Evidence map›Paper›PMID 25749445›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2015

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

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 read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  17. Heart-lung interaction in a model of COPD: importance of lung volume and direct ventricular interaction.American journal of physiology. Heart and circulatory physiology · 2016
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Mike StembridgeCardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom; mstembridge@cardiffmet.ac.uk.
Philip N AinslieCentre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia Okanagan Campus, Kelowna, Canada;
Michael G HughesCardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom;
Eric J StöhrCardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom;
James D CotterSchool of Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand;
Michael M TymkoCentre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia Okanagan Campus, Kelowna, Canada; Department of Biology, Mount Royal University, Calgary, Canada; and.
Trevor A DayDepartment of Biology, Mount Royal University, Calgary, Canada; and.
Akke BakkerMIRA Institute, University of Twente, Twente, The Netherlands.
Rob ShaveCardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom;

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AltitudeAdultCardiac OutputExerciseFemaleHumansMaleMyocardial ContractionRestStroke VolumeVentricular Dysfunction, Lefthypoxialeft ventricular mechanicsstroke volume

Identifiers

PMID25749445
PMCPMC4816416

What OpenQuestion holds

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.