Department of Genetics, Physical Anthropology and Animal Physiology, Faculty of Science and Technology, University of the Basque Country (UPV/EHU), Leioa, SPAIN.
Med Sci Sports Exerc. 2018 Feb;50(2):361-368. doi: 10.1249/MSS.0000000000001434.
This study aimed to investigate the association of candidate single nucleotide polymorphisms (SNP) with noncontact hamstring muscle injuries in elite soccer players and to create and validate a model to assess the risk of hamstring injury.
A total of 107 elite male outfield players were prospectively followed for six seasons. Players were genotyped for 37 SNP previously investigated in relation to musculoskeletal injuries. The association of SNP, previous injury, age, level of play, position, and anthropometric data with 129 hamstring injuries (413 observations) was investigated in the discovery phase (2010-2015), and a multivariable Cox frailty model was created using forward selection. The model's discriminative ability was tested in the validation phase (2015-2016, 31 injuries, 98 observations) using Harrell's C index.
Five SNP were found to be significantly associated with hamstring injury in a multivariable model: matrix metalloproteinase 3 rs679620 (A vs G, hazard ratio [HR] = 2.06, 95% confidence interval [CI] = 1.51-2.81), tenascin C rs2104772 (A vs T, HR = 1.65, 95% CI = 1.17-2.32), interleukin 6 rs1800795 (GG vs GC + CC, HR = 1.68, 95% CI = 1.11-2.53), nitric oxide synthase 3 rs1799983 (G vs T, HR = 1.35, 95% CI = 1.01-1.79), and hypoxia-inducible factor-1α rs11549465 (CC vs CT, HR = 2.08, 95% CI = 1.00-4.29). Age also entered the model (≥24 vs <24 yr, HR = 2.10, 95% CI = 1.29-3.42). The model showed acceptable discrimination in the discovery phase (C index = 0.74), but not in the validation phase (C index = 0.52).
Genetic variants appear to be involved in the etiology of hamstring injuries but were not found to have predictive value by themselves. Further research, increasing the number of genetic variants and including environmental factors in complex multifactorial risk models, is necessary.
本研究旨在探讨候选单核苷酸多态性(SNP)与精英足球运动员非接触性腘绳肌损伤的关系,并建立和验证一种评估腘绳肌损伤风险的模型。
前瞻性随访 107 名精英男性外场球员 6 个赛季。对 37 个先前与肌肉骨骼损伤相关的 SNP 进行了基因分型。在发现阶段(2010-2015 年),研究了 SNP、既往损伤、年龄、比赛水平、位置和人体测量数据与 129 例腘绳肌损伤(413 次观察)的关联,并使用向前选择创建了多变量 Cox 脆弱性模型。在验证阶段(2015-2016 年,31 例损伤,98 次观察)使用 Harrell 的 C 指数测试了该模型的判别能力。
在多变量模型中,有 5 个 SNP 与腘绳肌损伤显著相关:基质金属蛋白酶 3 rs679620(A 对 G,风险比[HR] = 2.06,95%置信区间[CI] = 1.51-2.81), tenascin C rs2104772(A 对 T,HR = 1.65,95% CI = 1.17-2.32),白细胞介素 6 rs1800795(GG 对 GC + CC,HR = 1.68,95% CI = 1.11-2.53),一氧化氮合酶 3 rs1799983(G 对 T,HR = 1.35,95% CI = 1.01-1.79)和缺氧诱导因子-1α rs11549465(CC 对 CT,HR = 2.08,95% CI = 1.00-4.29)。年龄也进入了模型(≥24 岁 vs <24 岁,HR = 2.10,95% CI = 1.29-3.42)。该模型在发现阶段具有可接受的判别能力(C 指数= 0.74),但在验证阶段(C 指数= 0.52)则不然。
遗传变异似乎与腘绳肌损伤的病因有关,但本身并没有预测价值。需要进一步研究,增加遗传变异的数量,并将环境因素纳入复杂的多因素风险模型中。