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肌肉雄激素受体含量而非全身激素与健康年轻男性抗阻训练诱导的骨骼肌肥大相关。

Muscle Androgen Receptor Content but Not Systemic Hormones Is Associated With Resistance Training-Induced Skeletal Muscle Hypertrophy in Healthy, Young Men.

作者信息

Morton Robert W, Sato Koji, Gallaugher Michael P B, Oikawa Sara Y, McNicholas Paul D, Fujita Satoshi, Phillips Stuart M

机构信息

Department of Kinesiology, McMaster University, Hamilton, ON, Canada.

Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.

出版信息

Front Physiol. 2018 Oct 9;9:1373. doi: 10.3389/fphys.2018.01373. eCollection 2018.

DOI:10.3389/fphys.2018.01373
PMID:30356739
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6189473/
Abstract

The factors that underpin heterogeneity in muscle hypertrophy following resistance exercise training (RET) remain largely unknown. We examined circulating hormones, intramuscular hormones, and intramuscular hormone-related variables in resistance-trained men before and after 12 weeks of RET. Backward elimination and principal component regression evaluated the statistical significance of proposed circulating anabolic hormones (e.g., testosterone, free testosterone, dehydroepiandrosterone, dihydrotestosterone, insulin-like growth factor-1, free insulin-like growth factor-1, luteinizing hormone, and growth hormone) and RET-induced changes in muscle mass ( = 49). Immunoblots and immunoassays were used to evaluate intramuscular free testosterone levels, dihydrotestosterone levels, 5α-reductase expression, and androgen receptor content in the highest- (HIR; = 10) and lowest- (LOR; = 10) responders to the 12 weeks of RET. No hormone measured before exercise, after exercise, pre-intervention, or post-intervention was consistently significant or consistently selected in the final model for the change in: type 1 cross sectional area (CSA), type 2 CSA, or fat- and bone-free mass (LBM). Principal component analysis did not result in large dimension reduction and principal component regression was no more effective than unadjusted regression analyses. No hormone measured in the blood or muscle was different between HIR and LOR. The steroidogenic enzyme 5α-reductase increased following RET in the HIR ( < 0.01) but not the LOR ( = 0.32). Androgen receptor content was unchanged with RET but was higher at all times in HIR. Unlike intramuscular free testosterone, dihydrotestosterone, or 5α-reductase, there was a linear relationship between androgen receptor content and change in LBM ( < 0.01), type 1 CSA ( < 0.05), and type 2 CSA ( < 0.01) both pre- and post-intervention. These results indicate that intramuscular androgen receptor content, but neither circulating nor intramuscular hormones (or the enzymes regulating their intramuscular production), influence skeletal muscle hypertrophy following RET in previously trained young men.

摘要

抗阻运动训练(RET)后肌肉肥大存在异质性的潜在因素在很大程度上仍不清楚。我们在12周RET训练前后,对接受抗阻训练的男性的循环激素、肌肉内激素以及与肌肉内激素相关的变量进行了检测。向后剔除法和主成分回归法评估了所提出的循环合成代谢激素(如睾酮、游离睾酮、脱氢表雄酮、双氢睾酮、胰岛素样生长因子-1、游离胰岛素样生长因子-1、促黄体生成素和生长激素)以及RET诱导的肌肉质量变化的统计学意义(n = 49)。免疫印迹法和免疫分析法用于评估12周RET训练中反应最高(HIR;n = 10)和最低(LOR;n = 10)的受试者的肌肉内游离睾酮水平、双氢睾酮水平、5α-还原酶表达以及雄激素受体含量。在最终模型中,无论是运动前、运动后、干预前还是干预后测量的激素,对于1型横截面积(CSA)、2型CSA或去脂去骨质量(LBM)的变化,均未始终表现出显著意义或始终被选中。主成分分析并未导致维度大幅降低,且主成分回归并不比未调整的回归分析更有效。HIR和LOR之间血液或肌肉中测量的激素没有差异。类固醇生成酶5α-还原酶在HIR组中RET训练后增加(P < 0.01),但在LOR组中未增加(P = 0.32)。雄激素受体含量在RET训练后未改变,但在HIR组中始终较高。与肌肉内游离睾酮、双氢睾酮或5α-还原酶不同,干预前后雄激素受体含量与LBM变化(P < 0.01)、1型CSA变化(P < 0.05)和2型CSA变化(P < 0.01)之间均存在线性关系。这些结果表明,在先前受过训练的年轻男性中,肌肉内雄激素受体含量而非循环激素或肌肉内激素(或调节其肌肉内产生的酶)影响RET训练后的骨骼肌肥大。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ad/6189473/5d35608a2251/fphys-09-01373-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ad/6189473/3178149ed1a7/fphys-09-01373-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ad/6189473/5c554f0f49d6/fphys-09-01373-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ad/6189473/0c0e77b29d5d/fphys-09-01373-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ad/6189473/5d35608a2251/fphys-09-01373-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ad/6189473/3178149ed1a7/fphys-09-01373-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ad/6189473/5c554f0f49d6/fphys-09-01373-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ad/6189473/0c0e77b29d5d/fphys-09-01373-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ad/6189473/5d35608a2251/fphys-09-01373-g004.jpg

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