Test Cyp Absorbtion Rate?

[earthdog]

Hi guys. Let's say that I inject my customary 100mg of test cyp weekly into the quad muscle on Friday morning. Later that day, I do a heavy squat workout. Will the exertion placed upon the quad muscle cause the cyp to be absorbed more quickly? Will I get a big spike the first couple of days, and then bottom out towards the end of the week? Hopefully the doctors will see this and respond.

 

[mranak]

The testosterone cypionate is quickly absorbed, but it is inactivated until the body removes all of the esters from it.

 

[SPE]

I've often wondered the same thing. The way I've posed the question is, "Does the half life of Testosterone Cypionate shorten with more muscle tissue breakdown from exercise?"

 

[chap]

I believe that once the oil is absorbed into the circulation, the ester is rapidly cleaved by enzymes in the bloodstream, while the oil is still in depot the ester is more slowly cleaved. I could be wrong but the mode of action is not simple and may be more than one phase.

 

[mranak]

I believe that once the oil is absorbed into the circulation, the ester is rapidly cleaved by enzymes in the bloodstream, while the oil is still in depot the ester is more slowly cleaved. I could be wrong but the mode of action is not simple and may be more than one phase.

I just read an explaination elsewhere that makes the claim that the ester causes the hormone to sit in depot in the muscle, so maybe I am mistaken. I'll be looking into this further, I guess.

 

[jboldman]

perhaps this will help. The exercise will likely have some but not a lot. This is for an injection of 140mg

jb

=========

 

[SWALE]

I should expect that squeezing the muscle would move more oil into the circulation. How much of a role dispersement from the injection site makes is unknown to me. However, the ester is cleaved, one group (or more) at a time, until only the backbone testosterone molecule is left. It has a half-life of "10-100 minutes" (they haven't been able to narrow it down within an order of magnitude). The test cyp, then the bare T molecule, are active until that point.

 

[earthdog]

I should expect that squeezing the muscle would move more oil into the circulation. How much of a role dispersement from the injection site makes is unknown to me.

Ok, that I understand.

However, the ester is cleaved, one group (or more) at a time, until only the backbone testosterone molecule is left. It has a half-life of "10-100 minutes" (they haven't been able to narrow it down within an order of magnitude). The test cyp, then the bare T molecule, are active until that point.

That part went right over my head! Can you run that by me again please?

 

[SWALE]

Okay. The test cyp molecule is active once it hits the bloodstream (ignoring for the time being any possible localized effect adjacent to the injection site) because it is being carried around the body and exposed to androgen receptors. The body possess enzymes which cleave off parts of the cypionate ester, until all that is left is the testosterone molecule. Then it, to, is broken down, according to its own half-life.

We cannot predict exactly how long a bolus of test cyp will remain active, but we we can average it out. The point where roughly half of it is still active is known as the "half-life". Another half-life goes by, and 1/4 is still working. Once more, and it is 1/8th of the original shot. On average.

I hope I did a better job of explaining it this time.

 

[earthdog]

Yes, thanks!

 

[chap]

Although I don't believe "half lifes" of drugs in the human body work quite as elegantly as radioactive isotopes, so it would surprise me if the rigid 1/2 then 1/2 again then 1/2 again model would actually follow so perfectly with these chemicals. I think half life may be a bit of a misnomer when it comes to biochemistry, or perhaps it is assumed that it is not a model of perfection.

 

[SWALE]

In a practical sense, that is exactly right.

The biological system presents great variation in activity level, overall health, isozymic make-up (the enzymes that process all this), metabolic differences, etc.

 

[mranak]

Okay. The test cyp molecule is active once it hits the bloodstream (ignoring for the time being any possible localized effect adjacent to the injection site) because it is being carried around the body and exposed to androgen receptors.

The testosterone cypionate molecule has binding affinity with the androgen receptors? And then the molecules between testosterone cypionate and the base testosterone would have binding affinity as well?

Interesting. Don't know how I missed all of this important data until now.

 

[chap]

Do you not actually mean, the test cyp molecule "becomes" active when it hits the bloodstream, as it is then rapidly cleaved giving the base testosterone molecule the ability to interact with the receptors.

I don't think you meant that the esterified molecule actually is able to interact with receptors as mranak is getting from your comment.

Can you clarify this important concept before I go putting these words in your mouth?

 

[SWALE]

I believe it does. No one has ever told me so, but it makes sense the physiological effects so soon status post injection would not be demonstrated were this not the case.

The molecule was capable already; but it has to be in the bloodstream and delivered near the androgen receptors to do its work.

Either way, it makes no difference. The effects are there.

 

[chap]

The theory I remember being espoused was that once in the bloodstream, esterified hormones are very rapidly cleaved, regardless of ester length, which could explain the quick results of an injection you mention. Therefore the time release effect we all expect from different esters is what is taking place in the depot.

 

[1cc]

Therefore the time release effect we all expect from different esters is what is taking place in the depot.

Please explain.

 

[chap]

I am by no means an expert on this, but I seem to remember that the esters affect the fat solubility, so the longer esters are more fat soluble, therefore they prefer to stay in depot longer, resisting absorption into the bloodstream.

Once an ester is cleaved the testosterone molecules are less fat soluble and become more easily picked up by the bloodstream.

That is one reason why short esters like propionate are so difficult to make in higher concentrations, as the solubility is so much poorer in oil than the longer esters (hence prop is usually 100mg/ml where cypionate can often be made as 300mg/ml easily)

If anyone has more expertise please jump in here.

 

[LiquidGib]

This is what I found in an article titled "All about Testosterone Esters":

An ester is a chain composed primarily of carbon and hydrogen atoms. This chain is typically attached to the parent steroid hormone at the 17th carbon position (beta orientation), although some compounds do carry esters at position 3 (for the purposes of this article it is not crucial to understand the exact position of the ester). Esterification of an injectable anabolic/androgenic steroid basically accomplishes one thing, it slows the release of the parent steroid from the site of injection. This happens because the ester will notably lower the water solubility of the steroid, and increase its lipid (fat) solubility. This will cause the drug to form a deposit in the muscle tissue, from which it will slowly enter into circulation as it is picked up in small quantities by the blood. Generally, the longer the ester chain, the lower the water solubility of the compound, and the longer it will take to for the full dosage to reach general circulation.



Esterification temporarily deactivates the steroid molecule. With a chain blocking the 17th beta position, binding to the androgen receptor is not possible (it can exert no activity in the body). In order for the compound to become active the ester must therefore first be removed. This automatically occurs once the compound has filtered into blood circulation, where esterase enzymes quickly cleave off (hydrolyze) the ester chain. This will restore the necessary hydroxyl (OH) group at the 17th beta position, enabling the drug to attach to the appropriate receptor. Now and only now will the steroid be able to have an effect on skeletal muscle tissue. You can start to see why considering testosterone cypionate much more potent than enanthate makes little sense, as your muscles are seeing only free testosterone no matter what ester was used to deploy it.

 

[SWALE]

Oh, thern that is news to me! Thank you.

Where did you find this article? Who wrote it?