Evidence map›Paper›PMID 30327870›Full record

ReviewEuropean journal of applied physiology2019

More than a 'speed gene': ACTN3 R577X genotype, trainability, muscle damage, and the risk for injuries.

Juan Del Coso, Danielle Hiam, Peter Houweling, Laura M Pérez, Nir Eynon, Alejandro Lucía

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in European journal of applied physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 7 pooled it
8.0field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 7 syntheses or guidelines pooled it, 86 citations in OpenAlex.

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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

6 authors at 5 institutions in 2 countries.

Juan Del CosoExercise Physiology Laboratory, Camilo José Cela University, Madrid, Spain. jdelcoso@ucjc.edu.ORCID http://orcid.org/0000-0002-5785-984X
Danielle HiamInstitute for Health and Sport (iHeS), Victoria University, Melbourne, Australia.
Peter HouwelingMurdoch Childrens Research Institute, Melbourne, Australia.
Laura M PérezUniversidad Europea de Madrid (Faculty of Sport Sciences) and Research Institute i+12, Madrid, Spain.
Nir EynonInstitute for Health and Sport (iHeS), Victoria University, Melbourne, Australia.
Alejandro LucíaUniversidad Europea de Madrid (Faculty of Sport Sciences) and Research Institute i+12, Madrid, Spain.
Murdoch Children's Research Institute · AUCamilo José Cela University · ESCentro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable · ESUniversidad Europea de Madrid · ESVictoria University · AU

Funding

Ministerio de Economía, Industria y Competitividad, Gobierno de España PI15/00558National Health & Medical Research Council APP1140644
6 · The paper itself

Abstract

A common null polymorphism (rs1815739; R577X) in the gene that codes for α-actinin-3 (ACTN3) has been related to different aspects of exercise performance. Individuals who are homozygous for the X allele are unable to express the α-actinin-3 protein in the muscle as opposed to those with the RX or RR genotype. α-actinin-3 deficiency in the muscle does not result in any disease. However, the different ACTN3 genotypes can modify the functioning of skeletal muscle during exercise through structural, metabolic or signaling changes, as shown in both humans and in the mouse model. Specifically, the ACTN3 RR genotype might favor the ability to generate powerful and forceful muscle contractions. Leading to an overall advantage of the RR genotype for enhanced performance in some speed and power-oriented sports. In addition, RR genotype might also favor the ability to withstand exercise-induced muscle damage, while the beneficial influence of the XX genotype on aerobic exercise performance needs to be validated in human studies. More information is required to unveil the association of ACTN3 genotype with trainability and injury risk during acute or chronic exercise.

Indexed as

GenotypeActininAthletic InjuriesAthletic PerformanceHumansMuscle, SkeletalMutation, MissenseMyalgiaActininACTN3 protein, humanAthletic performanceCommon human polymorphismGenomicsMuscle performanceα-Actinin-3 deficiency

Identifiers

PMID30327870
OpenAlexW2897420591

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.