Asthma & Allergy Research Group, Department of Medicine and Therapeutics, Ninewells Hospital & Medical School, University of Dundee, Dundee, Scotland, UK.
Clin Exp Allergy. 2010 May;40(5):731-7. doi: 10.1111/j.1365-2222.2010.03461.x. Epub 2010 Mar 1.
Elite swimmers have high rates of rhinoconjunctivitis and exercise-induced bronchoconstriction. Moreover, exposure to chlorine and chlorine metabolites is known to induce bronchial hyper-reactivity.
To assess the early and late effects of chlorine and exercise on the unified airway of elite swimmers, and to compare the response to mannitol and field-based exercise challenge.
The Scottish national squad underwent exhaled tidal (FE(NO)) and nasal (N(NO)) nitric oxide measurement, peak nasal inspiratory flow (PNIF), and forced expiratory volume in 1 s before, immediately after, and 4-6 h post-swimming. A sport-specific exercise test was carried out during an intensive lactate set (8 min at >/=80% maximum hear rate). All swimmers underwent mannitol challenge, and completed a health questionnaire.
N=61 swimmers were assessed: 8/59 (14%) of swimmers had a positive mannitol challenge. Nine out of 57 (16%) of swimmers had a positive exercise test. Only one swimmer was positive to both. Swimmers with a positive mannitol had a significantly higher baseline FE(NO) (37.3 vs. 18.0 p.p.b., P=0.03) than those with a positive exercise challenge. A significant decrease in FE(NO) was observed pre vs. immediate and delayed post-chlorine exposure: mean (95% CI) 18.7 (15.9-22.0) p.p.b. vs. 15.9 (13.3-19.1) p.p.b. (P<0.01), and 13.9 (11.5-16.7) p.p.b. (P<0.01), respectively. There were no significant differences in N(NO.) Mean PNIF increased from 142.4 L/min (5.8) at baseline to 162.6 L/min (6.3) immediately post-exposure (P<0.01). Delayed post-exposure PNIF was not significantly different from pre-exposure.
No association was found between mannitol and standardized field-based testing in elite swimmers. Mannitol was associated with a high baseline FE(NO); however, exercise/chlorine challenge was not. Thus, mannitol may identify swimmers with a 'traditional' inflammatory asthmatic phenotype, while field-based exercise/chlorine challenge may identify a swimmer-specific bronchoconstrictor response. A sustained fall in FE(NO) following chlorine exposure suggests that a non-cellular, perhaps neurogenic, response may be involved in this group of athletes.
精英游泳运动员患有鼻结膜炎和运动诱发的支气管收缩的比率很高。此外,接触氯和氯代谢物已知会引起支气管高反应性。
评估氯和运动对精英游泳运动员统一气道的早期和晚期影响,并比较甘露糖醇和基于现场的运动挑战的反应。
苏格兰国家队进行了呼出潮气流(FE(NO))和鼻(N(NO))一氧化氮测量、峰值鼻吸气流量(PNIF)和游泳前、游泳后即刻和 4-6 小时的用力呼气 1 秒(FEV1)。在高强度乳酸设置(8 分钟,> / = 80%最大心率)期间进行了特定于运动的运动测试。所有游泳运动员都接受了甘露糖醇挑战,并完成了健康问卷。
评估了 61 名游泳运动员:59 名游泳运动员中有 8/59(14%)的甘露糖醇挑战呈阳性。57 名游泳运动员中有 9/57(16%)的运动测试呈阳性。只有一名游泳运动员对两者均呈阳性。甘露糖醇阳性的游泳运动员的基线 FE(NO)明显更高(37.3 比 18.0 p.p.b.,P=0.03)比运动挑战阳性的游泳运动员。暴露于氯后,FE(NO)显著下降:预 vs. 即刻和延迟 post-chlorine exposure:平均(95%CI)18.7(15.9-22.0)p.p.b. vs. 15.9(13.3-19.1)p.p.b.(P<0.01),和 13.9(11.5-16.7)p.p.b.(P<0.01)。N(NO)没有显著差异。平均 PNIF 从基线时的 142.4 L/min(5.8)增加到暴露后即刻的 162.6 L/min(6.3)(P<0.01)。暴露后延迟的 PNIF与暴露前无显著差异。
在精英游泳运动员中,甘露糖醇和标准化现场测试之间未发现关联。甘露糖醇与高基线 FE(NO)相关;然而,运动/氯挑战并非如此。因此,甘露糖醇可能识别出具有“传统”炎症性哮喘表型的游泳运动员,而基于现场的运动/氯挑战可能识别出具有特定于游泳运动员的支气管收缩反应。暴露于氯后 FE(NO)持续下降表明,在这群运动员中可能涉及非细胞性,可能是神经源性的反应。