Evidence map›Paper›PMID 22461439›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012

Skeletal muscle mitochondrial density, gene expression, and enzyme activities in human heart failure: minimal effects of the disease and resistance training.

Michael J Toth, Mark S Miller, Kimberly A Ward, Philip A Ades

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  13. Frontiers in physiology · 2017
    Review
  14. Article
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  16. Article
  17. Exercise training in chronic heart failure: improving skeletal muscle O2 transport and utilization.American journal of physiology. Heart and circulatory physiology · 2015
    Review
  18. Article
  19. 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

4 authors at 1 institution in 1 country.

Michael J TothDepartment of Medicine, College of Medicine, University of Vermont, Burlington, VT, USA.
Mark S Miller
Kimberly A Ward
Philip A Ades
University of Vermont · US

Funding

Center for Neuroscience ExcellenceP30GM103498 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI PARSONS, RODNEY L · 2012 to 2015
$4.3M
Skeletal muscle contractile dysfunction in heart failureR01HL077418 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TOTH, MICHAEL J · 2006 to 2009
$1.5M
NCRR NIH HHS RR-00109NCRR NIH HHS RR-032135NHLBI NIH HHS HL-077418NHLBI NIH HHS R01 HL077418NIGMS NIH HHS GM-103498
6 · The paper itself

Abstract

Impaired skeletal muscle energetics could adversely affect physical and metabolic function in patients with heart failure (HF). The effect of HF on aspects of mitochondrial structure and function, independent of muscle disuse and other disease-related confounding factors, however, is unclear. Moreover, no study has evaluated whether resistance exercise training, a modality that increases functional capacity, might derive its benefits through modulation of mitochondrial structure and function. Thirteen HF patients and 14 age- and physical activity-matched controls were evaluated for skeletal muscle mitochondrial size/content, gene expression, and enzyme activity before and after an 18-wk resistance exercise-training program. At baseline, HF patients and controls had similar mitochondrial fractional areas, although HF patients had larger average mitochondrion size (P < 0.05) and a trend toward a reduced number of mitochondria (P ≤ 0.10). No differences in the expression of transcriptional regulators or cytochrome oxidase subunits or the activity of mitochondrial and cytosolic enzymes were noted. Relationships among transcriptional regulators suggested that networks controlling mitochondrial content and gene expression are intact. Resistance training increased (P < 0.01) mitochondrial transcription factor A expression in patients and controls, and this increase was related to improvements in muscle strength (P = 0.05). Training did not, however, alter mitochondrial size/content, enzyme activities, or expression of other transcriptional regulators. In conclusion, our results suggest that the HF syndrome has minimal effects on skeletal muscle mitochondrial biology when the confounding effects of muscle disuse and other disease-related factors are removed. Moreover, the beneficial effects of resistance training on physical function in HF patients and controls are likely not related to alterations in mitochondrial biology.

Indexed as

Gene Expression Regulation, EnzymologicResistance TrainingAgedEnzyme ActivationFemaleHeart FailureHumansMaleMitochondria, HeartMitochondria, MuscleMuscle, SkeletalMuscle StrengthOxygen Consumption

Identifiers

PMID22461439
PMCPMC3379153
OpenAlexW2123340661

What Socratic 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 Socratic graph.