Bronchial epithelial damage after a half-marathon in nonasthmatic amateur runners

Abstract

High neutrophil counts in induced sputum have been found in nonasthmatic amateur runners at rest and after a marathon, but the pathogenesis of airway neutrophilia in athletes is still poorly understood. Bronchial epithelial damage may occur during intense exercise, as suggested by investigations conducted in endurance-trained mice and competitive human athletes studied under resting conditions. To gain further information on airway changes acutely induced by exercise, airway cell composition, apoptosis, IL-8 concentration in induced sputum, and serum CC-16 level were measured in 15 male amateur runners at rest (baseline) and shortly after a half-marathon. Different from results obtained after a marathon, neutrophil absolute counts were unchanged, whereas bronchial epithelial cell absolute counts and their apoptosis increased significantly ( P < 0.01). IL-8 in induced sputum supernatants almost doubled postrace compared with baseline ( P < 0.01) and correlated positively with bronchial epithelial cell absolute counts ( R2 = 0.373, P < 0.01). Serum CC-16 significantly increased after all races ( P < 0.01). These data show mild bronchial epithelial cell injury acutely induced by intense endurance exercise in humans, extending to large airways the data obtained in peripheral airways of endurance-trained mice. Therefore, neutrophil influx into the airways of athletes may be secondary to bronchial epithelial damage associated with intense exercise.

The breathless adolescent asthmatic athlete

“…These findings were recently replicated in humans, as increased levels of bronchial epithelial cells were found in induced sputum of amateur endurance runners after repeated half-marathon races, in addition to apoptosis of bronchial cells after the races. Increased serum levels of Clara cell protein 16 and increased interleukin-8 levels in induced sputum supernatants were also found, demonstrating increased airway inflammation caused by participation in the half-marathon races [39]. These studies agree with the findings in induced sputum from swimmers and cold weather athletes reported by BOUGAULT et al [32].…”

Advances in asthma pathophysiology: stepping forward from the Maurizio Vignola experience

“…In healthy humans, studies on induced sputum cells at rest and after a marathon [76] or half-marathon [77] race documented that intense exercise caused mild epithelial injury and influx of neutrophils into the airways, possibly due to hyperosmolarity of the airway lining fluid secondary to the hyperpnoea of exercise. However, no significant activation of inflammatory cells occurred [76,77], in line with the anti-inflammatory effects of exercise documented in animal models. However, such inflammation could negatively affect airway muscle tone.…”

Oxidative stress and exercise-induced bronchoconstriction in elite athletes: does the interrelation exist?

“…На вопрос о генезе нейтрофилии мокроты у здо ровых марафонцев попробовали ответить L.Chimenti et al, изучив клеточный состав мокроты, наличие признаков апоптоза клеток, уровень интерлейкина 8 (IL 8) в мокроте и протеина клеток Клара (СС 16, маркера проницаемости микроциркуляторного рус ла легких) [33]. Установлено достоверное увеличение количества клеток цилиндрического эпителия брон хов с признаками апоптоза, показателя СС 16 и уд воение уровня IL 8 в мокроте у обследованных после соревнований по сравнению с исходными показате лями, однако количество нейтрофилов в мокроте спортсменов оставалось неизменным [33].…”

“…Установлено достоверное увеличение количества клеток цилиндрического эпителия брон хов с признаками апоптоза, показателя СС 16 и уд воение уровня IL 8 в мокроте у обследованных после соревнований по сравнению с исходными показате лями, однако количество нейтрофилов в мокроте спортсменов оставалось неизменным [33]. Причем по данным корреляционного анализа была опре делена положительная взаимосвязь уровня IL 8 с количеством реснитчатых клеток в образцах инду цированной мокроты [33]. Приведенные данные свидетельствуют о повреждающем действии продол жительной физической нагрузки на цилиндричес кий эпителий бронхов.…”

“…Приведенные данные свидетельствуют о повреждающем действии продол жительной физической нагрузки на цилиндричес кий эпителий бронхов. Нейтрофилия мокроты у ат летов, вероятно, носит вторичный характер по отношению к десквамации бронхиального эпителия при интенсивной физической нагрузке [33]. В свою очередь, индукция повреждения тканей и апоптоза клеток происходит с участием АФА (рис.…”