Fractional exhaled nitric oxide in the assessment of exercise-induced bronchoconstriction: A multicenter retrospective analysis of UK-based athletes.

Introduction: Exercise-induced bronchoconstriction (EIB) is not only highly prevalent in people with asthma, but can also occur independently, particularly in athletes. Fractional exhaled nitric oxide (FeNO) is an indirect biomarker of type 2 airway inflammation that has an established role in the assessment and management of asthma. The aim was to evaluate the value of FeNO in the assessment of EIB in athletes.

Pulmonary ventilation and gas exchange during prolonged exercise in humans: Influence of dehydration, hyperthermia and sympathoadrenal activity.

New Findings: What is the central question of the study? Ventilation increases during prolonged intense exercise, but the impact of dehydration and hyperthermia, with associated blunting of pulmonary circulation, and independent influences of dehydration, hyperthermia and sympathoadrenal discharge on ventilatory and pulmonary gas exchange responses remain unclear. What is the main finding and its importance? Dehydration and hyperthermia led to hyperventilation and compensatory adjustments in pulmonary CO and O exchange, such that CO output increased and O uptake remained unchanged despite the blunted circulation. Isolated hyperthermia and adrenaline infusion, but not isolated dehydration, increased ventilation to levels similar to combined dehydration and hyperthermia.

Diagnosis and management of allergy and respiratory disorders in sport: An EAACI task force position paper.

Allergy and respiratory disorders are common in young athletic individuals. In the context of elite sport, it is essential to secure an accurate diagnosis in order to optimize health and performance. It is also important, however, to consider the potential impact or consequences of these disorders, in recreationally active individuals engaging in structured exercise and/or physical activity to maintain health and well-being across the lifespan.

Physiological Function during Exercise and Environmental Stress in Humans-An Integrative View of Body Systems and Homeostasis.

Claude Bernard's (internal environment) and the associated concept of homeostasis are fundamental to the understanding of the physiological responses to exercise and environmental stress. Maintenance of cellular homeostasis is thought to happen during exercise through the precise matching of cellular energetic demand and supply, and the production and clearance of metabolic by-products. The mind-boggling number of molecular and cellular pathways and the host of tissues and organ systems involved in the processes sustaining locomotion, however, necessitate an integrative examination of the body's physiological systems.

Systemic but not local rehydration restores dehydration-induced changes in pulmonary function in healthy adults.

Water transport and local (airway) hydration are critical for the normal functioning of lungs and airways. Currently, there is uncertainty regarding the effects of systemic dehydration on pulmonary function. Our aims were ) to clarify the impact of exercise- or fluid restriction-induced dehydration on pulmonary function in healthy adults; and ) to establish whether systemic or local rehydration can reverse dehydration-induced alterations in pulmonary function.

Bronchial Provocation Testing for the Identification of Exercise-Induced Bronchoconstriction.

Exercise-induced bronchoconstriction (EIB) occurs in patients with asthma, children, and otherwise healthy athletes. Poor diagnostic accuracy of respiratory symptoms during exercise requires objective assessment of EIB. The standardized tests currently available are based on the assumption that the provoking stimulus to EIB is dehydration of the airway surface fluid due to conditioning large volumes of inhaled air.

Effect of Creatine Supplementation on the Airways of Youth Elite Soccer Players.

Introduction: Owing to its well-established ergogenic potential, creatine is a highly popular food supplement in sports. As an oral supplement, creatine is considered safe and ethical. However, no data exist on the safety of creatine on lung function in athletes.

Mechanisms and Biomarkers of Exercise-Induced Bronchoconstriction.

Exercise is a common trigger of bronchoconstriction. In recent years, there has been increased understanding of the pathophysiology of exercise-induced bronchoconstriction. Although evaporative water loss and thermal changes have been recognized stimuli for exercise-induced bronchoconstriction, accumulating evidence points toward a pivotal role for the airway epithelium in orchestrating the inflammatory response linked to exercise-induced bronchoconstriction.

Self-reported Symptoms after Induced and Inhibited Bronchoconstriction in Athletes.

Purpose: A change in the perception of respiratory symptoms after treatment with inhaled beta2 agonists is often used to aid diagnosis of exercise-induced bronchoconstriction (EIB). Our aim was to test the association between subjective ratings of respiratory symptoms and changes in airway caliber after induced and inhibited bronchoconstriction in athletes with EIB.

Methods: Eighty-five athletes with diagnosed or suspected EIB performed a eucapnic voluntary hyperpnea (EVH) challenge with dry air.

Urinary CC16 after challenge with dry air hyperpnoea and mannitol in recreational summer athletes.

Airway epithelial injury is regarded as a key contributing factor to the pathogenesis of exercise-induced bronchoconstriction (EIB) in athletes. The concentration of the pneumoprotein club cell (Clara cell) CC16 in urine has been found to be a non-invasive marker for hyperpnoea-induced airway epithelial perturbation. Exercise-hyperpnoea induces mechanical, thermal and osmotic stress to the airways.

Where to from here for exercise-induced bronchoconstriction: the unanswered questions.

The role of epithelial injury is an unanswered question in those with established asthma and in elite athletes who develop features of asthma and exercise-induced bronchorestriction (EIB) after years of training. The movement of water in response to changes in osmolarity is likely to be an important signal to the epithelium that may be central to the onset of EIB. It is generally accepted that the mast cell and its mediators play a major role in EIB and the presence of eosinophils is likely to enhance EIB severity.

Assessment of EIB: What you need to know to optimize test results.

Respiratory symptoms and asthma control questionnaires are poor predictors of the presence or severity of exercise-induced bronchoconstriction (EIB), and objective measurement is recommended. To optimize the chance of a positive test result, there are several factors to consider when exercising patients for EIB, including the ventilation achieved and sustained during exercise, water content of the inspired air, and the natural variability of the response. The high rate of negative exercise test results has led to the development of surrogates to identify EIB in laboratory or office settings, including eucapnic voluntary hyperpnea of dry air and inhalation of hyperosmolar aerosols.

Pathogenesis of exercise-induced bronchoconstriction.

This article presents the various potential mechanisms responsible for the development of exercise-induced bronchoconstriction (EIB). Although the etiology of EIB is multifactorial, and the physiologic processes involved may vary between individuals (especially between those with and without asthma), drying of the small airways with an associated inflammatory response seems prerequisite for EIB. Dysregulated repair processes following exercise-induced airway epithelial injury may also serve as basis for EIB development/progression.

Respiratory health of elite athletes - preventing airway injury: a critical review.

Elite athletes, particularly those engaged in endurance sports and those exposed chronically to airborne pollutants/irritants or allergens, are at increased risk for upper and lower airway dysfunction. Airway epithelial injury may be caused by dehydration and physical stress applied to the airways during severe exercise hyperpnoea and/or by inhalation of noxious agents. This is thought to initiate an inflammatory cascade/repair process that, ultimately, could lead to airway hyperresponsiveness (AHR) and asthma in susceptible athletes.

Assessment and prevention of exercise-induced bronchoconstriction.

The assessment of exercise-induced bronchoconstriction (EIB) in athletes requires the measurement of forced expiratory volume in 1 s (FEV(1)) before and after vigorous exercise or a surrogate of exercise such as eucapnic voluntary hyperpnoea (EVH) of dry air or mannitol dry powder. Exercise testing in a laboratory has a low sensitivity to identify EIB, and exercise testing in the field can be a challenge in itself particularly in cold weather athletes. The EVH test requires the subject to ventilate dry air containing ∼5% CO(2) for 6 min through a low-resistance circuit at a rate higher than that usually achieved on maximum exercise.

Airway injury during high-level exercise.

Airway epithelial cells act as a physical barrier against environmental toxins and injury, and modulate inflammation and the immune response. As such, maintenance of their integrity is critical. Evidence is accumulating to suggest that exercise can cause injury to the airway epithelium.

Hyperpnea-induced bronchoconstriction and urinary CC16 levels in athletes.

Purpose: Exercise-induced bronchoconstriction (EIB) is a common condition in both individuals with asthma and otherwise healthy elite athletes. Although excessive water loss by peripheral airways during hyperpnea is regarded as the initial trigger for EIB, the cascade of events that follows remains unclear. Our goal was to establish whether transient disruption of the airway epithelial barrier occurs after a short period of hyperpnea of dry air in athletes with EIB.

Effect of sodium cromoglycate on mast cell mediators during hyperpnea in athletes.

Introduction: The role of mast cells in the airway response to exercise and the benefit of sodium cromoglycate (SCG) in athletes are unclear.

Purpose: The purpose of this study was to clarify the role of mast cell mediators in the airway response to exercise in athletes and to investigate the effect of SCG.

Methods: Eleven athletes with exercise-induced bronchoconstriction (EIB+) and 11 without (EIB-) performed a eucapnic voluntary hyperpnea (EVH) test (a surrogate for exercise) 10 min after inhalation of a placebo or 40 mg of the mast cell stabilizing agent sodium cromoglycate.

Acute effects of beclomethasone on hyperpnea-induced bronchoconstriction.

Purpose: The aim of this study was to assess whether a single high dose of beclomethasone dipropionate (BDP) could blunt mast cell activation and bronchoconstriction after eucapnic voluntary hyperpnea (EVH).

Methods: In this model of exercise-induced bronchoconstriction (EIB), seven athletes with EIB and eight untrained subjects with mild asthma performed two EVH tests 5.5 h apart on the same day; the first challenge after inhalation of a placebo aerosol and the second 4 h after inhalation of BDP (1500 microg).

Asthma and the elite athlete: summary of the International Olympic Committee's consensus conference, Lausanne, Switzerland, January 22-24, 2008.

Respiratory symptoms cannot be relied on to make a diagnosis of asthma and/or airways hyperresponsiveness (AHR) in elite athletes. For this reason, the diagnosis should be confirmed with bronchial provocation tests. Asthma management in elite athletes should follow established treatment guidelines (eg, Global Initiative for Asthma) and should include education, an individually tailored treatment plan, minimization of aggravating environmental factors, and appropriate drug therapy that must meet the requirements of the World Anti-Doping Agency.

Airway injury as a mechanism for exercise-induced bronchoconstriction in elite athletes.

Exercise-induced bronchoconstriction (EIB) is a consequence of evaporative water loss in conditioning the inspired air. The water loss causes cooling and dehydration of the airway surface. One acute effect of dehydration is the release of mediators, such as prostaglandins, leukotrienes, and histamine, that can stimulate smooth muscle, causing contraction and a change in vascular permeability.

Bronchial challenges in athletes applying to inhale a beta2-agonist at the 2004 Summer Olympics.

Background: The International Olympic Committee Medical Commission required a medical justification for athletes to inhale a beta2-agonist before an event at the Summer Games in Athens in 2004.

Objective: We sought to establish the percentage of athletes applying to use an inhaled beta2-agonist on the basis of the results of objective tests to establish a diagnosis of asthma or exercise-induced bronchoconstriction. We also sought to compare this percentage with the percentage of athletes simply notifying the intention to use a beta2-agonist at the previous Summer Games in Sydney in 2000.

Exercise-induced bronchoconstriction: pathogenesis.

There is still active debate on the acute mechanism of exercise-induced bronchoconstriction (EIB). Although it is unlikely that vasoconstriction and hyperemia of the bronchial vasculature are essential events for EIB, it is likely that this vasculature enhances the airway response to dehydration and contributes to the pathogenesis of EIB, particularly in elite athletes. Accumulating evidence suggests that airway smooth muscle (ASM) becomes more sensitive as a result of repeated exposure to bulk plasma in response to airway injury from dehydration.