title: The ACTN3 genotype in soccer players in response to acute eccentric training.
abstract: Genetic factors can interfere with sporting performance. The identification of genetic predisposition of soccer players brings important information to trainers and coaches for individual training loads adjustment. Different responses to eccentric training could be observed by the genotype referred to as α-actinin-3 (ACTN3) in biomarkers of muscle damage, hormones and inflammatory responses. The aim of this study was to compare acute inflammatory responses, muscle damage and hormonal variations according to the eccentric training in soccer professional athletes with different genetic profiles of ACTN3 (XX, RX and RR). 37 soccer professional athletes (9 XX, 13 RX, 15 RR) were randomly divided into five stations associated to eccentric muscle contraction and plyometrics. Blood samples were taken from athletes pre-eccentric training, immediately after (post), 2- and 4-h post-eccentric training to determine hormone responses (cortisol and testosterone), muscle damage (CK and α-actin), and inflammatory responses (IL-6). After eccentric training, athletes XX presented higher levels for CK (4-h post), α-actin (post and 2-h post) and cortisol (post) compared to RR and RX athletes. However, RR and RX athletes presented higher levels of testosterone (post) and IL-6 (2 h post and 4 h post) compared to athletes XX. The main conclusion of this study is that professional soccer athletes homozygous to ACTN3XX gene are more susceptible to eccentric damage and present a higher catabolic state, demonstrated by metabolic, hormonal and immune responses post an eccentric training, in comparison to ACTN3RR and ACTN3RX groups.
authors.affiliation: Institute of Biomedicine (IBIOMED), University of León, León, Spain. empimenta@uol.com.br
authors.forename: Eduardo Mendonça
authors.initials: EM
authors.lastname: Pimenta
authors.forename: Daniel Barbosa
authors.initials: DB
authors.lastname: Coelho
authors.forename: Izinara Rosse
authors.initials: IR
authors.lastname: Cruz
authors.forename: Rodrigo Figueiredo
authors.initials: RF
authors.lastname: Morandi
authors.forename: Christiano Eduardo
authors.initials: CE
authors.lastname: Veneroso
authors.forename: Guilherme
authors.initials: G
authors.lastname: de Azambuja Pussieldi
authors.forename: Maria Raquel Santos
authors.initials: MR
authors.lastname: Carvalho
authors.forename: Emerson
authors.initials: E
authors.lastname: Silami-Garcia
authors.forename: José Antonio
authors.initials: JA
authors.lastname: De Paz Fernández
mesh_terms: D000185:Actinin / Q000235:genetics*; D000328:Adult; D000704:Analysis of Variance; D054874:Athletic Performance; D015415:Biomarkers / Q000097:blood; D001938:Brazil; D003402:Creatine Kinase / Q000097:blood; D020022:Genetic Predisposition to Disease; D006720:Homozygote; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D018836:Inflammation Mediators / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009119:Muscle Contraction; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009135:Muscular Diseases / Q000097:blood / Q000235:genetics / Q000503:physiopathology; D010641:Phenotype; D059385:Plyometric Exercise; D011110:Polymorphism, Genetic; D012916:Soccer; D013739:Testosterone / Q000097:blood; D013997:Time Factors; D055815:Young Adult
chemical_list: C118456:ACTN3 protein, human; D015415:Biomarkers; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D000185:Actinin; D013739:Testosterone; D003402:Creatine Kinase; D006854:Hydrocortisone