Check my Tren E/Test E cycle please

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    Check my Tren E/Test E cycle please


    4th cycle

    1st was test e @ 500/ week
    2nd was test e@ 500/ week plus dbol
    3rd was test e@ 600/week plus deca @ 300mg/ week


    Now I am looking to get on to the steroid with the best profile.
    Dianabol @ 50mgs week 1-4
    Test E @ 600mg/ week 1-12
    Tren E@ 300mg/ week 1-8
    Adex @ o.5mg/ eod
    caber @ 1mg/ week

    PCT
    Blast HCG@ 1000iu's weeks 14 and 15
    Clomid 100/75/75/50 16-20
    Nolva? Dont know if I need it.
    Any recommendations? Problems? What should I expect from this?

    I know tren ace is easier to change if you are having problems but i dont want to pin ED.

    Thanks

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    Your test is way too high. Man, do the research. With Tren you need only about 100mgs of test. Dbol and tren are good together. Tren E kind of sucks though. Tren seems to work best with shorter esters. I'd stick with Tren Ace, EOD.
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    Quote Originally Posted by DetroitHammer View Post
    Your test is way too high. Man, do the research. With Tren you need only about 100mgs of test. Dbol and tren are good together. Tren E kind of sucks though. Tren seems to work best with shorter esters. I'd stick with Tren Ace, EOD.
    I read that running high test with high tren was better just to bring on some more gains. So you are saying 100mg/week would suffice?
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    Anything else that should be fixed with this cycle?
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    [QUOTE="jman6;4588625"] I read that running high test with high tren was better just to bring on some more gains. So you are saying 100mg/week would suffice?[/QUOTE


    Ya it will give you more gains but also more sides.
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    Quote Originally Posted by jman6 View Post
    I read that running high test with high tren was better just to bring on some more gains. So you are saying 100mg/week would suffice?
    You will get zero gains with the increased test. The gains will come from the Tren. With 5 times the affinity to bind to the AR, Tren is going to push test out of the way as far as receptors go. The test you do inject that doesn't bind will give way to increase amortization hence more sides. You are wasting good test by injecting it with Tren. If you want more gains with the Tren use either Adrol or Dbol.
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    Quote Originally Posted by DetroitHammer View Post
    You will get zero gains with the increased test. The gains will come from the Tren. With 5 times the affinity to bind to the AR, Tren is going to push test out of the way as far as receptors go. The test you do inject that doesn't bind will give way to increase amortization hence more sides. You are wasting good test by injecting it with Tren. If you want more gains with the Tren use either Adrol or Dbol.
    Hmmm. So what about the last four weeks of my cycle then? Should I change the weeks on tren or test?
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    Oh man this thread is full of BS.
    1-dont blast you hcg- run it through your cycle at 250iu's-2x/week
    2-Tren e actually achieves higher blood levels than short esters so dont buy the BS that tren ace is stronger or better, that being said it may be prudent never havng run tren to go with ace since you do not know how you respond and if you have bad sides ace will clear quickly.
    3- The binding affinty /competition theory is total bull****. The only reason people run test lower is that it easier to manage sides that way. The key to sides management begins and ends with estrogen management It is the crux of managing your sides. Lower test, less e , easier sides management. That being said your adex dosing plan will more than do the job. The competition thing is total crap. In the presence of excess androgens the androgen receptor lifespan doubles as does the rate of production of new androgen receptors. The is no f-ing competition for chrsts sake.
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    Quote Originally Posted by StanleyG View Post
    Oh man this thread is full of BS.
    1-dont blast you hcg- run it through your cycle at 250iu's-2x/week
    2-Tren e actually achieves higher blood levels than short esters so dont buy the BS that tren ace is stronger or better, that being said it may be prudent never havng run tren to go with ace since you do not know how you respond and if you have bad sides ace will clear quickly.
    3- The binding affinty /competition theory is total bull****. The only reason people run test lower is that it easier to manage sides that way. The key to sides management begins and ends with estrogen management It is the crux of managing your sides. Lower test, less e , easier sides management. That being said your adex dosing plan will more than do the job. The competition thing is total crap. In the presence of excess androgens the androgen receptor lifespan doubles as does the rate of production of new androgen receptors. The is no f-ing competition for chrsts sake.
    I agree with you on almost all of this, except that I believe blasting hcg is more effective , because it will kick your nuts back up so by the time you start pct, the clomid wont be the only thing helping u. I know hcg is supposed to help you maintain natural test while on cycle, but I have heard that it becomes ineffective after a certain number off weeks
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    Quote Originally Posted by jman6 View Post
    I agree with you on almost all of this, except that I believe blasting hcg is more effective , because it will kick your nuts back up so by the time you start pct, the clomid wont be the only thing helping u. I know hcg is supposed to help you maintain natural test while on cycle, but I have heard that it becomes ineffective after a certain number off weeks
    different strokes with hcg. The way to avoid desesitization is a low dosing scheme like I prefer but you have to see what will work best for you. This method serves me well, blasting may serve you well.
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    And I suppose you have "clinical" studies to back up this BS? Your statement is reckless at best.

    Quote Originally Posted by StanleyG View Post
    3- The binding affinty /competition theory is total bull****. The only reason people run test lower is that it easier to manage sides that way. The key to sides management begins and ends with estrogen management It is the crux of managing your sides. Lower test, less e , easier sides management. That being said your adex dosing plan will more than do the job. The competition thing is total crap. In the presence of excess androgens the androgen receptor lifespan doubles as does the rate of production of new androgen receptors. The is no f-ing competition for chrsts sake.
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    Quote Originally Posted by DetroitHammer View Post
    And I suppose you have "clinical" studies to back up this BS? Your statement is reckless at best.
    Reckless? More like totally accurate perhaps. Im sorry if I offended, I didnt notice that you were one of the people that spouted off some of the ridiculous bull**** perpetrated here but hey if you were, too bad. Oh I just checked - stupid **** like tren pushing test out of the way is all i need to hear out of the likes of you not to waste my time arguing with ignorance. Been in the game longer, know way more, sometimes you should type less and read more and keep your mouth shut before spouting off crap like you posted. I suppose the pros are wasting good test when they inject 2grams of it with only 700mgs of tren .
    Look I came off harsh, but I also dont post about things I dont both have extensive firsthand experience with combined with a high level of knowledge as well. Its the way prudent advice is given. Broscience BS is what you posted- thats a fact.. Im sorry if I offended your ego or came across like a dick but I get tired of seeing it.
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    Quote Originally Posted by StanleyG View Post
    Reckless? More like totally accurate perhaps. Im sorry if I offended, I didnt notice that you were one of the people that spouted off some of the ridiculous bull**** perpetrated here but hey if you were, too bad. Oh I just checked - stupid **** like tren pushing test out of the way is all i need to hear out of the likes of you not to waste my time arguing with ignorance. Been in the game longer, know way more, sometimes you should type less and read more and keep your mouth shut before spouting off crap like you posted. I suppose the pros are wasting good test when they inject 2grams of it with only 700mgs of tren . Look I came off harsh, but I also dont post about things I dont both have extensive firsthand experience with combined with a high level of knowledge as well. Its the way prudent advice is given. Broscience BS is what you posted- thats a fact.. Im sorry if I offended your ego or came across like a dick but I get tired of seeing it.
    Just because it's your opinion doesn't make it accurate. Spouting of like a douchebag makes me think even less of your opinion. I doubt you've been in the game longer than DH btw. I'll takes his educated opinion over some broscience know-all any day of the week.
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    Just as I thought, just BS, nothing else. Sorry if I'm the only one to call you out on your totally ignorant rants but there are some newbees here that might actually think you know what you're talking about. But you don't. I'm not as easily fooled by self proclaimed AAS gurus, as yourself, but others may. Perhaps you can explain in clinical terminology your theory on up-regulation of ARs? I'd like to hear it for the comical value, knowing the utter nonsense of your misinformation.

    Quote Originally Posted by StanleyG View Post
    Reckless? More like totally accurate perhaps. Im sorry if I offended, I didnt notice that you were one of the people that spouted off some of the ridiculous bull**** perpetrated here but hey if you were, too bad. Oh I just checked - stupid **** like tren pushing test out of the way is all i need to hear out of the likes of you not to waste my time arguing with ignorance. Been in the game longer, know way more, sometimes you should type less and read more and keep your mouth shut before spouting off crap like you posted. I suppose the pros are wasting good test when they inject 2grams of it with only 700mgs of tren .
    Look I came off harsh, but I also dont post about things I dont both have extensive firsthand experience with combined with a high level of knowledge as well. Its the way prudent advice is given. Broscience BS is what you posted- thats a fact.. Im sorry if I offended your ego or came across like a dick but I get tired of seeing it.
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    Quote Originally Posted by Lukef2000 View Post
    Just because it's your opinion doesn't make it accurate. Spouting of like a douchebag makes me think even less of your opinion. I doubt you've been in the game longer than DH btw. I'll takes his educated opinion over some broscience know-all any day of the week.
    So perpetrating BS and misinfo is cool as long as you post nicey nice is ok- got it. Some people want the truth and facts, some are here to jerk each other off. Just remember that tren is in there pushing all that test away!! LOL Best of luck.
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    Quote Originally Posted by DetroitHammer View Post
    Just as I thought, just BS, nothing else. Sorry if I'm the only one to call you out on your totally ignorant rants but there are some newbees here that might actually think you know what you're talking about. But you don't. I'm not as easily fooled by self proclaimed AAS gurus, as yourself, but others may. Perhaps you can explain in clinical terminology your theory on up-regulation of ARs? I'd like to hear it for the comical value, knowing the utter nonsense of your misinformation.
    Well since im sure you wont be able to accurately interpret this I will reiterate. In the presence of excess androgens the ar receptor life span and rate of production of new androgen receptors both double. There is no freaking competition. There is no "test pushing tren out" Its nonsense so stop spouting it. The whole reason I posted is so newbs or anyone for that matter wouldnt go around repeating the ridiculous BS misinformation you posted. BTW this info has been around for around 20 years, not quite as long as I have been in the game. Scary you still spout the foolish BS you did.

    J Biol Chem. 1985 Jan 10;260(1):455-61.
    Mechanism of androgen-receptor augmentation. Analysis of receptor synthesis and degradation by the density-shift technique.
    Syms AJ, Norris JS, Panko WB, Smith RG.
    The ductus deferens smooth muscle tumor cell line (DDT1MF-2) contains receptors for, and is stimulated by, androgens. Cells cultured in the absence of androgens maintain a basal level of androgen receptors. Following incubation with various concentrations of the synthetic androgen methyltrienolone (R1881) for 1-6 h, the concentration of these receptors increased from 6.0 to 12.2 fmol/micrograms of DNA, while the equilibrium dissociation constant (Kd) of 0.5 nM for this steroid remained unchanged. The steroid-induced increase in androgen receptor levels was specific for androgens and dependent upon protein synthesis. The mechanism of receptor augmentation was examined by utilization of isotopically dense amino acids to determine rates of receptor appearance and degradation in the presence or absence of [3H]R1881. In the absence of androgens, the half-life of the androgen receptor was 3.1 h, with a rate constant (kD) of 0.22/h. In the presence of 1 nM [3H]R1881, however, the half-life was 6.6 h, with kD = 0.11/h. The rate constant for receptor synthesis (ks) in the absence or presence of [3H]R1881 was calculated to be 1.35 and 2.23 fmol/micrograms of DNA/h, respectively. Thus, androgen-induced androgen-receptor augmentation is explained by an increase both in receptor half-life and in rates of receptor synthesis.
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    When I get back this evening I'll address this drivel. I'm not surprised it impresses you and that you interpret it as fact.

    Quote Originally Posted by StanleyG View Post
    Well since im sure you wont be able to accurately interpret this I will reiterate. In the presence of excess androgens the ar receptor life span and rate of production of new androgen receptors both double. There is no freaking competition. There is no "test pushing tren out" Its nonsense so stop spouting it. The whole reason I posted is so newbs or anyone for that matter wouldnt go around repeating the ridiculous BS misinformation you posted. BTW this info has been around for around 20 years, not quite as long as I have been in the game. Scary you still spout the foolish BS you did.

    J Biol Chem. 1985 Jan 10;260(1):455-61.
    Mechanism of androgen-receptor augmentation. Analysis of receptor synthesis and degradation by the density-shift technique.
    Syms AJ, Norris JS, Panko WB, Smith RG.
    The ductus deferens smooth muscle tumor cell line (DDT1MF-2) contains receptors for, and is stimulated by, androgens. Cells cultured in the absence of androgens maintain a basal level of androgen receptors. Following incubation with various concentrations of the synthetic androgen methyltrienolone (R1881) for 1-6 h, the concentration of these receptors increased from 6.0 to 12.2 fmol/micrograms of DNA, while the equilibrium dissociation constant (Kd) of 0.5 nM for this steroid remained unchanged. The steroid-induced increase in androgen receptor levels was specific for androgens and dependent upon protein synthesis. The mechanism of receptor augmentation was examined by utilization of isotopically dense amino acids to determine rates of receptor appearance and degradation in the presence or absence of [3H]R1881. In the absence of androgens, the half-life of the androgen receptor was 3.1 h, with a rate constant (kD) of 0.22/h. In the presence of 1 nM [3H]R1881, however, the half-life was 6.6 h, with kD = 0.11/h. The rate constant for receptor synthesis (ks) in the absence or presence of [3H]R1881 was calculated to be 1.35 and 2.23 fmol/micrograms of DNA/h, respectively. Thus, androgen-induced androgen-receptor augmentation is explained by an increase both in receptor half-life and in rates of receptor synthesis.
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    Quote Originally Posted by DetroitHammer View Post
    When I get back this evening I'll address this drivel. I'm not surprised it impresses you and that you interpret it as fact.
    Before you try to act all hardass and call this drivel be prepared, its not drivel, its known fact on every experienced steroid board on the net, and it was brought to light by arguably the brightest mind to every address the topic of aas steroid use, cause, and effect, but hey if you cant dazzle them with brilliance go ahead and try to baffle them with bull****. It seems like that is what has been working for you up to this point here.
    You would be better served stating your tren pushing test out of the way comment wasnt accurate and the best reason to run test lower is sides management only... or at the very least not receptor competition or of all the assenine statements - "tren pushing out test" for goodness sake. Just think then you could give accurate advice AND accurate information and stop perpetrating total broscience BS.
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    Quote Originally Posted by StanleyG View Post
    Well since im sure you wont be able to accurately interpret this I will reiterate. In the presence of excess androgens the ar receptor life span and rate of production of new androgen receptors both double. There is no freaking competition. There is no "test pushing tren out" Its nonsense so stop spouting it. The whole reason I posted is so newbs or anyone for that matter wouldnt go around repeating the ridiculous BS misinformation you posted. BTW this info has been around for around 20 years, not quite as long as I have been in the game. Scary you still spout the foolish BS you did.

    J Biol Chem. 1985 Jan 10;260(1):455-61.
    Mechanism of androgen-receptor augmentation. Analysis of receptor synthesis and degradation by the density-shift technique.
    Syms AJ, Norris JS, Panko WB, Smith RG.
    The ductus deferens smooth muscle tumor cell line (DDT1MF-2) contains receptors for, and is stimulated by, androgens. Cells cultured in the absence of androgens maintain a basal level of androgen receptors. Following incubation with various concentrations of the synthetic androgen methyltrienolone (R1881) for 1-6 h, the concentration of these receptors increased from 6.0 to 12.2 fmol/micrograms of DNA, while the equilibrium dissociation constant (Kd) of 0.5 nM for this steroid remained unchanged. The steroid-induced increase in androgen receptor levels was specific for androgens and dependent upon protein synthesis. The mechanism of receptor augmentation was examined by utilization of isotopically dense amino acids to determine rates of receptor appearance and degradation in the presence or absence of [3H]R1881. In the absence of androgens, the half-life of the androgen receptor was 3.1 h, with a rate constant (kD) of 0.22/h. In the presence of 1 nM [3H]R1881, however, the half-life was 6.6 h, with kD = 0.11/h. The rate constant for receptor synthesis (ks) in the absence or presence of [3H]R1881 was calculated to be 1.35 and 2.23 fmol/micrograms of DNA/h, respectively. Thus, androgen-induced androgen-receptor augmentation is explained by an increase both in receptor half-life and in rates of receptor synthesis.
    Now you're sounding like the late, great Nandi. That man is rolling in his grave with all the crap that's out there these days.
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    Quote Originally Posted by tballz View Post
    Now you're sounding like the late, great Nandi. That man is rolling in his grave with all the crap that's out there these days.
    HA No freaking way. Thats exactly where this came from. Talk about missed, he is. If people only had any idea how he shaped the way people use aas today. Things he came up with 20 years ago are still solving issues & dispelling misconceptions today. Threads like this one make me miss him even more, where the young or new to steroids or even vets are fed a bunch of BS and then believe it and regurgitate it as fact. Dude above has no idea who he is attempting to dispute. Makes me laugh. They think I was a douche, Nandi's reply wouldnt have been near so kind in many ways! LOL
    You know Nandi and know some of his knowledge and the stuff he brought to the table you are pretty damn solid in my book.
    On all seriousness every person in or reading this thread would be well served goggling him and his postings from back in the day. There have to be more around here somewhere that knew him and all are using principles and strategies he came up with. Solid in scientific fact and real world experience. Smartest man on aas & ancillary uses, effects, sides and interactions I ever encountered, bar none.
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    Quote Originally Posted by StanleyG View Post
    HA No freaking way. Thats exactly where this came from. Talk about missed, he is. If people only had any idea how he shaped the way people use aas today. Things he came up with 20 years ago are still solving issues & dispelling misconceptions today. Threads like this one make me miss him even more, where the young or new to steroids or even vets are fed a bunch of BS and then believe it and regurgitate it as fact. Dude above has no idea who he is attempting to dispute. Makes me laugh. They think I was a douche, Nandi's reply wouldnt have been near so kind in many ways! LOL
    You know Nandi and know some of his knowledge and the stuff he brought to the table you are pretty damn solid in my book.
    On all seriousness every person in or reading this thread would be well served goggling him and his postings from back in the day. There have to be more around here somewhere that knew him and all are using principles and strategies he came up with. Solid in scientific fact and real world experience. Smartest man on aas & ancillary uses, effects, sides and interactions I ever encountered, bar none.
    I still go over to the forum he started back in 2002 or 2003, cuttingedgemuscle.com, and search out his stuff. He never answered a question without backing it up with a study.
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    Quote Originally Posted by tballz View Post
    I still go over to the forum he started back in 2002 or 2003, cuttingedgemuscle.com, and search out his stuff. He never answered a question without backing it up with a study.
    He is sorely missed and that forum was the best around years ago. I use it to ref things as well sometime just read and research. Place was 10 years ahead of its time.
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    Although I don't normally respond to trolls or jerks like you, I am making an exception. You can carry this on if you want, but unless you have something current and persuasive, just go away for the sake of the others. I can see through your BS, if others can't.

    The whole article you cite is about the half lives of ARs and the possible up-regulation of ARs, written 20 years ago, when the RNA strands and subsequent DNA strands forming a template through transcription were not well understood and hypothesizes drawn were suspect. The whole article actually struggles to explain why, on one hand the transcriptional activity appears to increase androgens in the presence of induced androgens while on the other hand imposing a self mediated stopping point, or down-regulation. Otherwise the more AAS you introduce and the longer you stayed on, the larger you would become with cancerous like growth of the ARs. Even the author of your citation admitted that the data, including his studies, were, “unfortunately the data are equivocal.”


    Even the study, which used isotopically dense amino acids to determine the rates of receptor appearance failed to adequately and accurately distinguish between sensitivity and appearance, but surmised through basal transcription data that not only was sensitivity increased (which I agree) but that production was also increased (something that lacks empirical data on). The logical explanation, assuming you’re following me thus far, is that in the presence of increased androgens the sensitivity of receptors is increased, but not the production of additional cells, but possibly the regeneration of the receptors or extension of half lives.

    This would explain two flaws in that 20 year old study. First, DNA, vice receptors, are genetically programmed and the mere introduction of increased androgens would not increase cell production or alter a persons DNA, but could desensitize the numerous cells that androgens would normally not bind to. It would also logically explain why we do not grow into the Hulk with more the introduction of increased androgens. The growth we experience at the on-set of AAS is the most growth a person will see. Subsequent cycles show only slightly more muscle alteration, but the initial growth, due to increased AR sensitivity, is responsible for the rapid growth. The explanation given in the article is weak at best and struggles to balance the dichotomy of increased AR production but only to a point, then abstract mediation takes over, something that makes no sense at all.

    The transcriptional activity of AR is affected by coregulators that influence a number of functional properties of AR, including ligand selectivity and DNA binding capacity. Unless they are rendered mutant, they are constrained by genetic predisposition and the increased production of AR’s is something that has not been adequately concluded.

    Having said that, let’s take up the argument about AR competition. We all know, or hope we do, that there will always be more receptors than androgens, but looking at the viable host receptors, tren will bind tighter to the AR than will test. And with five times the affinity to bind, it will be the dominant participant. Androgens have a very short window in which to bind. It’s not as if there are enough receptors to go around, so all androgens get a host receptor. It doesn’t work that way. If a person is on tren he needs to let the tren work and do its job. Your position that the only reason a person lowers his test is to reduce sides is ironically correct. Do you see the irony?


    Quote Originally Posted by StanleyG View Post
    Before you try to act all hardass and call this drivel be prepared, its not drivel, its known fact on every experienced steroid board on the net, and it was brought to light by arguably the brightest mind to every address the topic of aas steroid use, cause, and effect, but hey if you cant dazzle them with brilliance go ahead and try to baffle them with bull****. It seems like that is what has been working for you up to this point here.
    You would be better served stating your tren pushing test out of the way comment wasnt accurate and the best reason to run test lower is sides management only... or at the very least not receptor competition or of all the assenine statements - "tren pushing out test" for goodness sake. Just think then you could give accurate advice AND accurate information and stop perpetrating total broscience BS.
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    Quote Originally Posted by DetroitHammer View Post
    Although I don't normally respond to trolls or jerks like you, I am making an exception. You can carry this on if you want, but unless you have something current and persuasive, just go away for the sake of the others. I can see through your BS, if others can't.

    The whole article you cite is about the half lives of ARs and the possible up-regulation of ARs, written 20 years ago, when the RNA strands and subsequent DNA strands forming a template through transcription were not well understood and hypothesizes drawn were suspect. The whole article actually struggles to explain why, on one hand the transcriptional activity appears to increase androgens in the presence of induced androgens while on the other hand imposing a self mediated stopping point, or down-regulation. Otherwise the more AAS you introduce and the longer you stayed on, the larger you would become with cancerous like growth of the ARs. Even the author of your citation admitted that the data, including his studies, were, “unfortunately the data are equivocal.”


    Even the study, which used isotopically dense amino acids to determine the rates of receptor appearance failed to adequately and accurately distinguish between sensitivity and appearance, but surmised through basal transcription data that not only was sensitivity increased (which I agree) but that production was also increased (something that lacks empirical data on). The logical explanation, assuming you’re following me thus far, is that in the presence of increased androgens the sensitivity of receptors is increased, but not the production of additional cells, but possibly the regeneration of the receptors or extension of half lives.

    This would explain two flaws in that 20 year old study. First, DNA, vice receptors, are genetically programmed and the mere introduction of increased androgens would not increase cell production or alter a persons DNA, but could desensitize the numerous cells that androgens would normally not bind to. It would also logically explain why we do not grow into the Hulk with more the introduction of increased androgens. The growth we experience at the on-set of AAS is the most growth a person will see. Subsequent cycles show only slightly more muscle alteration, but the initial growth, due to increased AR sensitivity, is responsible for the rapid growth. The explanation given in the article is weak at best and struggles to balance the dichotomy of increased AR production but only to a point, then abstract mediation takes over, something that makes no sense at all.

    The transcriptional activity of AR is affected by coregulators that influence a number of functional properties of AR, including ligand selectivity and DNA binding capacity. Unless they are rendered mutant, they are constrained by genetic predisposition and the increased production of AR’s is something that has not been adequately concluded.

    Having said that, let’s take up the argument about AR competition. We all know, or hope we do, that there will always be more receptors than androgens,but looking at the viable host receptors, tren will bind tighter to the AR than will test. And with five times the affinity to bind, it will be the dominant participant. Androgens have a very short window in which to bind. It’s not as if there are enough receptors to go around, so all androgens get a host receptor. It doesn’t work that way. If a person is on tren he needs to let the tren work and do its job. Your position that the only reason a person lowers his test is to reduce sides is ironically correct. Do you see the irony?
    Wow you are good at baffling with BS. The amount of speculation in your post compared to this study is not even close, but hey you may have impressed many that do not know better with some big words , hell you even threw in speculative nonsense on ligand binding and transcriptional processes- or course you may not truly realize you did because you would have to fully understand- which you obviously do not - but hey kudos LOL. Some may be put off or impressed by you big words and BS, but not me.
    One simple basic example all will understand for you (oh I have more):
    If we take test with other steroids which have a lower binging affinity to the ar than test, are the effects (androgenic effects if you like) mediated or dismissed due to ar receptor competition? Or course not, it is ridiculous. In fact people cant take HUGE amounts of test with comparatively small amounts of less androgenic steroids yet the effects (again androgenic if you like) and impact off the lower dosed steroids, with a lower binding affinity is still felt, expressed, even documented, in essentially every way. It is the same with taking tren and test. There is no receptor competition. There are of course limiting factors to growth but viable ar's is NOT one of them.
    I implore you do not allow your ego and need to be correct cause you to perpetrate BS. People deserve to know the real deal not BS nonsense on why and how things work. Just stop, this is where it gets downright ridiculous. When people go to the lengths you just did to be right rather than accurate, broscience BS is spawned as the unknowing are impressed by the big words when sometimes the answer is as simple as my example above, or listening to people that have actually done **** instead of talked **** as well LOL.
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    I knew you wouldn't understand anything that was written above a third grade level. Didn't expect you too. You are a parasite on this board and I'm sure others. You apparently believe your own BS which is sad, but deserving. You're an idiot and if nothing else you were called out for the fool that you are. Now everyone can see you're just a loud mouth punk.

    Quote Originally Posted by StanleyG View Post
    Wow you are good at baffling with BS. The amount of speculation in your post compared to this study is not even close, but hey you may have impressed many that do not know better with some big words , hell you even threw in speculative nonsense on ligand binding and transcriptional processes- or course you may not truly realize you did because you would have to fully understand- which you obviously do not - but hey kudos LOL. Some may be put off or impressed by you big words and BS, but not me.
    One simple basic example all will understand for you (oh I have more):
    If we take test with other steroids which have a lower binging affinity to the ar than test, are the effects (androgenic effects if you like) mediated or dismissed due to ar receptor competition? Or course not, it is ridiculous. In fact people cant take HUGE amounts of test with comparatively small amounts of less androgenic steroids yet the effects (again androgenic if you like) and impact off the lower dosed steroids, with a lower binding affinity is still felt, expressed, even documented, in essentially every way. It is the same with taking tren and test. There is no receptor competition. There are of course limiting factors to growth but viable ar's is NOT one of them.
    I implore you do not allow your ego and need to be correct cause you to perpetrate BS. People deserve to know the real deal not BS nonsense on why and how things work. Just stop, this is where it gets downright ridiculous. When people go to the lengths you just did to be right rather than accurate, broscience BS is spawned as the unknowing are impressed by the big words when sometimes the answer is as simple as my example above, or listening to people that have actually done **** instead of talked **** as well LOL.
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    Wow! Welcome back DH. Been wondering where you were.
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    Quote Originally Posted by DetroitHammer View Post
    I knew you wouldn't understand anything that was written above a third grade level. Didn't expect you too. You are a parasite on this board and I'm sure others. You apparently believe your own BS which is sad, but deserving. You're an idiot and if nothing else you were called out for the fool that you are. Now everyone can see you're just a loud mouth punk.
    Ahh so when you are wrong you dont address the basic simple examples that prove it you go on the attack with personal insults. Nice.
    When someone see through your google garbage BS where you even contradict yourself because you really dont KNOW the info you google it, again you reply with a personal attack.
    Just admit you made a mistake, stop perpetrating BS nonsense about receptor competition and tren kicking out test, and stick with facts and what you really know and have personal experience with. Its simple. So simple a 3rd grader could understand it ;-)

    This is so f-ing ridiculous. If your contention was true NOTHING stacked with tren would act on the androgen receptor. Why even bother to take test at all if tren is simply pushing it out. You wouldnt. If it was true you would never stack an androgen with a lower binding affinity with one with a higher binding affinity and get the androgenic effects of the the compound with the lower ar binding affinity - yet you DO get the androgenic effects. Because there is no competition, there is no shortage of androgen receptors (viable as you choose to call them), that is quite simply not how it works, physiologically or in the real freaking world. Just STOP!
    Maybe you dont understand what you are doing. You see people read this and because of your BS facade & the way you come off people BELIEVE it. Then they follow it, then they repeat it and BS broscience 101 is in full effect. Stop. If you were on a predominantly steroid using board with experienced users you would be laughed off the board for posting what you did. This seem to be a younger board, I like it in fact, but people like you do it a disservice posting what you did and not just saying yeah your right when someone corrects you. I imagine you like being a big fish in a small pond and you prob even help some people but you also are taking about things and saying things you obviously do not understand or have personal experience with and doing this community a disservice.
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    Quote Originally Posted by DetroitHammer View Post
    I knew you wouldn't understand anything that was written above a third grade level. Didn't expect you too. You are a parasite on this board and I'm sure others. You apparently believe your own BS which is sad, but deserving. You're an idiot and if nothing else you were called out for the fool that you are. Now everyone can see you're just a loud mouth punk.
    Let's keep this civil. No need for name-calling. This is an awesome debate that everybody can learn from. I've seen this on other forums and the consensus is there is no receptor competition, however, if you have proof/studies to show otherwise let's see them...I love this stuff.
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    Subbed for lolz.
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    Quote Originally Posted by StanleyG View Post
    If your contention was true NOTHING stacked with tren would act on the androgen receptor. Why even bother to take test at all if tren is simply pushing it out. You wouldnt. If it was true you would never stack an androgen with a lower binding affinity with one with a higher binding affinity and get the androgenic effects of the the compound with the lower ar binding affinity - yet you DO get the androgenic effects. Because there is no competition, there is no shortage of androgen receptors (viable as you choose to call them), that is quite simply not how it works, physiologically or in the real freaking world.
    Seems right......
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    Quote Originally Posted by tballz View Post
    Seems right......
    Sex drive that's why you use base test.
    I'm just a dude chasing a dream
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    Quote Originally Posted by superbeast668 View Post
    Sex drive that's why you use base test.
    but wait how could you have a test base if test and tren are competing for receptors and tren "pushes the test out", oh wait you couldn't, yet we all know you can and do which is exactly why it is total bvll**** broscience being spouted off and there is no receptor competition and tren sure as hell in no way pushes test out of receptors. Thank You for stating the obvious and hopefully putting this nonsense garbage to rest.
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    Quote Originally Posted by StanleyG View Post
    but wait how could you have a test base if test and tren are competing for receptors and tren "pushes the test out", oh wait you couldn't, yet we all know you can and do which is exactly why it is total bvll**** broscience being spouted off and there is no receptor competition and tren sure as hell in no way pushes test out of receptors. Thank You for stating the obvious and hopefully putting this nonsense garbage to rest.
    You plain and simple need male hormone presence. You don't need 3 grams of test to one gram of tren.
    I'm just a dude chasing a dream
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    Quote Originally Posted by superbeast668 View Post
    You plain and simple need male hormone presence. You don't need 3 grams of test to one gram of tren.
    Never said you didnt, all I did is call BS on BS and it really is as simple as your test base post which essentially disproves the stupid nonsense someone trying baffle everyone with BS was trying to push off as true. Thats all.
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    Quote Originally Posted by superbeast668 View Post
    Sex drive that's why you use base test.
    You're misunderstanding the post altogether.
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    Quote Originally Posted by tballz View Post
    You're misunderstanding the post altogether.
    I fully understand both sides of the argument. Dh schooled him
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    Quote Originally Posted by superbeast668 View Post
    I fully understand both sides of the argument. Dh schooled him
    bwaaaaaahahahaha...he sure did! You obviously don't understand anything at all. Still laughing at that!!!!
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    *yawn*

    Sinha-Hikim I, Taylor WE, Gonzalez-Cadavid NF, Zheng W, Bhasin S. Androgen Receptor in Human Skeletal Muscle and Cultured Muscle Satellite Cells: Up-Regulation by Androgen Treatment. Journal of Clinical Endocrinology & Metabolism 2004;89(10):5245-55. Androgen Receptor in Human Skeletal Muscle and Cultured Muscle Satellite Cells: Up-Regulation by Androgen Treatment

    Androgens stimulate myogenesis, but we do not know what cell types within human skeletal muscle express the androgen receptor (AR) protein and are the target of androgen action. Because testosterone promotes the commitment of pluripotent, mesenchymal cells into myogenic lineage, we hypothesized that AR would be expressed in mesenchymal precursor cells in the skeletal muscle. AR expression was evaluated by immunohistochemical staining, confocal immunofluorescence, and immunoelectron microscopy in sections of vastus lateralis from healthy men before and after treatment with a supraphysiological dose of testosterone enanthate. Satellite cell cultures from human skeletal muscle were also tested for AR expression."


    Compliments of Dr Michael Scally - I suppose you wanna argue with him too or can your ego just let you shut your mouth and admit you are wrong DH. Sometimes you have to just know when to say when and move on. Oh and STOP perpetrating broscience BS as well......
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    Stanley is trying to say what would the point of running a test/tren/deca cycle if all tren is going to do is take up all the receptors since it is 5x as anabolic. There would be NO reason to run deca, but people do it all the time because tren doesnt hog every god damn receptor
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    Working the gun shop and motorcycles. I lurk from time to time, but didn't want to jump into a discussion without being able to reply back.

    Quote Originally Posted by wicked442 View Post
    Wow! Welcome back DH. Been wondering where you were.
  

  
 

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