. EIA is one of the first asthma symptoms and is the last to resolve after inhaled steroid treatment.
Symptoms of EIB:
Symptoms classically peak within 5-10 minutes after the cessation of moderate to intense exercise. It is suggested that during exercise surges in adrenaline are protective by stimulating bronchodilatation. After cessation of exercise adrenaline levels drop and mast cell mediator release occurs.
Symptoms of EIB are diverse, often not recognised and include:
- chest tightness
- shortness of breath
- dry cough
Others symptoms include prolonged difficulty in eliminating URTI’s, difficulty sleeping due to night symptoms & reduced performance.These symptoms will usually either resolve spontaneously or with the use of bronchodilators. 50% of patients with EIB are rendered refractory for the 2-4 hours after an event. The reason for this is unclear. It may be related to prostaglandins, and NSAID medications may abolish the refractory period. There may be a seasonal element to symptoms, and atopy is very important. There may be ↑ eosinophils in atopic athlete’s sputum. Winter athletes have been found to have ↑ neutrophils in their sputum (possibly because of respiratory tract trauma).
Diagnosis can be made via the use of:
- Clinical history (looking for the above symptoms)
- PEFR diary pre and post exercise and the bronchodilator response (although not entirely reliable and effort dependent).
- EVH challenge test (gold standard)
- Exercise challenge test
- Osmotic challenge tests- mannitol, hypertonic saline
- Allergen testing (SST, RAST, IgE) Total IgE serum levels can be used as a simple assessment of a patient’s allergic profile. Skin testing is for common allergens like dust mite, couch/rye/birch grass, and cats/dogs. If skin tests are positive (>3mm wheal) than should perform an IgE level plus a RAST test for that specific allergen.
Management begins with a thorough assessment of asthma triggers including animal dander, house dust mites, mould, smoke, and pollen, changes in the weather or airborne chemicals.
Asthma and EIB should be distinguished from associated disorders that cause respiratory symptoms during exercise including: fixed airway obstruction, laryngeal dysfunction, gastroesophageal reflux, and vocal cord dysfunction (VCD).
This should be used as adjunctive treatment, and there is no substitution for pharmacological therapy. Masks reduce severity of EIB; can recover 42 % of water at 16°C (more useful in colder countries). Nose breathing to increase resistance is not effective in all patients. It is difficult to do, especially during vigorous exercise (above 35 L / min). Exercise training effects still controversial. Increased fitness levels increase the threshold at which EIB occurs but won’t stop it.
Refractory period: This does not work in every athlete (~50%) and is not recommended as it may induce severe bronchospasm. Warm up before the actual exercise reduces asthma in subsequent exercise.
Dependent on level of exercise. Medications just before exercise are adequate. Some patients may require treatment with daily asthma therapy. NB: ALWAYS CHECK MEDICATIONS WITH YOUR SPORTS PHYSICIAN AS SOME MEDICATIONS ARE PROHIBITED, AND MAY RESULT IN AN ADVERSE DRUG TEST FINDING.
These are effective at relieving of asthma symptoms, and have been reported to improve pulmonary function in 90% of individuals with EIB. They bronchodilate, ↑ air flow, ↓vascular permeability and moderately inhibit mediator release. Studies have demonstrated no ergogenic properties of any IOC approved medication when used in therapeutic doses by the permitted route (oral consumption of beta agonists does have an anabolic effect).
Thought to block chloride ion flux into mast cells and prevent mast cell degranulation. Most effective within 2 hours of treatment and shown to prevent both early and late phase asthmatic reactions. It has no bronchodilating effects and cannot be used for acute episodes. Side effects: throat irritation, cough, transient bronchospasm. Precautions with abrupt withdrawal. Not restricted in sport.
They can give protection against EIB and do not show tolerance (unlike β2 agonists). As once daily oral tablets, often have better compliance in younger individuals, and they can reduce corticosteroid requirements. They have around a 50% mean effectiveness in inhibiting post-exercise bronchoconstriction (possibly due to other inflammatory mediators being responsible for symptoms). Leukotrienes are released from eosinophils in response to an increase in osmolarity and could feasibly cause transient migration of eosinophils to the airways. While treatment with inhaled steroids decreases eosinophil number, steroids do not prevent the contractile effects of leukotrienes. Thus, EIA may still occur if there are sufficient cells left containing this potent mediator.
Improve asthma symptoms by reducing airway inflammation and bronchial hyper-reactivity. They inhibit multiple segments of the asthmatic cascade, suppressing the generation of cytokines, reducing the population of airway eosinophils, and preventing inflammatory mediator release. They do not have an immediate bronchodilator effect, and are not effective when used prophylactically prior to exercise. 4 weeks treatment with corticosteroids 400 micrograms daily reduced EIA severity and increased lung function.
The main role of corticosteroids is that of maintenance therapy to help control asthma, but in doing so they act to reduce bronchial responsiveness to exercise, thereby reducing the propensity for EIA. Often used on a regular basis, with sodium cromoglycate or nedocromil sodium given just prior to exercise. Side-effects of oral candidiasis and dysphonia can be reduced by mouth washing following administration. Others are hoarseness, cough, rhinitis eczema, GIT upset, arrhythmia, headache, light-headedness, thirst, taste disturbance.
Anticholinergics (not used in EIB)
This blocks vagal tone and reflexes which mediate bronchoconstriction. Used alone it is not a powerful bronchodilator. Its duration is approximately 6 hours and can be used to augment β2 agonists. Side effects include blurred vision, precipitation of glaucoma and a dry mouth. Theophylline has no role in treating EIA.