Broncoespasmo induzido por exercício em corredores brasileiros de longa distância de elite

OBJETIVO: Determinar a prevalência de broncoespasmo induzido por exercício em corredores brasileiros de longa distância de elite e se há uma diferença na carga de treinamento entre atletas com e sem broncoespasmo induzido por exercício. MÉTODOS: Estudo transversal com corredores de longa distância de elite sem sintomas atuais de asma e sem diagnóstico de broncoespasmo induzido por exercício. Todos os participantes foram submetidos ao teste de hiperventilação voluntária eucápnica e ao teste cardiopulmonar de esforço máximo e responderam a questionários sobre sintomas de asma e atividade física para monitorizar sua carga de treinamento semanal. RESULTADOS: Dos 86 atletas do sexo masculino recrutados, 20 concordaram em participar do estudo, dos quais 5 (25%) foram diagnosticados com broncoespasmo induzido por exercício. Não foram evidenciadas diferenças entre os atletas com e sem broncoespasmo induzido por exercício em relação a características antropométricas, consumo de oxigênio de pico, valores basais de função pulmonar ou sintomas de asma relatados. A carga de treinamento semanal foi significativamente menor nos atletas com broncoespasmo induzido por exercício do que naqueles sem esse diagnóstico. CONCLUSÕES: Nesta amostra de corredores de longa distância brasileiros, a prevalência de broncoespasmo induzido por exercício foi alta.

Exercise-induced bronchoconstriction in elite long-distance runners in Brazil

Objective: To determine the prevalence of exercise-induced bronchoconstriction among elite long-distance runners in Brazil and whether there is a difference in the training loads among athletes with and without exercise-induced bronchoconstriction. Methods: This was a cross-sectional study involving elite long-distance runners with neither current asthma symptoms nor a diagnosis of exercise-induced bronchoconstriction. All of the participants underwent eucapnic voluntary hyperpnea challenge and maximal cardiopulmonary exercise tests, as well as completing questionnaires regarding asthma symptoms and physical activity, in order to monitor their weekly training load. Results: Among the 86 male athletes recruited, participation in the study was agreed to by 20, of whom 5 (25%) were subsequently diagnosed with exercise-induced bronchoconstriction. There were no differences between the athletes with and without exercise-induced bronchoconstriction regarding anthropometric characteristics, peak oxygen consumption, baseline pulmonary function values, or reported asthma symptoms. The weekly training load was significantly lower among those with exercise-induced bronchoconstriction than among those without. Conclusions: In this sample of long-distance runners in Brazil, the prevalence of exercise-induced bronchoconstriction was high.

Formaldehyde inhalation reduces respiratory mechanics in a rat model with allergic lung inflammation by altering the nitric oxide/cyclooxygenase-derived products relationship

Bronchial hyperresponsiveness is a hallmark of asthma and many factors modulate bronchoconstriction episodes. A potential correlation of formaldehyde (FA) inhalation and asthma has been observed; however, the exact role of FA remains controversial. We investigated the effects of FA inhalation on Ovalbumin (OVA) sensitisation using a parameter of respiratory mechanics. The involvement of nitric oxide (NO) and cyclooxygenase-derived products were also evaluated. The rats were submitted, or not, to FA inhalation (1%, 90 min/day, 3 days) and were OVA-sensitised and challenged 14 days later. Our data showed that previous FA exposure in allergic rats reduced bronchial responsiveness, respiratory resistance (Rrs) and elastance (Ers) to methacholine. FA exposure in allergic rats also increased the iNOS gene expression and reduced COX-1. L-NAME treatment exacerbated the bronchial hyporesponsiveness and did not modify the Ers and Rrs, while Indomethacin partially reversed all of the parameters studied. The L-NAME and Indomethacin treatments reduced leukotriene B4 levels while they increased thromboxane B2 and prostaglandin E2. In conclusion, FA exposure prior to OVA sensitisation reduces the respiratory mechanics and the interaction of NO and PGE2 may be representing a compensatory mechanism in order to protect the lung from bronchoconstriction effects.