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dc.contributor.authorGonzález-Alonso, José
dc.contributor.authorMora-Rodríguez, Ricardo
dc.contributor.authorCalbet, José Antonio Lopez
dc.contributor.authorKippelen, Pascale
dc.date.accessioned2023-10-17T07:18:13Z
dc.date.available2023-10-17T07:18:13Z
dc.date.created2023-03-10T12:37:04Z
dc.date.issued2023
dc.identifier.citationExperimental Physiology. 2023, 108(2), Side 188-206.en_US
dc.identifier.issn0958-0670
dc.identifier.urihttps://hdl.handle.net/11250/3096846
dc.descriptionThis 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.en_US
dc.description.abstractThe mechanisms driving hyperthermic hyperventilation during exercise are unclear. In a series of retrospective analyses, we evaluated the impact of combined versus isolated dehydration and hyperthermia and the effects of sympathoadrenal discharge on ventilation and pulmonary gas exchange during prolonged intense exercise. In the first study, endurance-trained males performed two submaximal cycling exercise trials in the heat. On day 1, participants cycled until volitional exhaustion (135 ± 11 min) while experiencing progressive dehydration and hyperthermia. On day 2, participants maintained euhydration and core temperature (Tc) during a time-matched exercise (control). At rest and during the first 20 min of exercise, pulmonary ventilation (VE), arterial blood gases, CO2 output and O2 uptake were similar in both trials. At 135 ± 11 min, however, VE was elevated with dehydration and hyperthermia, and this was accompanied by lower arterial partial pressure of CO2, higher breathing frequency, arterial partial pressure of O2, arteriovenous CO2 and O2 differences, and elevated CO2 output and unchanged O2 uptake despite a reduced pulmonary circulation. The increased VE was closely related to the rise in Tc and circulating catecholamines (R2 ≥ 0.818, P ≤ 0.034). In three additional studies in different participants, hyperthermia independently increased VE to an extent similar to combined dehydration and hyperthermia, whereas prevention of hyperthermia in dehydrated individuals restored VE to control levels. Furthermore, adrenaline infusion during exercise elevated both Tc and VE. These findings indicate that: (1) adjustments in pulmonary gas exchange limit homeostatic disturbances in the face of a blunted pulmonary circulation; (2) hyperthermia is the main stimulus increasing ventilation during prolonged intense exercise; and (3) sympathoadrenal activation might partly mediate the hyperthermic hyperventilation.en_US
dc.language.isoengen_US
dc.subjectblood gasesen_US
dc.subjectbody fluidsen_US
dc.subjecttemperatureen_US
dc.subjectventilationen_US
dc.titlePulmonary ventilation and gas exchange during prolonged exercise in humans: Influence of dehydration, hyperthermia and sympathoadrenal activityen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.rights.holder© 2023 The Authorsen_US
dc.source.pagenumber188-206en_US
dc.source.volume108en_US
dc.source.journalExperimental Physiologyen_US
dc.source.issue2en_US
dc.identifier.doi10.1113/EP090909
dc.identifier.cristin2133016
dc.description.localcodeInstitutt for fysisk prestasjonsevne / Department of Physical Performanceen_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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