After-course restoration of testosterone level steroidchoice.com

After-course restoration of testosterone level

William Llewellyn

Well, you experienced amazing 4-month course of Sustanon and Dianabol. You accumulated 9 kg of tremendous mass and you are very glad with your result. You can’t stop looking at yourself in the mirror. But now a problem starts devouring you. Your steroids will finish very soon (you know that you need a rest anyway) and your testes are of raisin size. Your body produces less testosterone than a 9-old girl and you try to understand what should be done in order to avoid painful after-course collapse which may deprive you of a part of hardly gained muscles. It seems that we have different opinions about how to restore the endogen production of testosterone after the course. Which one is the best? If you don’t have an exact understanding what is going on in your body and why some certain drugs help correct the situation, the choice of the right after-course therapy may be quite entangled. In this article I would like to discuss the role of antiestrogens and gonadotropin during this sensible period of time while designing an effective strategy of their administration.


Hypothalamus-hypophysis-testes or shortly HHT is a thermostat for the natural production of testosterone in your body. If you look at this in a simple way, too big amount of testosterone can burn out your oven. The insufficiency of it, on the other hand, will add heat. For the targets of our discussion we can imagine this regulating system as a system with three levels. Hypothalamus is at the top, where gonadotropin releasing hormone (GnRH) is produced when more testosterone is required. GnRH sends the signal to the second level of the arc, hyphophysis, which, in return, produces luteinizing hormone, LH for short. This hormone stimulates the testes (third level) to produce testosterone. Sex steroids (testosterone, estrogen) which are produced, are a balance and take part in negative feedback sending the signals (mostly to hypothalamus and hypophysis) to decrease the production of testosterone when too much amount of the hormone is present. Synthetic steroids, of course, suppress testosterone in the same way. This is a synopsis of the arc that regulates production of testosterone which is necessary for our further discussion because firstly we should look at the basic mechanisms before we will be able to understand why the natural restoration of HHT arc after the course is a slow process. Only then can we prepare an auxiliary therapy in order to overcome this.

Testes sensibility decrease

Although steroids suppress the production of testosterone mainly by decreasing the level of gonadotropic hormones, the main obstacle in HHT arc restoration after the rejection of the drugs is, amazingly, not LH itself. This problem became obvious in an investigation that was published in Acta Endocrinologica in 1975. It focused on blood parameters including testosterone and LH levels of men who used testosterone enanthate of 250 mg per week during 21 week. The participants were supervised for 18 more weeks after they stopped using drugs. In the beginning the level of LH was suppressed directly proportionally to the increase of testosterone level which was expected. However, the situation totally changed when steroids were no longer administrated (see pic. 1). The level of LH started to increase very fast (at third week) and at the same time the level of testosterone almost didn’t change for a long time. In fact, more than 10 weeks passed before some significant change started. This absence of relation explains that the problem in androgen level restoration is not the level of LH but in fact the atrophy and testes sensibility decrease to this hormone. After inactivity period testes, obviously, lost the mass (got atrophied) which made them unable to perform the work which is required by increased level of LH.

The role of antiestrogens

It is important to understand that antiestrogens themselves have no great affect on endogen testosterone restoration after the course. Usually they just stimulate the production of LH blocking the negative feedback of estrogens but as we see now, the level of LH also restores fast without them. In addition to this fact, there is no increased level of estrogens after the course which are blocked by antiestrogens because testosterone (already suppressed) is the main raw material for synthesis of estrogens at male athletes. As a result, estrogen level in serum will be lower and not higher. Any increase of estrogen level after the course will take place simultaneously with testosterone level increase, not before it (notice that there is an imbalance in the proportion of the levels of these hormones but this is a completely different topic). However, we can see why this fact can be easily missed. Medical literature has many references that antiestrogen drugs like Clomid and Nolvadex increase the levels of LH and testosterone and at normal conditions these drugs really increase endogen production of hormones blocking negative relation of estrogens. If we relate this with the fact that it is possible to find same amount of investigations which show that administration of steroids decreases level of LH and testosterone level, we could see that it is easy to conclude that we should focus on restoration of LH after the course. We would miss the real problem of testes sensibility decrease if we didn’t notice the real rate of restoration of the involved hormones. After this we immediately see the insignificant importance of antiestrogen drugs administration.