Evidence map›Paper›PMID 27913923›Full record

ArticleEuropean journal of applied physiology2017

ACTN3 X-allele carriers had greater levels of muscle damage during a half-ironman.

Juan Del Coso, Juan José Salinero, Beatriz Lara, César Gallo-Salazar, Francisco Areces, Carlos Puente, David Herrero

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In one paragraph

Article in European journal of applied physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 4 pooled it
3.3field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 4 syntheses or guidelines pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Alpha-Actinin-3 Deficiency Links Genetic Susceptibility to Renal Fibrosis: Evidence From Hemodialysis Patients and Murine Models.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  15. Effect ofGenes · 2021
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  18. Effect ofSports (Basel, Switzerland) · 2020
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  20. Genes · 2019
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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

7 authors at 2 institutions in 1 country.

Juan Del CosoExercise Physiology Laboratory, Camilo José Cela University, C/Castillo de Alarcon, 49, Villafranca del Castillo, 28692, Madrid, Spain. jdelcoso@ucjc.edu.ORCID http://orcid.org/0000-0002-5785-984X
Juan José SalineroExercise Physiology Laboratory, Camilo José Cela University, C/Castillo de Alarcon, 49, Villafranca del Castillo, 28692, Madrid, Spain.
Beatriz LaraExercise Physiology Laboratory, Camilo José Cela University, C/Castillo de Alarcon, 49, Villafranca del Castillo, 28692, Madrid, Spain.
César Gallo-SalazarExercise Physiology Laboratory, Camilo José Cela University, C/Castillo de Alarcon, 49, Villafranca del Castillo, 28692, Madrid, Spain.
Francisco ArecesExercise Physiology Laboratory, Camilo José Cela University, C/Castillo de Alarcon, 49, Villafranca del Castillo, 28692, Madrid, Spain.
Carlos PuenteExercise Physiology Laboratory, Camilo José Cela University, C/Castillo de Alarcon, 49, Villafranca del Castillo, 28692, Madrid, Spain.
David HerreroExercise Physiology Laboratory, Camilo José Cela University, C/Castillo de Alarcon, 49, Villafranca del Castillo, 28692, Madrid, Spain.
Camilo José Cela University · ESCamilo José Cela University · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAlpha-actinin-3, encoded by the ACTN3 gene, is an actin-binding protein with an important role in myofibril contraction and muscle force output. In humans, there is a relatively common deficiency of the α-actinin-3 due to homozygosity in a polymorphism of the ACTN3 gene (R577X, rs1815739), that has been related to decreased resistance to strain during voluntary muscle contractions. The purpose of this study was to investigate the influence of the ACTN3 genotype on the level of exercise-induced muscle damage attained by 23 experienced triathletes during an official half-ironman competition.

methodsBefore and after the race, a sample of venous blood was obtained and jump height was measured during a countermovement jump. The changes in serum creatine kinase (CK-MM isoform) were measured in the blood samples and muscle pain was measured with a visual analogue scale (0-10 cm). Data from RX heterozygotes and XX mutant homozygotes were grouped as X-allele carriers (n = 13) and compared to RR homozygotes (n = 10).

resultsRace time was very similar between groups (313 ± 31 vs. 313 ± 25 min; P = 0.45); however, pre-to-post-competition reduction in jump height was greater in X-allele carriers than RR homozygotes (-18.4 ± 11.4 vs. -8.2 ± 6.9%; P = 0.04). At the end of the race, X-allele carriers presented higher serum CK-MM concentrations (682 ± 144 vs. 472 ± 269 U/L; P = 0.03), and there was also a tendency for higher self-reported values of lower limb muscle pain (7.7 ± 1.1 vs. 6.3 ± 2.3 cm; P = 0.06).

conclusionsX-allele triathletes in the ACTN3 R577X polymorphism presented greater signs of exercise-induced muscle damage during a half-ironman race than RR homozygotes.

Indexed as

ExerciseHeterozygotePolymorphism, Single NucleotideActininAdolescentAdultAllelesCase-Control StudiesFemaleHumansMaleMiddle AgedMuscle FatigueActininACTN3 protein, humanEndurance performanceMuscle fatigueRhabdomyolysisSingle nucleotide polymorphismTriathlon

Identifiers

PMID27913923
OpenAlexW2557315984

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.