Evidence map›Paper›PMID 18202167›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2008

Skeletal muscle contractile protein function is preserved in human heart failure.

Yoko Okada, Michael J Toth, Peter Vanburen

Abstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Heart Failure-Induced Skeletal Muscle Wasting.Current heart failure reports · 2020
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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

3 authors at 1 institution in 1 country.

Yoko OkadaUniv. of Vermont, College of Medicine, Burlington, VT 05405, USA. vanburen@physiology.med.uvm.edu
Michael J Toth
Peter Vanburen
University of Vermont · US

Funding

Skeletal muscle contractile dysfunction in heart failureR01HL077418 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TOTH, MICHAEL J · 2006 to 2009
$1.5M
Myofibrillar Remodeling in Human Valvular Heart Disease:R01HL077637 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI VANBUREN, PETER C · 2004 to 2007
$1.5M
CONTRACTILE DYSFUNCTION IN ISCHEMIC HEART DISEASER01HL065586 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI VANBUREN, PETER C · 2000 to 2003
$1.3M
SKELETAL MUSCLE PROTEIN METABOLISM IN HEART FAILURER01AG017494 · NIA · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI TOTH, MICHAEL J · 1999 to 2001
$285k
NHLBI NIH HHS HL-077418NHLBI NIH HHS HL-65586NHLBI NIH HHS R01 HL065586NHLBI NIH HHS R01 HL077418NHLBI NIH HHS R01 HL077637NIA NIH HHS AG-17494
6 · The paper itself

Abstract

Skeletal muscle weakness is a common finding in patients with chronic heart failure (CHF). This functional deficit cannot be accounted for by muscle atrophy alone, suggesting that the syndrome of heart failure induces a myopathy in the skeletal musculature. To determine whether decrements in muscle performance are related to alterations in contractile protein function, biopsies were obtained from the vastus lateralis muscle of four CHF patients and four control patients. CHF patients exhibited reduced peak aerobic capacity and knee extensor muscle strength. Decrements in whole muscle strength persisted after statistical control for muscle size. Thin filaments and myosin were isolated from biopsies and mechanically assessed using the in vitro motility assay. Isolated skeletal muscle thin-filament function, however, did not differ between CHF patients and controls with respect to unloaded shortening velocity, calcium sensitivity, or maximal force. Similarly, no difference in maximal force or unloaded shortening velocity of isolated myosin was observed between CHF patients and controls. From these results, we conclude that skeletal contractile protein function is unaltered in CHF patients. Other factors, such as a decrease in total muscle myosin content, are likely contributors to the skeletal muscle strength deficit of heart failure.

Indexed as

AdultAgedAnimalsChronic DiseaseContractile ProteinsFemaleHeart FailureHumansIn Vitro TechniquesIsometric ContractionMaleMiddle AgedMuscle Fibers, Fast-TwitchMuscle Fibers, Slow-TwitchMuscle ProteinsMuscle, SkeletalContractile ProteinsMuscle ProteinsMyosin Heavy ChainsMyosin Light ChainsTroponin CTroponin ITroponin T

Identifiers

PMID18202167
PMCPMC2735408
OpenAlexW2141427431

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.