Evidence map›Paper›PMID 28771742›Full record

ArticleThe Journal of physiology2017

Experimental and modelling evidence of shortening heat in cardiac muscle.

Kenneth Tran, June-Chiew Han, Edmund John Crampin, Andrew James Taberner, Denis Scott Loiselle

Abstract read
In one paragraph

Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

19 citing papers in PubMed.

  1. Review
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  6. Sex differences in ventricular muscle energetics in a type 2 diabetic rat model.Cardiovascular diabetology. Endocrinology reports · 2025
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  11. Review
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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

5 authors.

Kenneth TranAuckland Bioengineering Institute, Auckland, New Zealand.ORCID 0000-0002-8651-3557
June-Chiew HanAuckland Bioengineering Institute, Auckland, New Zealand.ORCID 0000-0002-6396-7628
Edmund John CrampinSystems Biology Laboratory, Melbourne School of Engineering, Parkville, Australia.
Andrew James TabernerAuckland Bioengineering Institute, Auckland, New Zealand.
Denis Scott LoiselleAuckland Bioengineering Institute, Auckland, New Zealand.ORCID 0000-0002-6928-4019

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key pointsHeat associated with muscle shortening has been repeatedly demonstrated in skeletal muscle, but its existence in cardiac muscle remains contentious after five decades of study. By iterating between experiments and computational modelling, we show compelling evidence for the existence of shortening heat in cardiac muscle and reveal, mechanistically, the source of this excess heat. Our results clarify a long-standing uncertainty in the field of cardiac muscle energetics. We provide a revised partitioning of cardiac muscle energy expenditure to include this newly revealed thermal component. ABSTRACT: When a muscle shortens against an afterload, the heat that it liberates is greater than that produced by the same muscle contracting isometrically at the same level of force. This excess heat is defined as 'shortening heat', and has been repeatedly demonstrated in skeletal muscle but not in cardiac muscle. Given the micro-structural similarities between these two muscle types, and since we imagine that shortening heat is the thermal accompaniment of cross-bridge cycling, we have re-examined this issue. Using our flow-through microcalorimeter, we measured force and heat generated by isolated rat trabeculae undergoing isometric contractions at different muscle lengths and work-loop (shortening) contractions at different afterloads. We simulated these experimental protocols using a thermodynamically constrained model of cross-bridge cycling and probed the mechanisms underpinning shortening heat. Predictions generated by the model were subsequently validated by a further set of experiments. Both our experimental and modelling results show convincing evidence for the existence of shortening heat in cardiac muscle. Its magnitude is inversely related to the afterload or, equivalently, directly related to the extent of shortening. Computational simulations reveal that the heat of shortening arises from the cycling of cross-bridges, and that the rate of ATP hydrolysis is more sensitive to change of muscle length than to change of afterload. Our results clarify a long-standing uncertainty in the field of cardiac muscle energetics.

Indexed as

Energy MetabolismHot TemperatureModels, CardiovascularMyocardial ContractionAdenosine TriphosphateAnimalsCytoskeletonMaleRatsRats, Sprague-DawleyThermodynamicsAdenosine Triphosphatecardiac energeticscross-bridge modelpartitioning heat

Identifiers

PMID28771742
PMCPMC5621496

What OpenQuestion holds

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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.