Evidence map›Paper›PMID 20724360›Full record

ArticleThe Journal of physiology2010

Chronic heart failure decreases cross-bridge kinetics in single skeletal muscle fibres from humans.

Mark S Miller, Peter VanBuren, Martin M LeWinter, Joan M Braddock, Philip A Ades, David W Maughan, Bradley M Palmer, Michael J Toth

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
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

54 citing papers in PubMed, 74 citations in OpenAlex.

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  19. Influenza Infection has Fiber Type-Specific Effects on Cellular and Molecular Skeletal Muscle Function in Aged Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020
    Article
  20. Heart Failure-Induced Skeletal Muscle Wasting.Current heart failure reports · 2020
    Review
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

8 authors at 2 institutions in 2 countries.

Mark S MillerDepartment of Molecular Physiology, University of Vermont, Burlington, VT 05405, USA.
Peter VanBuren
Martin M LeWinter
Joan M Braddock
Philip A Ades
David W Maughan
Bradley M Palmer
Michael J Toth
Institute of Molecular Biology and Biophysics · RUUniversity of Vermont · US

Funding

WEIGHT MAINTENANCE AND PSYCHOLOGICAL BENEFITS OF EXERCISEM01RR000109 · NCRR · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI KIRKPATRICK, BETH DIANE · 1985 to 2010
$24.3M
Cardiomyocyte Zinc and its Regulation of Contraction-Relaxation FunctionR01HL086902 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI PALMER, BRADLEY M · 2008 to 2012
$1.9M
Skeletal muscle contractile dysfunction in heart failureR01HL077418 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TOTH, MICHAEL J · 2006 to 2009
$1.5M
Single Skeletal Muscle Fiber Mechanics and Myosin Kinetics in Human AgingK01AG031303 · NIA · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI MILLER, MARK STUART · 2008 to 2012
$611k
NCRR NIH HHS M01 RR000109NCRR NIH HHS RR-00109NHLBI NIH HHS HL-077418NHLBI NIH HHS HL-086902NHLBI NIH HHS R01 HL077418NHLBI NIH HHS R01 HL086902NIA NIH HHS AG-031303NIA NIH HHS K01 AG031303
6 · The paper itself

Abstract

Skeletal muscle function is impaired in heart failure patients due, in part, to loss of myofibrillar protein content, in particular myosin. In the present study, we utilized small-amplitude sinusoidal analysis for the first time in single human skeletal muscle fibres to measure muscle mechanics, including cross-bridge kinetics, to determine if heart failure further impairs contractile performance by altering myofibrillar protein function. Patients with chronic heart failure (n = 9) and controls (n = 6) were recruited of similar age and physical activity to diminish the potentially confounding effects of ageing and muscle disuse. Patients showed decreased cross-bridge kinetics in myosin heavy chain (MHC) I and IIA fibres, partially due to increased myosin attachment time (t(on)). The increased t(on) compensated for myosin protein loss previously found in heart failure patients by increasing the fraction of the total cycle time myosin is bound to actin, resulting in a similar number of strongly bound cross-bridges in patients and controls. Accordingly, isometric tension did not differ between patients and controls in MHC I or IIA fibres. Patients also had decreased calcium sensitivity in MHC IIA fibres and alterations in the viscoelastic properties of the lattice structure of MHC I and IIA fibres. Collectively, these results show that heart failure alters skeletal muscle contraction at the level of the myosin-actin cross-bridge, leading to changes in muscle mechanics which could contribute to impaired muscle function. Additionally, we uncovered a unique kinetic property of MHC I fibres, a potential indication of two distinct populations of cross-bridges, which may have important physiological consequences.

Indexed as

AgingFemaleHeart FailureHumansKineticsMaleMuscle ContractionMuscle Fibers, SkeletalMuscle, SkeletalMyosin Heavy ChainsMyosin Heavy Chains

Identifiers

PMID20724360
PMCPMC3000591
OpenAlexW1608092539

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.