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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Muscle Androgen Receptor Content but Not Hormones Determine Exercise Response
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<blockquote data-quote="madman" data-source="post: 127053" data-attributes="member: 13851"><p><strong><span style="color: rgb(184, 49, 47)">Muscle Androgen Receptor Content but Not Systemic Hormones Is Associated With Resistance Training-Induced Skeletal Muscle Hypertrophy in Healthy, Young Men</span></strong></p><p></p><p></p><p>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 resistancetrained 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, preintervention, 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.Unlikeintramuscular 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.<strong><span style="color: rgb(184, 49, 47)"> 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.</span></strong></p><p></p><p></p><p><strong>CONCLUSION</strong></p><p></p><p>We performed backward elimination and principal component regression on a relatively large cohort (n = 49) of resistance-trained men and conclude that the post-exercise AUC (i.e., acute transient net hormonal exposure) and resting hormone concentrations measured in the blood do not share common variance with RET-induced changes in muscle mass. That is, systemic hormone concentrations are not related to, or in any way predictive of, RET-induced changes in muscle mass. Performing subset analysis on the highest- and lowest responders revealed that androgen receptor content, not intramuscular androgen levels, does not change with RET in trained participants but is significantly higher in HIR than LOR to RET. This study, in conjunction with others (Bamman et al., 2007; Petrella et al., 2008; Davidsen et al., 2011; Eynon et al., 2013), provides evidence that the relative increase in skeletal muscle mass following RET is underpinned by local intramuscular factors and not systemic hormonal concentrations.</p></blockquote><p></p>
[QUOTE="madman, post: 127053, member: 13851"] [B][COLOR=rgb(184, 49, 47)]Muscle Androgen Receptor Content but Not Systemic Hormones Is Associated With Resistance Training-Induced Skeletal Muscle Hypertrophy in Healthy, Young Men[/COLOR][/B] 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 resistancetrained 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, preintervention, 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.Unlikeintramuscular 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.[B][COLOR=rgb(184, 49, 47)] 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.[/COLOR][/B] [B]CONCLUSION[/B] We performed backward elimination and principal component regression on a relatively large cohort (n = 49) of resistance-trained men and conclude that the post-exercise AUC (i.e., acute transient net hormonal exposure) and resting hormone concentrations measured in the blood do not share common variance with RET-induced changes in muscle mass. That is, systemic hormone concentrations are not related to, or in any way predictive of, RET-induced changes in muscle mass. Performing subset analysis on the highest- and lowest responders revealed that androgen receptor content, not intramuscular androgen levels, does not change with RET in trained participants but is significantly higher in HIR than LOR to RET. This study, in conjunction with others (Bamman et al., 2007; Petrella et al., 2008; Davidsen et al., 2011; Eynon et al., 2013), provides evidence that the relative increase in skeletal muscle mass following RET is underpinned by local intramuscular factors and not systemic hormonal concentrations. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
Muscle Androgen Receptor Content but Not Hormones Determine Exercise Response
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