exercise induced asthma

Exercise induced asthma: Take a deep breath - and learn to manage your asthma without falling foul of doping regulations

Asthma is an increasingly common chronic respiratory condition that is even commoner among athletes. New, stricter doping regulations mean that competitors who want to take prescribed drugs must now produce diagnostic evidence of need. But there are a number of other useful ways of controlling the condition and relieving its symptoms.

Asthma is characterised by a reversible narrowing of the airways, causing difficulty in breathing, which occurs in response to a trigger, or allergen (eg pollen, animal hair, dust). Prevalence rates for asthma in the general population vary from country to country: a recent study on 20,000 adults in Norway suggested a prevalence of diagnosed asthma of 9%(1), which is comparable with the 8% prevalence reported by the National Asthma Campaign for the UK(2). New Zealand has the highest rates of asthma internationally, with as many as 15% of adults affected(3).

In more than 80% of people with allergic asthma – and some with the non-allergic variety – the airway narrowing, technically known as bronchoconstriction, is also brought on by exercise, its severity peaking around 10 minutes after stopping exercise. Symptoms vary from person to person, but typically include wheezing, chest tightness, coughing, breathlessness and mucus production.

A recent review of exercise induced asthma (EIA) suggests a prevalence in élite athletes of between 10 and 50%, depending on the sport(4). Prevalence rates seem to be particularly high in cold-weather sports, for reasons which are explained later in this article(5).

The Medical Commission of the International Olympic Committee (IOC) has responded with suspicion to the increasing prevalence rates of EIA in athletes, and the consequently increased use of inhaled medication for its treatment. In September 2001 the IOC made it mandatory for all athletes who wished to use inhaled medication for asthma to produce diagnostic evidence. This ruling will be effective for the Athens Olympics later this year, and the IOC will no doubt watch with interest to see if reported prevalence rates among élite athletes change following the tougher approach to diagnosis.

But while it may be true that some athletes are using asthma medication unnecessarily, it is also possible that the high prevalence rates reported in certain sports may be linked to the competitive environment, of which there is more below.

But first let’s take a look at why asthma is triggered by exercise. The current consensus centres on one major trigger – airway drying (4). The high ventilatory flow rates associated with exercise are thought to induce a cascade of responses that begin with water loss from the airway surface liquid and a consequent change in the osmotic potential of the airway lining cells. When exercise stops, normal osmolarity is restored, but in people prone to asthma this process is accompanied by the release of inflammatory mediators from the affected cells, which trigger constriction of smooth muscle around the airways, causing them to narrow.

Why cold air triggers asthma

Many people with asthma find their exercise-induced attacks more severe in cold weather, probably because cold air is dryer than warm air. The greater prevalence of EIA in cold-weather sports is thought to be due to the chronic influence of airway drying and inflammation, which induce ‘airway remodelling’. This remodelling leads to a condition known as airway hyper-reactivity, in which the athlete becomes very sensitive to the effects of airway drying.

Other environmental stimuli, such as vehicle exhaust gases, chlorine and ice-resurfacing machine pollutants, may exacerbate EIA and also promote hyper-reactivity. Further systematic research is needed before clear linkages can be identified, but air pollution from vehicles is of growing concern generally, and evidence for a link between poor air quality and the increased incidence of hospital admissions from respiratory causes is strong (6). This is of particular concern in the context of the Athens Olympics, since Athens has very high levels of air pollution, especially during the summer months.

The IOC’s guidelines for the diagnosis of EIA require the use of ‘spirometric’ methods, which measure the volume of air inhaled and exhaled. People with normal airways do not show an improvement in their lung function when they take inhaled bronchodilator medication (beta2-agonists). However, asthmatics almost always do, and the IOC accepts a 15% increase in the forced expiratory volume in one second (FEV1) within 10 minutes of using a bronchodilator as a positive test for asthma. However, athletes may have very little chronic, pre-existing airway constriction, particularly if they are only responsive to exercise and therefore their lungs are normal for most of the time. Thus, the IOC also accepts the results of so-called ‘provocation challenges’.

Provocation challenges

Provocation challenges are of three main types, the simplest of which is a straightforward exercise test. The exercise must be of high intensity (>85% of maximum heart rate) and last for around six minutes, thus ensuring that the ventilatory requirement is sufficient to provoke airway drying. The main problem with an exercise challenge, though, is that the environmental conditions – eg a warm, humid day – may not favour a positive response, which could lead to a false negative result and a consequent inability to use asthma medication legally.

The second type of provocation challenge is a somewhat artificial but standardised method of inducing airway drying known as ‘eucapnic voluntary hypernoea’ (EVH), which requires the athlete to hyperventilate for six minutes into an apparatus supplying dry air. A positive diagnosis requires a 10% fall in FEV1 within 30 minutes of the provocation.

The third challenge involves inhalation of a substance that is known to trigger an inflammatory response in the airways of susceptible individuals (such as saline, mannitol, methacholine or histamine). However, the IOC regulations for diagnosis on the basis of an inhalation challenge are complex, and it is not the preferred method.

For all of these tests, the athlete must have ceased taking any of the following prescribed medications:

  • short-acting beta2-agonists 12 hours before the test;
  • long-acting beta2-agonists 48 hours before;
  • corticosteriods (anti-inflammatory) 72 hours before.

Because athletes must be deprived of their medication, EIA provocation challenges should only be conducted by appropriately qualified individuals, under conditions where medical support is available.

If you suspect that you, or one or more athletes that you are working with, are affected by EIA or airway hyper-responsiveness, there are some preliminary assessments that can be made without the need for expensive equipment or personnel.

The first thing you need is a simple mechanical peak expiratory flow meter (such as the Mini-Wright peak flow meter). These can be obtained from pharmacies as well as from a large number of outlets that trade over the internet (just type ‘peak expiratory flow meter’ into any search engine). You – or the person experiencing the symptoms – should then monitor and record your peak flow performance throughout the day for a week, especially before and after conditions that appear to be related to the development of symptoms (eg exposure to animals, or exercise).

After exercise, peak flow should be monitored at 5, 10, 15 and 30 minutes. If the peak flow falls consistently and by more than 20% after exercise or in response to another environmental factor, medical advice should be sought in order to confirm the diagnosis and obtain treatment. If the peak flow does not fall consistently but symptoms persist, referral for further medical assessment should be considered, as there are other causes of asthma-like symptoms.

Inspiratory stridor – a related problem affecting vocal cords

At this point, it is worth mentioning that there is a growing awareness of an asthma-like condition known as ‘inspiratory stridor’(7). The symptoms of this condition are very similar to asthma, but provocation challenges fail to elicit any changes in lung function, despite severe breathlessness and inspiratory ‘wheeze’. The dysfunction in athletes affected by stridor appears to be related to an abnormal vocal cord function. During inspiration, the vocal cords are supposed to abduct (move apart) in order to facilitate unimpeded inflow of air. If they do not part completely, the cords induce an increased resistance to breathing, with obvious repercussions.

The management of EIA depends on the competitive status of the individual athlete. Athletes who are in competition should refer to the rules of their governing body for up-to-date guidance on permissible pharmacological management of EIA.

The goal of any management strategy is to minimise the symptoms, reduce the risk of exacerbation and optimise the athlete’s ability to compete to the limits of his or her potential. The most obvious mode of management is pharmacological (medication), but for those in competition this requires an intimate knowledge of the doping regulations for their particular sport. No competitive athlete should take a prescribed treatment for their EIA without first referring to the most recent version of these regulations. As well as making sure that the proposed medication is not banned, the athlete must also ‘qualify’ for its use – ie meet the criteria for diagnosis of EIA laid down by their sport. Only once these requirements are met is it safe to take medication for EIA.

Drug treatment for EIA

Pharmacological management of EIA must be undertaken under the supervision of a physician, since there are large variations between individuals which call for a highly individualised approach(4). The principal weapons in the pharmacological armoury are as follows:

  • Bronchodilators (beta2-agonists). Frequently know as ‘reliever’ medication, beta2-agonists relax the muscles around the airways, dilating them and reducing their resistance to airflow. Short-acting beta2-agonists can be used up to four times daily and are most effective when taken immediately before exercise or in response to the development of acute of EIA. If EIA is mild and infrequent, this may be the only pharmacological treatment required. Otherwise, it may be necessary to supplement the treatment with…
  • Corticosteriods. Known as ‘preventer’ medication, corticosteroids suppress the chronic inflammation associated with asthma. Reducing inflammation will improve pre-exercise lung function as well as reducing the sensitivity of the airways to EIA. For athletes with mild EIA, a once daily dose of inhaled corticosteroid may be the only medication required to manage EIA effectively.

Non-pharmacological management includes the following:

  • Warm-up. It has been known for years that many asthmatics 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’. Refractoriness means that 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 offers a simple and easily-implemented management technique for those in whom it works;
  • Dietary modification. Although the relationship between food tolerance and asthma has been studied for many years, and positive relationships have been identified, the effects of dietary modification on EIA has only recently been examined (9).

One of the earliest dietary components linked to asthma was salt. Recent evidence suggests that restricting salt intake reduces the severity of the post-exercise decline in lung function in people with asthma after just one week(10). At the start of the study, the subject’s FEV1 declined by 27% post-exercise, but after one week on a diet restricted to 1,500mg/day of sodium, the post- exercise fall in FEV1 was only 9%.

By contrast, a high sodium diet has been found to exacerbate post-exercise falls in FEV1(11). Studies examining the relative contributions of sodium and chloride to the severity of EIA suggest that both are involved(9). The recommended daily allowance for sodium for reducing hypertension is 2,400mg/day, which is considerably higher than the effective range for EIA attenuation (1,000-1,800mg/day). The restriction of salt intake therefore offers a simple non-pharmacological approach to the management of EIA.

Fish oils have also been studied for their potential role in alleviating EIA. These are rich sources of omega-3 polyunsaturated fatty acids (PUFAs), which are thought to damp down inflammatory responses. The link between fish oils and asthma was based on the low prevalence of asthma in Eskimo populations, which have high intakes of fish oils(9).

A recent study on the effects of three weeks’ supplementation with fish oil capsules on EIA in élite athletes produced some encouraging findings. The researchers compared a normal diet with a placebo diet and a fish oil-supplemented diet and found that fish oil supplementation reduced the post-exercise fall in FEV1 from 17% on the normal diet to just 3%(12). These preliminary data suggest that fish oil supplementation may offer another non-pharmacological approach to management of EIA.

Free radicals and the benefits of antioxidant vitamins

The damaging role of free radicals and the protective effects of antioxidants in sport is currently receiving a great deal of attention. Since inflammatory cells produce oxidants and asthma is an inflammatory disease, the role of antioxidants in EIA has naturally been investigated. The principle antioxidant vitamins are C and E, and recent studies have demonstrated beneficial effects of both.

Preliminary data from one study suggests that three weeks’ supplementation with a combination of vitamin C (500 mg/day) and vitamin E (33 IU/day) can reduce the post-exercise fall in FEV1 by 10%(13). An earlier study examining the effect of vitamin C (500mg) alone, with a much shorter supplementation period of just 90 minutes, showed a halving of the post-exercise fall in FEV1, from 20% to 10%(14).

Thus, it appears that antioxidant vitamins also offer some protection from EIA, although not all subjects appear to respond to supplementation(15), and the differential effects of vitamins C and E are unknown, as is the optimum supplementation regimen.

Because of its well-known ergogenic effects, caffeine supplementation has been used by athletes for many years. This has led the IOC to establish a limit on caffeine consumption, which is defined by its concentration in urine – no greater than 12 mg/ml.

Caffeine as a bronchodilator

It has been known for many years that caffeine is a bronchodilator(16), and two studies have specifically examined the effects of caffeine on EIA. In one, researchers observed a reduction in the severity of the post-exercise fall in FEV1 from 24% to just 10% after subjects consumed 7mg per kg of body mass of caffeine (~50mg, or three strong cups of coffee) two hours before an exercise challenge(17). In another, using an EVH test and a stronger caffeine dose of 10 mg/kg, researchers observed a similar effect on bronchoconstriction, with the fall in FEV1 reduced from 17% to 7%(18).

However, lower doses of caffeine (3.5 to 5 mg/kg) have not been shown to have a significant influence on EIA. And, unfortunately for competitive athletes, the doses which do seem to offer protection would probably give rise to urine concentrations of caffeine in excess of the IOC doping limit.

Since, additionally, caffeine is also a diuretic, its use for the management of EIA is not recommended, especially as other dietary modifications are neither banned by the IOC nor associated with any known negative side effects.

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(19), and this has been demonstrated directly in people with asthma.

One research group has conducted a number of studies examining the influence of specific inspiratory muscle resistance training (IMT) on symptoms, respiratory effort and consumption of medication in asthmatics. And they have come up with some impressive results, with subjects showing huge reductions in their consumption of both beta2-agonists and their ratings of breathlessness(20, 21). Unfortunately, no studies have yet examined the influence of IMT on EIA per se, and it is very unlikely that it has a direct effect on the severity of bronchoconstriction.

Nevertheless, it seems that IMT alleviates the principal symptom of bronchoconstriction (breathlessness). In addition, recent studies on non-asthmatics have shown that IMT is ergogenic (see PP171, Oct 2002) and also reduces respiratory and whole body effort sensations. Improvements in time trial performance and reductions in inspiratory muscle fatigue have been demonstrated by well controlled studies(22-24).

For athletes with asthma (for whom the work of breathing may be higher), IMT may offer even greater improvements in performance as well as symptom control. However, further research is needed to fully understand the beneficial effects of IMT in asthma.

In summary, the first step in the effective management of EIA is early recognition, and any athlete who repeatedly experiences asthma-like symptoms should seek a definitive diagnosis. For those who do have EIA, there are a number of management options, including dietary and training manipulations, as well as drugs.

For competitive athletes whose asthma falls short of the IOC criteria for pharmacological management, the non-pharmacological approaches outlined in this article offer the only means of minimising the negative impact of mild EIA on their ability to fulfil their sporting potential.

Alison McConnell

References

  1. Eur Respir J 21:468-72, 2003
  2. National Asthma Campaign, www.asthma.org.uk/pros/publications.php, 2001
  3. Lancet 351 (9111):1225-32, 1998
  4. Sports Med 32: 583-600, 2002
  5. Dickinson and Harries, ABC of Sports Medicine, 2004
  6. Eur Respir J 22:802-8, 2003
  7. Chest 124:1602-5, 2003
  8. Med Sci Sports Exerc 26:951-6, 1994
  9. Sports Med 33:671-681, 2003
  10. Med Sci Sports Exerc 35:S10, 2003
  11. Med Sci Sports Exerc 32;1815-9, 2000
  12. Am J Resp Crit Care Med 168:1181-9, 2003
  13. Med Sci Sports Exerc 34:S155, 2003
  14. Ann Allergy 49:146-51, 1982
  15. Arch Pediatr Adolesc Med 151:367-70, 1997
  16. Cochrane Review, 2001 www.cochrane.org/cochrane/revabstr/AB001112.htm
  17. Chest 97:1083-5, 1990
  18. Chest 99:1374-7, 1991
  19. Sports Med, 34(2), McConnell & Romer (in press), Jan 2004
  20. Chest 102:1357-61, 1992
  21. Can Respir J 9:307-12, 2002
  22. Med Sci Sports Exerc 33:803-9, 2001
  23. Int J Sports Med 23:353-60, 2003
  24. Med Sci Sports Exerc 34:785-92, 2003

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