schwellington
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There is much talk on the net about roids some people know what they are talking about, and some well are just reinforcing myths. One thing I hear about all the time is the topic of androgen receptors or (ARs). It seems many people still believe that over the course of a cycle ARs downgrade this just isnt the case. People argue the downgrade point because of the fact there comes a time growth slows or stops though the dose of testosterone hasn't changed.
It also stems from the fact that we know other receptors of the body do downgrade. Take ephedrine for example, it binds to beta-receptors, over a period of time the number of receptors on a target cell begins to decrease. This is due to a decrease in the half-life of receptor proteins without a decrease in the rate that the cell is making new receptors which leads to a decrease in the potency of a given dose.
The above happens with many substances and receptors but androgen receptors are very different. Many studies that are coming out these days show in the presence of high concentrations of testosterone receptors up regulate to consume the higher amounts of testosterone in the body. When you stop growing it is not because of down regulation and here is why.
Most everyone knows a little about how steroids work increased protein synthesis right? Well there is much more to it than that. They also increase the activity of satellite cells, GH and igf-1, also increase new myofiber formation.
In one study I read a 500mg injection of testosterone per week increased GH levels by 18% and IGF-1 levels by 15% that shows a powerful effect! Activation of satellite cells by testosterone requires IGF-1 and as a loop effect aromatized test that turns to estrogen again increases IGF-1 so each plays off the other with the end result being increased satellite cell production. This leads to a greater capacity for protein synthesis by increasing fusion of satellite cells to existing fibers.
Proliferation of satellite cells is needed in order to meet the needs of thousands of muscle cells all potentially requiring additional nuclei. Differentiation is necessary in order for the new nucleus to behave as a nucleus of muscle origin. The number of myonuclei directly determines the capacity of a muscle cell to manufacture proteins, including androgen receptors.
So you see the increased test levels actually increase satellite cells which in turn down the road increase receptors. It also seems the higher the dose the more the activity of satellite cells increase. That doesn't mean jump right in to 2-3g doses of test you have to build up receptors over time. All jumping up to a huge amount of test will do is give you an estrogen level of a tranny queen who happens to have muscle lol.
Here are a few quotes to support my claims
Endocrinology (1990) 126 1165. In fibroblasts cultured from human genital skin which contained very low amounts of 5-alpha reductase, 2 nanomolar tritium-labeled testosterone [which is sufficient to saturate ARs] produced a 34% increase in androgen receptors as measured by specific AR binding, the best assay method known, and 20 nanomolar tritium-labeled testosterone produced an increase of 64% in number of ARs.
J Steroid Biochemistry and Molecular Biology (1990) 37 553. In cultured adipocytes, methyltrienolone and testosterone demonstrated marked up regulation of AR content upon administration of androgen. 10 nanomolar methyltrienolone increased AR content (as measured by binding to radiolabeled androgen) by more than five times, relative to zero androgen.
J Steroid Biochemistry and Molecular Biology (1993) 45 333. In cultured smooth muscle cells from the penis of the rat, mRNA production was found to be up regulated by high dose testosterone (100 nanomolar) or DHT. When 5-alpha reducatase was inhibited by finasteride, thus blocking metabolism to DHT, AR mRNA production was down regulated in response to testosterone. Blockage of the aromatization pathway to estrogen by fadrozole eliminated this downregulation effect. Estradiol itself was found to down regulate AR mRNA production in these cells.
Endocrinol Japan (1992) 39 235. One nanomolar DHT was demonstrated to increase AR protein by over 100% within 24 hours, relative to zero androgen level. The half life of the AR was demonstrated to increase from 3.3 h to 7.5 h as a result of the androgen administration.
Endocrinology (1996) 137 1385. 100 nanomolar testosterone was found to increase AR levels in vitro in muscle satellite cells, myotubes, and muscle-derived fibroblasts.
The main reason growth stops when the dose remains the same is the body doesn't like change, it will fight you every step of the way. When you increase the amount of anabolic hormones, catabolic hormones will rise as well. When the concentration of catabolic hormones is high enough growth is off set or even stops. When that happens you can do one of two things. Stop taking gear so the body can return to normal or increase the amount of test to once more be in an anabolic state. The increase in receptors is the reason you can use more and more test every cycle, and the funny thing is these receptors once built will hang around for a very long time even years ever increasing your ability to build muscle
It also stems from the fact that we know other receptors of the body do downgrade. Take ephedrine for example, it binds to beta-receptors, over a period of time the number of receptors on a target cell begins to decrease. This is due to a decrease in the half-life of receptor proteins without a decrease in the rate that the cell is making new receptors which leads to a decrease in the potency of a given dose.
The above happens with many substances and receptors but androgen receptors are very different. Many studies that are coming out these days show in the presence of high concentrations of testosterone receptors up regulate to consume the higher amounts of testosterone in the body. When you stop growing it is not because of down regulation and here is why.
Most everyone knows a little about how steroids work increased protein synthesis right? Well there is much more to it than that. They also increase the activity of satellite cells, GH and igf-1, also increase new myofiber formation.
In one study I read a 500mg injection of testosterone per week increased GH levels by 18% and IGF-1 levels by 15% that shows a powerful effect! Activation of satellite cells by testosterone requires IGF-1 and as a loop effect aromatized test that turns to estrogen again increases IGF-1 so each plays off the other with the end result being increased satellite cell production. This leads to a greater capacity for protein synthesis by increasing fusion of satellite cells to existing fibers.
Proliferation of satellite cells is needed in order to meet the needs of thousands of muscle cells all potentially requiring additional nuclei. Differentiation is necessary in order for the new nucleus to behave as a nucleus of muscle origin. The number of myonuclei directly determines the capacity of a muscle cell to manufacture proteins, including androgen receptors.
So you see the increased test levels actually increase satellite cells which in turn down the road increase receptors. It also seems the higher the dose the more the activity of satellite cells increase. That doesn't mean jump right in to 2-3g doses of test you have to build up receptors over time. All jumping up to a huge amount of test will do is give you an estrogen level of a tranny queen who happens to have muscle lol.
Here are a few quotes to support my claims
Endocrinology (1990) 126 1165. In fibroblasts cultured from human genital skin which contained very low amounts of 5-alpha reductase, 2 nanomolar tritium-labeled testosterone [which is sufficient to saturate ARs] produced a 34% increase in androgen receptors as measured by specific AR binding, the best assay method known, and 20 nanomolar tritium-labeled testosterone produced an increase of 64% in number of ARs.
J Steroid Biochemistry and Molecular Biology (1990) 37 553. In cultured adipocytes, methyltrienolone and testosterone demonstrated marked up regulation of AR content upon administration of androgen. 10 nanomolar methyltrienolone increased AR content (as measured by binding to radiolabeled androgen) by more than five times, relative to zero androgen.
J Steroid Biochemistry and Molecular Biology (1993) 45 333. In cultured smooth muscle cells from the penis of the rat, mRNA production was found to be up regulated by high dose testosterone (100 nanomolar) or DHT. When 5-alpha reducatase was inhibited by finasteride, thus blocking metabolism to DHT, AR mRNA production was down regulated in response to testosterone. Blockage of the aromatization pathway to estrogen by fadrozole eliminated this downregulation effect. Estradiol itself was found to down regulate AR mRNA production in these cells.
Endocrinol Japan (1992) 39 235. One nanomolar DHT was demonstrated to increase AR protein by over 100% within 24 hours, relative to zero androgen level. The half life of the AR was demonstrated to increase from 3.3 h to 7.5 h as a result of the androgen administration.
Endocrinology (1996) 137 1385. 100 nanomolar testosterone was found to increase AR levels in vitro in muscle satellite cells, myotubes, and muscle-derived fibroblasts.
The main reason growth stops when the dose remains the same is the body doesn't like change, it will fight you every step of the way. When you increase the amount of anabolic hormones, catabolic hormones will rise as well. When the concentration of catabolic hormones is high enough growth is off set or even stops. When that happens you can do one of two things. Stop taking gear so the body can return to normal or increase the amount of test to once more be in an anabolic state. The increase in receptors is the reason you can use more and more test every cycle, and the funny thing is these receptors once built will hang around for a very long time even years ever increasing your ability to build muscle
