Exercise induced bronchoconstriction is a condition that can affect people at any level of exercise, from children to Olympic athletes (Mahler 1993). Bronchoconstriction following exercise has been documented since the second century (Rundell and Jenkinson 2002) and exercise will trigger asthma in most individuals with chronic asthma and in some
10 individuals who do not have asthma (Weiler 1996). Asthma has been an increasing public health issue over the past 40 years and affects a significant proportion of the global population. The World Health Survey states that on a global scale the prevalence rate of doctor diagnosed asthma is 4.3% (To, et al. 2012). In 2004, the Global Initiative for Asthma (GIBA) combined data from the Phase 1 International Study of Asthma and Allergies (ISAAC) collected from 1992-1996 and the European Community Respiratory Health Survey (ECRHS) from 1988-1994 to generate a global estimate of asthma burden.
The report estimated that 300 million people worldwide have asthma, and projected that this number would increase to 400 million by 2025, as countries develop. In the UK, 5.4 million people are currently receiving treatment for asthma this amounts to 1.1 million children (1 in 11) and 4.3 million adults (1 in 12) (Asthma UK Accessed on 12.06.2013).
The data highlight the global burden of asthma and the increase in prevalence in western societies. Thus if the occurrence of asthma is increasing, there will be an associated rise in the prevalence of EIB.
Asthma and airway hyperreposnsiveness are amongst the most common chronic medical conditions reported by Olympic athletes with a prevalence of 7-8% (Kippelen, et al. 2012) although large variations exist between sports (Fitch 2012). In the general population up to 80% of clinically recognised asthmatics can experience EIB (Anderson and Holzer 2000). The prevalence of EIB has been reported in a non-elite population of 230 middle and high school athletes (11 – 18 years old) from a range of sports (Rupp, Guill and Brudno 1992). Following the completion of an exercise challenge, 29% of the athletes were identified as EIB positive based on a post-exercise drop in FEV1 of greater than 15%;
11 all had been previously undiagnosed (Rupp, Guill and Brudno 1992). This study documents the prevalence in sub-elite athletes however with greater training loads associated with elite level sport it may predispose a greater risk of EIB in this population. Elite athletes have been shown to have a greater prevalence of airway hyper-responsiveness compared to a control population (Langdeau, et al. 2000). The athletes had a 49% prevalence of airway hyperresponsiveness compared with 28% of the sedentary participants (P = 0.009).
Within elite sportsmen and women there has been a steady increase in the number of athletes reporting symptoms associated with EIB. Reports from a screening programme organised by the US Olympic Committee found that 57 out of 597 (9.5%) American Olympic Athletes in the 1984 summer games reported suffering from EIB or asthma (Voy 1986). A high prevalence of asthma was also reported at the 1996 Olympic Games. Six hundred and ninety nine athletes completed a medical history questionnaire, 107 reported (15.3%) a previous diagnosis of asthma, 97 (13.9%) recorded the use of asthma medication at some time in the past, and 73 (10.4%) of the athletes were currently taking medication.
One hundred and seventeen (16.7%) reported the use of asthma medication, a diagnosis of asthma, or both (Weiler, Layton and Hunt 1998). These studies show both prevalence and medication usage amongst elite athletes is high. Critically these two studies are solely questionnaire based, and no attempts were made to verify or assess EIB by any other forms other than symptoms alone. A diagnosis of EIB through symptoms alone has been shown to be unreliable (Rundell, et al. 2001a, Holzer, Anderson and Douglass 2002) and likely result in both false-positive and false-negative results. Many elite athletes have high thresholds for pain, and often view pain and discomfort as a normal part of training.
12 Therefore many may neither consider EIB as abnormal nor realise it can be detrimental to performance (Rundell, Wilber and Lemanske Jr 2002). This suggests that elite athletes should be routinely screened for EIB using a suitable bronchial provocation challenge (See section 2.4).
Using the bronchial provocation challenge of methacholine, 49% of 100 competitive athletes exhibited airway hyper-responsiveness compared to 28% of sedentary subjects (Langdeau, et al. 2000), highlighting the greater risk of EIB within an athletic population.
The bronchial provocation challenge of eucapnic voluntary hyperventilation (EVH) has been shown to diagnose previously undiagnosed athletes (Dickinson, McConnell and Whyte 2011). With high prevalence rates amongst elite athletes this has led to a concomitant rise in the use of β2-agonist medication. Of all the athletes competing in the 2002 winter Olympic Games, 5.2% used inhaled β2-agonists and 4.2% in the 2004 Olympic Games (Anderson, et al. 2006, Anderson, et al. 2003, Fitch 2006). See section 2.5 for more details on pharmacological therapy.
High prevalence’s of EIB have been reported in the Great Britain Olympic Teams at the 2000 and 2004 Olympic Games. Prior to the IOC requirement for bronchial provocation testing as evidence for asthma and EIB medical forms of the 2000 Team GB squad (152 Male, 120 Female) assessed prevalence. 21.2% of the squad reported as suffering from asthma (Dickinson, et al. 2005). Prior to the 2004 Olympic Games, British athletes selected to compete in Team GB (165 men, and 106 women) were recruited for bronchial provocation testing. Athletes were only tested for asthma if they had a previous diagnosis of EIB, reported symptoms of EIB or were referred for testing by a team medical officer.
13 Diagnosis was made in accordance with the International Olympic Committee – Medical Commission requirements of a positive bronchodilator (increase in FEV1 of ≥ 15%
following 200 µg of short-acting β2-agonist) or bronchoprovocation test (decrease in FEV1
≥ 10% from the pre challenge value). Fifty six of the 271 (20.7%) athlete’s tested from the 2004 Team GB received a positive diagnosis. Sixty two athletes had previously been diagnosed with asthma and were prescribed asthma medication; 13 of the 62 (21%) then failed to produce a positive test for asthma. The results show prevalence in elite-athletes is likely to be sport and environment dependent (Table 2. 1) with the highest rates reported amongst swimmers and cyclists, these studies highlight the need for continued monitoring and accurate diagnosis so correct support and medication can be offered to our elite athletes.
14 Table 2. 1 Prevalence of asthma in the British squads at the 2000 and 2004 Olympic Games. Reproduced with permission from Dickinson, et al. (2005).
2000 2004
Some of the highest rates of EIB are found among winter sports athletes who may be chronically exposed to dry, cold air. Following assessment of medical history data and a methacholine challenge, plus two symptoms identified via medical history, asthma was found to be prevalent in 33 of 47 (70%) Swedish cross country skiers, compared to just 1 of 29 non-skiing controls (Larsson, et al. 1993). Sue-Chu et al. (1996) provided further evidence of the high prevalence of EIB in cross country skiers. Self-reported symptoms of asthma were prevalent in 46% of 118 Norwegian skiers, and 51% of 53 Swedish skiers.
Following methacholine testing, 14% of the Norwegian skiers, and 43% of Swedish skiers suffered with airway hyperresponsiveness (Sue-Chu, Larsson and Bjermer 1996). The differences in bronchial hyperresponsiveness between the Norwegian and Swedish skiers
15 were attributed to the differing geographical locations and subsequently greater exposure to cold air in the Swedish skiers. It has been suggested that the combination of demanding training at low temperatures and repeated inhalation of cold air may be a pathogenic factor in asthma in this population of athletes (Larsson, et al. 1993); it has been termed “ski asthma” and could be a normal physiological response to extreme environmental stimuli (Bjermer and Larsson 1996, Sue-Chu, et al. 1999). It has been suggested that cross country skiers are an extreme subtype of exercise induced asthmatics, and chronic exposure to cold dry air at high ventilation rates can lead to significant thickening of the bronchial sub-epithelial basement membrane, which is similar to that seen in chronic asthmatics (Karjalainen, et al. 2000)
Indoor winter sports competitors also experience a high prevalence of EIB and asthma like symptoms, and have been shown to have a great degree of small airway dysfunction (Rundell, et al. 2001a, Rundell, et al. 2001b). This high prevalence has been attributed to the inhalation of cold dry air and the high-emissions of pollutants from the ice resurfacing machines.
Studies of endurance based summer sports also show a high prevalence of EIB. A prevalence of 15-23% has been reported in endurance and distance runners and has been associated with atopy, allergy, and asthma (Tikkanen and Helenius 1994, Helenius, et al.
1998). Elite male and female distance runners who were initially classified as atopic (n=39) or non-atopic (n=19) based on skin prick tests of 10 airborne allergens were assessed for EIB. Lung function was assessed following an outdoor 2000 m run at 85% of their individual maximum heart rate during the winter season (mean temperature −6.6°C) and
16 during the summer pollen season (Helenius, Tikkanen and Haahtela 1998). FEV1 was measured immediately post, and at 4, 10, and 20 minutes post exercise. EIB (defined as a post exercise drop in FEV1 of 10%) was observed in 9% of the runners in either summer or winter. When the group’s mean change in FEV1 minus 2 standard deviations was taken as lower limit (a reduction of 6.5% or more in FEV1) 26% of runners had probable EIB in either the winter or pollen season. A high proportion of long distance runners have been shown to suffer from asthma; 17% of long distance runners reported physician diagnosed asthma compared to 8% of speed and power athletes, and 3% of controls (Helenius, Tikkanen and Haahtela 1997). For athletes competing and training in indoor swimming pools, the prevalence of EIB is also high, attributed to the chlorine compounds in swimming pools (Helenius and Haahtela 2000). In a sample of 738 swimmers, overall prevalence of EIB was 13.4%, in 165 competing at international level, 21% had EIB. The prevalence was less amongst the 537 lower level swimmers at 11.2% (Potts 1996), and therefore could be dependent upon training and competition intensity.
It is clear that exercise induced asthma is highly prevalent amongst asthmatics and elite athletes. The increase in asthma prevalence over the last 30 years has been linked to environmental changes and improved hygiene with fewer children experiencing childhood infections (Umetsu, et al. 2002). However the specific early life infections that limit T-helper type 2 (Th-2)-biased inflammation and asthma are not fully understood. Asthma can result from aeroallergen induced inflammation driven by Th-2 response and mediated by the cytokines IL-4, IL-5, and IL-13, as opposed to T-helper 1 cells which secrete IL-2 and
17 interferon-γ (Woodruff, et al. 2009, Barnes 2001). The airway cells and their mediators are discussed in section 2.2.2.
Advances in optimal diagnosis and novel treatment methods aimed at athletic populations may help to reduce the burden of the condition and improve the management for these individuals.