Role of expiratory flow limitation in determining lung volumes and ventilation during exercise

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Deutscher übersetzter Titel:Rolle der Exspirations-Leistungsgrenze in der Bestimmung von Lungenvolumina und Ventilation unter koerperlicher Belastung
Autor:McClaran, S.R.; Wetter, T.J.; Pegelow, D.F.; Dempsey, J.A.
Erschienen in:Journal of applied physiology
Veröffentlicht:86 (1999), 4, S. 1357-1366, Lit.
Format: Literatur (SPOLIT)
Publikationstyp: Zeitschriftenartikel
Medienart: Gedruckte Ressource
Sprache:Englisch
ISSN:8750-7587, 0021-8987, 0161-7567, 1522-1601
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Erfassungsnummer:PU199905309220
Quelle:BISp

Abstract des Autors

We determined the role of expiratory flow limitation (EFL) on the ventilatory response to heavy exercise in six trained male cyclists (maximal O2 uptake = 65+/-8 (range 55-74) ml/kg/min) with normal lung function. Each subject completed four progressive cycle ergometer tests to exhaustion in random order: two trials while breathing N2O2 (26% O2-balance N2), one with and one without added dead space, and two trials while breathing HeO2 (26% O2-balance He), one with and one without added dead space. EFL was defined by the proximity of the tidal to the maximal flow-volume loop. With N2O2 during heavy and maximal exercise, 1) EFL was present in all six subjects during heavy (19+/-2% of tidal volume (VT) intersected the maximal flow-volume loop) and maximal exercise (43+/-8% of VT), 2) the slopes of the ventilation (deltaVE) and peak esophageal pressure responses to added dead space (e.g., deltaVE/deltaPETCO2, where PETCO2 is end-tidal PCO2) were reduced relative to submaximal exercise, 3) end-expiratory lung volume (EELV) increased and end-inspiratory lung volume reached a plateau at 88-91% of total lung capacity, and 4) VT reached a plateau and then fell as work rate increased. With HeO2 (compared with N2O2) breathing during heavy and maximal exercise, 1) HeO2 increased maximal flow rates (from 20 to 38%) throughout the range of vital capacity, which reduced EFL in all subjects during tidal breathing, 2) the gains of the ventilatory and inspiratory esophageal pressure responses to added dead space increased over those during room air breathing and were similar at all exercise intensities, 3) EELV was lower and end-inspiratory lung volume remained near 90% of total lung capacity, and 4) VT was increased relative to room air breathing. We conclude that EFL or even impending EFL during heavy and maximal exercise and with added dead space in fit subjects causes EELV to increase, reduces the VT, and constrains the increase in respiratory motor output and ventilation. Verf.-Referat