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dc.contributor.authorStembridge, Mike
dc.contributor.authorAinslie, Philip
dc.contributor.authorStöhr, Eric J.
dc.contributor.authorTymko, Michael
dc.contributor.authorDay, Trevor A.
dc.contributor.authorBakker, Akke
dc.contributor.authorHughes, Michael G.
dc.contributor.authorSmith, K.J
dc.contributor.authorWillie, C.K.
dc.contributor.authorLewis, N.C.S.
dc.contributor.authorShave, Rob
dc.identifier.citationStembridge, M., Ainslie, P.N., Hughes, M.G., Stöhr, E.J., Cotter, J.D., Tymko, M.M., Day, T.A., Bakker, A. and Shave, R. (2015) 'Intrinsic ventricular function does not explain reduced stroke volume at rest and during exercise at high altitude', Japanese Journal of Physical Fitness and Sports Medicine, 64(1), p.112. DOI: 10.7600/jspfsm.64.112.en_US
dc.descriptionArticle published in Journal of Applied Physiology on 25 January 2015, freely available at:
dc.description.abstractIntroduction: Both impaired systolic dysfunction and myocardial relaxation have previously been advanced as possible mechanisms contributing to decreased stroke volume (SV) at high altitude (HA). To determine whether myocardial performance is a limiting factor in the generation of SV at HA, we assessed left ventricular (LV) mechanics due to their close relationship with filling and ejection. Methods: Left ventricular volumes and mechanics were assessed using echocardiography in 10 healthy participants (aged 32 ± 2; mean ± SEM) at rest and during incremental exercise up to 50% peak power at sea level (SL; 344 m) and after ascent to 5050m. Arterial oxygen saturation (SaO2) was assessed using pulse oximetry. Data were analysed using a repeated measures analysis of variance and post-hoc tests with Bonferroni correction. Alpha was set at 0.05. Results: Ascent to altitude was associated with a significant reduction in resting (SaO2=81%) and exercise (SaO2=72%) arterial oxygen saturation. In contrast to SL, LV end-diastolic volume (EDV) was lower at rest (104±6 vs. 128 ± 6 ml, p=0.004) and did not increase from rest to exercise despite a greater untwisting velocity and preserved coupling of systolicdiastolic twist velocities (r2=0.99 and r2=0.98 at SL and HA,respectively). Furthermore, whilst an increase in resting ejection fraction (EF; 6%), LV twist (43%), and apical circumferential strain (17%) was observed at HA, resting SV was significantly lower (60 ± 3 vs. 70 ± 3 ml, all p<0.05). With exercise at HA, the increase in SV was limited (12 ml vs. 22 ml), and LV twist failed to augment. Discussion: In conclusion, in vivo diastolic relaxation, as assessed by LV untwist velocity, was not impaired despite moderate-severe hypoxemia at HA. The increase in EF observed previously and in the current study alongside greater LV twist may represent a mechanism by which SV is protected in the presence of a reduced EDV. However, higher resting LV twist and apical circumferential strain reduce the functional mechanical reserve normally available at SL. Consequently, whilst hypoxia does not suppress systolic function per se, the ability of the LV to respond to an exercise challenge at HA is limited.en_US
dc.publisherJapanese Society of Physical Fitness and Sports Medicineen_US
dc.relation.ispartofseriesJapanese Journal of Physical Fitness and Sports Medicine;
dc.titleIntrinsic ventricular function does not explain reduced stroke volume at rest and during exercise at high altitudeen_US
rioxxterms.funderCardiff Metropolitan Universityen_US
rioxxterms.identifier.projectCardiff Metropolian (Internal)en_US

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