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dc.contributor.authorFagoni, Nazzareno
dc.contributor.authorBruseghini, Paolo
dc.contributor.authorAdami, Alessandra
dc.contributor.authorCapelli, Carlo
dc.contributor.authorLador, Frederic
dc.contributor.authorMoia, Christian
dc.contributor.authorTam, Enrico
dc.contributor.authorBringard, Aurélien
dc.contributor.authorFerretti, Guido
dc.date.accessioned2021-06-04T12:28:33Z
dc.date.available2021-06-04T12:28:33Z
dc.date.created2021-01-20T13:16:23Z
dc.date.issued2020
dc.identifier.citationInternational Journal of Sports Medicine. 2020, 41(4), 209-218.en_US
dc.identifier.issn0172-4622
dc.identifier.urihttps://hdl.handle.net/11250/2757967
dc.descriptionThis article is available under the Creative Commons CC-BY-NC-ND license and permits non-commercial use of the work as published, without adaptation or alteration provided the work is fully attributed.en_US
dc.description.abstractWe hypothesised that vagal withdrawal and increased venous return interact in determining the rapid cardiac output (CO) response (phase I) at exercise onset. We used lower body negative pressure (LBNP) to increase blood distribution to the heart by muscle pump action and reduce resting vagal activity. We expected a larger increase in stroke volume (SV) and smaller for heart rate (HR) at progressively stronger LBNP levels, therefore CO response would remain unchanged. To this aim ten young, healthy males performed a 50 W exercise in supine position at 0 (Control), −15, −30 and −45 mmHg LBNP exposure. On single beat basis, we measured HR, SV, and CO. Oxygen uptake was measured breath-by-breath. Phase I response amplitudes were obtained applying an exponential model. LBNP increased SV response amplitude threefold from Control to −45 mmHg. HR response amplitude tended to decrease and prevented changes in CO response. The rapid response of CO explained that of oxygen uptake. The rapid SV kinetics at exercise onset is compatible with an increased venous return, whereas the vagal withdrawal conjecture cannot be dismissed for HR. The rapid CO response may indeed be the result of two independent yet parallel mechanisms, one acting on SV, the other on HR.en_US
dc.language.isoengen_US
dc.subjectcardiac outputen_US
dc.subjectheart rateen_US
dc.subjectkinetics and exercise transienten_US
dc.subjectLBNPen_US
dc.subjectoxygen uptakeen_US
dc.subjectstroke volumeen_US
dc.titleEffect of lower body negative pressure on phase I cardiovascular responses at exercise onseten_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.rights.holder© Georg Thieme Verlag KGen_US
dc.source.pagenumber209-218en_US
dc.source.volume41en_US
dc.source.journalInternational Journal of Sports Medicineen_US
dc.source.issue4en_US
dc.identifier.doi10.1055/a-1028-7496
dc.identifier.cristin1875491
dc.description.localcodeInstitutt for fysisk prestasjonsevne / Department of Physical Performanceen_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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