OuchThatHurts
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This is ridiculous. All of this is to create a long-lasting reservoir of testosterone with an intramuscular injection. We're talking in this thread about long and short esters, not testosterone or testosterone base (or TNE as it's called). Some in-plasma testosterone is obviously converted to estrogen via aromatization but esterified testosterone is created artificially with the process of esterification to increase the weight of the molecule and improve the solubility in OIL (fat) so it can be placed in depot via intramuscular injection. The longer the ester, the better the solubility and greater hydrophobicity of the esterified testosterone (the solute) to create a longer delivery mechanism.
In reality, the release rate is not very steady. It's very high in the beginning and then rapidly falls to a lower level and only then slowly drops as the size of the reservoir diminishes. Where it becomes somewhat different is in the time it takes to diminish. With longer esters, each subsequent reservoir that is created acts similarly so by the 3rd or 4th dose, you have several reservoirs releasing their payload (testosterone x) simultaneously and their effect is cumulative and eventually reaches a high level and stays that way (steady-state plasma level). The time it takes the ester to be cleaved is of no consequence. Because the level high, steadily for such a long period, more is converted and reduced along with metabolization. With shorter esters, which are absorbed more quickly, there is less time at very high plasma levels and less time for aromatization and 5-alpha reduction to occur throughout the body. Not a lot less, just a bit less. Enough though, for some people to notice somewhat less estrogenic side effects (water retention, etc). The amount of aromatization that occurs in adipose tissue is so tiny that it is unlikely to account for what some people notice as the difference between long and short esterified testosterone - particularly people with low amounts of adipose tissue.
In reality, the release rate is not very steady. It's very high in the beginning and then rapidly falls to a lower level and only then slowly drops as the size of the reservoir diminishes. Where it becomes somewhat different is in the time it takes to diminish. With longer esters, each subsequent reservoir that is created acts similarly so by the 3rd or 4th dose, you have several reservoirs releasing their payload (testosterone x) simultaneously and their effect is cumulative and eventually reaches a high level and stays that way (steady-state plasma level). The time it takes the ester to be cleaved is of no consequence. Because the level high, steadily for such a long period, more is converted and reduced along with metabolization. With shorter esters, which are absorbed more quickly, there is less time at very high plasma levels and less time for aromatization and 5-alpha reduction to occur throughout the body. Not a lot less, just a bit less. Enough though, for some people to notice somewhat less estrogenic side effects (water retention, etc). The amount of aromatization that occurs in adipose tissue is so tiny that it is unlikely to account for what some people notice as the difference between long and short esterified testosterone - particularly people with low amounts of adipose tissue.
That's why I thought he had wrote that statement as he keeps mentioning how test is not active until it hits the blood etc. But to say test e is not an anabolic hormones is plain silly to me. He's way overthinking things imo. As you say test is anabolic. The ester is not anabolic. The two called are both anabolic and non anabolic at different times. So obviously test e is an anabolic hormone. Sounds pretty simple but just the ay I look at it.