Check my Tren E/Test E cycle please
- 08-02-2014, 11:56 PM
Check my Tren E/Test E cycle please
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
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.
- 08-03-2014, 04:22 PM
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.
- 08-03-2014, 09:00 PM
08-03-2014, 09:01 PM
Anything else that should be fixed with this cycle?
08-03-2014, 09:02 PM
[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.
08-03-2014, 09:07 PM
08-03-2014, 10:23 PM
08-04-2014, 03:38 PM
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.
08-05-2014, 02:08 PM
08-05-2014, 03:51 PM
08-05-2014, 07:58 PM
08-05-2014, 11:20 PM
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.
08-06-2014, 04:03 AM
08-06-2014, 07:17 AM
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.
08-06-2014, 07:19 AM
08-06-2014, 07:26 AM
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.
08-06-2014, 07:56 AM
08-06-2014, 08:28 AM
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.
08-06-2014, 10:04 AM
08-06-2014, 10:49 AM
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.
08-06-2014, 10:52 AM
08-06-2014, 11:53 AM
08-06-2014, 08:30 PM
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?
08-07-2014, 06:54 AM
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.
08-07-2014, 07:47 AM
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.
08-07-2014, 07:58 AM
Wow! Welcome back DH. Been wondering where you were.
08-07-2014, 08:55 AM
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.
08-07-2014, 09:47 AM
08-07-2014, 10:05 AM
Subbed for lolz.
I'm just a dude chasing a dream
08-07-2014, 11:38 AM
08-07-2014, 02:15 PM
08-07-2014, 03:00 PM
08-07-2014, 03:52 PM
08-07-2014, 03:58 PM
08-07-2014, 04:02 PM
08-07-2014, 04:04 PM
08-07-2014, 04:10 PM
08-07-2014, 04:18 PM
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......
08-07-2014, 06:20 PM
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
08-07-2014, 06:59 PM
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