Exercise-induced asthma and exercise-related respiratory problems are important for both the asthmatic child and adolescent, as well as for actively competing athletes. For the asthmatic child it is important both for their self-perception and development that they undertake and enjoy physical activity; indeed it may even be a means of mastering their asthma. However, the present chapter will be limited to matters relevant to the competing athlete.

Asthma and allergy represent increasing problems for the actively competing athlete with an increasing prevalence of exercise-induced asthma (EIA) or exercise-induced bronchoconstriction (EIB) reported, especially among elite endurance athletes [1-3]. Exercise-induced asthma and exercise-induced bronchoconstriction are terms used to describe the transient narrowing of the airways that follows vigorous exercise. The term EIA is used to describe symptoms and signs of asthma provoked by exercise and EIB for the reduction in lung function which may be demonstrated after an exercise test or a naturally occurring exercise.

In 1989 it was reported for the first time that high-level endurance training by adolescent swimmers increased nonspecific bronchial hyper-responsiveness (BHR) to histamine depending on the intensity of the physical training. Nine years later the finding of inflammatory changes in bronchial biopsies from young skiers was reported from Trondheim. The effect of intensive physical activity may be enhanced by untoward environmental conditions during the activity, such as cold ambient temperatures for winter sports and organic chlorine products from indoor swimming pools in swimmers. It should also be emphasized that the present day heavy training and intense physical activity during competitions reached by elite athletes due to their extremely high level of physical fitness and maximum oxygen uptake (V’O_2max), make it increasingly difficult to discriminate between physiological and pathological limitations to maximum exercise.

Sixty-seven of 597 American Olympic Athletes (who collectively won 41 medals) for the Los Angeles 1984 summer Olympic Games suffered from EIA or asthma. This was followed by reports of high prevalences of asthma from later Olympic Games; in 1996 an asthma prevalence of 45% was reported in cyclists and mountain bikers compared with none in divers and weightlifters. However, these reports were almost all questionnairebased without attempts objectively to verify the presence of EIB by exercise tests or other means. Later, the prevalence of BHR to metacholine (49%) in 100 competitive athletes of various sports was compared with that of sedentary subjects (28%). The prevalence of BHR varied in athletes performing their sports in cold air, dry air, humid air or combinations of these. Subsequently, reports on the use of inhaled drugs after applications for their use in the three latest Olympic Games suggested that 5.2% of all participating athletes used inhaled β₂-agonists in the Winter Olympic Games in 2002 and 4.2% in the Summer Olympics in 2004. From data collected over the three latest Summer Olympic Games, in Atlanta 1996, Sydney 2000 and Athens 2004, it appears that the use of inhaled b₂-agonists is highest in endurance sports, with cycling top (15.4% of all competitors), followed by the triathlon and by swimming.

In 1993, it was reported that 23 of 42 elite cross country skiers had a combination of BHR and asthma symptoms compared with only one of 23 referents. This was followed by reports of high prevalences in Norwegian and Swedish skiers, in competitive figure skaters, in elite cold-weather athletes and among participants in the 1998 American Olympic National team for winter sports, including gold medalists.

BHR to methacholine (PD_{20-methacholine} < 16.3 mmol) was found in 35.5% of the Norwegian national female soccer team, and 56% of Canadian professional football players had a positive bronchodilator test (increase in FEV₁ 12%) to inhaled salbutamol [4]. Among American track and field athletes, 10% of men and 23% of women suffered from EIB after a national competitive event with higher incidences after long-distance events.

Helenius and Haahtela in a series of studies on Finnish elite track and field athletes reported physician diagnosed asthma in 17% of long-distance runners, 8% of speed and power athletes and 3% of controls. They also reported total asthma (current asthma, physician diagnosed asthma or BHR) in 23% of the athletes compared with 4% of the controls, current asthma in 14% compared with 2% among controls and a positive skin prick test in 48% of the athletes compared with 36% among controls. Among swimmers they found a high prevalence of BHR (48%) to histamine. Employing the objective criteria for diagnosing asthma and/or bronchial hyper-responsiveness as ruled by the IOC, Medical Comission, Dickinson reported prevalences among UK participants in the Olympic Games in 2000 and 2004 to be 21.2 and 20.7%, respectively, with a positive bronchoprovocation or bronchodilator test.

Thus it can be concluded that elite athletes, especially active in endurance sports, have a high prevalence of asthma and bronchial hyper-responsiveness. We will enquire if this is due to type of physical activity in itself, or due to environmental exposures during the performance of sports.

In relationship to individual sports, there is limited evidence and it is necessary to combine knowledge based upon different types of sports performed in different environments in order to reach an understanding about the relevant pathogenetic mechanisms.

Exposures may be related to the environmental conditions under which the sport is performed, or to particular aspects of the type of sport itself. These exposures may have a direct relationship to the pathogenetic mechanisms at work in causing asthma and related problems in many athletes in particular types of sport. As above, asthma and bronchial responsiveness develop more frequently in endurance sports than in speed and power sports and sports related to esthetic performance. In particular these sports have in common prolonged and increased ventilation during training and competition. This was recently shown experimentally in an Italian study of training mice, with signs of wearing in the mucous membranes after exercising compared with nonexercising mice. Another animal study of competing Alaskan sled dogs participating in a 1100 mile endurance race demonstrated intraluminal debris by bronchoscopy 12-24 hours after completing the race with higher numbers of macrophages and neutrophils in bronchoalveolar lavage as compared with control, nonracing dogs.

Physical activity may cause several different conditions in the respiratory tract. Exerciseinduced asthma is most important, occurring most often in asthmatics who are not taking inhaled steroids. EIA will typically occur shortly after exercise with bronchial obstruction occurring within a few minutes after exercise or after reducing the intensity of exercise. The dyspnoea will typically be expiratory and with audible wheeze on auscultation.

Other respiratory conditions are also related to physical activity and sports, representing the important differential diagnoses to EIA and EIB in an athlete. Studies have demonstrated that most of the elite athletes referred for respiratory problems do not suffer from asthma or exercise-induced asthma, but rather from some of the differential diagnostic conditions.

One frequent differential diagnosis is exercise-induced inspiratory stridor or exercise-induced vocal chord dysfunction. The symptoms consist of inspiratory stridor occurring during maximum exercise, and ceasing when exercise is terminated unless hyperventilation is maintained by the patient. In such cases, there are audible inspiratory sounds from the laryngeal area, and bronchodilators or other asthma medication will not help. This condition most often occurs in young well-trained athletic girls from approximately 15 years of age. Symptoms only occur during maximum exercise. The symptoms are probably due to the relatively small crosssectional area of the laryngeal orifice, which may be even further reduced by the negative pressure created by the strong inspiratory flow during heavy exercise. One possible differential diagnosis to this syndrome is paradoxical movement of the vocal chords with adduction during inspiration, sometimes occurring without exercise. The diagnosis of vocal chord dysfunction/exercise induced inspiratory stridor can be made clinically and confirmed and differentiated by direct fibreoptic laryngoscopy during exercise.

Swimming-induced pulmonary edema is another differential diagnosis to EIA. Swimming-induced pulmonary edema occurs in well-trained swimmers after a heavy swimming session. The condition was reported in 70 previously healthy swimmers, who developed typical symptoms of pulmonary edema together with a restrictive pattern in pulmonary function, remaining for up to one week after the swimming incident.

In addition, other chronic disorders including heart diseases as well as other chronic respiratory diseases may impact upon physical performance and represent a possible differential diagnosis to exercise-induced asthma. Over- and underweight may also influence the diagnosis, but rarely concerns athletes.

Poor physical fitness or overtraining may represent other possible differential diagnoses to EIA. This is especially so when physical fitness and exercise performance are not up to the expectations of the athletes – or their trainers or parents. A lack of success in sports is often attributed to asthma even if this is not actually the case.

Finally, exercise-induced arterial hypoxemia occurs in many athletes, especially in those who are highly trained. It is thought to be due to limitations in diffusion and ventilation-perfusion inequality during exercise. In the healthy lung, the former (limited diffusion) is thought to be due to a rapid red blood cell transit time through the pulmonary capillary bed. Physical training improves muscle strength and endurance, with increased ionotrophic and chronotrophic capacities of the cardiovascular system but no such effects occur in the respiratory tract. Ventilatory requirement rises with no alteration in the capacity of the airways and the lungs to produce higher flow rates or higher tidal volumes, and there is little or no change in the pressure-generating capability of inspiratory muscles. The result is exercise-induced arterial hypoxemia which may occur in up to 50% of highly trained athletes. This reduction in arterial oxygen saturation may be confused with EIA.

Thus several differential diagnoses to EIA exist. Whatever the cause for the respiratory difficulties, it is important to make a thorough examination and rule out possible differential diagnoses as this has important implications for treatment.

The following procedure is recommended in the examination of the athlete with respiratory problems. The diagnostic criteria are identical to those of the usual asthmatic patient. However, due to criteria set by the Medical Commission of the IOC, certain modifications must be made.

The following diagnostic procedure is recommended.