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receiptor site question

buldog9

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Apr 6, 2007
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When staying on after say 4 or 5 months does it do any good to change the type of aas as for as the receiptor [being more receptive]site is concerned. I am close to what I want to acheve but need about 2 more months at the rate I am going. I need to know if I should stay on or lay off 5 or 6 weeks and then get back on for 8 to 10 weeks. My gains are slowing but BF% is still droping [about 8%] I want to gain another 5 or 6 lbs of muscle and lose about the same in BF.I have lost about 25 lbs of fat and gained about 17 lbs of muscle. I know 17 lbs is a good gain and to excepct 5 more lbs of lean muscle is stretching it in a normal cycle but I am only trying to get back to where I was so muscle memory will come into play. I am 52 and want to get back to where I was at 28.Normaly I would just lay off for a while and get back on but work will start to come into play soon and I want to get what I can as soon as I can.
 
Receptor sites do not degrade, it's a BB'ing myth that just wont die.

If you have gained a certain amount of muscle, then you may need more AAS to continue to gain, in the same way you need more protein and cals to continue to gain.
 
Receptor sites do not degrade, it's a BB'ing myth that just wont die.

If you have gained a certain amount of muscle, then you may need more AAS to continue to gain, in the same way you need more protein and cals to continue to gain.

Is that true with igf....
 
Receptor sites do not degrade, it's a BB'ing myth that just wont die.

If you have gained a certain amount of muscle, then you may need more AAS to continue to gain, in the same way you need more protein and cals to continue to gain.

well said!

i dont buy the receptor site bs either....
 
from personal experience..

The last cycle i ran was 6months in length.

about half way to 3/4s of the way through, i switched esters from cyp to enth.

I definately noticed a "surge" once the enth kicked in. increase in strength and slight increase in weight, after my weight gain had pretty much plateaued.

however i will say this... i believe the cyp dose i was running was around 600mg per week and when i ran the enth i jumped up to 750mg. so it could have just been a result of the increase in dossage.
 
Is that true with igf....

I am not hugely experienced with IGF but have read a fair bit from trusted people who are.

I don't know if it is posted on this forum, but Grunt76 had written a pretty concise bit on IGF and receptor downgrading.

If it is not on here, let me know and I'll link it for you, it is on many forums, and a good read.
 
from personal experience..

The last cycle i ran was 6months in length.

about half way to 3/4s of the way through, i switched esters from cyp to enth.

I definately noticed a "surge" once the enth kicked in. increase in strength and slight increase in weight, after my weight gain had pretty much plateaued.

however i will say this... i believe the cyp dose i was running was around 600mg per week and when i ran the enth i jumped up to 750mg. so it could have just been a result of the increase in dossage.

Without a doubt mate, there is no difference between cyp and enth (well 1 carbon in their Estered state), they are both test, and the ester needs to be cleaved off before they become active in the body.
 
from personal experience..

The last cycle i ran was 6months in length.

about half way to 3/4s of the way through, i switched esters from cyp to enth.

I definately noticed a "surge" once the enth kicked in. increase in strength and slight increase in weight, after my weight gain had pretty much plateaued.

however i will say this... i believe the cyp dose i was running was around 600mg per week and when i ran the enth i jumped up to 750mg. so it could have just been a result of the increase in dossage.

ya even if there were a receptor site it would be the same for test en and test cyp. i belive...
 
Hmmm, I've been wondering this as well since I had to start my next cycle a bit earlier than planned and was worried that I wouldn't get anything out of it if my receptors hadn't recovered or whatever. Now I'm not so worried about it.
 
read this study, "Testosterone administration to older men improves muscle function:molecular and physiological mechanisms". interesting points are that AR expression increased "upregulated" at 1 month. And returned to baseline "downregulated" at the 6 month point.This was with at or slightly above HRT doses. Based off of this i never really understood the whole switching of esters or even compounds. The steroids basically attach to the receptor. Some better than others but the effects are the same plus or minus the estrogen effects, meaning testosterone builds muscle, boldenone builds muscle also, same effects just different drugs, one produces more estrogen sides the other does'nt..
 
Without a doubt mate, there is no difference between cyp and enth (well 1 carbon in their Estered state), they are both test, and the ester needs to be cleaved off before they become active in the body.

If I remember correct enanthate has a slightly higher % of test. He also mentioned that he increased the dosage which was probably the difference.
 
If I remember correct enanthate has a slightly higher % of test. He also mentioned that he increased the dosage which was probably the difference.

Yes it does, the Cyp ester is 8 carbons, and the enth ester 7, which in the real world would not make a noticeable difference.

I think it is the upping of the dose that did the trick.

Per 100mg of compound, this is the approx amount of actual test once the ester is taken into account.

Testosterone Enanthate: 70mg

Testosterone Cypionate: 69mg

So as you see the difference is practically none.
 
I think you're all right. Test is test and he increased his dosage by 25% (not including a small difference from the different esters). That's a substantial increase. Regarding receptors, there are myths flying around some truth so let me offer up what I know and maybe it will make things clearer. When you talk about receptor up/downregulation it doesn't have much to do with the receptor itself but rather the AMOUNT of receptors. A cell is upregulated if the overall density (or number of receptors) increases and the same cell is downregulated if the amount of receptors decreases. I think what gets confused here is something entirely different and refers to receptor sensitivity. Your body's cells could be androgen receptor upregulated and cells could be highly dense with receptors but the sensitivity of the receptors can be very low. This applies to many types of receptors. I don't see any reason why androgen receptors would be different.
 
Last edited:
Nice post, Ouch!

Let me add this, too. Receptors are just folded up proteins with amino acid sequences arranged to allow for a certain type of folding and reactivity with other chemical compounds.

To "clear" receptors, either we have to intoduce a competitive inhibitor that binds the receptor more stongly (meaning it has better affinity for the receptor), actually remove the receptor from the nuclear or cell membrane, or allow drug levels to drop so low that many fewer receptors are bound with drug.

Remember, too, that receptors, being proteins manufactured in the cell, have a life just as any cell or cell component does, and are constantly being replaced, and as Ouch said, added or pulled off the membrane in upregulation or downregulation.

It seems that many people think of the receptors as a static, fixed entity that just sits there waiting to be filled or "cleared' - this is an imcomplete and inaccurate picturre of the way these work.

Finally, the percentage of drug (dosing per mg or ml) is less important than the percentage and amount that's free vs bound. Only free drug fraction can be used by the cell, not that bound. In the case of test, about 2% is free and 98% is bound, unless we do something with a competitive inhibitor of higher affinity to displace bound drug.
 
Finally, the percentage of drug (dosing per mg or ml) is less important than the percentage and amount that's free vs bound. Only free drug fraction can be used by the cell, not that bound. In the case of test, about 2% is free and 98% is bound, unless we do something with a competitive inhibitor of higher affinity to displace bound drug.

Enter Insulin, proviron, and stinging Nettle/Nettle root....3 totally different compounds alltogether that all have a curious side effect relating to the above
 
Enter Insulin, proviron, and stinging Nettle/Nettle root....3 totally different compounds alltogether that all have a curious side effect relating to the above

DC, can you please go into how stinging Nettle/Nettle root is used?
 
Enter Insulin, proviron, and stinging Nettle/Nettle root....3 totally different compounds alltogether that all have a curious side effect relating to the above

DC, can you please go into this a bit more, especially stinging nettle root? Have always been interested in your views/theories on drugs. Thanks.
 
Enter Insulin, proviron, and stinging Nettle/Nettle root....3 totally different compounds alltogether that all have a curious side effect relating to the above

i have found the proviron and insulin wothout a doubt will increase the free, but i have read all about the nettle on a's board and have tried it and havent had too much sucess with it...
 
KM, etc do you guys know of anything "natural", something like stinging nettle root or any "supplement" that can somewhat effectively reduce Shbg (increase free test)? Obviously i'm not talking to the degree of insulin and proviron, though, but anything that you have found?
 
KM, etc do you guys know of anything "natural", something like stinging nettle root or any "supplement" that can somewhat effectively reduce Shbg (increase free test)? Obviously i'm not talking to the degree of insulin and proviron, though, but anything that you have found?
Does tribulus do that?
 

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