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      Maximal exercise does not increase ventilation heterogeneity in healthy trained adults

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          Abstract

          The effect of exercise on ventilation heterogeneity has not been investigated. We hypothesized that a maximal exercise bout would increase ventilation heterogeneity. We also hypothesized that increased ventilation heterogeneity would be associated with exercise‐induced arterial hypoxemia ( EIAH). Healthy trained adult males were prospectively assessed for ventilation heterogeneity using lung clearance index ( LCI), S cond, and S acin at baseline, postexercise and at recovery, using the multiple breath nitrogen washout technique. The maximal exercise bout consisted of a maximal, incremental cardiopulmonary exercise test at 25 watt increments. Eighteen subjects were recruited with mean ±  SD age of 35 ± 9 years. There were no significant changes in LCI, S cond, or S acin following exercise or at recovery. While there was an overall reduction in SpO 2 with exercise (99.3 ± 1 to 93.7 ± 3%, P <  0.0001), the reduction in SpO 2 was not associated with changes in LCI, S cond or S acin. Ventilation heterogeneity is not increased following a maximal exercise bout in healthy trained adults. Furthermore, EIAH is not associated with changes in ventilation heterogeneity in healthy trained adults.

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          Exercise-induced arterial hypoxemia.

          P. Wagner, Robert J. Dempsey (1999)
          Exercise-induced arterial hypoxemia (EIAH) at or near sea level is now recognized to occur in a significant number of fit, healthy subjects of both genders and of varying ages. Our review aims to define EIAH and to critically analyze what we currently understand, and do not understand, about its underlying mechanisms and its consequences to exercise performance. Based on the effects on maximal O(2) uptake of preventing EIAH, we suggest that mild EIAH be defined as an arterial O(2) saturation of 93-95% (or 3-4% 25-30 Torr) and inadequate compensatory hyperventilation (arterial PCO(2) >35 Torr) commonly contribute to EIAH, as do acid- and temperature-induced shifts in O(2) dissociation at any given arterial PO(2). In turn, expiratory flow limitation presents a significant mechanical constraint to exercise hyperpnea, whereas ventilation-perfusion ratio maldistribution and diffusion limitation contribute about equally to the excessive A-a DO(2). Exactly how diffusion limitation is incurred or how ventilation-perfusion ratio becomes maldistributed with heavy exercise remains unknown and controversial. Hypotheses linked to extravascular lung water accumulation or inflammatory changes in the "silent" zone of the lung's peripheral airways are in the early stages of exploration. Indirect evidence suggests that an inadequate hyperventilatory response is attributable to feedback inhibition triggered by mechanical constraints and/or reduced sensitivity to existing stimuli; but these mechanisms cannot be verified without a sensitive measure of central neural respiratory motor output. Finally, EIAH has detrimental effects on maximal O(2) uptake, but we have not yet determined the cause or even precisely identified which organ system, involved directly or indirectly with O(2) transport to muscle, is responsible for this limitation.
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            Ventilation heterogeneity is a major determinant of airway hyperresponsiveness in asthma, independent of airway inflammation.

            Bruce Thompson, Sylvia Verbanck, C Salome … (2007)
            Airway hyperresponsiveness is the ability of airways to narrow excessively in response to inhaled stimuli and is a key feature of asthma. Airway inflammation and ventilation heterogeneity have been separately shown to be associated with airway hyperresponsiveness. A study was undertaken to establish whether ventilation heterogeneity is associated with airway hyperresponsiveness independently of airway inflammation in subjects with asthma and to determine the effect of inhaled corticosteroids on this relationship. Airway inflammation was measured in 40 subjects with asthma by exhaled nitric oxide, ventilation heterogeneity by multiple breath nitrogen washout and airway hyperresponsiveness by methacholine challenge. In 18 of these subjects with uncontrolled symptoms, measurements were repeated after 3 months of treatment with inhaled beclomethasone dipropionate. At baseline, airway hyperresponsiveness was independently predicted by airway inflammation (partial r2 = 0.20, p<0.001) and ventilation heterogeneity (partial r2 = 0.39, p<0.001). Inhaled corticosteroid treatment decreased airway inflammation (p = 0.002), ventilation heterogeneity (p = 0.009) and airway hyperresponsiveness (p<0.001). After treatment, ventilation heterogeneity was the sole predictor of airway hyperresponsiveness (r2 = 0.64, p<0.001). Baseline ventilation heterogeneity is a strong predictor of airway hyperresponsiveness, independent of airway inflammation in subjects with asthma. Its persistent relationship with airway hyperresponsiveness following anti-inflammatory treatment suggests that it is an important independent determinant of airway hyperresponsiveness. Normalisation of ventilation heterogeneity is therefore a potential goal of treatment that may lead to improved long-term outcomes.
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              Noninvasive assessment of airway alterations in smokers: the small airways revisited.

              M Meysman, Walter Vincken, Saul M. Paiva … (2004)
              It has been shown that structural changes in small airways of smokers with average smoking histories greater than 35 pack-years could be reflected in the single-breath washout test. The more sophisticated multiple breath washout test (MBW) has the potential to anatomically locate the affected small airways in acinar and conductive lung zones through increased phase III slope indices S(acin) and S(cond), respectively. Pulmonary function, S(acin), and S(cond) were obtained in 63 normal never-smokers and in 169 smokers classified according to smoking history ( 30 pack-years). Compared with never-smokers, significant changes in S(acin) (p = 0.02), S(cond) (p < 0.001), and diffusing capacity (DL(CO); p < 0.001) were detected from greater than 10 pack-years onwards. Spirometric abnormality was significant only from greater than 20 pack-years onwards. In smokers with greater than 30 pack-years and DL(CO) less than 60% predicted, the presence of emphysema resulted in disproportionally larger S(acin) than S(cond) increases. We conclude that S(cond) and S(acin) can noninvasively detect airway changes from as early as 10 pack-years onwards, locating the earliest manifestations of smoking-induced small airways alterations around the acinar entrance. In these early stages, the associated DL(CO) decrease may be a reflection of ventilation heterogeneity rather than true parenchymal destruction. In more advanced stages of smoking-induced lung disease, differential patterns of S(acin) and S(cond) are characteristic of the presence of parenchymal destruction in addition to peripheral airways alterations.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Physiol Rep
                Journal ID (iso-abbrev): Physiol Rep
                Journal ID (doi): 10.1002/(ISSN)2051-817X
                Journal ID (publisher-id): PHY2
                Journal ID (hwp): physreports
                Title: Physiological Reports
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2051-817X
                Publication date (Electronic): 06 April 2016
                Publication date Collection: April 2016
                Volume: 4
                Issue: 7 ( doiID: 10.1111/phy2.2016.4.issue-7 )
                Electronic Location Identifier: e12747
                Affiliations
                [ 1 ] Department of MedicineMonash University MelbourneAustralia
                [ 2 ] Allergy, Immunology & Respiratory MedicineThe Alfred MelbourneAustralia
                [ 3 ] Department of Respiratory MedicineFiona Stanley Hospital PerthAustralia
                Author notes
                [*] [* ] Correspondence

                Dr Jeremy Wrobel, Department of Respiratory Medicine, Fiona Stanley Hospital, 11 Robin Warren Drive, Murdoch, Australia.

                Tel: +61 8 6152 2222

                Fax: + 61 8 6152 4084

                E‐mail: jeremy.wrobel@ 123456health.wa.gov.au

                Article
                Publisher ID: PHY212747
                DOI: 10.14814/phy2.12747
                PMC ID: 4831321
                PubMed ID: 27044853
                SO-VID: d542b8ff-ee3b-41b9-b621-bdd21f9b23a6
                Copyright © © 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 16 December 2015
                Date revision received : 01 March 2016
                Date accepted : 02 March 2016
                Page count
                Pages: 10
                Categories
                Subject: Original Research
                Subject: Original Research
                Custom metadata
                source-schema-version-number 2.0
                component-id phy212747
                cover-date April 2016
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.8.6 mode:remove_FC converted:14.04.2016

                Keywords: cardiopulmonary exercise test,hypoxemia,lung clearance index,multiple breath nitrogen washout,ventilation inhomogeneity
                Data availability:
                Keywords: cardiopulmonary exercise test, hypoxemia, lung clearance index, multiple breath nitrogen washout, ventilation inhomogeneity

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