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Swimmers asthma 7 th, April, 2008 Joseph Cummiskey MD Respiratory Physician Member IOC, MC Consensus meeting on asthma in sport Member of Task Force of.

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1 Swimmers asthma 7 th, April, 2008 Joseph Cummiskey MD Respiratory Physician Member IOC, MC Consensus meeting on asthma in sport Member of Task Force of the ERS & EAACI on Diagnosis of asthma in sport IOC ASTHMA CONSENSUS CONFERENCE

2 Outline of my talk Definition of asthma Definition of asthma Diagnosis of asthma in elite athletes Diagnosis of asthma in elite athletes Etiology of asthma in swimmers Etiology of asthma in swimmers WADA rules in asthma treatment WADA rules in asthma treatment IOC ASTHMA CONSENSUS CONFERENCE

3 Exercise is good for your health Asthma, exercise and the environment Air Quality and Asthma: The Summer Outdoor/Indoor and the Winter Indoor Athlete

4 DEFINITION of asthma-1 Two main definitions of asthma have been used. Two main definitions of asthma have been used. The first is the classification of asthma as a manifestation of atopy, thereby including eczema and raised levels of IgE in the definition. The first is the classification of asthma as a manifestation of atopy, thereby including eczema and raised levels of IgE in the definition. The second approach is by defining asthma in the form of induced bronchial hyperreactivity, without reference to atopy. The second approach is by defining asthma in the form of induced bronchial hyperreactivity, without reference to atopy. Atopic and non-atopic asthma Atopic and non-atopic asthma

5 DEFINITION of asthma-2 Does this mean there are 2 distinct forms of asthma involving distinctly different immunopathological processes? Does this mean there are 2 distinct forms of asthma involving distinctly different immunopathological processes? Th 1 type cells express CXC chemokine receptor (CXCR)-3 CXC chemokine receptor (CXCR)-3 CC chemokine receptor (CCR)-5 CC chemokine receptor (CCR)-5 Th 2 type cells express CCR3, CCR4, CCR8 CCR3, CCR4, CCR8 Mast cells release PGD-2 and LTC-4 and histamine that works on the smooth muscle cells Mast cells release PGD-2 and LTC-4 and histamine that works on the smooth muscle cells

6 DEFINITION of asthma-3 We must ask the question early on “do we want to approach asthma as a single syndrome (lumper) or do we want various forms of asthma (splitter)”. We must ask the question early on “do we want to approach asthma as a single syndrome (lumper) or do we want various forms of asthma (splitter)”. Asthma is phenotypically heterogenous Asthma is phenotypically heterogenous Asthma is a multifaceted disease Asthma is a multifaceted disease Asthma maybe a systemic inflammatory disorder that includes the GI tract Asthma maybe a systemic inflammatory disorder that includes the GI tract Splitters would say Splitters would say Lymphocyte v eosinophil infiltrate in the airways Should we be using less ICS in neutrophil asthma Apotosis of leukocytes is blocked by ICS

7 DEFINITION of asthma-4 Brochoconstriction various with various stimulants: Brochoconstriction various with various stimulants: INDIRECTExercise, EVH, DIRECTHypertonic saline, Mannitol Methacholine, bromide v chloride, Response to therapy Response to therapyICS Beta-2 sympathomimetics

8 Diagnosis of Asthma in Elite Athletes Respiratory symptoms such as recurrent breathlessness, cough, wheezing, chest tightness and excessive mucous production are common in athletes and may be suggestive of asthma. Respiratory symptoms such as recurrent breathlessness, cough, wheezing, chest tightness and excessive mucous production are common in athletes and may be suggestive of asthma. As these symptoms alone cannot be relied upon for making a diagnosis of asthma and clinical examination may be normal, objective tests are required to confirm the diagnosis. As these symptoms alone cannot be relied upon for making a diagnosis of asthma and clinical examination may be normal, objective tests are required to confirm the diagnosis.

9 Diagnosis of Asthma in Elite Athletes These tests would include spirometry (forced expiratory volume in one second FEV1). These tests would include spirometry (forced expiratory volume in one second FEV1). Athletes may have an FEV1 within or above the normal range, this does not exclude variable airway obstruction. Athletes may have an FEV1 within or above the normal range, this does not exclude variable airway obstruction. If airway obstruction is present, spirometry should be repeated after inhalation of a bronchodilator to test for reversibility. If airway obstruction is present, spirometry should be repeated after inhalation of a bronchodilator to test for reversibility. In the absence of airflow limitation, a bronchial provocation test, to establish the presence of bronchial hyperresponsiveness, is needed. In the absence of airflow limitation, a bronchial provocation test, to establish the presence of bronchial hyperresponsiveness, is needed. If the results of these tests are negative other disorders should be considered. If the results of these tests are negative other disorders should be considered.

10 PFT in asthma This clinical syndrome must have the clinical diagnosis of asthma supplemented with the addition of Pulmonary Function Tests (to ERS and / or ATS standards). This clinical syndrome must have the clinical diagnosis of asthma supplemented with the addition of Pulmonary Function Tests (to ERS and / or ATS standards). The percentage changes in PFT are as follows The percentage changes in PFT are as follows resting pulmonary function tests, (12% bronchodilation above the predicted or the athletes resting FEV-1) resting pulmonary function tests, (12% bronchodilation above the predicted or the athletes resting FEV-1) non-pharmacological challenge (10% bronchoconstriction) non-pharmacological challenge (10% bronchoconstriction) Exercise or Exercise or Eucapnic Voluntary Hyperventilation tests Eucapnic Voluntary Hyperventilation tests pharmacological stimulation tests pharmacological stimulation tests (20% bronchoconstriction at a Methacholine dose of < 4 mg/ml) (20% bronchoconstriction at a Methacholine dose of < 4 mg/ml) (15% bronchoconstriction to a Mannitol test) (15% bronchoconstriction to a Mannitol test) (15% bronchoconstriction to a 4.5% saline challenge) (15% bronchoconstriction to a 4.5% saline challenge)

11 Environmental aspects of asthma in elite athletes The major environmental factors which could influence airway function in elite athletes are allergens and ambient conditions such as temperature, humidity and air quality. Because of the high minute ventilation during exercise, the effects of these exposures may be more marked in athletes. Exposures of importance to the athlete include seasonal and perennial allergens, dry / cold air, chlorine derivatives in swimming pools, ozone and combustion derived pollutants, such as oxides of nitrogen and particulate matter.

12 Etiology of asthma in swimmers Atopy Atopy FH, high eosinophil count, high IgE, symptoms spontaneously at night and without provocation FH, high eosinophil count, high IgE, symptoms spontaneously at night and without provocation Training Training Damage the airways Damage the airways Damage the lung vasculature esp capillaries Damage the lung vasculature esp capillaries Environment Environment Chorides Chorides

13 Is sport health damaging ? – probably – yes !!

14 Training as a cause of Asthma in Elite Athletes Long-term intense endurance training may be associated with an increased risk of development of airway hyperresponsiveness and asthma in the elite athlete. Long-term intense endurance training may be associated with an increased risk of development of airway hyperresponsiveness and asthma in the elite athlete. Environmental factors, such as allergens, chlorine derivatives, pollutants or cold air exposure may contribute to the development of airway inflammation and functional changes. Their penetration into the airways will be enhanced by the high ventilation required during intense exercise. Environmental factors, such as allergens, chlorine derivatives, pollutants or cold air exposure may contribute to the development of airway inflammation and functional changes. Their penetration into the airways will be enhanced by the high ventilation required during intense exercise. The changes in lung function and airway responsiveness may be partly reversible after cessation of long-term endurance training. The changes in lung function and airway responsiveness may be partly reversible after cessation of long-term endurance training. More research is necessary on how to prevent or minimise the adverse effects of long-term training on the airways, particularly the effects of environmental exposure on airway structure and function. More research is necessary on how to prevent or minimise the adverse effects of long-term training on the airways, particularly the effects of environmental exposure on airway structure and function.

15 Training Powerful systemic inflammatory stress Powerful systemic inflammatory stress Multi-organ adaptation (except the lung) Multi-organ adaptation (except the lung) Pulmonary pressures Pulmonary pressures -I> lung injury Transient interstitial edema Transient interstitial edema

16 Training as a cause of asthma Mechanical damage to the airways ? air or exercise Mechanical damage to the airways ? air or exercise In exercise it may be the pattern of breathing: rough and deep i.e. trauma to the airways In exercise it may be the pattern of breathing: rough and deep i.e. trauma to the airways Exhale against water resistance Exhale against water resistance High lung function (130% predicted volumn and flows) High lung function (130% predicted volumn and flows) Alveoli are large but not the capillaries, high haemoglobin Alveoli are large but not the capillaries, high haemoglobin

17 CT & MR images of exercise- induced Pulmonary Edema Interstitial edema, peribronchial edema,transient, increased lung water, only occurs in top athletes, ? vascular injury

18 asthma Weekly swimming in indoor chlorinated pools – is associated with increased frequency of asthma especially among children with a family history of asthma Weekly swimming in indoor chlorinated pools – is associated with increased frequency of asthma especially among children with a family history of asthma A. Bernard et al. Lung hyperpermeability and asthma prevalence in schoolchildren: unexpected associations with the attendance at indoor chlorinated pools (Occ Envir Med 2003; 60: 385-) 1881 børn i alderen 5-8 år.

19 The Pool Chlorine Hypothesis “rise in childhood asthma results from exposure to chloramines in the air of indoor pools” “rise in childhood asthma results from exposure to chloramines in the air of indoor pools” Nitrogen trichloride (trichloramine) Nitrogen trichloride (trichloramine) Chloramines formed from NH3 + HOCl Chloramines formed from NH3 + HOCl Probability of developing asthma is strongly linked to pool attendance before 6-7 years of age (Bernard et al. 2006) Probability of developing asthma is strongly linked to pool attendance before 6-7 years of age (Bernard et al. 2006) Elevated eNO is strongly associated with indoor pool attendance (Bernard et al. 2006) Elevated eNO is strongly associated with indoor pool attendance (Bernard et al. 2006) Finnish Olympic swimmers: 36%-79% bronchial hyperresponsiveness to methacholine or histamine (Helenius & Haahtela 2000) Finnish Olympic swimmers: 36%-79% bronchial hyperresponsiveness to methacholine or histamine (Helenius & Haahtela 2000)

20 The Pool Chlorine Hypothesis A 5 year follow-up study (Helenius et al. 2002). A 5 year follow-up study (Helenius et al. 2002). Current asthma (bronchial responsiveness & exercise-induced symptoms) in swimmers increased during swimming career and decreased after stopping. Current asthma (bronchial responsiveness & exercise-induced symptoms) in swimmers increased during swimming career and decreased after stopping. Sputum EOS increased in active swimmers, tended to decrease in “past swimmers”. Sputum EOS increased in active swimmers, tended to decrease in “past swimmers”.

21 The Pool Chlorine Hypothesis NCl 3 exposure and oxidative stress (Varraso et al. 2002) NCl 3 exposure and oxidative stress (Varraso et al. 2002) Plasma GSH-Px activity increased Plasma GSH-Px activity increased Acts as anti-oxidant Acts as anti-oxidant Reduces lipid hydroperoxides to alcohols 2GSH + H 2 O 2 → GSSG + 2H 2 0 Reduces lipid hydroperoxides to alcohols 2GSH + H 2 O 2 → GSSG + 2H 2 0 SOD activity increased Dismutates superoxide to O 2 & H 2 O 2 Dismutates superoxide to O 2 & H 2 O 2 Fast rx that out-competes NO (which forms peroxynitrite with O 2 - ) Fast rx that out-competes NO (which forms peroxynitrite with O 2 - )

22 COMEAP statement Suggestive but evidence is insufficent Suggestive but evidence is insufficent Not thr cause of asthma epidemic Not thr cause of asthma epidemic The least chlorine possible for an adequate anti-microbial effect The least chlorine possible for an adequate anti-microbial effect Further research is necessary Further research is necessary

23 WADA Because of the widespread use and potential for misuse of inhaled beta 2 agonists by athletes, there was consensus to continue the strict control of the use of this class of drugs in sport.

24 WADA rules for asthma All beta 2 agonists and in particular oral preparations are prohibited. Inhaled corticosteroids and some inhaled beta 2 agonists can be used in accordance with the relevant section of the Therapeutic Use Exemption (TUE) process. Systemic corticosteroids are prohibited and also require a TUE.

25 Thank you Questions? If the chairman wishes If the chairman wishes IOC ASTHMA CONSENSUS CONFERENCE

26

27 DEFINITION of asthma A set of guidelines for A set of guidelines for General Physicians General Physicians Respiratory physicians Respiratory physicians Follow-up of asthma and its degree of control Follow-up of asthma and its degree of control Clinical ACT asthma control test, correlates well with inflammatory e NO Clinical ACT asthma control test, correlates well with inflammatory e NO Inflammatorye Nitric Oxide Inflammatorye Nitric Oxide Physiologic FEV-1 correlates poorly with the other 2 Physiologic FEV-1 correlates poorly with the other 2

28 Value of swimming A program of swimming for asthmatics A program of swimming for asthmatics No asthma exacerbations in 20 years of swimming in asthmatics. No asthma exacerbations in 20 years of swimming in asthmatics. Majority have asthma after 24 years. Majority have asthma after 24 years. FH was positive for asthma FH was positive for asthma Endurance sport in summer and winter Endurance sport in summer and winter Symptoms and a positive ahr test Symptoms and a positive ahr test 40-50% active swimmers 40-50% active swimmers 12-30% past swimming i.e. some loose it others will not 12-30% past swimming i.e. some loose it others will not Super dosing of the pool with chorine was used the night before weekly training for 20 years. Super dosing of the pool with chorine was used the night before weekly training for 20 years. IOC ASTHMA CONSENSUS CONFERENCE

29 Asthmatic children and adolescents (n = 46) swimming training for five months Physical work capacity (PWC 170 ) treadmill run increased 11% (mean); controls 3.9% Post exercise-induced asthma (running challenge) unchanged; mean post-exercise decrease in FEV 1 33% (mean) pre-swim training and 32.1% post training IOC ASTHMA CONSENSUS CONFERENCE 2008

30 Asthmatic children and adolescents (aged 9 to 16 years: n = 46) undertook five months of supervised swimming training. Outcomes Decreased asthma Decreased asthma Reduced medication Reduced medication Increased lung volumes (p < 0.01) Increased lung volumes (p < 0.01) Program fitness in childhood remains thro life Program fitness in childhood remains thro life Above benefits were proportional to the distance swum IOC ASTHMA CONSENSUS CONFERENCE 2008

31 Asthmatic children and adolescents (aged 9-16 years: n = 46) undertook five months of supervised swimming training. Outcomes Improved posture (p < 0.01) Improved posture (p < 0.01) Reduced body fat (p <0.05) Reduced body fat (p <0.05) Increased distance swum in 9 min Increased distance swum in 9 min Less protecting parents Less protecting parents Fitch Morton Blanksby Arch Dis Childh 1976; 51: IOC ASTHMA CONSENSUS CONFERENCE 2008

32 Elite swimming athletes 5/7 CDN swimmers + EVH (>20%) 5/7 CDN swimmers + EVH (>20%) Most have no childhood history of asthma/atopy Most have no childhood history of asthma/atopy Not consistent symptomatology Not consistent symptomatology Many do not feel limited in the pool Many do not feel limited in the pool Compelling evidence of changes in AHR with time Compelling evidence of changes in AHR with time IOC ASTHMA CONSENSUS CONFERENCE

33 Treatment Past experience with elite athletes Past experience with elite athletes Current recommendations Current recommendations Future recommendations Future recommendations

34 Past experience of beta 2 agonists use in Elite Athletes There are good data now available on athletes who seek approval to use a beta 2 agonist. There are good data now available on athletes who seek approval to use a beta 2 agonist. These data arise from the recent Winter and Summer Olympic Games and from World IAAF championships in athletics. These data arise from the recent Winter and Summer Olympic Games and from World IAAF championships in athletics. While most applications for the Games came from those competing in endurance sports this was not a universal finding. While most applications for the Games came from those competing in endurance sports this was not a universal finding. The geographical distribution of the applications closely relates to the reported prevalence of asthma in those countries. The geographical distribution of the applications closely relates to the reported prevalence of asthma in those countries. Over the last 5 years there has been a significant increase in the proportion of athletes using inhaled corticosteroids in conjunction with a beta 2 adrenoceptor agonist. A minority of athletes are now relying on a beta 2 agonist alone to manage their condition. A minority of athletes are now relying on a beta 2 agonist alone to manage their condition.

35 Treatment of Asthma in Elite Athletes The management of the athlete with asthma should follow current national or international guidelines (eg Global INitiative for Asthma-GINA). The management of the athlete with asthma should follow current national or international guidelines (eg Global INitiative for Asthma-GINA). At present, there is no evidence that management of asthma in athletes should differ from non athletes. At present, there is no evidence that management of asthma in athletes should differ from non athletes. However, some specific issues should be considered for the high-level athlete. However, some specific issues should be considered for the high-level athlete. The prevention and management of exercise induced bronchoconstriction is a key issue in athletes. The prevention and management of exercise induced bronchoconstriction is a key issue in athletes. They may also be exposed to high levels of allergens and environmental irritants during training and competition because of high ventilation rates. Dry/cold air may be a particular problem for some athletes. They may also be exposed to high levels of allergens and environmental irritants during training and competition because of high ventilation rates. Dry/cold air may be a particular problem for some athletes.

36 Treatment of Asthma in Elite Athletes Athletes should be offered Asthma education in order to develop self management skills and ensure appropriate use of medication including inhaler technique. Athletes should be offered Asthma education in order to develop self management skills and ensure appropriate use of medication including inhaler technique. Individualised action plans for the management of exacerbations, asthma monitoring and follow-up are important. Individualised action plans for the management of exacerbations, asthma monitoring and follow-up are important. The non-pharmacological management of asthma in athletes is important. The non-pharmacological management of asthma in athletes is important. This includes identifying and avoiding asthma triggers whenever possible and especially during training. This includes identifying and avoiding asthma triggers whenever possible and especially during training. Warm-up may help to reduce exercise-induced bronchoconstriction. Warm-up may help to reduce exercise-induced bronchoconstriction.

37 Treatment of Asthma in Elite Athletes Drug treatment of asthma in athletes should follow standard guidelines: treatment should be individualised to achieve asthma control. Drug treatment of asthma in athletes should follow standard guidelines: treatment should be individualised to achieve asthma control. The effects of treatment should be monitored. The effects of treatment should be monitored. Any medications prescribed should comply with World Anti-Doping Agency (WADA) regulations. Any medications prescribed should comply with World Anti-Doping Agency (WADA) regulations.

38 Treatment of Asthma in Elite Athletes Inhaled corticosteroids are the most effective drugs for long term control and prevention of asthma and EIB. IOC ASTHMA CONSENSUS CONFERENCE

39 Treatment of Asthma in Elite Athletes Inhaled beta 2 agonists are the most effective drugs for immediate inhibition of exercise-induced bronchoconstriction (EIB) and for relieving intermittent symptoms of asthma. Inhaled beta 2 agonists are the most effective drugs for immediate inhibition of exercise-induced bronchoconstriction (EIB) and for relieving intermittent symptoms of asthma. However, tolerance (or tachyphylaxis) to the effects of beta agonists develops rapidly when used frequently. However, tolerance (or tachyphylaxis) to the effects of beta agonists develops rapidly when used frequently. Athletes who use short- or long-acting beta-agonists on a daily basis should be advised that their effectiveness to prevent EIB will partially diminish. Athletes who use short- or long-acting beta-agonists on a daily basis should be advised that their effectiveness to prevent EIB will partially diminish. Frequent use of beta-agonists may also increase the bronchoconstrictor response to exercise and allergens. Frequent use of beta-agonists may also increase the bronchoconstrictor response to exercise and allergens. Strategies to avoid these problems could include restricting beta-agonists to infrequent use, use of alternative treatments for preventing exercise-induced bronchoconstriction and ensuring adequate treatment of underlying asthma with inhaled corticosteroids. Strategies to avoid these problems could include restricting beta-agonists to infrequent use, use of alternative treatments for preventing exercise-induced bronchoconstriction and ensuring adequate treatment of underlying asthma with inhaled corticosteroids. Long acting beta agonists should never be used as monotherapy. Long acting beta agonists should never be used as monotherapy.

40 Future of beta 2 agonists in elite athletes Beta 2 agonists are likely to remain the most effective bronchodilators available in the foreseeable future. Beta 2 agonists are likely to remain the most effective bronchodilators available in the foreseeable future. However, they may have a less important role in the management of asthma because exercise induced bronchoconstriction should be better controlled by use of other therapies such as ICS, LT inhibitors, chromates and monoclonal antibodies against IgE. However, they may have a less important role in the management of asthma because exercise induced bronchoconstriction should be better controlled by use of other therapies such as ICS, LT inhibitors, chromates and monoclonal antibodies against IgE. Such therapies are likely to target the production, release and effects of the mediators of bronchoconstriction. Such therapies are likely to target the production, release and effects of the mediators of bronchoconstriction. Ideally, beta agonists should be reserved for occasional use and breakthrough symptoms. Better strategies to avoid the development of beta 2 agonists tolerance need to be developed. Ideally, beta agonists should be reserved for occasional use and breakthrough symptoms. Better strategies to avoid the development of beta 2 agonists tolerance need to be developed.

41 History of Beta - 2 Sympathomimetics at the Olympic Games Pre-1972Allowed 1972Prohibited 1976-’84Permitted with notification Not necessary to report Permitted with notification Application reviewed by an international independent panel 2006On a specified list

42 Most commonly used, allowed if notified, drug in sport Rising Prevalence of use of anti-asthma drugs in all competing athletes Applications Approved Applications Approved LA (1980)1.7%1.7% LA (1980)1.7%1.7% Atlanta (1996)3.6%3.6% Atlanta (1996)3.6%3.6% Nagano(1998)5.6%5.6% Nagano(1998)5.6%5.6% Sydney(2000)5.7%5.7% Sydney(2000)5.7%5.7% SLC(2002)6.3%5.2% SLC(2002)6.3%5.2% Athens(2004)4.6%4.2% Athens(2004)4.6%4.2% Turino(2006)8.4%7.8% Turino(2006)8.4%7.8%

43 Where have we come from 1999The 3 IOC, MC premises highlighted 1999The 3 IOC, MC premises highlighted 2001WADA aTUE for asthma 2001WADA aTUE for asthma 2002International panel at an Olympic Games 2002International panel at an Olympic Games 2004Preregistration of use ofsympathomimetics (stimulants) 2004Preregistration of use ofsympathomimetics (stimulants) 2005European Academic Respiratory Physician input in ERS and EAACI article (ERS monograph, vol 10, no.33, Nov 2005) 2005European Academic Respiratory Physician input in ERS and EAACI article (ERS monograph, vol 10, no.33, Nov 2005) 2006EOC, MC publish a one page diagnostic criteriae for asthma 2006EOC, MC publish a one page diagnostic criteriae for asthma 2006The above published articles quoted by WADA and IOC, MC associated paper 2006The above published articles quoted by WADA and IOC, MC associated paper 2007Interfederal FIMS sports consultation 2007Interfederal FIMS sports consultation 2007Presentation of the above papers at FIMS, ECSS, National and other International meetings with good feedback on the criteria for asthma diagnosis 2007Presentation of the above papers at FIMS, ECSS, National and other International meetings with good feedback on the criteria for asthma diagnosis 2008IOC, MC consensus statement 2008IOC, MC consensus statement

44 Prior to 1999

45 History from 2001

46 Consensus meeting 2008


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