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dc.contributor.authorStöhr, Eric J.
dc.contributor.authorStembridge, Mike
dc.contributor.authorEsformes, Joseph I.
dc.date.accessioned2016-11-25T16:50:02Z
dc.date.available2016-11-25T16:50:02Z
dc.date.issued2015-05-01
dc.identifier.citationStöhr, E.J., Stembridge, M. and Esformes, J.I. (2015) 'In vivo human cardiac shortening and lengthening velocity is region dependent and not coupled with heart rate:‘longitudinal’strain rate markedly underestimates apical contribution', Experimental Physiology, 100(5), pp.507-518.en_US
dc.identifier.issn0958-0670
dc.identifier.urihttp://hdl.handle.net/10369/8196
dc.descriptionThis article was published in Experimental Physiology on 6 May 2015 (online), freely available at http://dx.doi.org/10.1113/EP085081en_US
dc.description.abstractNew Findings •What is the central question of this study? Regulation of cardiac function is typically achieved by changes in heart rate (HR) and cardiac shortening velocity (strain rate; SR), but their interdependence in vivo remains poorly understood. •What is the main finding and its importance? Using resistance exercise to increase heart rate and arterial resistance physiologically in humans and measuring regional cardiac SR (at the base and apex), we found that HR and SR were not strictly coupled because SR at the base and apex responded differently, despite the same HR. Importantly, our data show that the region-averaged ‘longitudinal’ SR, which is currently popular in the clinical setting, markedly underestimates the contribution of the apex. The fundamental importance of cardiac shortening and lengthening velocity (i.e. strain rate; SR) has been demonstrated in vitro. Currently, the interdependence between in vivo SR and HR is poorly understood because studies have typically assessed region-averaged ‘longitudinal’ strain rate, which is likely to underestimate the apical contribution, and have used non-physiological interventions that may also have been influenced by multicollinearity caused by concomitant reductions in arterial resistance. Resistance exercise acutely raises HR, blood pressure and arterial resistance and transiently disassociates these cardiovascular factors following exercise. Therefore, we measured SR, HR, blood pressure and arterial resistance in nine healthy men (aged 20 ± 1 years) immediately before, during and after double-leg-press exercise at 30 and 60% of maximal strength. Resistance exercise caused a disproportionate SR response at the left ventricular base and apex (interaction effect, P < 0.05). Consequently, associations between HR and regional peak SR were inconsistent and mostly very weak (r2 = 0.0004–0.24). Likewise, the areas under the curve for systolic and diastolic SR and their relationship with systolic and diastolic duration were variable and weak. Importantly, region-averaged ‘longitudinal’ SR was identical to basal SR, thus, markedly underestimating the apical contribution. In conclusion, in vivo HR and SR are not strictly coupled in healthy humans, which is explained by the region-specific responses of SR that are not captured by ‘longitudinal SR’. This novel observation emphasizes the independent role of in vivo SR in overall cardiac function during stress and may cause a ‘revival’ of SR as a marker of regional left ventricular (dys)function.en_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofseriesExperimental Physiology;
dc.rightsNon-Commercial
dc.subjectStrain rateen_US
dc.subjectheart rateen_US
dc.subjectexerciseen_US
dc.titleIn vivo human cardiac shortening and lengthening velocity is region-dependent and not coupled with heart rateen_US
dc.typeArticleen_US
dc.identifier.doihttp://dx.doi.org/10.1113/EP085081
dcterms.dateAccepted2015-03-04
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.startdate2016-11-25
rioxxterms.funder.project37baf166-7129-4cd4-b6a1-507454d1372een_US


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