Department of Kinesiology, Muscle Physiology Laboratory, San Francisco State University, San Francisco, California.
Department of Pharmacy Practice, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, Michigan.
J Strength Cond Res. 2020 Jun;34(6):1574-1580. doi: 10.1519/JSC.0000000000003185.
Bagley, JR, Burghardt, KJ, McManus, R, Howlett, B, Costa, PB, Coburn, JW, Arevalo, JA, Malek, MH, and Galpin, AJ. Epigenetic responses to acute resistance exercise in trained vs. sedentary men. J Strength Cond Res 34(6): 1574-1580, 2020-Acute resistance exercise (RE) alters DNA methylation, an epigenetic process that influences gene expression and regulates skeletal muscle adaptation. This aspect of cellular remodeling is poorly understood, especially in resistance-trained (RT) individuals. The study purpose was to examine DNA methylation in response to acute RE in RT and sedentary (SED) young men, specifically targeting genes responsible for metabolic, inflammatory, and hypertrophic muscle adaptations. Vastus lateralis biopsies were performed before (baseline), 30 minutes after, and 4 hours after an acute RE bout (3 × 10 repetitions at 70% 1 repetition maximum [1RM] leg press and leg extension) in 11 RT (mean ± SEM: age = 26.1 ± 1.0 years; body mass = 84.3 ± 0.2 kg; leg press 1RM = 412.6 ± 25.9 kg) and 8 SED (age = 22.9 ± 1.1 years; body mass = 75.6 ± 0.3 kg; leg press 1RM = 164.8 ± 22.5 kg) men. DNA methylation was analyzed through methylation sensitive high-resolution melting using real-time polymerase chain reaction. Separate 2 (group) × 3 (time) repeated-measures analyses of variance and analyses of covariance were performed to examine changes in DNA methylation for each target gene. Results showed that acute RE (a) hypomethylated LINE-1 (measure of global methylation) in RT but not SED, (b) hypermethylated metabolic genes (GPAM and SREBF2) in RT, while lowering SREBF2 methylation in SED, and (c) did not affect methylation of genes associated with inflammation (IL-6 and TNF-α) or hypertrophy (mTOR and AKT1). However, basal IL-6 and TNF-α were lower in SED compared with RT. These findings indicate the same RE stimulus can illicit different epigenetic responses in RT vs. SED men and provides a molecular mechanism underpinning the need for differential training stimuli based on subject training backgrounds.
巴格利,JR,伯加德,KJ,麦克马纳斯,R,豪利特,B,科斯塔,PB,科伯恩,JW,阿雷瓦洛,JA,马利克,MH 和加尔平,AJ。急性抗阻运动对训练有素与久坐男性的 DNA 甲基化反应。J 力量与调理研究 34(6):1574-1580,2020-急性抗阻运动(RE)改变 DNA 甲基化,这是一种影响基因表达并调节骨骼肌适应的表观遗传过程。细胞重塑的这一方面尚不清楚,特别是在抗阻训练(RT)个体中。本研究的目的是检测 RT 和久坐(SED)年轻男性急性 RE 后的 DNA 甲基化反应,特别是针对代谢、炎症和肥大肌肉适应的基因。在一次急性 RE 运动(3×10 次重复,70%1 重复最大[1RM]腿推和腿伸展)前后 30 分钟和 4 小时,对 11 名 RT(平均±SEM:年龄=26.1±1.0 岁;体重=84.3±0.2kg;腿推 1RM=412.6±25.9kg)和 8 名 SED(年龄=22.9±1.1 岁;体重=75.6±0.3kg;腿推 1RM=164.8±22.5kg)男性的股外侧肌进行活检。通过实时聚合酶链反应使用甲基化敏感高分辨率熔解进行 DNA 甲基化分析。进行了 2(组)×3(时间)重复测量方差分析和协方差分析,以检查每个靶基因的 DNA 甲基化变化。结果表明,急性 RE(a)在 RT 中使 LINE-1 低甲基化(整体甲基化的测量),但在 SED 中没有,(b)在 RT 中使代谢基因(GPAM 和 SREBF2)高甲基化,同时降低 SED 中的 SREBF2 甲基化,(c)不影响与炎症(IL-6 和 TNF-α)或肥大(mTOR 和 AKT1)相关的基因的甲基化。然而,SED 中的基础 IL-6 和 TNF-α 低于 RT。这些发现表明,相同的 RE 刺激可以在 RT 与 SED 男性中引起不同的表观遗传反应,并为基于受试者训练背景的不同训练刺激提供了分子机制。