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

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          Abstract

          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. The authors review the evidence relating to prevention or reduction of the risk of AHR/asthma development. Appropriate measures should be implemented when athletes exercise strenuously in an attempt to attenuate the dehydration stress and reduce the exposure to noxious airborne agents. Environmental interventions are the most important. Non-pharmacological strategies can assist, but currently, pharmacological measures have not been demonstrated to be effective. Whether early prevention of airway injury in elite athletes can prevent or reduce progression to AHR/asthma remains to be established.

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          Most cited references84

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          Diagnosis and management of cough executive summary: ACCP evidence-based clinical practice guidelines.

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            Long-term inhaled corticosteroids in preschool children at high risk for asthma.

            It is unknown whether inhaled corticosteroids can modify the subsequent development of asthma in preschool children at high risk for asthma. We randomly assigned 285 participants two or three years of age with a positive asthma predictive index to treatment with fluticasone propionate (at a dose of 88 mug twice daily) or masked placebo for two years, followed by a one-year period without study medication. The primary outcome was the proportion of episode-free days during the observation year. During the observation year, no significant differences were seen between the two groups in the proportion of episode-free days, the number of exacerbations, or lung function. During the treatment period, as compared with placebo use, use of the inhaled corticosteroid was associated with a greater proportion of episode-free days (P=0.006) and a lower rate of exacerbations (P<0.001) and of supplementary use of controller medication (P<0.001). In the inhaled-corticosteroid group, as compared with the placebo group, the mean increase in height was 1.1 cm less at 24 months (P<0.001), but by the end of the trial, the height increase was 0.7 cm less (P=0.008). During treatment, the inhaled corticosteroid reduced symptoms and exacerbations but slowed growth, albeit temporarily and not progressively. In preschool children at high risk for asthma, two years of inhaled-corticosteroid therapy did not change the development of asthma symptoms or lung function during a third, treatment-free year. These findings do not provide support for a subsequent disease-modifying effect of inhaled corticosteroids after the treatment is discontinued. (ClinicalTrials.gov number, NCT00272441.). Copyright 2006 Massachusetts Medical Society.
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              Ultrafine particle deposition in humans during rest and exercise.

              Ultrafine particles (diameter < 100 nm) may be important in the health effects of air pollution, in part because of their predicted high respiratory deposition. However, there are few measurements of ultrafine particle deposition during spontaneous breathing. The fractional deposition for the total respiratory tract of ultrafine carbon particles (count median diameter = 26 nm, geometric standard deviation = 1.6) was measured in 12 healthy subjects (6 female, 6 male) at rest (minute ventilation 9.0 +/- 1.3 L/min) using a mouthpiece exposure system. The mean +/- SD fractional deposition was 0.66 +/- 0.11 by particle number and 0.58 +/- 0.13 by particle mass concentration, similar to model predictions. The number deposition fraction increased as particle size decreased, reaching 0.80 +/- 0.09 for the smallest particles (midpoint count median diameter = 8.7 nm). No gender differences were observed. In an additional 7 subjects (2 female, 5 male) alternating rest with moderate exercise (minute ventilation 38.1 +/- 9.5 L/min), the deposition fraction during exercise increased to 0.83 +/- 0.04 and 0.76 +/- 0.06 by particle number and mass concentration, respectively, and reached 0.94 +/- 0.02 for the smallest particles. Experimental deposition data exceeded model predictions during exercise. The total number of deposited particles was more than 4.5-fold higher during exercise than at rest because of the combined increase in deposition fraction and minute ventilation. Fractional deposition of ultrafine particles during mouth breathing is high in healthy subjects, and increases further with exercise.
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                Author and article information

                Journal
                Br J Sports Med
                Br J Sports Med
                bjsports
                bjsm
                British Journal of Sports Medicine
                BMJ Group (BMA House, Tavistock Square, London, WC1H 9JR )
                0306-3674
                1473-0480
                1 June 2012
                29 April 2012
                : 46
                : 7
                : 471-476
                Affiliations
                [1 ]Centre for Sports Medicine & Human Performance, Brunel University, Uxbridge, UK
                [2 ]School of Sports Science, Exercise and Health, Faculty of Life Sciences, University of Western Australia, Crawley, Western Australia, Australia
                [3 ]Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia
                [4 ]Faculté des Sciences du Sport, Université Droit et Santé de Lille 2, Lille, France
                [5 ]Centre de recherche de l’Institut universitaire de cardiologie et de pneumologie de Québec, Quebec, Canada
                [6 ]Medical Affairs, Pharmaxis, Exton, Pennsylvania, USA
                [7 ]Department of Thoracic Medicine, St Olavs Hospital, University Hospital of Trondheim, Trondheim, Norway
                [8 ]Department of Circulation and Imaging, Norwegian University of Science and Technology, Trondheim, Norway
                [9 ]Division of Sports Medicine, School of Human Kinetics, University of British Columbia, Vancouver, Canada
                Author notes
                Correspondence to Pascale Kippelen, Brunel University, Centre for Sports Medicine & Human Performance, Uxbridge UB8 3PH, UK; pascale.kippelen@ 123456brunel.ac.uk
                Article
                bjsports-2012-091056
                10.1136/bjsports-2012-091056
                3371227
                22522585
                326a5a09-5f0f-494c-b92a-4e12894785e5
                Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license. See: http://creativecommons.org/licenses/by-nc/2.0/ and http://creativecommons.org/licenses/by-nc/2.0/legalcode.

                History
                : 9 February 2011
                : 6 March 2012
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