Impaired myocardial function does not explain reduced left ventricular filling and stroke volume at rest or during exercise at high altitude

verfasst von: Mike Stembridge, Philip N. Ainslie, Michael G. Hughes, Eric J. Stöhr, James D. Cotter, Michael M. Tymko, Trevor A. Day, Akke Bakker, Rob Shave
Abstract: Stembridge M, Ainslie PN, Hughes MG, Stöhr EJ, Cotter JD, Tymko MM, Day TA, Bakker A, Shave R. Impaired myocardial function does not explain reduced left ventricular filling and stroke volume at rest or during exercise at high altitude. J Appl Physiol 119: 1219-1227, 2015. First published March 6, 2015; doi:10.1152/japplphysiol.00995.2014.-Impaired myocardial systolic contraction and diastolic relaxation have been suggested as possible mechanisms contributing to the decreased stroke volume (SV) observed at high altitude (HA). To determine whether intrinsic myocardial performance is a limiting factor in the generation of SV at HA, we assessed left ventricular (LV) systolic and diastolic mechanics and volumes in 10 healthy participants (aged 32 ± 7; mean ± SD) at rest and during exercise at sea level (SL; 344 m) and after 10 days at 5,050 m. In contrast to SL, LV end-diastolic volume was ∼19% lower at rest (P = 0.004) and did not increase during exercise despite a greater untwisting velocity. Furthermore, resting SV was lower at HA (∼17%; 60 ± 10 vs. 70 ± 8 ml) despite higher LV twist (43%), apical rotation (115%), and circumferential strain (17%). With exercise at HA, the increase in SV was limited (12 vs. 22 ml at SL), and LV apical rotation failed to augment. For the first time, we have demonstrated that EDV does not increase upon exercise at high altitude despite enhanced in vivo diastolic relaxation. The increase in LV mechanics at rest may represent a mechanism by which SV is defended in the presence of a reduced EDV. However, likely because of the higher LV mechanics at rest, no further increase was observed up to 50% peak power. Consequently, although hypoxia does not suppress systolic function per se, the capacity to increase SV through greater deformation during submaximal exercise at HA is restricted.
Externe Organisation(en): Cardiff Metropolitan University
University of British Columbia
University of Otago
Mount Royal University
University of Twente
Typ: Artikel
Journal: Journal of applied physiology
Band: 119
Seiten: 1219-1227
Anzahl der Seiten: 9
ISSN: 8750-7587
Publikationsdatum: 11.2015
Publikationsstatus: Veröffentlicht
Peer-reviewed: Ja
ASJC Scopus Sachgebiete: Physiologie, Physiologie (medizinische)
Elektronische Version(en): https://doi.org/10.1152/japplphysiol.00995.2014 (Zugang: Geschlossen)
http://hdl.handle.net/10369/8180 (Zugang: Offen)

BibTeX

@article{9f645ac81cc44002b5b237e7d313d713,
title = "Impaired myocardial function does not explain reduced left ventricular filling and stroke volume at rest or during exercise at high altitude",
abstract = "Stembridge M, Ainslie PN, Hughes MG, St{\"o}hr EJ, Cotter JD, Tymko MM, Day TA, Bakker A, Shave R. Impaired myocardial function does not explain reduced left ventricular filling and stroke volume at rest or during exercise at high altitude. J Appl Physiol 119: 1219-1227, 2015. First published March 6, 2015; doi:10.1152/japplphysiol.00995.2014.-Impaired myocardial systolic contraction and diastolic relaxation have been suggested as possible mechanisms contributing to the decreased stroke volume (SV) observed at high altitude (HA). To determine whether intrinsic myocardial performance is a limiting factor in the generation of SV at HA, we assessed left ventricular (LV) systolic and diastolic mechanics and volumes in 10 healthy participants (aged 32 ± 7; mean ± SD) at rest and during exercise at sea level (SL; 344 m) and after 10 days at 5,050 m. In contrast to SL, LV end-diastolic volume was ∼19% lower at rest (P = 0.004) and did not increase during exercise despite a greater untwisting velocity. Furthermore, resting SV was lower at HA (∼17%; 60 ± 10 vs. 70 ± 8 ml) despite higher LV twist (43%), apical rotation (115%), and circumferential strain (17%). With exercise at HA, the increase in SV was limited (12 vs. 22 ml at SL), and LV apical rotation failed to augment. For the first time, we have demonstrated that EDV does not increase upon exercise at high altitude despite enhanced in vivo diastolic relaxation. The increase in LV mechanics at rest may represent a mechanism by which SV is defended in the presence of a reduced EDV. However, likely because of the higher LV mechanics at rest, no further increase was observed up to 50% peak power. Consequently, although hypoxia does not suppress systolic function per se, the capacity to increase SV through greater deformation during submaximal exercise at HA is restricted.",
keywords = "Hypoxia, Left ventricular mechanics, Stroke volume",
author = "Mike Stembridge and Ainslie, {Philip N.} and Hughes, {Michael G.} and St{\"o}hr, {Eric J.} and Cotter, {James D.} and Tymko, {Michael M.} and Day, {Trevor A.} and Akke Bakker and Rob Shave",
year = "2015",
month = nov,
doi = "10.1152/japplphysiol.00995.2014",
language = "English",
volume = "119",
pages = "1219--1227",
journal = "Journal of applied physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "10",
}