Details
| Originalsprache | Englisch |
|---|---|
| Seiten (von - bis) | 1219-1227 |
| Seitenumfang | 9 |
| Fachzeitschrift | Journal of applied physiology |
| Jahrgang | 119 |
| Ausgabenummer | 10 |
| Frühes Online-Datum | 15 Nov. 2015 |
| Publikationsstatus | Veröffentlicht - Nov. 2015 |
| Extern publiziert | Ja |
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.
ASJC Scopus Sachgebiete
- Biochemie, Genetik und Molekularbiologie (insg.)
- Physiologie
- Medizin (insg.)
- Physiologie (medizinische)
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in: Journal of applied physiology, Jahrgang 119, Nr. 10, 11.2015, S. 1219-1227.
Publikation: Beitrag in Fachzeitschrift › Artikel › Forschung › Peer-Review
}
TY - JOUR
T1 - Impaired myocardial function does not explain reduced left ventricular filling and stroke volume at rest or during exercise at high altitude
AU - Stembridge, Mike
AU - Ainslie, Philip N.
AU - Hughes, Michael G.
AU - Stöhr, Eric J.
AU - Cotter, James D.
AU - Tymko, Michael M.
AU - Day, Trevor A.
AU - Bakker, Akke
AU - Shave, Rob
PY - 2015/11
Y1 - 2015/11
N2 - 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.
AB - 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.
KW - Hypoxia
KW - Left ventricular mechanics
KW - Stroke volume
UR - http://www.scopus.com/inward/record.url?scp=84947266680&partnerID=8YFLogxK
U2 - 10.1152/japplphysiol.00995.2014
DO - 10.1152/japplphysiol.00995.2014
M3 - Article
C2 - 25749445
AN - SCOPUS:84947266680
VL - 119
SP - 1219
EP - 1227
JO - Journal of applied physiology
JF - Journal of applied physiology
SN - 8750-7587
IS - 10
ER -