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 (n = 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; n = 10) and lowest- (LOR; n = 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 (P < 0.01) but not the LOR (P = 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 (P < 0.01), type 1 CSA (P < 0.05), and type 2 CSA (P < 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.
Highlights
MATERIALS AND METHODSThere is substantial individual variability in resistance exercise training (RET)-induced skeletal muscle hypertrophy (Hubal et al, 2005; Davidsen et al, 2011)
We found that high responders (HIR) had increased 5α-reductase content following 12 weeks of RET and had significantly higher androgen receptor content, which did not change with RET, than low responders (LOR) both prior to- and after-RET (Figure 3)
Consistent with previous work, we propose instead that the magnitude of RET-induced skeletal muscle hypertrophy is modulated in part by intramuscular androgen receptor content (Figure 4) and likely other intramuscular variables
Summary
There is substantial individual variability in RET-induced skeletal muscle hypertrophy (Hubal et al, 2005; Davidsen et al, 2011). The post-exercise rise in circulating, presumably anabolic, hormones (e.g., T, GH, and IGF-1) are believed to be causative in determining RET-induced skeletal muscle hypertrophy (Kraemer et al, 2017; Mangine et al, 2017). The RETinduced increase in intramuscular androgen receptor content has been significantly correlated with RET-induced muscle hypertrophy (Ahtiainen et al, 2011; Mitchell et al, 2013). It may be that an increase in intramuscular androgens and/or their receptors, via an autocrine mechanism, are important in determining RET-induced hypertrophy
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
