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When one begins his 1st cycle aka a novice...they say to limit the dosage to something low(not sure about the duration), why is this? Then it seems the cycles following the 1st one are increased in dosage. Is this because the body develops a tolerance to that low dosage and the only way to increase gains is to up the dosage every cycle thereon? Is it harmful to start off at a high dosage for your 1st cycle? Let me know what you guys think, thanks i appreciate your time and effort :)
The 1st cycle is mostly to see how your body reacts to the subject. 1st cycle should always be a test-only cycle 400-500mg/WK, preferbly test e or cyp IMO. 10-12 weeks is mostly suggested for a 1st cycle and I agree.
but is the reason people increase the dosages on their cycles due to the fact that the body builds a tolerance to previous dosages? :unsure:
Quote:
Originally Posted by WannabePro
dont you think they'd up the dose because they're, in fact, BIGGER than they previously were?? plus they know how the body responds to that specific dose so they feel that they can up the dose a bit.
So what you're saying is the more muscle mass you acquire, the dosage has to be increased?Quote:
Originally Posted by wolfyEVH
Quote:
Originally Posted by WannabePro
it probably necessarily doesnt mean exactly that, but some people think that the more gear you use, the more gains you will see. i have yet to see any studies on multiple cycles using the same low amount, i know people rave about the low dose cycle (bask8kace).....until i see some proof that increasing dosage is unnecessary, i'd up the dose myself.......you know what you can handle after your first cycle, so you'll wanna increase the dose the next cycle and try to accomplish what you did before. JMO.
Personally i think you just need to see how your body reacts to the juice, for me it took a couple of years experimenting as there are so many different types of juice and combinations and cycles. After years of trying what works for me, i stuck with 1 particular thing i liked and thats me really, as i dont have the same goals as everyone else obviously my view will be different I dont count numbers anymore but i have never had to use more than i was using 5 years ago to be honest to get the same effect, some people do take more and more, and they can probably take it but i think there is a limit, safest way to find it for me was to work my way up, and when i found the sides were too much, then i cut back to find what i called a tolerable time while i was on.
You have to way up the pros and the cons, like am i prepared to lose all my hair, **** my prostrate, hurt my joints/ligaments from lifting too much or taking too much gear just so i can gain a lb more?? when you find your own level, then i would just stick with that, some people can tolerate anything, some people cant, thats why there is no one answer to this question
peace
thats the truth right there. People experiment first cycle to see how they react, and then up dosages to get better gains, but only to a certain level. At some point, as he said, you have to weigh the costs to the benefits, and decide if it is worth it to you to gain the few extra pounds!Quote:
Originally Posted by The Original Jason
weight is a factor when using steroids. Im not sure about the tolerance idea. That would mean what?? Your body learns to metabolize it faster or more efficiantly. Or that the hormone will converted to other hormones more easily?? Im pretty sure that the later doesnt happen to me. I have been cycling 2+ grams a week for a few cycles now and dont have any problem with gyno or my body aromitizing my gear.
By the way untill I see a 250-300lbs guys advocating low dose cycles Ill stick with my way of cycling. I want to be 300lbs some day and im not gonna get there doing less than a gram a week.
Next post is an article about receptors, it wont answer all your questions but will help you figure out how it works.
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.
after i asked you to post in this forum about 14 hours ago, how come you finally decided too? oh wait....the super super mod posted and you posted right after him!!! "as he said?" haha what a kiss a$$ lolol....just giving you a hard time haha....Quote:
Originally Posted by angelxterminator
[QUOTE=OJ]no need to quote everything so long it makes the place look untidy:)QUOTE]
whoa ...i'll get started on chapter 1 of this novel tomorrow if you dont mind lol. I really need some sleep. i'll read it tomorrow and let you know what ive learned. thanks for the incredible help and effort !!!
Quote:
Originally Posted by WannabePro
Exactly. It's directly connected.
so for example,Quote:
So what you're saying is the more muscle mass you acquire, the dosage has to be increased?
someone who starts out at say 135lb should take say 500mg week of test and 400mg week of deca and say 40mg day of dbol.
then someone whos starting out at say 270lb should start on 1g test 800mg deca and 80mg dbol per day?
sorry thats bull****, its not about weight at all
you can read 1000 posts back of people asking for juice advise and i dont think you will once read someone asking what weight are you before they decide what dosage that person should use.
I started off at 180ish and am currently 250ish, still using same dosages
peace
juicing is sort of simple and complex at the same time - each person reacts slightly differently but the basic concept is inviolable - the further you are from your maximum natural limit, the more juice you will need to grow. Thats why some newbies can gain a solid 20lbs on a first low dose cycle - they are far from their max potential - now if they are at the very limit of their natural levels, they might do better with a little more - but the next round will need to increase if they have reached the limit with the level of juice they have - most people dont really reach their limits the first time or two and probably start juicing before natural limits and thats why they can stay with 500mg per week for 3 cycles or so - but eventually, you have to up it if you want to grow further - its also why people who are far beyond their limits pretty much stay on at some doseage level.
did you start working out at the same time you started using juice?Quote:
Originally Posted by The Original Jason
what i was trying to say. you said it better.Quote:
Originally Posted by CYCLEON
i've tried arguing this before and got flamed to high heaven.Quote:
Originally Posted by CYCLEON
very complicated it seems. Lots of expermental doses before the the right one is found.Quote:
Originally Posted by CYCLEON
NOW when someone cycles a drug such as dbol, that drug can only be taken for so long before the body becomes immune to it so im assuming the androgen receptors are blocked from this drug. I guess what im trying to say is that we know this because we stop making gains from this particular drug but its hard to know if yous stack another androgenic steroid with it. So if taking for example 50mg of anadrol, after a while it stops working. Will other androgenic drugs be effected by this in the sense that the strentgh of the drug with be decreased because the androgen receptors have been filled by the anadrol to whatever extent they did to the AAS receptors?
Denkall produces a product called DENKADIOL. Which supposedly unblocks the receptors. What's your thought on this jason? thanksQuote:
Originally Posted by The Original Jason
i try not to get too complicated, after all juicing is very simple really, we just are complicated people lol. Personally i would never bother with stuff like that, i have used ketotifen before with clen but it used to knock me to sleep so i stopped. If your just the average juicer doing cycles on and off as you need to, dont think you need to bother about receptors. The more you talk about it, the more confused you will get.
i personally dont think receptors get "blocked" or downregulated however you want to put it, thats just my personal view
peace
Quote:
Originally Posted by WannabePro
it really isnt - based upon your stats, my guess is that you can still make good gains at 1 gram of test + 4-500mgs of deca + orals - now once you hit say 280-285 at 11% you are going to need to boost it up 25% or so perhaps to get that next 10-15 lbs of solid gain
Thanks Jason, i heard Deca is the only drug out there that you can take year long without becoming immune to it.Quote:
Originally Posted by The Original Jason
*oh by the way, since you are a super super moderator, i think that avatar needs to be changed to JASON (witht the hockey mask), CYLEON has that scary ICON and so does the mod with the CYCLOPS eye. and you're above them (super super) haha.....you need to make your presense felt and scare and intimidate us like cycleon and the cyclops eye guy lol
oic, but that is purely "hypothetical" right? I know you're very smart, and i dont mean to offend your intelect by any means. But once someone finds that dosage range, and keeps making gains every cycle. there is no need to up the anny right? this guy said he's used the same dose for 5 years because he keeps making gains of it. your thoughts please. thanks cycleon.Quote:
Originally Posted by CYCLEON
oh by the way, your avatar looks like that dragon beast from Lord of the Rings 1, whered u get it?
Receptor downgrade is a largely myth.
Humans given 15 mg of oxandrolone daily for 5 days, had their skeletal muscle AR density almost double.
In another study, when exposed to testosterone ( in vitro), skeletal muscle AR expression increased quite a bit.
In another study, older men were given testosterone to bring their testosterone levels into the medium-high range. Androgen Reeptor (expression) more than doubled after the first month, however, by 6 months it returned to baseline; Baseline...but not below. Downregulated? Hardly. And we're talking about 6 months that this took....not the typical 3 month cycle most guys run.
References (in order):
J Clin Endocrinol Metab. 1999 Aug;84(8):2705-11.
Short-term oxandrolone administration stimulates net muscle protein synthesis in young men.
Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR, Ferrando AA
Endocrinology. 1996 Apr;137(4):1385-94.
Testosterone up-regulates androgen receptors and decreases differentiation of porcine myogenic satellite cells in vitro
Doumit ME, Cook DR, Merkel RA.
Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7
of course if your still making gains, it makes common sense that you dont need to up the doses, however i highly doubt you will be using exactly same compounds over and over again unless your like me lol, and i doubt that.
as hooker posted, totally agree receptor downreg makes great pubtalk and big up urself with your mates in gym, however its b/s
peace
good point there. Well if that is the case, then why do drugs stop working after a period of time. You cant take anadrol or dbol for 20 weeks with consistent gains. The gains stop after a short period of time, so the drug probably has stop working because the gains stop coming. I know most normal people dont stay on 17aa's for that long but think about it. These drugs will not work forever. there is a reason. your thoughts?Quote:
Originally Posted by hooker
Any answer to that would be mostly speculation.
Quote:
Originally Posted by WannabePro
You don't become immune to test. If this were true.. we'd shrivle up within months of being born and turn to girls.
You stop making gains because the amount of test you're taking supports x amount of muscle. You take more, you build/sustain more. You take less, you build/sustain less.
We all agree that receptor sites dont down regulate.. But we are not in agreement with the weight factor. So if its not receptor down regulation and weight is not a factor. What is it then???