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Asthma in sport: athletes should take heed of WADA guidelines
Exercise-induced asthma is a relatively common condition, which affects tens of thousands of athletes worldwide. However, those using asthma medication need to be aware of the new WADA guidelines that have just come into force. Alison McConnell explains
On 1 January 2009, a new set of World Anti-Doping Agency (WADA) guidelines came into force. For the majority of athletes this event is of limited consequence, but for the 20% or so who have asthma and/or exercise-induced asthma (EIA), it heralds a change to the way that they seek approval to use their asthma medications.
The new 2009 guidelines contain a change to the mandatory International Standard for Therapeutic Use Exemptions (TUEs), bringing them into line with the standards established by the International Olympic Committee prior to the Salt Lake City Olympics in 2002. To quote WADA on the objective of this change, ‘The purpose of the International Standard for TUEs is to ensure that the process of granting therapeutic use exemptions is harmonised across sports and countries… The Code permits athletes and their physicians to apply for therapeutic use exemptions (TUE) i.e. permission to use, for therapeutic purposes, substances or methods contained in the List of Prohibited Substances or Methods whose use is otherwise prohibited’. Since asthma medications remain on the list of prohibited substances, athletes wishing to use them require a TUE.
In a nutshell, a TUE is generally required by all athletes who compete nationally or internationally. The implication for national and international level athletes currently using asthma medications is that they must now obtain a TUE from either their National Anti-Doping Organisation (NADO) or the international federation for their sport; for example, the UK NADO is UK Sport. In the US and Australia, the respective NADOs are the US Anti-Doping Agency and the Australian Sports Anti-Doping Authority.
In operational terms, WADA oversees this process and reserves the right to reverse the decisions made by, say UK Sport, if it considers that the granting or refusal of a TUE did not comply with the International Standard for TUEs. Further details of the WADA guidelines and UK Sport’s procedures are available on their respective websites (links are provided at the end of this article), including guidance on the levels of competition that require a TUE. UK Sport also encourages athletes to speak with their national governing body to check whether they are required to apply for a TUE before competing in their sport.
So if you find that you need to obtain a TUE, what exactly are the implications? The TUE is normally submitted to the athlete’s NADO or international federation (depending upon the athlete’s level of competition) by the athlete or by medical personnel with responsibility for the athlete’s care.
Previously (pre-2009), TUE applications for asthma medications required the prescribing medical practitioner to complete a TUE application form, which included their diagnosis. This previous system did not require the diagnosis to be based upon objective evidence. However, the new International Standard for TUEs requires that athletes wishing to use medication in the form of an inhaled beta-2 agonist (also known as ‘bronchodilator’, ‘rescue’ or ‘reliever’ inhaler) to demonstrate that they have asthma or EIA by providing clear objective evidence. In other words, as well as a detailed medical history, the application must include quantitative evidence from lung function testing, ie spirometry (see figure 1).
What constitutes quantitative evidence of asthma or EIA? There are essentially two distinct tests that are considered to provide ‘proof’ of a legitimate requirement for the use of a beta-2 agonist. The first is an increase in the forced expiratory volume in one second (FEV1) of 12% or more following the inhalation of a therapeutic dose of a beta-2 agonist. Measurements of lung function are made before, and 10 minutes after, administration of a beta-2 agonist, and the FEV1 is compared. The TUE application must be accompanied by a full spirometry report, including flow-volume loop tracings. Figure 1 shows an example of such a tracing.
Since it is not uncommon for athletes with EIA to have normal resting lung function (and a negative response to the first test), there is also provision for ‘bronchoprovocation challenge’ testing. This means that the airways can be subjected to stimuli that trigger a response akin to EIA. In order to understand how these tests trigger an EIA response, it is helpful at this point to explain how EIA is triggered ‘naturally’.
Causes of EIA and diagnosis
Asthma and exercise-induced asthma (EIA) are the most common chronic condition affecting the sporting population (see Summary for more details). Asthma is defined as ‘a chronic inflammatory disorder of the airways’ (Global Initiative for Asthma, 1995), the cardinal symptoms of which are wheezing, breathlessness, chest tightness and cough. These symptoms are the result of airway narrowing in response to an inflammatory trigger.
Exercise is believed to trigger bronchoconstriction (narrowing of the airways) because it leads to dehydration of the lung’s airways (1), which induces inflammation. Symptoms peak around 10 minutes after stopping exercise. Inhaled air contains relatively little moisture, so when it enters the lungs, it’s not only warmed, it’s also humidified. This moisture is drawn out of the airway lining cells, causing them to dehydrate. When exercise stops, the cells rehydrate, and it is this dehydration and rehydration process that leads to a cascade of biochemical changes that will ultimately trigger bronchoconstriction in a susceptible individual. The degree to which a given bout of exercise provokes bronchoconstriction is dependent upon exercise intensity (how much air washes in and out of the lungs), and the temperature and humidity of the inhaled air. Cold air is very dry, and therefore causes faster and more severe dehydration, especially of small airways. In contrast, warm humid environments (such as swimming pools) are less provocative from a dehydration perspective (but see the caveat below). The principal stimulus to EIA is believed to be dehydration.
Testing for EIA
With the above mechanistic basis in mind, there are three recommended methods of ‘challenging’ the airways in order to test for EIA. These are as follows:
1. Eucapnic voluntary hyperventilation
challenge(2): This test involves breathing dry air at a level of breathing that is equivalent to 30 times the athlete’s FEV1 for at least six minutes. This test simulates the dehydrating effect that high levels of breathing during exercise exert on the airways, and is therefore highly specific to EIA. Lung function is measured at discrete time intervals for up to 30 minutes after cessation of hyperventilation. A positive diagnosis is made with a fall in FEV1 greater than 10% from baseline at two or more time points post-challenge.
2. Mannitol challenge (3): Mannitol is a harmless sugar that is inhaled progressively increasing doses to induce airway dehydration. Dehydration occurs because the sugar particles that are deposited in the airways draw moisture from the airway lining cells, dehydrating them in a similar way to exercise. Mannitol therefore triggers EIA in a very similar way to exercise, but without all the ‘puffing and panting’. In this respect a mannitol challenge is also a very specific test of EIA. Lung function is measured after each dose, and compared to the baseline value. A positive diagnosis is made with a fall in FEV1 greater than 15% from baseline at any inhaled dose or a 10% incremental fall in FEV1 between doses.
3. Exercise challenge: This is the most specific test of EIA and normally consists of a single bout of exercise lasting a minimum of six minutes at an intensity equivalent to 80-90% of maximal heart rate. However, this can be the least reliable challenge, since its outcome is highly dependent upon environmental conditions. Because the trigger for EIA is airway dehydration, the response to an exercise challenge is highly dependent upon the magnitude of ventilatory response achieved during the challenge bout of exercise, as well as the water content of the inhaled air. If the test is undertaken in, say, an air conditioned laboratory, airway dehydration may be insufficient to trigger EIA. However, an exercise challenge that is conducted in the athletes’ competitive environment, eg, snow clad mountains, may provide the only setting in which EIA is triggered. A positive diagnosis is made with a fall in FEV1 greater than 10% from baseline at two or more time points post-exercise.
Selection of the test will be ‘situation specific’, and dependent upon the facilities that are available to the athlete and physician.
At the start of this article I indicated that roughly 20% of athletes might be affected by the new WADA guidelines. For example, in the UK, Asthma UK estimates the prevalence of asthma in the general population to be around 10%. The figure of 20% for prevalence of EIA amongst elite athletes is based upon UK Olympians(4), and is one that therefore surprises athletes and the general public alike. So the question arises, why should athletes be more susceptible to EIA?
No one knows for certain, and research is underway to find out, but one plausible hypothesis relates to the phenomenon of ‘airway trauma’(5). Cross-sectional analysis of different sports points to a greater prevalence of EIA in endurance and winter sports, as well as those sports where training and competing takes place in environments where the air contains irritants, such as chlorinated swimming pools(6). In these sports, prevalence can be as high as 40 or even 50%. The unacceptably high levels of EIA prevalence confirm the need for accurate diagnosis and appropriate management of the condition, which may be one reason that WADA has taken the stance that it has – ie the recognition that not only does testing weed out those who are taking medication unnecessarily, but also those who need medication for a condition that they may not realise they have!
Professor Alison McConnell (BSc, MSc, PhD) is Professor of applied physiology at Brunel University, a Fellow of the American College of Sports Medicine and a British Association of Sport & Exercise Sciences accredited sport scientist
1. J Allergy Clin Immunol 106: 453-9, 2000
2. Br J Sports Med 35: 344-7, 2001
3. Respir Res 10: 4, 2009
4. Thorax 60: 629-32, 2005
5. Sports Med 35: 565-74, 2005
6. Allergy 63: 685-94, 2008