Androgen Receptors
So, the key and the lock, the lock and the key. The key is supposed to open the lock, but in reality, things are not always smooth. The key may or may not fit into the lock. But even if the key fits into the lock, it may not necessarily open it.
Or there may be significant difficulties with opening – this can happen even if you have a nearly exact copy of the key. If there is already a key in the lock, you cannot insert a second one – this is understandable, but it is worth clarifying just in case.
It's almost the same with hormones and receptors. Almost every hormone has its own unique receptor. For testosterone and dihydrotestosterone, it is the androgen receptor.
The hormone molecule binds to its receptor and activates it, after which the pair participates in some "action".
But there are also substances whose molecules bind wonderfully to the receptor, but nothing happens: they simply block the receptor and prevent it from performing its mission (antiandrogens and progestins).
I will repeat once more: the analogy with the key and the lock is used very often. And I think it is because of this analogy that the concept of "clogged receptors" was born.
Indeed: foreign substances can get into a regular lock – it can get clogged in the most literal sense of the word, and then it will be impossible to insert the key into it.
Could something similar happen with receptors? In fact, nothing like this can happen with receptors, as they are simply large protein molecules. And molecules cannot "rest," "deteriorate," or get "clogged" – they are always ready for a chemical reaction.
You do not think that molecules, for example, of sulfuric acid will not react with metals because they are "clogged," "tired," or do not want to participate in this "mess," do you?
Number of Receptors and Tissue Sensitivity
Now, to the most interesting part. Receptors, like any other protein molecules, can break down and be recreated. Moreover, all protein molecules have a certain half-life, meaning they must "die" after a certain period and then "come back to life."
At the same time, the number of receptors can change: decrease or increase – thus regulating the sensitivity of tissues to certain hormones.
We all know the word "insulin resistance": it means a decrease in sensitivity to insulin, which occurs due to a reduction in the number of its specific receptors on the cell surface.
This is how the body reacts to an excess of insulin in the blood. But perhaps the body will react in the same way to an excess of testosterone in the blood if it (or its analogs) was introduced from outside?
Androgen Receptors and AAS
So, maybe the word "clogged" hides precisely the decrease in the number of androgen receptors during the "cycle"? And this is where the most interesting part begins.
For a while, scientists did indeed believe that in response to injections (or oral intake) of testosterone or its analogs, the number of androgen receptors in most tissues decreases.
But as early as 1999, it was definitively established: when using synthetic androgens, the number of AR in a number of tissues not only does not decrease but even significantly increases!
This happens primarily due to a sharp increase in the half-life of AR in the presence of androgens: from three hours it increases almost to ten – more than three times.
This applies to androgens themselves and anabolic steroids that exhibit androgenic activity. It is not entirely clear how androgen receptors behave when only testosterone analogs completely devoid of androgenic activity – nandrolone, for example, or boldenone – are present in the blood.
But in the presence of testosterone, methyltestosterone, trenbolone, stanozolol, drostanolone, and so on, the number of AR in most tissues – including muscle tissue – increases. Once again: it increases!
It's Not About the Receptors
Everyone is more or less familiar with the term "steroid plateau." This is not a fiction – the decrease in the effectiveness of androgenic anabolic steroids (AAS) over time indeed occurs. However, not only for them – decreased effectiveness is characteristic of many medications.
But if we talk about AAS, this effect is by no means explained by problems with androgen receptors. So, what then? It is worth starting with the fact that a living organism is an ideal self-regulating system. It can maintain its internal state within acceptable limits under the most unfavorable conditions.
Moreover, it must do this if it wants to stay alive. The body tries to neutralize any interference by activating defensive mechanisms. These are activated even when we know that the interference is necessary and without it, the body may die.
In the case of an excess of synthetic androgens or their analogs in the blood, the body responds by increasing the synthesis and secretion of sex hormone-binding globulin. Since only free molecules can penetrate the cell and bind to the androgen receptor, the body tries to bind as many of them "hand and foot" as possible.
At the same time, the activity of aromatase increases, so even free molecules of testosterone are not guaranteed to reach the cell – they may well turn into estradiol molecules. Usually, this restructuring takes the body a little over three weeks – this is where the idea of short "cycles" came from.
Although there are other ways to trick the body: they include the simple increase in dosages and the inclusion of new drugs in the "cycle."
Conclusion
I have outlined only the general contours of the problem and merely hinted at ways to solve it. As for the androgen receptors… You know, there is a saying, "Don't blame the mirror if your face is crooked" – Nikolai Vasilievich Gogol even chose it as an epigraph for his play "The Government Inspector."
So, there's no point in blaming the androgen receptors for something they are definitely not responsible for. This certainly will not help solve your problems with "cycles."
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