Evidence map›Paper›PMID 22180761›Full record

ArticleBiophysical reviews2011

Mechanisms Of Residual Force Enhancement In Skeletal Muscle: Insights From Experiments And Mathematical Models.

Stuart G Campbell, Kenneth S Campbell

Abstract read
In one paragraph

Article in Biophysical reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–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

20 citing papers in PubMed.

  1. The distinctive mechanical and structural signatures of residual force enhancement in myofibers.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Article
  3. Eccentric muscle contractions: from single muscle fibre to whole muscle mechanics.Pflugers Archiv : European journal of physiology · 2023
    Review
  4. Article
  5. Article
  6. An Innovative Assessment of the Dynamics of Facial Movements in Surgically Managed Unilateral Cleft Lip and Palate Using 4D Imaging.The Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association · 2020
    Article
  7. Muscle thixotropy-where are we now?Journal of applied physiology (Bethesda, Md. : 1985) · 2019
    Review
  8. Article
  9. Article
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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

2 authors.

Stuart G CampbellDepartment of Physiology and the Center for Muscle Biology, University of Kentucky, Lexington, Kentucky.
Kenneth S Campbell

Funding

Kentucky Center for Clinical and Translational ScienceUL1TR001998 · NCATS · UNIVERSITY OF KENTUCKY · PI HARTMANN, KATHERINE E, KERN, PHILIP A · 2016 to 2025
$34.2M
Kentucky Center for Clinical and Translational ScienceUL1TR000117 · NCATS · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2012 to 2015
$13.3M
Myocardial Stiffness in Diastolic Heart FailureR01HL090749 · NHLBI · UNIVERSITY OF KENTUCKY · PI CAMPBELL, KENNETH S · 2008 to 2012
$1.6M
NCATS NIH HHS UL1 TR000117NCATS NIH HHS UL1 TR001998NHLBI NIH HHS R01 HL090749
6 · The paper itself

Abstract

A skeletal muscle that is stretched while contracting will produce more force at steady state than if it is stretched passively and then stimulated to contract. This phenomenon is known as residual force enhancement and has been widely studied since its description more than sixty years ago. The idea that the mechanical properties of a muscle are governed not just by its present length but also by its length at earlier time points has far reaching implications since muscles stretch and shorten routinely in normal use. In this review, we present the experimental and theoretical advances that have been made toward understanding the mechanisms that underlie residual force enhancement. In the past ten years, experiments and models have focused on essentially three candidate mechanisms for residual force enhancement: (half-) sarcomere inhomogeneity, activity of so-called 'passive' mechanical elements in the sarcomere (titin), and the intrinsic properties of myosin crossbridges. Evidence, both computational and experimental, is accumulating for each of these mechanisms such that a final description of the phenomenon seems attainable in the near future. We conclude that computational models that incorporate more than one putative mechanism may ultimately facilitate reconciliation of the growing number of ideas and experimental data in this field.

Identifiers

PMID22180761
PMCPMC3237401

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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.