Testosterone Propionate Treatment Reverses Myocardial Antioxidant Defenses

Genetic Freak

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Androgens Increase Oxidative Stress in Heart Tissue

This study shows that in adolescent male rats: (1) all potentially beneficial effects of endurance training on the enzymatic components of the antioxidant defence system in the heart left ventricle are reversed by chronic high-dose testosterone propionate treatment and (2) none of the potentially detrimental effects of the training on the left ventricular antioxidant barrier are considerably counteracted by this treatment. These results imply that anabolic androgen use among adolescents, either alone or in combination with endurance training, may elevate oxidative stress-related risk to cardiac health.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085793/pdf/12012_2011_Article_9105.pdf

Interestingly, serum TT levels in the rats treated with the lower TP dose were, 9 days after the last dose, several times higher than those found during the first week following the injection of the same TP dose to naıve young adult male rats (Langfort et al., unpublished data). This shows extensive buildup of serum testosterone with weekly TP doses, which is in clear contrast with the need for administration of TP at 2- to 3-day intervals in humans with the aim of attaining reasonably stable TT levels.
 
I wonder if the ester is specific as they don't report others, and if this should seriously change the way everyone doses testosterone... If test p is building up with weekly (or less) dosing, would that also mean that longer esters build up with weekly dosing also (since weekly test e dosing is by far the most common test supplementation routine). I would be interested to see if there is other studies with similar results, also with longer esters to see if it translates...
 
Thanks for posting GF.

Pretty much what we'd expect to see I think. However some surprises include:

"there was no statistically significant interaction between endurance training and TP treatment effects on either the LV MDA or LV nonenzymatic antioxidants’ levels. This result shows additivity of these manipulations and suggests no benefit, in terms of cardioprotection, from endurance training when combined with AAS use. In line with our observations, it has been shown that nandrolone decanoate treatment interferes with cardiac renin-angiotensin system and impairs the beneficial effect of another type of aerobic training (swimming) in young adult rats."

While this again supports the use of an ARB to block the effect of AAS on cardiac RAS, I'm not entirely convinced that even without it, endurance training will have no benefit in humans. It's shameful they won't perform these studies on willing participants.

Of interest in highlighting the difficulties with the rodent model was the finding that exogenous TP had little effect on rat E2 - this is rarely the case in humans and may have something to do with the distribution and concentration of fat and aromatase.

Also the finding that total test was more a reliable marker than free test of biological activity was interesting, though I wonder whether it really has any implications for humans:

"The traditional view holds that only FT represents biologically active testosterone. However, there was a high positive correlation between serum TT and FT levels in this study, and the correlation coefficients between the other indices measured and FT or TT level were, pair wise, remarkably similar (not shown), except that there was no significant correlation between serum FT and E2 levels (R = 0.22, P = 0.18 ). Thus, our data support the view that serum TT accurately reflects biologically active testosterone in adolescent rats."
 
. In line with our observations, it has been shown that nandrolone decanoate treatment interferes with cardiac renin-angiotensin system and impairs the beneficial effect of another type of aerobic training (swimming) in young adult rats."

"The traditional view holds that only FT represents biologically active testosterone".



Regards nandrolone interfering with cardiac renin-angiotensin system, could this contribute to elevated BP synonymous with nandrolone..?

Regarding free test: It is generally accepted that it is the unbound or free hormone that is biologically active, and that hormone binding delays metabolism and provides a circulating reservoir of hormones. More recently, it has been suggested that the specific binding globulins are not just passive transporters but may interact with membrane receptors and that hormone binding to the globulins initiates a signal transduction pathway..
 
Well, not just Nandrolone but all AAS, yes. AAS effects on RAS is one of the key things we've been discussing on here regarding the deleterious cardiac side effects and the recommendation to use an ARB.

I've read a few papers discussing the functional aspects of the globulin complex (an idea which seems pretty obvious when you think about it), but it'll be nice to see some more in vivo stuff. And also the implications to TRT protocols, given how physiological reactions to different ratios of FT and TT are likely to be diverse. We may see some people needing much larger (or indeed smaller) doses to attain comparable physiological effects without the risk of harm.
 
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