please help with tren a/test prop cycle

[kaptainkeezy04]

my friend informs me that "Tren will win out for receptor sites over test every time. Any dosage higher than that of your tren is basically a waste." I was planning on shooting 75mg of test prop and 50mg of tren ace every day, but according to the information he has given me, which he says he got from vets/mods on another board, 25mg of prop would be wasted every day. what do you guys think?

[OnTheSauce]

Then all pros would run baby doses. You have a ton of receptors. Use what u want. Personally id swap your dose to 75 Tren and 30 test p. Less sides with higher tren

[Lunk1]

The battling for or filling of receptors is a bunk myth. Slap your friend and tell him to join the site where all the kool kids hang out

Receptors are being reproduced every few hours on average and there are more than enough to go around.

The only part he got right is that higher doses of test are not needed, he just had the why part wrong.

Break down your stats and cycle experience again would ya???

[Alinjr]

100 tren/100 test

[stpete]

my friend informs me that "Tren will win out for receptor sites over test every time. Any dosage higher than that of your tren is basically a waste." I was planning on shooting 75mg of test prop and 50mg of tren ace every day, but according to the information he has given me, which he says he got from vets/mods on another board, 25mg of prop would be wasted every day. what do you guys think?

He's wrong. Very wrong. Those dosages are fine for first time. you could also avoid from being a pin cushion and pin eod if you want. I haven't noticed a single difference from ed to eod.

[anahny]

He's wrong. Very wrong. Those dosages are fine for first time. you could also avoid from being a pin cushion and pin eod if you want. I haven't noticed a single difference from ed to eod.

I personally like to run tren a@ 100mg and test p 50mg eod. Awesome results.

[Bk2]

I would recommend 100 test / 75 mg tren

[Knockout_Power]

The battling for or filling of receptors is a bunk myth. Slap your friend and tell him to join the site where all the kool kids hang out

haha ^^^this

then, do what you wish. Just know that tren is much more potent per volume so why do a bunch of test when the tren can do the work. Dont need a lot. You can see great gains on 350-400/wk tren and a simple 200-250/wk test dose. Combine this with the right diet and just let it amaze

[DanB]

my friend informs me that "Tren will win out for receptor sites over test every time. Any dosage higher than that of your tren is basically a waste." I was planning on shooting 75mg of test prop and 50mg of tren ace every day, but according to the information he has given me, which he says he got from vets/mods on another board, 25mg of prop would be wasted every day. what do you guys think?

Copy/paste from Atomoni's post yesterdayAll anabolic steroids bind to androgen receptors. So yes, it binds to the same receptors as Tren , which binds to the same receptors as Testosterone , which binds to the same receptors as Methandrostenolone , which binds to the same receptors as Stanozolol does, etc. etc. etc. Understand?

And by the way, your plan is utterly useless. Androgen receptors do not saturate, nor do they downregulate. Receptor downregulation and saturation is a COMPLETE MYTH that has been disproven in clinical studies. The diminishing gains experienced in the later parts of a cycle do not result from the myth of 'receptor saturation'. As a matter of fact, the exact OPPOSITE happens when you use anabolic steroids .

The myth of receptor saturation has been disproven in a number of studies I saw, where it was noted that the number of androgen receptors actually INCREASED in response to supraphysiological doses of anabolic steroids and grew FASTER in individuals administered high doses of AAS. There is no such thing as androgen receptor 'downregulation', 'burnout', or the need to 'clean' receptors. All of those propositions sound absolutely absurd in the face of the evidence brought forth by the medical studies I am going to cite here that all display total opposite operation regarding how androgen receptors work.

Now, some people might be wondering still why the effectiveness of anabolic steroids simply decrease and level out over time as well as over the course of a cycle. Well, the reason why we 'cycle' is of course to avoid any long term damage from using supraphysological amounts of AAS. We all already know this. The idea with cycling is to get on, make your gains, and then get off before the body can, for the lack of a better term, 'catch on' to what is going on. With prolonged use of AAS, not only can you encounter permanent health issues, but the effectiveness of the anabolic steroid decreases over time, but NOT because of receptor 'downregulation' or 'saturation' or 'burn out' or whatever quirky whaky name you want to give it. The reason gains diminish over time is for a couple of primary reasons:

1. It happens because your body has begun secreting and producing hormones and proteins that are antagonistic to the anabolic steroids you are using (this is what I meant, going back to what I said about your body 'catching on'). Hormones and proteins such as: cortisol, myostatin, SHBG, estrogen and various other factors all increase the longer you are on a cycle. The only way to prevent this is either to use ancilliaries that will somewhat combat the rise of these antagonistic devices, OR to simply get off cycle and allow the body to 'normalize' itself.

2. Lets be realistic here. A 5'10" 170lb. male at 10% bodyfat hopping on a cycle is going to obviously be able to slap on a whole lot more amount of muscle mass than a 5'10" 210 lbs. at 10% bodyfat. The latter subject has far more muscle mass on him, and therefore is closer to his genetic limitations than the former subject. The more cycles you do, the more mass you gain, the closer you reach your limit and therefore the slower the gains will come on every subsequent cycle. If you were to build yourself up to 225 lbs. at 10% bodyfat, and lets say you are very close to your genetic limit... and suddenly a life situation strikes and you lose a lot of muscle, leaving you at lets say 180 lbs., if you were to do a cycle to get yourself back up, the gains would then be dramatic again. Muscle growth never really occurs in a linear consistent fashion. If that were the case, we'd all be champion bodybuilders after a handful of cycles.

Read this:

Taking issue with the idea of androgen receptor down-regulation.
By Bryan Haycock MS.

There is as much misinformation about steroids as there is good information had among bodybuilding enthusiasts. Go to any gym and you will hear some kid spouting off to his buddies about how steroids do this, or how they do that, or whatever. This soon starts somewhat of a pissing contest (excuse the expression) as to who knows more about steroids. It's the same kind of titillating and infectious banter that adolescent boys get into about girls and sex. With steroid banter you hear all the popular terms like Deca , Test, GH, gyno , zits, raisins, "h-u-u-u-ge", roid, freak, monster, roid-rage, "I knew this guy once", etc., etc.. If by some rare chance they are smart and have been reading this or some other high quality bodybuilding site on the net, they may actually get a few details right. More often than not they know just enough to be dangerous. Fortunately steroids haven't proven to be all that dangerous. Not only that, but most of these guys who are infatuated with steroids won't ever use or even see them except in magazines.

This kind of ego driven gym talk doesn't really bother me until they begin giving advice to other clueless people who actually have access to them. Spewing out steroid lingo gives other less experienced kids the impression that these kids actually know what they are talking about. That's how all of the psuedo-science folklore about steroids perpetuates. This is also why most people who actually use steroids know little about them. This last fact should bother anyone who cares about bodybuilding and/or bodybuilders.

I started out with this article planning on giving some textbook style explanation as to why using steroids doesn't down regulate androgen receptors (AR). Then after considering some of my critics views that I tend to write articles that hardly anyone can read, I decided to write an easy to read, yet informative explanation about what androgens actually do and how this precludes androgen receptor down regulation. I still have a few references but not so many that it looks like a review paper.

Androgen receptors down-regulate….Don't they?
One misunderstood principle of steroid physiology is the concept of androgen receptors (AR), sometimes called "steroid receptors", and the effects of steroid use on their regulation. It is commonly believed that taking androgens for extended periods of time will lead to what is called AR "down regulation". The premise for this argument is; when using steroids during an extended cycle , you eventually stop growing even though the dose has not decreased. This belief has persisted despite the fact that there is no scientific evidence to date that shows that increased levels of androgens down regulates the androgen receptor in muscle tissue.

The argument for AR down-regulation sounds pretty straightforward on the surface. After all, we know that receptor down-regulation happens with other messenger-mediated systems in the body such as adrenergic receptors. It has been shown that when taking a beta agonist such as Clenbuterol , the number of beta-receptors on target cells 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.) This leads to a decrease in the potency of a given dose. Subsequently, with fewer receptors you get a smaller, or diminished, physiological response. This is a natural way for your body to maintain equilibrium in the face of an unusually high level of beta-agonism.

In reality this example using Clenbuterol is not an appropriate one. Androgen receptors and adrenergic receptors are quite different. Nevertheless, this is the argument for androgen receptor down-regulation and the reasoning behind it. The differences in the regulation of ARs and adrenergic receptors in part show the error in the view that AR down-regulate when you take steroids . Where adrenergic receptor half-life is decreased in most target cells with increased catecholamines, AR receptors half-live's are actually increased in many tissues in the presence of androgens.1

Let me present a different argument against AR down-regulation in muscle tissue. I feel that once you consider all of the effects of testosterone on muscle cells you come to realize that when you eventually stop growing (or grow more slowly) it is not because there is a reduction in the number of androgen receptors.

Testosterone : A multifaceted anabolic
Consider the question, "How do anabolic steroids produce muscle growth?" If you were to ask the average bodybuilding enthusiast I think you would hear, "steroids increase protein synthesis." This is true, however there is more to it than simple increases in protein synthesis. In fact, the answer to the question of how steroids work must include virtually every mechanism involved in skeletal muscle hypertrophy. These mechanisms include:

Enhanced protein synthesis

Enhanced protein synthesis

Enhanced growth factor activity (e.g. GH, IGF -1, etc.)

Enhanced activation of myogenic stem cells (i.e. satellite cells)

Enhanced myonuclear number (to maintain nuclear to cytoplasmic ratio)

New myofiber formation

Starting with enhanced growth factor activity, we know that testosterone increases GH and IGF-1 levels. In a study by Fryburg the effects of testosterone and stanozolol were compared for their effects on stimulating GH release.2 Testosterone enanthate (only 3 mg per kg per week) increased GH levels by 22% and IGF-1 levels by 21% whereas oral stanozolol (0.1mg per kg per day) had no effect whatsoever on GH or IGF-1 levels. This study was only 2-3 weeks long, and although stanozolol did not effect GH or IGF-1 levels, it had a similar effect on urinary nitrogen levels.

What does this difference in the effects of testosterone and stanozolol mean? It means that stanozolol may increase protein synthesis by binding to AR receptors in existing myonuclei, however, because it does not increase growth factor levels it is much less effective at activating satellite cells and therefore may not increase satellite cell activity nor myonuclear number directly when compared to testosterone esters. I will explain the importance of increasing myonuclear number in a moment, first lets look at how increases in GH and IGF-1 subsequent to testosterone use effects satellite cells.

Don't forget Satellite cells!
Satellite cells are myogenic stem cells, or pre-muscle cells, that serve to assist regeneration of adult skeletal muscle. Following proliferation (reproduction) and subsequent differentiation (to become a specific type of cell), satellite cells will fuse with one another or with the adjacent damaged muscle fiber, thereby increasing the number of myonuclei for fiber growth and repair. Proliferation of satellite cells is necessary 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.

In order to better understand what is physically happening between satellite cells and muscle cells, try to picture 2 oil droplets floating on water. The two droplets represent a muscle cell and a satellite cell. Because the lipid bilayer of cells are hydrophobic just like common oil droplets, when brought into proximity to one another in an aqueous environment, they will come into contact for a moment and then fuse together to form one larger oil droplet. Now whatever was dissolved within one droplet (i.e. nuclei) will then mix with the contents of the other droplet. This is a simplified model of how satellite cells donate nuclei, and thus protein-synthesizing capacity, to existing muscle cells.

Enhanced activation of satellite cells by testosterone requires IGF-1. Those androgens that aromatize are effective at not only increasing IGF-1 levels but also the sensitivity of satellite cells to growth factors.3 This action has no direct effect on protein synthesis, but it does lead to a greater capacity for protein synthesis by increasing fusion of satellite cells to existing fibers. This increases the number of myonuclei and therefore the capacity of the cell to produce proteins. That is why large bodybuilders will benefit significantly more from high levels of androgens compared to a relatively new user.

Testosterone would be much less effective if it were not able to increase myonucleation. There is finite limit placed on the cytoplasmic/nuclear ratio, or the size of a muscle cell in relation to the number of nuclei it contains.4 Whenever a muscle grows in response to training there is a coordinated increase in the number of myonuclei and the increase in fiber cross sectional area (CSA). When satellite cells are prohibited from donating viable nuclei, overloaded muscle will not grow.5,6 Clearly, satellite cell activity is a required step, or prerequisite, in compensatory muscle hypertrophy, for without it, a muscle simply cannot significantly increase total protein content or CSA.

More myonuclei mean more receptors
So it is not only true that testosterone increases protein synthesis by activating genetic expression, it also increases the capacity of the muscle to grow in the future by leading to the accumulation of myonuclei which are required for protein synthesis. There is good reason to believe that testosterone in high enough doses may even encourage new fiber formation. To quote the authors of a recent study on the effects of steroids on muscle cells:

"Intake of anabolic steroids and strength-training induce an increase in muscle size by both hypertrophy and the formation of new muscle fibers. We propose that activation of satellite cells is a key process and is enhanced by the steroid use."7

Simply stated, supraphysiological levels of testosterone give rise to increased numbers of myonuclei and thereby an increase in the number of total androgen receptors per muscle fiber. Keep in mind that I am referring to testosterone and testosterone esters. Not the neutered designer androgens that people take to avoid side effects . This is not an argument to rapidly increase the dosages you use. It takes time for these changes to occur and the benefits of higher testosterone levels will not be immediately realized.

Maintenance of the kind of muscle mass seen in top-level bodybuilders today requires a given level of androgens in the body. That level will vary from individual to individual depending on their genetics. Nevertheless, if the androgen level drops, or if they were to "cycle off" the absolute level of lean mass will also drop. Likewise, as the level of androgens goes up, so will the level of lean mass that individual will be able to maintain. All of this happens without any evidence of AR down regulation. More accurately it demonstrates a relationship between the amount of androgens in the blood stream and the amount of lean mass that you can maintain. This does not mean that all you need is massive doses to get huge. Recruitment of satellite cells and increased myonucleation requires consistent "effective" training, massive amounts of food, and most importantly, time. Start out with reasonable doses. Then, as you get bigger you can adjust your doses upwards.

References:

Kemppainen JA, Lane MV, Sar M, Wilson EM. Androgen receptor phosphorylation, turnover, nuclear transport, and transcriptional activation. Specificity for steroids and antihormones. J Biol Chem 1992 Jan 15;267(2):968-74

Fryburg DA., Weltman A., Jahn LA., et al: Short-term modulation of the androgen milieu alters pulsatile, but not exercise- or growth hormone releasing hormone -stimulated GH secretion in healthy men: Impact of gonadal steroid and GH secretory changes on metabolic outcomes. J Clin Endocrinol. Metab. 82(11):3710-37-19, 1997

Thompson SH., Boxhorn LK., Kong W., and Allen RE. Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin -like growth factor-I. Endocrinology. 124:2110-2117, 1989

Rosenblatt JD, Yong D, Parry DJ., Satellite cell activity is required for hypertrophy of overloaded adult rat muscle. Muscle Nerve 17:608-613, 1994

Rosenblatt JD, Parry DJ., Gamma irradiation prevents compensatory hypertrophy of overloaded extensor digitorum longus muscle. J. Appl. Physiol. 73:2538-2543, 1992

Phelan JN, Gonyea WJ. Effect of radiation on satellite cell activity and protein expression in overloaded mammalian skeletal muscle. Anat. Rec. 247:179-188, 1997

Kadi F, Eriksson A, Holmner S, Thornell LE. Effects of anabolic steroids on the muscle cells of strength-trained athletes. Med Sci Sports Exerc 1999 Nov;31(11):1528-34
This is why I don't support long cycle lengths. If anything, they're simply a waste of the money you spent on your gear as positive returns simply diminish after the 8-10 week mark (and it varies between people). The longer you remain on, the more your body will flood itself with hormones and proteins that are antagonistic to muscle growth and the AAS you are using.

[kaptainkeezy04]

haha ^^^this

then, do what you wish. Just know that tren is much more potent per volume so why do a bunch of test when the tren can do the work. Dont need a lot. You can see great gains on 350-400/wk tren and a simple 200-250/wk test dose. Combine this with the right diet and just let it amaze

right on!