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I've been on since june, and im staying on for another 2-3 monthes im doin 25 weeks of test at 750-1000mg , im also doin gh, just started 600mg a week of deca, 400mg of tren, 200mg of winny, and goin back on masteron 400mg a week the last 4 weeks. My question ive been on right now for around 14 weeks, results are starting to slow down, why??? also should i keep seeing results or have i reached a platau. Why is this
I dont calim to know everything about gear so this is only my estimation on your situation. If you have been on for 14 weeks then your body is probably maxing out its ability to grow. How much weight have you gained? For every lb of lbm your body has gained its another lb that has to be maintained, nourished, sustained. if you have gained say 10lbs then suddenly your body has to deal with carrying around 10lbs more muscle. The body likes to be in homeostasis and the rapid weight gain has offset it. So to gain even more is going to become more and more difficult as your body is struggling to adapt to its rapid change in size, needs etc.Quote:
Originally Posted by HumanPerfection1
JMHO.
I second that.
Dam, that's a lot of gear. Hope this isn't your first cycle!
Holy crap, thats alot of gear man.......one would think that if you were experienced enough to be using that much then you would be experienced enough to have the answer to your question
LOL! Interesting perspective Dalton! Makes sense tho...Quote:
Originally Posted by Dalton5
last time i kept switching drugs every 10 weeks, worked good
Bumpin this, if you neede 4000 cal a day to get 10 lbs, you need to add calories to support the additional 10 lbs. You should try to up your food intake at least another 500-100 calories. That is why it gets tough to grow on really long cycles I believe, it gets hard to consume enough food.Quote:
Originally Posted by Prime
IMO that doesnt completely explain it though.. I would like to hear "expert" opinion.. Does the androgen receptor down regulation play a role in this?
There is an excellent article about the "myth" of receptor site saturation with high test cycles. If you can't find it, pm me, I think I have stored here somwhere, I always save the interesting shit. Was posted sometime in the last 2 weeks.Quote:
Originally Posted by stupidhippo
Damn , he must be preparing for the Mr. Olympia ! That or trying to do what some of the old pros have done with their own Super Suicidal Steroid Stack !!! LOL
If you don't change your training routine your results will plateau. That goes for natural and non-natural lifters. I have to cycle my volume, intensity, lifts, and rep ranges pretty much every month in order to keep gaining.
i change up my routein every 6 weeks, imma try eating even more, lol im walking around and cant even look at food im eating so much lol
jesus that's alot of gear...
didn't see any mention of u getting bloodwork done... do u??? with that much gear it wld b a good idea...
i agree
well saidQuote:
Originally Posted by Dalton5
Quote:
Originally Posted by johan
How far are the growth periods apart?
if you know what you are doing juice like there is no tomorrow just remeber to cycle off my boy was on 7 diff types of juice for 5 months at one time he knew what he was doing. maybe you are becoming immune to it??? think of that???
i think you just need to come off for a while. how many cycles have you run and of what?
no sense whatsoever.Quote:
Originally Posted by suav
humanperfection is the guy going for all those comps and titles. he's 22 and he's been working out for 14yrs remember!! he knows whats up
if u " juice like there is no tomorrow" there very well cld be no tomorrow... even if u know what u r doing u need to use your head.. this isn't aspirin your fuking around with ... aas is potent shit.. it needs to be treated as such..Quote:
Originally Posted by suav
haha lol :7up: people were telling me to not trake primo winni fina,,,and i was goona take hell of alot lower dose than that but its also my first cycle..how can you handle so many drugs at such high dosses at once/???? :scratch:Quote:
Originally Posted by HumanPerfection1
test/winny/tren is a great stack. I get blood work done every 6 weeks, My liver values were slightly high from dbol and halo. yes im 22, its 4 years not 14 years, im not little hurcules. Im working my ass off, I wanna do the nyc hurcules in june.
So post your pics, Your story switches all the time. Stick with one lie and run with it.
sure, anyway does anyone have any interesting articles on the receptor cell theory
thats a lot of gear bro
I thought so.Quote:
Originally Posted by HumanPerfection1
and whats everyones thoughts on it
i have one pic in my other thread, its a few monthes old, and i could care less, if you have any good advice to offer i'd love to hear it, if not, hit the gym.Quote:
Originally Posted by IBdmfkr
Learn how to cycle more efficiently, diet properly and train to maximize gains. Obviously you do not know how to follow one, if not all three of these things. Otherwise you would not be asking the question stated above. A very novice question for such an advanced individual like yourself.Quote:
Originally Posted by HumanPerfection1
honestly, this doesent happen when i switch drugs, my diet is near perfect, my training is near perfect so's my rest, those ends are covered. Maybe up the dose of gh from 4ius to 6ius???
DietQuote:
Originally Posted by HumanPerfection1
fvck it 10ius. then see what grows. :rolleyes: your not growing on GH...real GH :bs:
GH isn't quite as impressive as you might think at an early age. 4ius/day for 6 months and I'm quite disappointed.
Shock the muscles. Good advice.Quote:
Originally Posted by redmeat
Quote:
Originally Posted by IBdmfkr
did u run juice with it
Symatech does.Send him a PM and ask.He posted one a while back,I'll look for it.Quote:
Originally Posted by HumanPerfection1
~Pinnacle~
Yes, But I found I did like it during PCT seeing it helps with catabolism.Quote:
Originally Posted by HumanPerfection1
Here's one posted by SYMATECH....
Receptor Down Regulation
Brian Haycock
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 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…
In part 2 we will discuss the role of satellite cells and myonuclei and how testosterone (androgens) activates these systems to create muscle growth far beyond what simple activation of the androgen receptor can produce.
In part 1 of this article we discussed the mistake of thinking about androgen receptors (testosterone receptors) in the same way we think of other receptors such as beta-receptors. Beta-receptors down regulate in response to beta-adrenergic stimulation whereas there is good evidence that androgen receptors increase in numbers in response to androgens. We also discussed the various affects of testosterone on muscle growth. Testosterone does far more than simply increase the rate of protein synthesis!
Now in part 2 we will finish our discussion of androgen receptor regulation as it pertains to the way muscle cells grow. The very mechanism of real muscle growth opens the door for increased androgen receptor number in response to testosterone treatment.
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.
Another group of researchers are quoted as saying:
"…it is intriguing to speculate that the upregulation of AR levels via the administration of pharmacological amounts of androgens might convert some muscles that normally have a minor or no response to muscles with enhanced androgen responsiveness"(8)
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. It does shed some light however on the proportional differences between natural and androgen assisted bodybuilders physiques.
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:
1. 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
2. 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
3. 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
4. Rosenblatt JD, Yong D, Parry DJ., Satellite cell activity is required for hypertrophy of overloaded adult rat muscle. Muscle Nerve 17:608-613, 1994
5. Rosenblatt JD, Parry DJ., Gamma irradiation prevents compensatory hypertrophy of overloaded extensor digitorum longus muscle. J. Appl. Physiol. 73:2538-2543, 1992
6. 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
7. 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
8. Antonio J, Wilson JD, George FW. Effects of castration and androgen treatment on androgen-receptor levels in rat skeletal muscles. J Appl Physiol. 1999 Dec;87(6):2016-9.
Yea, thats it, up the dose, up the doses on everything you take, and your only 22?? At this rate, you won't live to see 32.. Good luck, and if you need that much juice for that long..maybe you don't have that genetic edge to be a pro. I'm 6'5" and 283 pounds...been lifting for 17 years and juiced 10 years and I never had to take that much...wow...good luck bro. :aajack:Quote:
Originally Posted by HumanPerfection1