Exercise-induced dehydration alters pulmonary function but does not modify airway responsiveness to dry air in athletes with mild asthma.

Local airway water loss is the main physiological trigger for exercise-induced bronchoconstriction (EIB). Our aim was to investigate the effects of whole body water loss on airway responsiveness and pulmonary function in athletes with mild asthma and/or EIB. Ten recreational athletes with a medical diagnosis of mild asthma and/or EIB completed a randomized, crossover study. Pulmonary function tests, including spirometry, whole body plethysmography, and diffusing capacity of the lung for carbon monoxide (DlCO), were conducted before and after three conditions: 1) 2 h of exercise in the heat with no fluid intake (dehydration), 2) 2 h of exercise with ad libitum fluid intake (control), and 3) a time-matched rest period (rest). Airway responsiveness was assessed 2 h postexercise/rest via eucapnic voluntary hyperpnea (EVH) to dry air. Exercise in the heat with no fluid intake induced a state of mild dehydration, with a body mass loss of 2.3 ± 0.8% (SD). After EVH, airway narrowing was not different between conditions: median (interquartile range) maximum fall in forced expiratory volume in 1 s was 13 (7-15)%, 11 (9-24)%, and 12 (7-20)% in dehydration, control, and rest conditions, respectively. Dehydration caused a significant reduction in forced vital capacity (300 ± 190 ml, P = 0.001) and concomitant increases in residual volume (260 ± 180 ml, P = 0.001) and functional residual capacity (260 ± 250 ml, P = 0.011), with no change in DlCO Mild exercise-induced dehydration does not exaggerate airway responsiveness to dry air in athletes with mild asthma/EIB but may affect small airway function.NEW & NOTEWORTHY This study is the first to investigate the effect of whole body dehydration on airway responsiveness. Our data suggest that the airway response to dry air hyperpnea in athletes with mild asthma and/or exercise-induced bronchoconstriction is not exacerbated in a state of mild dehydration. On the basis of alterations in lung volumes, however, exercise-induced dehydration appears to compromise small airway function.

A standard, single dose of inhaled terbutaline attenuates hyperpnea-induced bronchoconstriction and mast cell activation in athletes.

Release of bronchoactive mediators from mast cells during exercise hyperpnea is a key factor in the pathophysiology of exercise-induced bronchoconstriction (EIB). Our aim was to investigate the effect of a standard, single dose of an inhaled ß2-adrenoceptor agonist on mast cell activation in response to dry air hyperpnea in athletes with EIB. Twenty-seven athletes with EIB completed a randomized, double-blind, placebo-controlled, crossover study. Terbutaline (0.5 mg) or placebo was inhaled 15 min prior to 8 min of eucapnic voluntary hyperpnea (EVH) with dry air. Pre- and postbronchial challenge, urine samples were analyzed by enzyme immunoassay for 11ß-prostaglandin F2α (11ß-PGF2α). The maximum fall in forced expiratory volume in 1 s of 14 (12-20)% (median and interquartile range) following placebo was attenuated to 7 (5-9)% with the administration of terbutaline (P < 0.001). EVH caused a significant increase in 11ß-PGF2α from 41 (27-57) ng/mmol creatinine at baseline to 58 (43-72) ng/mmol creatinine at its peak post-EVH following placebo (P = 0.002). The rise in 11ß-PGF2α was inhibited with administration of terbutaline: 39 (28-44) ng/mmol creatinine at baseline vs. 40 (33-58) ng/mmol creatinine at its peak post-EVH (P = 0.118). These data provide novel in vivo evidence of mast cell stabilization following inhalation of a standard dose of terbutaline prior to bronchial provocation with EVH in athletes with EIB.

Effect of terbutaline on hyperpnoea-induced bronchoconstriction and urinary club cell protein 16 in athletes.

Repeated injury of the airway epithelium caused by hyperpnoea of poorly conditioned air has been proposed as a key factor in the pathogenesis of exercise-induced bronchoconstriction (EIB) in athletes. In animals, the short-acting ß2-agonist terbutaline has been shown to reduce dry airflow-induced bronchoconstriction and the associated shedding of airway epithelial cells. Our aim was to test the efficacy of inhaled terbutaline in attenuating hyperpnoea-induced bronchoconstriction and airway epithelial injury in athletes. Twenty-seven athletes with EIB participated in a randomized, double-blind, placebo-controlled, crossover study. Athletes completed an 8-min eucapnic voluntary hyperpnoea (EVH) test with dry air on two separate days 15 min after inhaling 0.5 mg terbutaline or a matching placebo. Forced expiratory volume in 1 s (FEV1) and urinary concentration of the club cell (Clara cell) protein 16 (CC16, a marker of airway epithelial perturbation) were measured before and up to 60 min after EVH. The maximum fall in FEV1 of 17 ± 8% (SD) on placebo was reduced to 8 ± 5% following terbutaline (P < 0.001). Terbutaline gave bronchoprotection (i.e., post-EVH FEV1 fall <10%) to 22 (81%) athletes. EVH caused an increase in urinary excretion of CC16 in both conditions (P < 0.001), and terbutaline significantly reduced this rise (pre- to postchallenge CC16 increase 416 ± 495 pg/µmol creatinine after placebo vs. 315 ± 523 pg/µmol creatinine after terbutaline, P = 0.016). These results suggest that the inhalation of a single therapeutic dose of terbutaline offers significant protection against hyperpnoea-induced bronchoconstriction and attenuates acute airway epithelial perturbation in athletes.

Misdiagnosis of exercise-induced bronchoconstriction in professional soccer players.

BACKGROUND: Physicians typically rely heavily on self-reported symptoms to make a diagnosis of exercise-induced bronchoconstriction (EIB). However, in elite sport, respiratory symptoms have poor diagnostic value. In 2009, following a change in international sports regulations, all elite athletes suspected of asthma and/or EIB were required to undergo pulmonary function testing (PFT) to permit the use of inhaled ß(2)-agonists. The aim of this study was to examine the diagnostic accuracy of physician diagnosis of asthma/EIB in English professional soccer players. METHODS: Sixty-five players with a physician diagnosis of asthma/EIB were referred for pulmonary function assessment. Medication usage and respiratory symptoms were recorded by questionnaire. A bronchial provocation test with dry air was conducted in 42 players and a mannitol challenge in 18 players. Five players with abnormal resting spirometry performed a bronchodilator test. RESULTS: Of the 65 players assessed, 57 (88%) indicated regular use of asthma medication. Respiratory symptoms during exercise were reported by 57 (88%) players. Only 33 (51%) of the players tested had a positive bronchodilator or bronchial provocation test. Neither symptoms nor the use of inhaled corticosteroids were predictive of pulmonary function tests' outcome. CONCLUSION: A high proportion of English professional soccer players medicated for asthma/EIB (a third with reliever therapy only) do not present reversible airway obstruction or airway hyperresponsiveness to indirect stimuli. This underlines the importance of objective PFT to support a symptoms-based diagnosis of asthma/EIB in athletes.

Effect of inspired air conditions on exercise-induced bronchoconstriction and urinary CC16 levels in athletes.

Injury to the airway epithelium has been proposed as a key susceptibility factor for exercise-induced bronchoconstriction (EIB). Our goals were to establish whether airway epithelial cell injury occurs during EIB in athletes and whether inhalation of warm humid air inhibits this injury. Twenty-one young male athletes (10 with a history of EIB) performed two 8-min exercise tests near maximal aerobic capacity in cold dry (4°C, 37% relative humidity) and warm humid (25°C, 94% relative humidity) air on separate days. Postexercise changes in urinary CC16 were used as a biomarker of airway epithelial cell perturbation and injury. Bronchoconstriction occurred in eight athletes in the cold dry environment and was completely blocked by inhalation of warm humid air [maximal fall in forced expiratory volume in 1 s = 18.1 ± 2.1% (SD) in cold dry air and 1.7 ± 0.8% in warm humid air, P < 0.01]. Exercise caused an increase in urinary excretion of CC16 in all subjects (P < 0.001), but this rise in CC16 was blunted following inhalation of warm humid air [median CC16 increase pre- to postchallenge = 1.91 and 0.35 ng/µmol in cold dry and warm humid air, respectively, in athletes with EIB (P = 0.017) and 1.68 and 0.48 ng/µmol in cold dry and warm humid air, respectively, in athletes without EIB (P = 0.002)]. The results indicate that exercise hyperpnea transiently disrupts the airway epithelium of all athletes (not only in those with EIB) and that inhalation of warm moist air limits airway epithelial cell perturbation and injury.

Effect of endurance training on lung function: a one year study.

OBJECTIVE: To identify in a follow up study airway changes occurring during the course of a sport season in healthy endurance athletes training in a Mediterranean region. METHODS: Respiratory pattern and function were analysed in 13 healthy endurance trained athletes, either during a maximal exercise test, or at rest and during recovery through respiratory manoeuvres (spirometry and closing volume tests). The exercise test was conducted on three different occasions: during basic endurance training and then during the precompetition and competitive periods. RESULTS: During the competitive period, a slight but non-clinically significant decrease was found in forced vital capacity (-3.5%, p = 0.0001) and an increase in slope of phase III (+25%, p = 0.0029), both at rest and after exercise. No concomitant reduction in expiratory flow rates was noticed. During maximal exercise there was a tachypnoeic shift over the course of the year (mean (SEM) breathing frequency and tidal volume were respectively 50 (2) cycles/min and 3.13 (0.09) litres during basic endurance training v 55 (3) cycles/min and 2.98 (0.10) litres during the competitive period; p < 0.05). CONCLUSIONS: This study does not provide significant evidence of lung function impairment in healthy Mediterranean athletes after one year of endurance training.

Undiagnosed exercise-induced bronchoconstriction in ski-mountaineers.

Because the practise conditions put the ski-mountaineering athletes potentially at risk for exercise-induced bronchoconstriction (EIB), this study was conducted to estimate the prevalence of EIB in this population. Thirty-one highly-trained ski-mountaineers with racing experience participating in the race were evaluated. EIB was determined after a European race at high altitude and frigid conditions. Pre-race investigations included pulmonary function measurements and a questionnaire enquiring about i) training habits, ii) respiratory history during training and/or competition. Pulmonary function was also tested after the race. None of the athletes reported a basal airway obstruction. Two groups were determined after post-race airway response: i) EIB (+) group exhibiting a fall in FEV (1) > or = 10 % (n = 15) and ii) EIB (-) without fall in FEV (1) or fall < 10 % (n = 16). Neither training habits nor baseline lung function were associated with the post-race airway response. Six of the 31 ski-mountaineers had a previous physician-made diagnosis of asthma and/or EIB, nevertheless 23 of our athletes complained about at least one characteristic symptom of asthma during practise. Four of our 15 EIB (+) had a previous physician-made diagnosis of asthma/EIB indicating that 73 % of EIB (+) athletes were undiagnosed for EIB. The proportion of allergic athletes was not significantly different between EIB (+) and EIB (-). This study showed that approximatively half of highly-trained ski-mountaineers with racing experience can develop EIB after a race and that 73 % of them are unaware of the problem.

Is hemoglobin desaturation related to blood viscosity in athletes during exercise?

Several studies have suggested that athletes with low hemoglobin saturation during exercise may experience impaired pulmonary blood gas exchange during maximal exercise. Blood viscosity may be implicated in exercise-induced pulmonary hemorrhage in race horses. We hypothesized that blood rheology may contribute to impaired gas exchange and reduced hemoglobin saturation during exercise in humans. A group of 20 highly trained endurance athletes participated in this study, 9 with low hemoglobin saturation during exercise (Low-SpO (2) group) and 11 with normal hemoglobin saturation (High-SpO (2) group). All subjects performed a progressive exercise test conducted to V.O (2max). Venous blood was sampled at rest, 50 % V.O (2max) and maximal exercise. Blood viscosity (etab) was measured at very high shear rate (1000 s (-1)) and 37 degrees C with a falling ball viscometer. The erythrocyte rigidity coefficient, "Tk", was calculated using the Dintenfass equation. At rest, no significant difference in etab was observed between the two groups (3.00 +/- 0.08 mPa . s vs. 3.01 +/- 0.04 mPa . s for the Low-SpO (2) and High-SpO (2) group, respectively). At 50 % V.O (2max) and maximal exercise, etab was higher in Low-SpO (2) (p < 0.01). Tk decreased in High-SpO (2) (p < 0.01) but remained unchanged in the other group during testing. The greater increase in etab in the Low-SpO (2) group during exercise may therefore have been due to the lack of reduction in Tk. As suggested by previous studies, the greater increase in blood viscosity in athletes with low hemoglobin saturation may lead to vascular shear stress. Whether this could impair the blood gas barrier and result in exercise-induced hypoxemia requires further study.

Asthma and exercise-induced bronchoconstriction in amateur endurance-trained athletes.

High-level endurance training contributes to the development of asthma and exercise-induced bronchoconstriction but the effect of moderate endurance training on airway function remains to be determined. The aim of this study was to evaluate the prevalence of physician-diagnosed asthma and/or exercise-induced bronchoconstriction in moderately endurance-trained athletes. Ninety-five Mediterranean amateur endurance-trained athletes filled out a questionnaire about respiratory disorders and underwent a resting spirometry. Mean training volume was 10 h per week. The prevalence of asthma was found to be 4.2 %. All the athletes with asthma plus another one (5.3 %) reported having exercise-induced bronchoconstriction. These percentages are in the same range as those from the general population and much lower than those observed in elite endurance athletes. In contrast to elite athletes, our amateur endurance-trained athletes seem not exposed to a higher risk of asthma or exercise-induced bronchoconstriction than the general population. We suggest that 10 h per week of moderate endurance training in a temperate climate area does not lead to respiratory disease.

[Asthma in athletes]. / L'asthme chez l'athlète.

INTRODUCTION: Numerous recent studies have shown that the risk of developing asthma or exercise-induced asthma is increased in the athletic population, particularly in endurance-trained athletes at national and international level. STATE OF ART: According to the literature, this could be explained by both hyperventilation during exercise and increased airway exposure to inhaled allergens, pollutants and/or cold dry air. However this form of asthma seems to differ from classical asthma. PERSPECTIVES: In the future, the establishment of rigorous controls - via a detailed description of symptoms and documentation of objective measurements such as resting spirometry, bronchial hyperreactivity and reversibility - should allow early detection of respiratory problems in athletes and enable to provide an adequate treatment. CONCLUSIONS: Although asthma and exercise-induced asthma are particularly common among athletes, if appropriately detected and treated, these disorders should not constitute a limiting factor in exercise performance.