Evidence map›Paper›PMID 19919996›Full record

ArticleCirculation. Heart failure2009

Mechanisms underlying skeletal muscle weakness in human heart failure: alterations in single fiber myosin protein content and function.

Mark S Miller, Peter Vanburen, Martin M Lewinter, Stewart H Lecker, Donald E Selby, Bradley M Palmer, David W Maughan, Philip A Ades, Michael J Toth

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation. Heart failure, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 12% 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

66 citing papers in PubMed, 2 syntheses or guidelines pooled it, 95 citations in OpenAlex.

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6 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Mark S MillerDepartments of Molecular Physiology and Biophysics and Medicine, University of Vermont, College of Medicine, Burlington, Vt, USA.
Peter Vanburen
Martin M Lewinter
Stewart H Lecker
Donald E Selby
Bradley M Palmer
David W Maughan
Philip A Ades
Michael J Toth
Beth Israel Deaconess Medical Center · US

Funding

WEIGHT MAINTENANCE AND PSYCHOLOGICAL BENEFITS OF EXERCISEM01RR000109 · NCRR · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI DUMAS, JULIE A · 1985 to 2010
$24.3M
Proteomics Core for Neuroscience P20 RR16435P20RR016435 · NCRR · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI SPEES, JEFFREY L · 2001 to 2010
$23.5M
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 P20 RR016435NCRR NIH HHS RR-00109NCRR NIH HHS RR-16435NHLBI NIH HHS HL-077418NHLBI NIH HHS R01 HL077418NIA NIH HHS AG-031303NIA NIH HHS K01 AG031303
6 · The paper itself

Abstract

backgroundPatients with chronic heart failure (HF) frequently experience skeletal muscle weakness that limits physical function. The mechanisms underlying muscle weakness, however, have not been clearly defined. METHODS AND

resultsThis study examined the hypothesis that HF promotes a loss of myosin protein from single skeletal muscle fibers, which in turn reduces contractile performance. Ten patients with chronic HF and 10 controls were studied. Muscle atrophy was not evident in patients, and groups displayed similar physical activity levels, suggesting that observed differences reflect the effects of HF and not muscle atrophy or disuse. In single muscle fibers, patients with HF showed reduced myosin heavy chain protein content (P<0.05) that manifested as a reduction in functional myosin-actin cross-bridges (P<0.05). No evidence was found for a generalized loss of myofilament protein, suggesting a selective loss of myosin. Accordingly, single muscle fiber maximal Ca(2+)-activated tension was reduced in myosin heavy chain I fibers in patients (P<0.05). However, tension was maintained in myosin heavy chain IIA fibers in patients because a greater proportion of available myosin heads were bound to actin during Ca(2+) activation (P<0.01).

conclusionsCollectively, our results show that HF alters the quantity and functionality of the myosin molecule in skeletal muscle, leading to reduced tension in myosin heavy chain I fibers. Loss of single fiber myosin protein content represents a potential molecular mechanism underlying muscle weakness and exercise limitation in patients with HF.

Indexed as

Muscle ContractionMuscle StrengthActin CytoskeletonActinsAgedCase-Control StudiesChronic DiseaseDown-RegulationExercise ToleranceFemaleHeart FailureHumansMaleMiddle AgedMuscle Fibers, SkeletalMuscle WeaknessActinsMyosin Heavy Chains

Identifiers

PMID19919996
PMCPMC2782533
OpenAlexW2159978090

What OpenQuestion holds

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LicenceTDM
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.