Exercise-induced whole-body dehydration does not affect airway responsiveness in athletes but may impair small airway function

Exercise-induced bronchoconstriction (EIB) is the transient narrowing of the airways that occurs during or shortly after strenuous exercise. Loss of water from the airway surface, due to the conditioning of large volumes of air during exercise, is the main physiological stimulus for EIB. We proposed that exercise-induced whole-body dehydration would interfere with hydration of the airways and, consequently, increase the risk and/or severity of EIB. We also investigated the effects of whole-body dehydration on resting lung function

Effect of endurance training on lung function: A one year study

The official published version can be accessed from the link below.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

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

This article is made available through the Brunel Open Access Publishing Fund and is distributed by the Creative Commons CC-BY 3.0 license, under which all are free to reuse or distribute the article under the condition that this original publication must be cited.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 β2-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.World Anti Doping Agenc

A proposal to account for the stimulus, the mechanism and the mediators released in exercise-induced bronchoconstriction

Exercise induced bronchoconstriction (EIB) describes the transient narrowing of the airways that follows vigorous exercise. It commonly occurs in children and adults who have asthma and in elite athletes. The primary stimulus is proposed to be loss of water, by evaporation, from the airway surface due to conditioning inspired air. The mechanism, whereby this evaporative loss of water provokes contraction of the bronchial smooth muscle, is thought to be an increase in osmolarity of the airway surface liquid. The increase in osmolarity causes mast cells to release histamines, prostaglandins, and leukotrienes. It is these mediators that contract smooth muscle causing the airways to narrow

A proposal to account for the stimulus, the mechanism, and the mediators released in exercise-induced bronchoconstriction

Exercise induced bronchoconstriction (EIB) describes the transient narrowing of the airways that follows vigorous exercise. It commonly occurs in children and adults who have asthma and in elite athletes. The primary stimulus is proposed to be loss of water, by evaporation, from the airway surface due to conditioning inspired air. The mechanism, whereby this evaporative loss of water provokes contraction of the bronchial smooth muscle, is thought to be an increase in osmolarity of the airway surface liquid. The increase in osmolarity causes mast cells to release histamines, prostaglandins, and leukotrienes. It is these mediators that contract smooth muscle causing the airways to narrow

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

Background: Local airway water loss is the main physiological trigger for exercise induced bronchoconstriction (EIB). Aim: To investigate the effects of whole-body water loss on airway responsiveness and pulmonary function in athletes with mild asthma and/or EIB. Methods: Ten recreational athletes with a doctor diagnosis of mild asthma and/or EIB completed a randomized, cross-over study. Pulmonary function tests (spirometry, whole body plethysmography and diffusing capacity for carbon monoxide [DLCO]) were conducted before and after three conditions: i) 2 h exercise in the heat with no fluid intake (dehydration); ii) 2 h exercise with ad libitum fluid intake (control); and iii) time-matched rest period (rest). Airway responsiveness was assessed 2 h post-exercise/rest via eucapnic voluntary hyperpnea (EVH) to dry air. Results: Exercise in the heat with no fluid intake induced a state of mild dehydration, with a mean 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 sec was 13 (7–15)%, 11 (9–24)% and 12 (7–20)% in the 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. Conclusion: Mild exercise induced dehydration does not exaggerate airway responsiveness to dry air in athletes with mild asthma/EIB, but may affect small airway function.This study was supported by the European Hydration Institute Student Research Grant Scheme

Physiological function during exercise and environmental stress in humans: An integrative view of body systems and homeostasis

Copyright: © 2022 by the authors. Claude Bernard’s milieu intérieur (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. This integrative approach can be used to identify whether function and cellular homeostasis are maintained or compromised during exercise. In this review, we discuss the responses of the human brain, the lungs, the heart, and the skeletal muscles to the varying physiological demands of exercise and environmental stress. Multiple alterations in physiological function and differential homeostatic adjustments occur when people undertake strenuous exercise with and without thermal stress. These adjustments can include: hyperthermia; hyperventilation; cardiovascular strain with restrictions in brain, muscle, skin and visceral organs blood flow; greater reliance on muscle glycogen and cellular metabolism; alterations in neural activity; and, in some conditions, compromised muscle metabolism and aerobic capacity. Oxygen supply to the human brain is also blunted during intense exercise, but global cerebral metabolism and central neural drive are preserved or enhanced. In contrast to the strain seen during severe exercise and environmental stress, a steady state is maintained when humans exercise at intensities and in environmental conditions that require a small fraction of the functional capacity. The impact of exercise and environmental stress upon whole-body functions and homeostasis therefore depends on the functional needs and differs across organ systems.Brunel Open Access Publishing Fund

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. The aim of this project was to evaluate the effects of a standard course of creatine on the airways of youth elite athletes. Methods Nineteen elite soccer players, 16-21 yr old, completed a stratified, randomized, double-blind, placebo-controlled, parallel-group trial. The creatine group (n = 9) ingested 0.3 g·kg-1⋅d-1 of creatine monohydrate (CM) for 1 wk (loading phase) and 5 g·d-1 for 7 wk (maintenance phase), and the placebo group (n = 10) received the same dosages of maltodextrin. Airway inflammation (assessed by exhaled nitric oxide, FENO) and airway responsiveness (to dry air hyperpnoea) were measured pre- and postsupplementation. Results Mild, unfavorable changes in FENO were noticed by trend over the supplementation period in the CM group only (P = 0.056 for interaction, η2 = 0.199), with a mean group change of 9 ± 13 ppb in the CM group versus -5 ± 16 ppb in the placebo group (P = 0.056, d = 0.695). Further, the maximum fall in forced expiratory volume in 1 s after dry air hyperpnoea was larger by trend postsupplementation in the CM group compared with the placebo group: 9.7% ± 7.5% vs 4.4% ± 1.4%, respectively (P = 0.070, d = 0.975). These adverse effects were more pronounced when atopic players only (n = 15) were considered. Conclusion On the basis of the observed trends and medium to large effect sizes, we cannot exclude that creatine supplementation has an adverse effect on the airways of elite athletes, particularly in those with allergic sensitization. Further safety profiling of the ergogenic food supplement is warranted