Can someone explain why testosterone esters have to "kick in" ?

[DaMan]

When it comes to total T, the exogenous essentially becomes endogeneous once it's in you. One mg of exogenous T will raise total T (around) 2 ngs. Let's presume your natural endo T is 400 ngs. If you took a hit of 200 mgs of T that will raise will raise it another 400 ngs equating to a total of 800ngs. Thta's only double, I know. (Math has never been my best subject) But there are other factors. For one thing, the immediate hit causes a much bogger spike. A blood test taken one hour after administration might show a total T closer to 2000. Once you piss a few times, it comes down and settles in the aformentioned range for a few days until it slowly dissapates.
Considering the half lfe, once you take a second shot just a week later (And these are super-low dosages) your total T will still be way above that of mortal men.

Does that clear anything up or did I just make it more confused?

Most of it made sense... so 1mg of T increases endo-T by 2ng/dl. Sounds plausible.

But I still don't see exactly what value becomes quadrupled (or doubled)... 2ng/dl is not 2x1mg ... (well, not necessarily), since it's nanograms per deciliter and is a relative measure whereas the milligram is an absolute one... i.e. if you have a 10cc vial of 200mg/ml test and add 2000mg of test then you have around 360mg/ml of test (I'm not using a calculator here), so the 2000mg almost doubled it, but if you only had a 5cc value and added the same, 2000mg would more than quadruple it... so each mg of added test does not raise already-present test by a constant value, but rather a relative and variable one... if that made sense...

Again I'm curious about the scientific explanation behind it, not really the mathematical one... i.e. which T value is multiplied (not just raised) due to what biological factor/process...

 

[Nelson Montana]

My head hurts.


I think the confusion comes from the term "quadrupled" when in fact, it is the total T that is simply higher e.g. "raised."

 

[DrJMW]

Without getting into the numbers, here is a short explanation of the pharmacokinetics:

Testosterone esters are less polar than free testosterone. Testosterone esters in oil injected intramuscularly are absorbed slowly from the lipid phase; thus testosterone enanthate can be given at intervals of two to four weeks.

Testosterone in plasma is 98 percent bound to a specific testosterone-estradiol binding globulin, and about two percent is free. Generally, the amount of this sex-hormone binding globulin in the plasma will determine the distribution of testosterone between free and bound forms, and the free testosterone concentration will determine its half-life.

About 90 percent of a dose of testosterone is excreted in the urine as glucuronic and sulfuric acid conjugates of testosterone and its metabolites; about six percent of a dose is excreted in the feces, mostly in the unconjugated form. Inactivation of testosterone occurs primarily in the liver. Testosterone is metabolized to various 17-keto steroids through two different pathways. There are considerable variations of the half-life of testosterone as reported in the literature, ranging from 10 to 100 minutes.

In responsive tissues, the activity of testosterone appears to depend on reduction to dihydrotestosterone, which binds to cytosol receptor proteins. The steroid-receptor complex is transported to the nucleus where it initiates transcription events and cellular changes related to androgen action.

 

[Peyomp]

In laymans terms the ester acts simular to a time release vitamin pill. When you inject your test levels do increase fairly steady. The ester must be broken down before the test is free to work in the system. Faster acting esters like prop break down much quicker, where as enth will break down and release the free test at a much slower rate. The reason people call it a kick in point is that it takes time to build up to higher free test /blood consentration in the body and that is the point were you start to feel the most effects of the test in your system. If you frontload you will reach the kick in point (test/blood level Consentration of noticalbe effect) quicker because while the break down rate remains the same there is more estered test being broken down at the same time.

If this is the case and the halflife of testosterone suspension is very short, then it seems like testosterone esters would need a dosage that is... MUCH higher than is needed. Because as soon as one molecule gets snipped and is active, its gone only minutes later. I think you are wrong. Must be...

I donut understand.

 

[Peyomp]

Without getting into the numbers, here is a short explanation of the pharmacokinetics:

Testosterone esters are less polar than free testosterone. Testosterone esters in oil injected intramuscularly are absorbed slowly from the lipid phase; thus testosterone enanthate can be given at intervals of two to four weeks.

Testosterone in plasma is 98 percent bound to a specific testosterone-estradiol binding globulin, and about two percent is free. Generally, the amount of this sex-hormone binding globulin in the plasma will determine the distribution of testosterone between free and bound forms, and the free testosterone concentration will determine its half-life.

About 90 percent of a dose of testosterone is excreted in the urine as glucuronic and sulfuric acid conjugates of testosterone and its metabolites; about six percent of a dose is excreted in the feces, mostly in the unconjugated form. Inactivation of testosterone occurs primarily in the liver. Testosterone is metabolized to various 17-keto steroids through two different pathways. There are considerable variations of the half-life of testosterone as reported in the literature, ranging from 10 to 100 minutes.

In responsive tissues, the activity of testosterone appears to depend on reduction to dihydrotestosterone, which binds to cytosol receptor proteins. The steroid-receptor complex is transported to the nucleus where it initiates transcription events and cellular changes related to androgen action.

First of all thanks everyone for the good replies.

Question though: Can testosterone enanthate not bind as effectively to the androgen receptor because it is not as polar?

I guess there are also other mechanisms of action, that aren't even known... so its hard to say, eh?

 

[brotheriron]

There does seem to be a big misconception that enanthate take 4 weeks to kick in. I only use it for a week normally, and i notice in the first week. Totally agree with nelson.
Also i get comments telling me that sus takes 4 weeks to start working???? Someone ought to tell these guys the truth. Maybe they just get really shit gear
bro

 

[Superfrk]

Here is a link to an article on this site that should help out.

http://www.elitefitness.com/articledata/esters.html

It shows how different test ester are in fact different and how the longer acting the ester is the heavier molecular structure is meaning MG/MG there is less test present.

All of it is a fairly complicated and my post above was not ment to be definative, Just to offer a very basic understanding in simple terms.

Peyomp,

If this is the case and the halflife of testosterone suspension is very short, then it seems like testosterone esters would need a dosage that is... MUCH higher than is needed. Because as soon as one molecule gets snipped and is active, its gone only minutes later. I think you are wrong. Must be... "

The doses are much higher to a point, You would not want to inject 500mg of prop all at once, like you would a longer acting ester. The half life deals with rate of decay or in this case the rate at which the free test is released though the break down of molecule or what is being refered to as sniping of the molecule. With prop for example the rate of release of active free test is much quicker than the rate of release of free test with an eth ester. It is not how quickly the body is able to use the free test but how fast the free test is being released to become active for the body to use. The test is not released all at one time it is being released at a set rate based on the structure of the molecule thought the decay process. Just like with carbon dateing the carbon molecule has a set decay rate. The same is true for the molecule chain that determains the ester.

 

[Austrian]

Question though: Can testosterone enanthate not bind as effectively to the androgen receptor because it is not as polar?

only pure testosterone can bind to anything, the ester - any ester - has to be detached by the esterase enzyme to make the testosterone molecule active. read: click me

i 've found a chart which compares the blood plasma concentrations after one shot of testoviron depot with another enanthate product:

click me

It peaks somewhere around the 3rd day and the depot is exhausted after ~14 days. If you do another shot before this date you will get a higher peak and higher concentrations afterwards and so on. Depending on how much concentration you need to feel something you will reach the "kick in" after the amount of shots it takes to reach that level.

I have no idea how long it takes for the presence of the hormone to actually translate into noticeable gains.