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dc.contributor.authorStuckless, Troy
dc.contributor.authorVermeulen, Tyler
dc.contributor.authorBrown, Courtney
dc.contributor.authorBoulet, Lindsey
dc.contributor.authorShafer, Brooke
dc.contributor.authorWakeham, Denis
dc.contributor.authorSteinback, Craig
dc.contributor.authorAyas, Najib
dc.contributor.authorFloras, John
dc.contributor.authorFoster, Glen
dc.date.accessioned2020-05-22T08:36:15Z
dc.date.available2020-05-22T08:36:15Z
dc.date.issued2019-12-05
dc.identifier.citationStuckless, T.J., Vermeulen, T.D., Brown, C.V., Boulet, L.M., Shafer, B.M., Wakeham, D.J., Steinback, C.D., Ayas, N.T., Floras, J.S. and Foster, G.E. (2020) 'Acute intermittent hypercapnic hypoxia and sympathetic neurovascular transduction in men', The Journal of Physiology, 598(3), pp.473-487.en_US
dc.identifier.issn1469-7793
dc.identifier.urihttp://hdl.handle.net/10369/11042
dc.descriptionArticle published in The Journal of Physiology on 05 December 2019, available at: https://doi.org/10.1113/JP278941.en_US
dc.description.abstractAcute intermittent hypercapnic hypoxia (IH) induces long‐lasting elevations in sympathetic vasomotor outflow and blood pressure in healthy humans. It is unknown whether IH alters sympathetic neurovascular transduction (sNVT), measured as the relationship between sympathetic vasomotor outflow and either forearm vascular conductance (FVC; regional sNVT) or diastolic blood pressure (systemic sNVT). We tested the hypothesis that IH augments sNVT by exposing healthy males to 40 consecutive 1 min breathing cycles, each comprising 40 s of hypercapnic hypoxia (urn:x-wiley:00223751:media:tjp13923:tjp13923-math-0001: +4 ± 3 mmHg above baseline; urn:x-wiley:00223751:media:tjp13923:tjp13923-math-0002: 48 ± 3 mmHg) and 20 s of normoxia (n = 9), or a 40 min air‐breathing control (n = 7). Before and after the intervention, lower body negative pressure (LBNP; 3 min at –15, –30 and –45 mmHg) was applied to elicit reflex increases in muscle sympathetic nerve activity (MSNA, fibular microneurography) when clamping end‐tidal gases at baseline levels. Ventilation, arterial pressure [systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP)], brachial artery blood flow (urn:x-wiley:00223751:media:tjp13923:tjp13923-math-0003BA), FVC (urn:x-wiley:00223751:media:tjp13923:tjp13923-math-0004BA/MAP) and MSNA burst frequency were measured continuously. Following IH, but not control, ventilation [5 L min–1; 95% confidence interval (CI) = 1–9] and MAP (5 mmHg; 95% CI = 1–9) were increased, whereas FVC (–0.2 mL min–1 mmHg–1; 95% CI = –0.0 to –0.4) and mean shear rate (–21.9 s–1; 95% CI = –5.8 to –38.0; all P < 0.05) were reduced. Systemic sNVT was increased following IH (0.25 mmHg burst–1 min–1; 95% CI = 0.01–0.49; P < 0.05), whereas changes in regional forearm sNVT were similar between IH and sham. Reductions in vessel wall shear stress and, consequently, nitric oxide production may contribute to heightened systemic sNVT and provide a potential neurovascular mechanism for elevated blood pressure in obstructive sleep apnoea.en_US
dc.description.sponsorshipNSERC, CFI, HSFC, MSFHRen_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofseriesThe Journal of Physiology;
dc.titleAcute intermittent hypercapnic hypoxia and sympathetic neurovascular transduction in menen_US
dc.typeArticleen_US
dc.identifier.doihttps://doi.org/10.1113/JP278941
dcterms.dateAccepted2019-12-03
rioxxterms.funderCardiff Metropolitan Universityen_US
rioxxterms.identifier.projectCardiff Metropolian (Internal)en_US
rioxxterms.versionAMen_US
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden_US
rioxxterms.licenseref.startdate2020-05-22
rioxxterms.freetoread.startdate2020-12-05
rioxxterms.funder.project37baf166-7129-4cd4-b6a1-507454d1372een_US


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