European Respiratory Society

Asthma, airway inflammation and epithelial damage in elite athletes

K-H. Carlsen

In recent years there has been special focus on the increased occurrence of asthma and bronchial responsiveness among top athletes within endurance sports. As early as 1989, an increase in nonspecific bronchial responsiveness after heavy endurance training was found in young competitive swimmers 1. Later, reports were made concerning increased prevalence of asthma and bronchial hyperresponsiveness to metacholine among top cross-country skiers 2, 3. Reports came from Trondheim (Norway) regarding inflammatory changes in bronchial biopsies appearing during a winter season in young competitive cross-country skiers 4, 5. These studies confirmed that both bronchial responsiveness and airway inflammation increased through heavy endurance training 15.

In the Olympic arena, such reports were confirmed by Voy 6, who reported a prevalence of exercise-induced asthma of 11% among the American summer Olympic athletes of 1984; this increased to >20% among the American participants in the 1996 summer Olympic Games, and was especially high among cyclists and mountain bikers 7. K. Fitch (who supplied some of the data presented in 8) reported that the use of asthma drugs and, in particular, inhaled β2-agonists, was highest in cross-country skiing and speed-skating followed by cycling, Nordic combined (both cross-country skiing and ski jumping) and swimming during the last three summer Olympics and the last three winter Olympics 8.

In the present issue of the European Respiratory Journal, Bougault et al. 9 report findings from a study of induced sputum and cell counts of eosinophils and neutrophils in swimmers and cold-air athletes (cross-country skiers, speed skaters and biathletes), as compared to healthy controls and controls with asthma. The study participants had a mean age of 19–22 yrs; the two groups of athletes had a mean of 10 yrs of training. Details are not given as to how the athletes were recruited, other than that they were high-level athletes. Bougault et al. 9 could not find any correlation between bronchial hyperresponsiveness (BHR) to metacholine and age and number of years of training; however, the athletes in the study were still at an early stage in their career as compared with other studies, which showed increased prevalence of asthma 2 and increased prevalence of BHR to metacholine 10 among elite athletes with increasing age and duration of training. Bougault et al. 9 reported that 69% of swimmers and 28% of cold-air athletes suffered from BHR to metacholine. An increased number of bronchial epithelial cells and neutrophils was found in induced sputum, with neutrophil counts being independent of the presence of BHR. In contrast, eosinophils were only increased among both swimmers and cold-air athletes with the presence of BHR, and correlated with BHR in swimmers only. It is of great interest that the sputum neutrophil counts correlated with number of training hours per week.

The study by Bougault et al. 9 clearly demonstrates the effect of heavy endurance training upon the respiratory tract. The findings of the study show both increased bronchial epithelial cells and an increased number of neutrophils among the athletes, as well as a rise in the number of eosinophils in athletes with BHR. These findings demonstrate the wear-and-tear effect that may be caused by increased ventilation during endurance training, as well as increased airways inflammation due to training. These findings are in line with results from bronchial biopsies from skiers 4, 5, as well as with the results of the study by Helenius et al. 11, who also reported increased levels of eosinophils and neutrophils, as well as increased concentrations of sputum eosinophil peroxidase and human neutrophil lipocalin in induced sputum from swimmers. The findings of Bougault et al. 9 are also supported by animal studies. Chimenti et al. 12 compared the bronchial mucosa of trained mice with that of sedentary mice. Bronchiolar epithelium of trained mice showed progressive loss of ciliated cells, and increased apoptosis and proliferation. In another study, Davis et al. 13 performed bronchoscopy and bronchoalveolar lavage in elite racing sled dogs 24–48 h after completion of a 1,100-mile endurance race in Alaska (USA). Of the 59 dogs examined, 48 showed abnormal accumulations of intra-luminal debris, and bronchalveolar lavage obtained after the race showed significantly higher nucleated macrophage and eosinophil counts as compared with sedentary control dogs. These studies suggest, in the same way as Bougault et al. 9, that increased ventilation during repeated heavy exercise causes stress to the airway epithelium and increases airway mucosal inflammation. Environmental agents, such as exposure to cold air and organic chlorine products, will probably increase this stress, increasing bronchial responsiveness.

The environment in which the sports performance takes place is important for the development of bronchial hyperresponsiveness as measured by the reaction to methacholine or histamine, airways inflammation and respiratory epithelial damage in endurance athletes. This is the case for several types of sports 14 but particularly for cross-country skiers and swimmers 8, as in the study of Bougault et al. 9. Actively competing swimmers are particularly exposed to organic chlorine products used to disinfect the water in indoor swimming pools 15. Bernard et al. 16 have also focused upon exposure in indoor swimming pools and found that there is a relationship between the number of hours spent in indoor swimming pools when growing up and the risk of asthma development in pre-school children and schoolchildren 17. Serum levels of surfactant proteins A and B 16 as well as of Clara cell proteins 18 have been related to lung damage induced by pool attendance during childhood. Bernard et al. 19 also reported an increased risk of asthma related to attendance at outdoor chlorinated pools.

A link therefore remains between respiratory symptoms, bronchial hyperresponsiveness to metacholine/histamine and airway inflammation in athletes, occurring in particular environmental conditions and documented in several studies 8, and the risk of developing asthma in physically active children. However, this is so much more obvious in top athletes due to their intensive, repetitive training and high ventilation rates. This underlines the need to understand the pathogenesis of asthma and bronchial hyperresponsiveness occurring in elite athletes, as exemplified in the paper of Bougault et al. 9 in the present issue of European Respiratory Journal.

Statement of interest

A statement of interest for K-H. Carlsen can be found at