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ABSTRACT: McAuley, ABT, Hughes, DC, Tsaprouni, LG, Varley, I, Suraci, B, Bradley, B, Baker, J, Herbert, AJ, and Kelly, AL. Genetic associations with acceleration, change of direction, jump height, and speed in English academy football players. J Strength Cond Res 38(2): 350-359, 2024-High-intensity movements and explosive actions are commonly assessed during athlete development in football (soccer). Although many environmental factors underpin these power-orientated traits, research suggests that there is also a sizeable genetic component. Therefore, this study examined the association of 22 single-nucleotide polymorphisms (SNPs) with acceleration, change of direction, jump height, and speed in academy football players. One hundred and forty-nine, male, under-12 to under-23 football players from 4 English academies were examined. Subjects performed 5-, 10-, 20-, and 30-m sprints, countermovement jumps (CMJs), and the 5-0-5 agility test. Simple linear regression was used to analyze individual SNP associations, whereas both unweighted and weighted total genotype scores (TGS; TWGS) were computed to measure the combined influence of all SNPs. To control for multiple testing, a Benjamini-Hochberg false discovery rate of 0.05 was applied to all genotype model comparisons. In isolation, the GALNT13 (rs10196189) G allele and IL6 (rs1800795) G/G genotype were associated with faster (â¼4%) 5-, 10-, and 20-m sprints and higher (â¼16%) CMJs, respectively (p < 0.001). Furthermore, the TGS and TWGS significantly correlated with all performance assessments, explaining between 6 and 33% of the variance (p < 0.001). This study demonstrates that some genetic variants are associated with power-orientated phenotypes in youth football players and may add value toward a future polygenic profile of physical performance.
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Futebol , Adolescente , Masculino , Humanos , Aceleração , Academias e Institutos , AlelosRESUMO
BACKGROUND: Technical capabilities have significant discriminative and prognostic power in youth football. Although, many factors influence technical performance, no research has explored the genetic contribution. As such, the purpose of this study was to examine the association of several single nucleotide polymorphisms (SNPs) with technical assessments in youth football players. METHODS: Fifty-three male under-13 to under-18 outfield football players from two Category 3 English academies were genotyped for eight SNPs. Objective and subjective technical performance scores in dribbling, passing, and shooting were collated. Simple linear regression was used to analyse individual SNP associations each variable, whereas both unweighted and weighted total genotype scores (TGSs; TWGSs) were computed to measure the combined influence of all SNPs. RESULTS: In isolation, the ADBR2 (rs1042714) C allele, BDNF (rs6265) C/C genotype, DBH (rs1611115) C/C genotype, and DRD1 (rs4532) C allele were associated with superior (8-10%) objective dribbling and/or shooting performance. The TGSs and/or TWGSs were significantly correlated with each technical assessment (except subjective passing), explaining up to 36% and 40% of the variance in the objective and subjective assessments, respectively. CONCLUSIONS: The results of this study suggest inter-individual genetic variation may influence the technical capabilities of youth football players and proposes several candidate SNPs that warrant further investigation.
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Desempenho Atlético , Futebol Americano , Futebol , Adolescente , Humanos , Masculino , Polimorfismo de Nucleotídeo Único , Genótipo , AlelosRESUMO
The purpose of this study was to examine differences in the genotype frequency distribution of thirty-three single nucleotide variants (SNVs) between youth development phase (YDP) and professional development phase (PDP) academy football players. One hundred and sixty-six male football players from two Category 1 and Category 3 English academies were examined within their specific age phase: YDP (n = 92; aged 13.84 ± 1.63 years) and PDP (n = 74; aged 18.09 ± 1.51 years). Fisher's exact tests were used to compare individual genotype frequencies, whereas unweighted and weighted total genotype scores (TGS; TWGS) were computed to assess differences in polygenic profiles. In isolation, the IL6 (rs1800795) G allele was overrepresented in PDP players (90.5%) compared to YDP players (77.2%; p = 0.023), whereby PDP players had nearly three times the odds of possessing a G allele (OR = 2.83, 95% CI: 1.13-7.09). The TGS (p = 0.001) and TWGS (p < 0.001) were significant, but poor, in distinguishing YDP and PDP players (AUC = 0.643-0.694), with PDP players exhibiting an overall more power-orientated polygenic profile. If validated in larger independent youth football cohorts, these findings may have important implications for future studies examining genetic associations in youth football.
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Atletas , Futebol , Adolescente , Humanos , Masculino , Alelos , Variação GenéticaRESUMO
In this chapter we discuss the past, present and future of clinical biomarker development. We explore the advent of new technologies, paving the way in which health, medicine and disease is understood. This review includes the identification of physicochemical assays, current regulations, the development and reproducibility of clinical trials, as well as, the revolution of omics technologies and state-of-the-art integration and analysis approaches.
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Medicina de Precisão , Inteligência Artificial , Biomarcadores/análise , HumanosRESUMO
The aim of this review was to assess the association of ACTN3 R577X and ACE I/D polymorphisms with athlete status in football and determine which allele and/or genotypes are most likely to influence this phenotype via a meta-analysis. A comprehensive search identified 17 ACTN3 and 19 ACE studies. Significant associations were shown between the presence of the ACTN3 R allele and professional footballer status (OR = 1.35, 95% CI: 1.18-1.53) and the ACE D allele and youth footballers (OR = 1.18, 95% CI: 1.01-1.38). More specifically, the ACTN3 RR genotype (OR = 1.48, 95% CI: 1.23-1.77) and ACE DD genotype (OR = 1.29, 95% CI: 1.02-1.63) exhibited the strongest associations, respectively. These findings may be explained by the association of the ACTN3 RR genotype and ACE DD genotype with power-orientated phenotypes and the relative contribution of power-orientated phenotypes to success in football. As such, the results of this review provide further evidence that individual genetic variation may contribute towards athlete status and can differentiate athletes of different competitive playing statuses in a homogenous team-sport cohort. Moreover, the ACTN3 R577X and ACE I/D polymorphisms are likely (albeit relatively minor) contributing factors that influence athlete status in football.
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Actinina , Peptidil Dipeptidase A , Polimorfismo Genético , Futebol , Humanos , Actinina/genética , Alelos , Genótipo , Peptidil Dipeptidase A/genética , Futebol/fisiologiaRESUMO
Genetic variation is responsible for a large amount of the inter-individual performance disparities seen in sport. As such, in the last ten years genetic association studies have become more common; with one of the most frequently researched sports being football. However, the progress and methodological rigour of genetic association research in football is yet to be evaluated. Therefore, the aim of this paper was to identify and evaluate all genetic association studies involving football players and outline where and how future research should be directed. Firstly, a systematic search was conducted in the Pubmed and SPORTDiscus databases, which identified 80 eligible studies. Progression analysis revealed that 103 distinct genes have been investigated across multiple disciplines; however, research has predominately focused on the association of the ACTN3 or ACE gene. Furthermore, 55% of the total studies have been published within the last four years; showcasing that genetic association research in football is increasing at a substantial rate. However, there are several methodological inconsistencies which hinder research implications, such as; inadequate description or omission of ethnicity and on-field positions. Furthermore, there is a limited amount of research on several key areas crucial to footballing performance, in particular; psychological related traits. Moving forward, improved research designs, larger sample sizes, and the utilisation of genome-wide and polygenic profiling approaches are recommended. Finally, we introduce the Football Gene Project, which aims to address several of these limitations and ultimately facilitate greater individualised athlete development within football.
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Desempenho Atlético/fisiologia , Estudos de Associação Genética/estatística & dados numéricos , Futebol/fisiologia , Actinina/genética , Adolescente , Adulto , Desempenho Atlético/psicologia , Proteínas de Ciclo Celular/genética , Criança , Epigênese Genética , Feminino , Variação Genética , Estudo de Associação Genômica Ampla/estatística & dados numéricos , Humanos , Masculino , Proteínas Oncogênicas/genética , Peptidil Dipeptidase A/genética , Futebol/psicologia , Esportes , Adulto JovemRESUMO
Smoking is a major risk factor in many diseases. Genome wide association studies have linked genes for nicotine dependence and smoking behavior to increased risk of cardiovascular, pulmonary, and malignant diseases. We conducted an epigenome wide association study in peripheral-blood DNA in 464 individuals (22 current smokers and 263 ex-smokers), using the Human Methylation 450 K array. Upon replication in an independent sample of 356 twins (41 current and 104 ex-smokers), we identified 30 probes in 15 distinct loci, all of which reached genome-wide significance in the combined analysis P < 5 × 10(-8). All but one probe (cg17024919) remained significant after adjusting for blood cell counts. We replicated all 9 known loci and found an independent signal at CPOX near GPR15. In addition, we found 6 new loci at PRSS23, AVPR1B, PSEN2, LINC00299, RPS6KA2, and KIAA0087. Most of the lead probes (13 out of 15) associated with cigarette smoking, overlapped regions of open chromatin (FAIRE and DNaseI hypersensitive sites) or/and H3K27Ac peaks (ENCODE data set), which mark regulatory elements. The effect of smoking on DNA methylation was partially reversible upon smoking cessation for longer than 3 months. We report the first statistically significant interaction between a SNP (rs2697768) and cigarette smoking on DNA methylation (cg03329539). We provide evidence that the metSNP for cg03329539 regulates expression of the CHRND gene located circa 95 Kb downstream of the methylation site. Our findings suggest the existence of dynamic, reversible site-specific methylation changes in response to cigarette smoking , which may contribute to the extended health risks associated with cigarette smoking.
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Metilação de DNA , Polimorfismo de Nucleotídeo Único , Fumar/efeitos adversos , Adulto , Idoso , Idoso de 80 Anos ou mais , Ilhas de CpG , Epigênese Genética , Feminino , Estudo de Associação Genômica Ampla , Humanos , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Locos de Características Quantitativas , Análise de Sequência de RNARESUMO
Post-translational modifications of histones, particularly acetylation, are associated with the regulation of inflammatory gene expression. We used two animal models of inflammation of the bowel and biopsy samples from patients with Crohn's disease (CD) to study the expression of acetylated histones (H) 3 and 4 in inflamed mucosa. Acetylation of histone H4 was significantly elevated in the inflamed mucosa in the trinitrobenzene sulfonic acid model of colitis particularly on lysine residues (K) 8 and 12 in contrast to non-inflamed tissue. In addition, acetylated H4 was localised to inflamed tissue and to Peyer's patches (PP) in dextran sulfate sodium (DSS)-treated rat models. Within the PP, H3 acetylation was detected in the mantle zone whereas H4 acetylation was seen in both the periphery and the germinal centre. Finally, acetylation of H4 was significantly upregulated in inflamed biopsies and PP from patients with CD. Enhanced acetylation of H4K5 and K16 was seen in the PP. These results demonstrate that histone acetylation is associated with inflammation and may provide a novel therapeutic target for mucosal inflammation.