can your body become resistent to steroids

[gangers]

just wanna know if my body will become resistent to steroids ????

[Dukkit]

correct me if im wrong Vets, but your receptors will downgrade. thats why after awhile, guys up their doses to get the same results. hence... taking a good amount of time off. in order for your bodies hormones to regulate and your receptors to clean out.

[hdd123]

just wanna know if my body will become resistent to steroids????

Actually every drugs used in prolonged periods, can cause some addiction.

[sphincter]

Actually every drugs used in prolonged periods, can cause some addiction.

addiction? reallY? care to back up your statement by any sort of psuedo science?

there are plenty ofdrugs and compounds that do not cause addiction of any kind under prolonged use. As mentioned, the body may become resistant to the compound thereby requiring higher dosing but this by no means constitutes and addiction.

[Atomini]

correct me if im wrong Vets, but your receptors will downgrade. thats why after awhile, guys up their doses to get the same results. hence... taking a good amount of time off. in order for your bodies hormones to regulate and your receptors to clean out.

Nope, receptors do not downregulate nor do they "saturate" as it was once commonly theorized. A recent study has disproven this. They discovered that muscle cells, in the presence of supraphysiological amounts of androgens actually grow MORE receptors even FASTER on the muscle cells. So now the only logical reason why gains stop and/or slow down on cycle is because of the other proteins and counter-hormones the body produces to counter the high amounts of exogenous androgens (stuff like SHBG, cortisol, estrogen, etc.), not because of 'receptor saturation'.

So yes, your body does become resistant to the muscle-building effects of AAS. This is one of the many reasons why we cycle.

[millionairemurph]

Nope, receptors do not downregulate nor do they "saturate" as it was once commonly theorized. A recent study has disproven this. They discovered that muscle cells, in the presence of supraphysiological amounts of androgens actually grow MORE receptors even FASTER on the muscle cells. So now the only logical reason why gains stop and/or slow down on cycle is because of the other proteins and counter-hormones the body produces to counter the high amounts of exogenous androgens (stuff like SHBG, cortisol, estrogen, etc.), not because of 'receptor saturation'.

So yes, your body does become resistant to the muscle-building effects of AAS. This is one of the many reasons why we cycle.

Wow, good info! thanks brother

[Phate]

Nope, receptors do not downregulate nor do they "saturate" as it was once commonly theorized. A recent study has disproven this. They discovered that muscle cells, in the presence of supraphysiological amounts of androgens actually grow MORE receptors even FASTER on the muscle cells. So now the only logical reason why gains stop and/or slow down on cycle is because of the other proteins and counter-hormones the body produces to counter the high amounts of exogenous androgens (stuff like SHBG, cortisol, estrogen, etc.), not because of 'receptor saturation'.

So yes, your body does become resistant to the muscle-building effects of AAS. This is one of the many reasons why we cycle.

could you cite this information or paste the study, i'm not saying your wrong i'm just interested in reading the study, i love this type of stuff

[ShadetreeJones]

Nope, receptors do not downregulate nor do they "saturate" as it was once commonly theorized. A recent study has disproven this. They discovered that muscle cells, in the presence of supraphysiological amounts of androgens actually grow MORE receptors even FASTER on the muscle cells. So now the only logical reason why gains stop and/or slow down on cycle is because of the other proteins and counter-hormones the body produces to counter the high amounts of exogenous androgens (stuff like SHBG, cortisol, estrogen, etc.), not because of 'receptor saturation'.

So yes, your body does become resistant to the muscle-building effects of AAS. This is one of the many reasons why we cycle.

Now thats good stuff. Well researched and well spoken. Phenomenal.

[Atomini]

could you cite this information or paste the study, i'm not saying your wrong i'm just interested in reading the study, i love this type of stuff

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

[Phate]

sweet, thanks bro, gonna definitely print and add to my "steroid book"

[Atomini]

sweet, thanks bro, gonna definitely print and add to my "steroid book"

For sure, and tell as many people as you can. SO many people today still believe in the 'receptor downregulation' or 'saturation' theory. It's been proved to be complete bullshit.

[Phate]

for sure, i'll keep this link in my arsenal of stuff, if you haven't noticed i like posting links to good threads for people to read and i'll add this one

[Schmidty]

Nope, receptors do not downregulate nor do they "saturate" as it was once commonly theorized. A recent study has disproven this. They discovered that muscle cells, in the presence of supraphysiological amounts of androgens actually grow MORE receptors even FASTER on the muscle cells. So now the only logical reason why gains stop and/or slow down on cycle is because of the other proteins and counter-hormones the body produces to counter the high amounts of exogenous androgens (stuff like SHBG, cortisol, estrogen, etc.), not because of 'receptor saturation'.

So yes, your body does become resistant to the muscle-building effects of AAS. This is one of the many reasons why we cycle.

+1... I wonder if u regulated all of these during ur cycle u would keep growing. SHBG can be regulated by provirion, estrogen has countless things, same with cortisol. HMM???

[Atomini]

+1... I wonder if u regulated all of these during ur cycle u would keep growing. SHBG can be regulated by provirion, estrogen has countless things, same with cortisol. HMM???

Yeah I see where you're definitely coming from, but you gotta remember that even though you use proviron , the body will always catch on and then at some point start secreting even MORE SHBG.

There are also other processes the body increases or decreases besides the aformentioned (cortisol, estrogen, SHBG).

You also have to understand that with each cycle done, you have added more and more muscle to your frame. And in many people, surpassing their genetic potential in doing so. As the bigger you get, the harder your body aims to bring it self to its set weight, simply because the human body can only pack on so much muscle, as we all have a limit and as we get closer and closer to that limit, it gets more and more difficult to put on muscle. What I mean is look at it this way: 20 pounds worth of gains on a 180 pound person is alot, but not on someone thats 250 pounds, or at least not as much. That's why for a first cycle, you always see amazing gains and then subsequent cycles after that it becomes less and less and harder and harder. And this has nothing to do with receptors or counteracting hormones, it just has to do with the limit of muscle that can be packed onto a human frame. Am I making sense?

[Phate]

perfect sense, AS are in actuality a stepping stone, not the final solution, follow my logic on this and tell me if i'm way off, keep in mind that i have nothing to base this off of, i'm just daydreaming so to speak

when our bodies are close to their genetic potential then gains slow down and it is then that most of us use AS to attain a higher level of muscularity then normally would be possible

but even AS can only go so far, so as they reach their limit of synthetic growth enhancement we would need something even more potent then AS to allow us to traverse our chemically enhanced limits to another level

using that logic AS are just stepping stone, though since nothing more potent exists we'll have to wait before we hypothesize on that "higher level"

[james21]

maybe if you shoot them in your "VAINS"

[hdd123]

addiction? reallY? care to back up your statement by any sort of psuedo science?

there are plenty ofdrugs and compounds that do not cause addiction of any kind under prolonged use. As mentioned, the body may become resistant to the compound thereby requiring higher dosing but this by no means constitutes and addiction.

No, u ****in' asshole! I s...UPS I'm really sorry for pelting u with rough words. But u must know that I mentioned not dietary supplements or weak prohormones, but I meaned real medicions (ya know- all those pain killers, narcotic medicions, psichotropic drugs and even...STEROIDS (yes they WERE also listed in one professional book of medicine as substances that may cause even physical addiction)). Second, high dosage as cause of addiction is constant only then, if the drug used for prolonged periods (it also depends on what kind of drug is it). But anyway, even quite small dose (if used for a very long time) may cause some addiction, which symptomes might appear, when it's considered to drop it right- then.

[Big]

Don't believe everything you read about steroids , I've read some ridiculous stuff, I don't post it as fact.

[hdd123]

Don't believe everything you read about steroids, I've read some ridiculous stuff, I don't post it as fact.

Yeah, there might be some overstates or, or else though...not always. Also everyone might react very individual to roids or other substances + genetics dictates also it's rulles.
But the testimony, that steroids can't make u addicted, might be also quite bullshit...these corticosteroids...u must know, that after long term use (and especially in high doses), when u tryin to come of rapidly u might get thrashing withdrawal syndrome or this might turn even more lethal. But even if u're coming off step by step u're feelin as a wasted piece of shit. So don't rate the worse sides of roids too low. If steroids used in cycles and not too long and u don't increase intake so rapidly it might be much safer. But in my opinion, when the roids stoped to use for starting pct and the body has became lax to pruduce something by itself, it still might be some kind of addiction.

[naturalsux]

some good info in here.