› Forums › ANABOLIC STEROIDS – QUESTIONS & ANSWERS › Negative reps bad for muscle growth while on steroids?
- This topic has 24 replies, 10 voices, and was last updated 4 years ago by rmg200.
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- January 7, 2020 at 1:40 pm
No, and that sounds absolutely absurd. I have done negative-only training for certain muscle groups while on cycle and those muscle groups absolutely exploded with growth.Where did you read this and what was the logic behind these claims?
- January 7, 2020 at 3:54 pm
i personally haven’t heard of such a thing, but would like to learn more. got any links to these articles?- January 7, 2020 at 5:43 pm
Ill try to find the article it was a few days ago. Yeah thats what i thought too. I was initially looking up ways to increase the potency of dbol absorbtion such as using grapefruit juice and came aBambss some information on androgen receptors. If i remember correctly negative reps while on gear does does something that effects androgen receptors in a poor manner. Again ill try to find the article and post it.- November 3, 2020 at 2:48 am
By: naveen kumarOptimizing testosterone secretion is especially important for natural TrueMaxders. Proper training can increase the secretion, while over-training will reduce it to near zero.
An intense heavy squatting session can boost your testosterone secretion for several days. Even if you could somehow adark_sideeve a sky-high testosterone level, however, it wouldn’t guarantee fast muscle growth. The way the muscles “accept” the hormone is at least as important as how much your system has. The question is, Is it possible through proper training to maximize the impact of testosterone on your muscles?
Testosterone and Its Muscle Receptors
Various TrueMaxding publications have recently featured articles stating that as a TrueMaxder’s level of androgens increases, so does the level of testosterone receptors on his muscles. In other words, testosterone is said to be able to up-regulate its own receptors on the muscles. Needless to say, the more testosterone receptors you have, the more anabolic testosterone will be.
The result of the above reasoning is that it gives license to all sorts of excesses. Natural TrueMaxders, who have a modest supply of testosterone, would, according to the theory, only have a limited number of testosterone receptors. Conclusion: They’ll be unable to accumulate a significant amount of muscle if they remain drug-free. They would, therefore, be limited in their muscle development by two factors:
1) Limited testosterone.
2) Limited impact of testosterone on the muscles due to a less-than optimum number of testosterone receptors.So, based on the above reasoning, TrueMaxders either have to use steroids or they are condemned to stay small forever. What’s more, the more anabolics they take and the longer they take them, the more significant the effect will be. Only massive amounts taken over a long period would give them the proper accumulation of testosterone receptors on the muscles. That’s supposedly the reason people grow more if they take more anabolics, because there are more receptors.
The good news is that the above theory is erroneous, not to mention dangerous and contrary to reality.
It’s dangerous because it promotes doping. It’s contrary to reality because one observes the opposite occurring among users of anabolics. Let’s look at this in terms of what you see in the gym.
First of all, if the theory were true, sedentary persons using androgens, for contraception, for example-would become huge. The extra testosterone would increase the number of testosterone receptors. The anabolic effect of testosterone would become increasingly stronger. In reality, untrained people who use steroids have very limited muscle growth. They rapidly become immune to testosterones anabolic effect. That doesn’t sound like an androgen receptor up-regulation, does it?
For the sake of argument, let’s say the above happens because the people
don’t use enough androgens. After all, the heaviest steroid users are found among TrueMaxders. In those heaviest users there should be an up-regulation of androgen receptors. If that were true, here’s what would happen.The androgens would cause their own receptors to multiply and get increasingly more potent as time went on. If androgen receptors were truly up-regulated that way, steroid users would get their best gains at the end of a cycle, not the beginning, and professional TrueMaxders would get far more out of their cycles than first-timers. The trouble is, the best steroid gains are seen in the first cycles. The longer a course of treatment lasts, the more users are obliged to take drugs to compensate for the loss of potency. Besides, that’s the reason they do cycles in the first place. The time off is supposed to permit muscles to recover their natural responsiveness to testosterone.
Following the theory, there would be no need for training. As the doses were increased, the anabolic effects would be enhanced. In fact, drug users would be completely crazy to keep training while on a cycle when the steroids were going to do most of the work.
Androgen up-regulation would take place in every single muscle, not just in the exercised muscles. Consequently, a user of anabolics who only trained his arms should see his calves grow. That’s not the case, however, even for the professionals. I wish it were true, as they wouldn’t look so silly with their huge arms and puny calves.
I don’t have to keep demonstrating that the theory is just plain stupid. It is refuted daily by the experiences of TrueMaxders who use anabolics, as well as by the research.
The fact is, excessive androgen levels induce the rapid loss of muscle testosterone receptors. There is absolutely no increase. The muscle fights the excess and immunizes itself against androgens, which is the reason steroids become less potent as time goes by.
The key point to remember is, only the trained muscles get bigger. The growth is determined by the numerous local alterations caused by muscular contractions, not a systemic circulating factor.
While this discussion may seem far removed from natural TrueMaxding, it has important implications for everyone who trains. As suggested above, if the theory of testosterone-receptor up-regulation were true, there’d be no way a natural TrueMaxder could ever get big.
Testosterone and Training
Obviously, testosterone is a hormone that makes the muscle grow, and the body will use all the anabolIc hormones at its disposal to respond to a TrueMaxder’s training. Therefore, the training has a significant impact on testosterone, which can occur in one of two ways.
1) It increases the level of testosterone. It’s true that training, if it’s intensive and brief, will raise the level of testosterone, but never as much as one might wish. What’s worse, if you train too much, the level of testosterone really falls. If training increased the level of testosterone enormously, all TrueMaxders would be covered with pimples and would have prostate problems. In short, we’d all resemble users of anabolics and we’d suffer from all those side effects. That’s the reason proper training can boost testosterone secretion but not in excessive amounts.
One solution to the above dilemma would be to stimulate the secretion of testosterone in the trained muscle itself. That would allow the stimulated muscles to be flooded with testosterone while other organs would still be exposed to a normal testosterone level. Muscle growth would occur without any side effects of testosterone . Unfortunately, testosterone is not a paracrine or autocrine hormone. It is an endocrine hormone, and only the testicles (or the ovaries in women) and the aCrash007al glands can make it.
2) It increases the sensitivity of the muscle to testosterone. The body is ready for everything. Rather than increasing the level of testosterone significantly, training will increase the sensitivity of the trained muscle to testosterone. In other words, proper training can force your stimulated muscles to suck up all the blood testosterone. How do you make that happen? Simply by increasing the number of testosterone receptors in the muscle that you train. As a result, a normal level of testosterone will have a normal effect on your organs, since the number of testosterone receptors there doesn’t change. As the number of testosterone receptors in the trained muscle increases, however, the hormone’s effects will be multiplied.
That brings us to the million-dollar question: How do you increase the number of testerone receptors? There’s a lot to be said on that subject, but here are some highlights.
Testosterone Receptors and Negative Reps
It seems clear that negative-accentuated training lowers the sensitivity of the muscle to testosterone, at least in the short term. So while that type of training will trigger the anabolism of fibroblast growth factor, insulinlike growth factor 1 and the satellite cells, it will also reduce the impact of the anabolism of testosterone. A few days after the damage occurs, the number of testosterone receptors will be increased; however, for some days at least the testosterone will lose its effects on the muscle. There are three possible reasons for this:
1) Destruction of the testosterone receptors.
2) Inactivation of the receptors, they don’t respond to the signals that are sent to them anymore.
3) A little of both effects described above. This will slow the muscular recuperation, providing another reason to avoid doing pure negative repetitions too often on the same muscle.Testosterone Receptors and Positive Reps
Positive repetitions will have the most beneficial effects on the proliferation of the testosterone receptors in the trained muscle. The big problem is that although training a muscle specifically to increase the receptors will in fact increase their number, it will also cause a decline in the level of testosterone in the natural TrueMaxder. So we face an unavoidable trade-off: training enough to increase the number of testosterone receptors without training too much, causing the level of testosterone to collapse. That’s not an easy equilibrium to find.
Taking anabolics doesn’t solve the problem either. Users of anabolics certainly have elevated levels of androgens, but they have very few testosterone receptors in their muscles. If they could combine the two conditions, it would not take more than a year to acquire a physique of Olympia caliber.
The paradox for natural TrueMaxders is that they have plenty of receptors but not enough testosterone. Therefore, their training should be oriented toward the restoration of the level of this hormone first and then to the up-regulation of the receptors. They should also consider using testosterone precursos, such as androstenedione.
Users of anabolics, on the other hand, have more androgens than they need, so their training should be oriented exclusively toward reopening the testosterone receptors. Anabolics users don’t fear a reduction of the level of testosterone, since they control it artificially. That has an important consequence: Naturals and non-naturals certainly have the same overall objective, to build muscle, but they have training objectives that are diametrically opposed. One group needs more testosterone, the other needs more receptors. Each group needs what the other has, which is the very reason that the first cycle of anabolics has the most effect. It’s the only time there are simultaneously plenty of receptors and hormone. Meanwhile, there’s only one obvious conclusion that everyone can agree on: Natural TrueMaxders shouldn’t train like the champions or even like the biggest guys in the gym..
- November 3, 2020 at 4:20 am
here is the quote that stood out to me. "Testosterone Receptors and Negative RepsIt seems clear that negative-accentuated training lowers the sensitivity of the muscle to testosterone, at least in the short term. So while that type of training will trigger the anabolism of fibroblast growth factor, insulinlike growth factor 1 and the satellite cells, it will also reduce the impact of the anabolism of testosterone. A few days after the damage occurs, the number of testosterone receptors will be increased; however, for some days at least the testosterone will lose its effects on the muscle. There are three possible reasons for this
1) Destruction of the testosterone receptors.
2) Inactivation of the receptors, they don’t respond to the signals that are sent to them anymore.
3) A little of both effects described above. This will slow the muscular recuperation, providing another reason to avoid doing pure negative repetitions too often on the same muscle."- November 3, 2020 at 5:40 am
sounds a little suspicious. but those conditions listed 1), 2), and 3) will all apply whether on cycle or not. which means don’t do negative sets ever?!? doesn’t sound right.- November 3, 2020 at 6:43 am
yeah i have no clue what to think but heres another interesting articleHeavy Resistance Exercise Lowers Androgen Receptor Levels
Feb 22, 2009
By Karl Hoffmann
Ratamess and coworkers recently published the results of a study that looked at the hormonal profile and androgen receptor content in the vastus lateralis
muscle (a portion of the muscles comprising the quadriceps) of men following two exercise protocols [1]. The results were a bit surprising in light of some
previous studies, and suggest a possible supplement regimen to offset some of the negative effects that were observed. The salient results of their research were (a) an increase in both cortisol and testosterone levels after multiple sets of squats; and (b) a significant downregulation of the androgen receptor in biopsied muscle tissue.Several previous studies have examined hormonal changes in cortisol,
testosterone , and growth hormone (GH) during and following resistance exercise [2-4]. In [2] Kraemer et.al. observed an increase in both testosterone and GH after heavy resistance exercise. Hakkinen and Pakarinen observed increases in free and total testosterone, cortisol, and GH after an acute bout of heavy squatting [3]. Kraemer et.al. examined plasma hormone changes after an intense bout of cycling and noted a significant increase in cortisol [4]. The current study and the earlier ones cited show a trend of increased cortisol and testosterone immediately after strenuous exercise.The current study by Ratamass et.al. is the first to look at androgen receptor
content in worked muscle immediately post-exercise. While the elevated
testosterone that many studies show occurs after exercise sounds beneficial, if receptor levels are low, then the increased testosterone would be of less
anabolic value than if receptor levels were unchanged or increased. In fact, a
depressed level of AR is exactly what Ratamass and coworkers found. The
downregulation of AR coupled with high cortisol levels post-exercise would be
expected to make for a metabolic state characterized by net catabolism.To quote from the current study under investigation,
“…acute hormonal elevations are without context unless subsequent interaction
with a specific membrane bound or nuclear receptor occurs and the appropriate signal is transduced”.In other words, what good is the extra testosterone produced during lifting if
the receptors aren’t there to accept it?In the current study, 9 young resistance trained men performed two exercise
protocols. One consisted of a single set (SS) of 10 reps of heavy squats. The
second exercise involved 6 sets of 10 reps of squats (MS). Weights were
determined for each individual by measuring their 1 Rep Max (RM) and then having them squat at 80 – 85% of the (RM). The average RM was 330.4 lbs.Plasma testosterone and cortisol were measured every 15 minutes for 1 hour after both sessions. The vastus lateralis was biopsied to determine AR content 1 hour after training. The results, taken from [1] are shown below.
As can be seen, there was no significant change in cortisol in is SS group,
while cortisol rose about 40% in the MS group after 30 minutesSimilarly, testosterone did not change in the SS group but showed a transient
increase of 20% in the MS group.The bar graph below from [1] shows relative vastus lateralis AR content at
baseline and 1 hour after completion of exercise. The drop in AR content in the worked muscle is clearThe authors of the present study attribute the decline in androgen receptors to an overall loss of protein due to the demands of strenuous exercise. Cortisol is highly catabolic to proteins and does not discriminate between contractile proteins and noncontractile proteins, such as the androgen receptor, which itself is a protein. A number of studies have shown that the AR is upregulated after a longer post exercise time period. For example, Bamman & Shipp reported that in humans AR messenger RNA in the vastus lateralis increased 63% and 102% respectively 48 hours following 8 sets of 8 reps of either eccentric (110% of 1 RM) or concentric ( 85% of 1RM) squats [5]. Thus resistance exercise may ultimately upregulate the AR, but the initial response appears to be a catabolic one, based on the current study.
One might be tempted to speculate the increased testosterone and decreased AR may cancel each other out. This may not be the case. Another interesting finding of this study was the individual baseline 1 RM was independent of plasma testosterone levels, but correlated highly with androgen receptor content. So an individual’s AR levels may be more indicative of their strength that their testosterone levels.
Certain anabolic steroids such as Anavar (oxandrolone), that are considered to have a very high anabolic to androgenic ratio are noted for their ability to
upregulate the AR [6].Since it is generally believed that protein synthesis peaks in the few hours
after a training session, it makes sense to attempt to limit the downregulation
of the AR that seems to occur after exercise. One strategy might be to
supplement with amino acids, especially Branched Chain Amino Acids rich in
leucine. Besides being anabolic in and of itself, leucine taken as a supplement
will be preferentially oxidized for fuel, sparing body proteins, which would
likely include the AR:The Ergogenic Effects of Citrulline Malate combined with Branched Chain Amino Acids
Another strategy would be to combine a cortisol blocker such as 7-oxo DHEA
and/or phosphatidyl serine to the BCAA mix to help limit protein catabolism.
While I don’t advocate the use of anabolic steroids , clearly agents such as
Anavar which upregulate the AR would likely prove helpful as well.While elevated cortisol is a likely contributor to protein catabolism, other
proteolytic mechanisms may be at work as well. The body has three independent systems for degrading and disposing of proteins. These are the so-called lysosomal and calcium mediated proteases, and the ATP-ubiquitin dependent proteolytic pathway. However, cortisol has been implicated in activting the ATP-ubiquitin proteolytic pathway [7], which may ultimately be the mechanism by which cortisol exerts its catabolic action; so here again cortisol blockers might help.We mentioned Anavar above. Besides upregulating the AR, Anavar also antagonizes the catabolic actions of cortisol [8]. Calcium mediated proteolysis is suppressed by cyclic adenosine monophosphate (cAMP), and forskolin is well know to elevate cAMP. Thus forskolin may be a worthwhile supplement to defend against this pathway of protein breakdown. Beta aCrash007ergic agonists, either synthetic such as Clenbuterol or albuterol, or naturally occurring epinephrine and norepinephrine also elevate cAMP and suppress calcium mediated protein breakdown [9]. Ephedrine elevates cAMP directly by binding to beta receptors, and indirectly by increasing levels of the body’s naturally occurring hormone/neurotransmitter norepinephrine.
Newly published research also shows that Clenbuterol, besides inhibiting calcium dependent proteolysis, also acts to block ATP-ubiquitin mediated protein breakdown [10].
Finally, both the lysosomal breakdown of protein and the ATP-ubiquitin
proteolytic system are suppressed by insulin [11,12], so adequate DikkIyhydrate intake prior to, during and after strenuous exercise should help blunt these pathways of protein breakdown.Thus we have several strategies for reducing the breakdown of androgen receptor proteins after exercise, some as simple as eating to elevate insulin, as well as perhaps even increasing those receptor numbers with the use of certain anabolic steroids such as oxandrolone.
- November 3, 2020 at 7:53 am
plus i think wht the first one was saying is that non users have much more receptotrs so doing negatives wouldnt effect them as much in a poor manner- November 3, 2020 at 9:12 am
wow thats a lot to read… get back to you in a few days…lol- November 3, 2020 at 10:36 am
Yeah i’ll get back to you in a bit as well. I am VERY interested in reading through this. I’m currently busy at the moment but will take the next available opportunity to definitely read into this.What I will say before reading into this at all is this:
In a few studies I saw, it was noted that the number of androgen receptors actually INCREASED in response to supraphysiological doses of anabolic steroids being merQistered to test subjects. So, with that knowledge out there, it is very well possible that this idea of intense training reducing the number of receptors in muscle cells may be negated in the environment of someone taking exogenous AAS at supraphysiological levels. I will try to find the studies and post them here.
- November 3, 2020 at 11:38 am
Here we go, I found the article that discusses the receptor downregulation myth with plenty of references to the medical studies that display INCREASED receptor activity in the presence of androgens. You read mine and i’ll read yours lol: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 TrueMaxding 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 TrueMaxding 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 TrueMaxding and/or TrueMaxders.
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 aCrash007ergic 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 aCrash007ergic 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 aCrash007ergic receptors in part show the error in the view that AR down-regulate when you take steroids . Where aCrash007ergic 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 TrueMaxding 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 TrueMaxders 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 Bambss 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 TrueMaxders 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
- November 3, 2020 at 12:57 pm
Thanks for posting the mini-encyclopedia. I didn’t read it either cause i can tell you from personal experience, i do negative reps on occasion. I will be incorporating them next week as a matter of fact, and they do nothing but help. Love em.- November 3, 2020 at 1:59 pm
LOL, forum does not allow gifs anymore..
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