Evidence map›Paper›PMID 15083369›Full record

Trial reportEuropean journal of applied physiology2004

Exploration of myostatin polymorphisms and the angiotensin-converting enzyme insertion/deletion genotype in responses of human muscle to strength training.

Martine A I Thomis, Wim Huygens, Sofie Heuninckx, Monique Chagnon, Hermine H M Maes, Albrecht L Claessens, Robert Vlietinck, Claude Bouchard, Gaston P Beunen

Abstract readClinical TrialRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in European journal of applied physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 85 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. An intron variant of the GLI family zinc finger 3 (GLI3) gene differentiates resistance training-induced muscle fiber hypertrophy in younger men.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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  10. Review
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  14. The ACE gene and human performance: 12 years on.Sports medicine (Auckland, N.Z.) · 2011
    Review
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  17. Article
  18. Association between ACE D allele and elite short distance swimming.European journal of applied physiology · 2009
    Article
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  20. 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

9 authors at 3 institutions in 3 countries.

Martine A I ThomisDepartment of Sport and Movement Sciences, Faculty of Physical Education and Physiotherapy, Katholieke Universiteit Leuven, Tervuursevest 101, 3001, Leuven, Belgium. martine.thomis@flok.kuleuven.ac.be
Wim Huygens
Sofie Heuninckx
Monique Chagnon
Hermine H M Maes
Albrecht L Claessens
Robert Vlietinck
Claude Bouchard
Gaston P Beunen
KU Leuven · BEPennington Biomedical Research Center · USVirginia Commonwealth University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study explores the associations between polymorphisms in two candidate genes-myostatin gene (MSTN or GDF8) and angiotensin-converting enzyme (ACE) gene-with interindividual differences in human muscle mass and strength responses to strength training. The MSTN AluI A55T (exon 1), BanII K153R, TaqI E164 K and BstNI P198A (all in exon 2) markers and the ACE insertion (I)/deletion (D) polymorphism were typed in 57 males [22.4 (3.7) years] who participated in a 10-week, high-resistance training program for the elbow flexors. Maximal strength, and maximal isometric and concentric elbow flexor torques were measured at baseline and after training. Information on muscle cross-sectional area of the upper arm was obtained by computer tomography scans. Only one individual was heterozygous for the MSTN BanII K153R variant. No allelic variant was detected at the other MSTN sites in this population. For the ACE I/D polymorphism, no evidence was found for an association of the D or I allele with baseline strength, isometric and concentric torque or arm muscle cross-sectional area [analysis of covariance (ANCOVA) 0.25< P<0.97]. Responses to the strength-training program were not associated with the ACE I/D genotype (ANCOVA 0.057< P<0.70). Borderline significance was found for larger strength gains in dynamic flexion torques for I/I genotypes. This study therefore does not support the hypothesis that an increased muscle fiber hypertrophic effect of strength training is present in D-allele carriers.

Indexed as

Adaptation, PhysiologicalAdultDNA Transposable ElementsExerciseFemaleGene Expression RegulationGenotypeHumansMaleMuscle ContractionMuscle, SkeletalMyostatinPeptidyl-Dipeptidase APhysical Education and TrainingPhysical ExertionPolymorphism, GeneticDNA Transposable ElementsMSTN protein, humanMyostatinPeptidyl-Dipeptidase ATransforming Growth Factor beta

Identifiers

PMID15083369
OpenAlexW1977671873

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.