Electromyographic, cerebral, and muscle hemodynamic responses during intermittent, isometric contractions of the biceps brachii at three submaximal intensities

dc.contributor.authorBhambhani, Yagesh
dc.contributor.authorFan, Jui Lin
dc.contributor.authorPlace, Nicolas
dc.contributor.authorRodríguez Falces, Javier
dc.contributor.authorKayser, Bengt
dc.contributor.departmentIngeniería Eléctrica y Electrónicaes_ES
dc.contributor.departmentIngeniaritza Elektrikoa eta Elektronikoaeu
dc.date.accessioned2018-09-04T06:43:49Z
dc.date.available2018-09-04T06:43:49Z
dc.date.issued2014
dc.description.abstractThis study examined the electromyographic, cerebral and muscle hemodynamic responses during intermittent isometric contractions of biceps brachii at 20, 40, and 60% of maximal voluntary contraction (MVC). Eleven volunteers completed 2 min of intermittent isometric contractions (12/min) at an elbow angle of 90° interspersed with 3 min rest between intensities in systematic order. Surface electromyography (EMG) was recorded from the right biceps brachii and near infrared spectroscopy (NIRS) was used to simultaneously measure left prefrontal and right biceps brachii oxyhemoglobin (HbO2), deoxyhemoglobin (HHb), and total hemoglobin (Hbtot). Transcranial Doppler ultrasound was used to measure middle cerebral artery velocity (MCAv) bilaterally. Finger photoplethysmography was used to record beat-to-beat blood pressure and heart rate. EMG increased with force output from 20 to 60% MVC (P < 0.05). Cerebral HbO2 and Hbtot increased while HHb decreased during contractions with differences observed between 60% vs. 40% and 20% MVC (P < 0.05). Muscle HbO2 decreased while HHb increased during contractions with differences being observed among intensities (P < 0.05). Muscle Hbtot increased from rest at 20% MVC (P < 0.05), while no further change was observed at 40 and 60% MVC (P > 0.05). MCAv increased from rest to exercise but was not different among intensities (P > 0.05). Force output correlated with the root mean square EMG and changes in muscle HbO2 (P < 0.05), but not changes in cerebral HbO2 (P > 0.05) at all three intensities. Force output declined by 8% from the 1st to the 24th contraction only at 60% MVC and was accompanied by systematic increases in RMS, cerebral HbO2 and Hbtot with a leveling off in muscle HbO2 and Hbtot. These changes were independent of alterations in mean arterial pressure. Since cerebral blood flow and oxygenation were elevated at 60% MVC, we attribute the development of fatigue to reduced muscle oxygen availability rather than impaired central neuronal activation.en
dc.format.extent11 p.
dc.format.mimetypeapplication/pdfen
dc.identifier.doi10.3389/fphys.2014.00190
dc.identifier.issn1664-042X (Electronic)
dc.identifier.urihttps://academica-e.unavarra.es/handle/2454/30437
dc.language.isoengen
dc.publisherFrontiers Mediaen
dc.relation.ispartofFrontiers in Physiology, 5:190en
dc.relation.publisherversionhttps://doi.org/10.3389/fphys.2014.00190
dc.rights© 2014 Bhambhani, Fan, Place, Rodriguez-Falces and Kayser. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.en
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/
dc.subjectBiceps forceen
dc.subjectElectromyographyen
dc.subjectCerebral blood flow and oxygenationen
dc.subjectMuscle blood flow and oxygenationen
dc.titleElectromyographic, cerebral, and muscle hemodynamic responses during intermittent, isometric contractions of the biceps brachii at three submaximal intensitiesen
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublication
relation.isAuthorOfPublication8ebfa8e7-2a2b-41eb-a0c2-f82e9b6f39dc
relation.isAuthorOfPublication.latestForDiscovery8ebfa8e7-2a2b-41eb-a0c2-f82e9b6f39dc

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