Couto Mariana, Silva Diana, Delgado Luis, Moreira André
Allergy, Asthma & Sports Unit, Immunoallergology Department, Centro Hospitalar São João EPE/Faculty of Medicine, University of Porto, Porto, Portugal.
Acta Med Port. 2013 Jan-Feb;26(1):56-60. Epub 2013 Apr 24.
Olympic level athletes present an increased risk for asthma and allergy, especially those who take part in endurance sports, such as swimming or running, and in winter sports. Classical postulated mechanisms behind EIA include the osmotic, or airway-drying, hypothesis. Hyperventilation leads to evaporation of water and the airway surface liquid becomes hyperosmolar, providing a stimulus for water to move from any cell nearby, which results in the shrinkage of cells and the consequent release of inflammatory mediators that cause airway smooth muscle contraction. But the exercise-induced asthma/bronchoconstriction explanatory model in athletes probably comprises the interaction between environmental training factors, including allergens and ambient conditions such as temperature, humidity and air quality; and athlete's personal risk factors, such as genetic and neuroimmuneendocrine determinants. After the stress of training and competitions athletes experience higher rate of upper respiratory tract infections (URTI), compared with lesser active individuals. Increasing physical activity in non-athletes is associated with a decreased risk of URTI. Heavy exercise induces marked immunodepression which is multifactorial in origin. Prolonged, high intensity exercise temporarily impairs the immune competence while moderate activity may enhance immune function. The relationship between URTI and exercise is affected by poorly known individual determinants such genetic susceptibility, neurogenic mediated immune inflammation and epithelial barrier dysfunction. Further studies should better define the aetiologic factors and mechanisms involved in the development of asthma in athletes, and propose relevant preventive and therapeutic measures.
奥运水平的运动员患哮喘和过敏的风险增加,尤其是那些参加耐力运动(如游泳或跑步)以及冬季运动的运动员。运动诱发哮喘(EIA)背后的经典假设机制包括渗透或气道干燥假说。过度通气导致水分蒸发,气道表面液体变得高渗,刺激水分从附近的任何细胞中移出,导致细胞收缩,进而释放引起气道平滑肌收缩的炎症介质。但运动员运动诱发哮喘/支气管收缩的解释模型可能包括环境训练因素(包括过敏原和温度、湿度及空气质量等环境条件)与运动员个人风险因素(如遗传和神经免疫内分泌决定因素)之间的相互作用。与活动较少的人相比,运动员在训练和比赛的压力下上呼吸道感染(URTI)的发生率更高。在非运动员中增加身体活动与降低URTI风险相关。剧烈运动可诱发明显的免疫抑制,其起源是多因素的。长时间的高强度运动暂时损害免疫能力,而适度活动可能增强免疫功能。URTI与运动之间的关系受遗传易感性、神经源性介导的免疫炎症和上皮屏障功能障碍等鲜为人知的个体决定因素影响。进一步的研究应更好地确定运动员哮喘发病的病因因素和机制,并提出相关的预防和治疗措施。