Anabolic reference guide 6th issue

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anabolic reference guide 6th issue

This does nothing with regard to inhibition of the hypothalamus and pituitary. And if the cortisol-blocking theory were true, we also would expect that persons with abnormally low cortisol ought to be quite muscular. The analogy is just great! While this may seem perhaps an overly strong condemnation of that view, please consider that the claims for downregulation seen in books such as Anabolic Reference Guide 6th Issue , World Anabolic Review, Underground Steroid Handbook, etc.

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For example, differentiation of satellite cells of muscle into mature muscle cells might be a non-AR mediated activity. There are I think at least two: Range of measurement First, the question is, downregulation relative to what? When 5-alpha reducatase was inhibited by finasteride, thus blocking metabolism to DHT, AR mRNA production was downregulated in response to testosterone. The argument that AAS use alone, without training, will not produce a championship physique proves nothing with respect to how the androgen receptor is regulated. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. Virilizing activities in female rat fetuses also showed a trend of potencies different from trends of binding affinities to the AR.

It is only moderately toxic to the liver but can cause a marked disturbance in the body's endogenous production of testosterone. Athletes claim that this drug produces dramatic size and strength increases.

It can be stacked with a number of different steroids and yield even greater results. Cypionate is the most popular testosterone used by athletes and is still produced domestically under the brand name Depo-Testosterone and under numerous manufacturers labels with the generic name. Effective dosages for men are in the range of ccs per week. This product is a long acting injectable testosterone that is widely used amongst athletes. Like all testosterones, it is highly androgenic, highly anabolic, aromatizes easily, and is moderately toxic to the liver.

Some athletes claim that enanthate does not have as much "kick" as cypionate. However, enanthate only needs to be administered once every 10 days as opposed to cypionate's weekly injections. This yields greater convenience and cost effectiveness. Effective dosages range from 1 to 3 ccs every 10 days. Enanthate is still manufactured domestically and is available in several European versions. Gator could you send me the sample 4day menu from the anabolic reference guide.

I remember that book. I wrote a paper on steroids in college and most of the info came from it. EAS was all I used in the late 90's.

Just wondering why you would want information so dated, just like the guy or something. I asked back in Check out when I started this thread. The sample cycles were cool to check out. I love looking at what was the "standard" at that time and what is now. It will be the same way 10 yrs from now.

Well, today we know that it does do that but also shuts ya down. Loved the book at the time. It was cutting edge. Muscle Media as well by Bill Phillips.

Users Browsing this Thread. Anabolic Effects of PGF2. Ergogenic use of anabolic steroids. By thatotherguy in forum Anabolic Steroids and Bodybuilding Articles. Isn't it also true that exogenous testosterone administration lowers SHBG as long as E2 is controlled? I am talking about high doses not testosterone replacement therapy TRT doses.

So I still believe this is the reason when on high doses. Users Browsing this Thread. Steroid Action - Is it in the receptor? Featuring anabolic steroid information, anabolic steroid drug profiles, anabolic steroid articles, live discussion forums and much more.

All times are GMT The time now is Register Help Remember Me? A lot has been said in regards to clearing the receptors and I thought now would be a good time to delve into this subject and simplify things. Basically, one must view the receptor sites as parking spaces. Envision a slew of parking spaces that are all empty.

Now we are going to call these parking spaces your receptor sites and we shall call steroids the cars. Now I want you to imagine one of those old 's style drive up hamburger stands where the girls come up in roller skates and take your order. Typically one would order a burger, fries and a coke--ah the food of the gods--the waitress would take the order, go bring the information to the cook, who would in-turn make the food and the waitress would then bring the food to you and you would then begin eating which is the whole reason you came to the hamburger stand in the first place.

I think everyone can easily understand that. Which means everyone can easily understand all they need to know about the receptor sites because they do the exact same thing. We will keep with this hamburger stand model and explain what happens when you inject steroids and they begin to go to work. Remember how I said steroids were like the cars and the parking spaces were like the receptor sites?

Well it is basically that simple. When you inject testosterone or any one of it's anabolic or androgenic derivatives, you are sending a whole slew of "cars" into your system. Now these "cars" are on a mission--just like you would be if you were hungry and heading to a hamburger stand.

They have orders to place with the cells, but before they can place them they must first find a parking space. Now let's say you have never used steroids before. If this were the case, it would be very much like a hamburger stand that was having a grand opening The steroids cars enter the system and come to a brand new hamburger stand called your cells.

Now these cells have never previously been open to the boat-load of anabolics that are now present in the system because they previously only dealt with what your body naturally produced. However, there are lots of extra parking spaces that can be utilized and so the steroids park themselves into these spaces. Once they are parked a "waitress" called CYCLICl AMP literally crosses the cellular membrane which is totally impenetrably to anything else and takes the order from the steroid.

The order is quite simple: The "waitress" then crosses back through the cellular membrane and brings the order to the "cook" called the Nucleus who begins to fill it by ordering its helpers called Ribosomes to produce muscle protein.. Now different steroids will have slightly different orders in that some may have a bigger order for the cook to fill--such as testosterone. The thing you have to realize is that a lot of times, after the order is placed, the steroid does not necessarily leave the parking space and make it available to other steroids This is why you do not continually grow by injecting bigger and bigger doses of steroids.

Now it would not be so bad if all the parking spaces were taken by "cars" that were sending orders to the cook, because that is when you grow. The problem is when there are "cars" that are no longer sending orders and on top of that have dead batteries which is preventing them from exiting the receptors parking space. This is what the whole point of this article is This will result in new muscle mass!

First and foremost, is to plan sensible courses. This is why I am an advocate of short courses designed in such a fashion as to have all drugs out of the system by the end of the cycle and then allow for a week off time in which you are totally clean. If you stay on these monster month courses, you just wind up screwing yourself and requiring that much longer of an off period.

The longer you are on, the more the body recognizes that there is "too much" in the system and will begin to take counter measures. Now with this in mind, how can we help get the cars out of there? Well WE actually cannot, but the body can and will. Basically as time goes by, the body will free up the parking spaces just like a tow truck would remove a dead car from a parking space.

However, you are at the mercy of time in this situation which is why it is important to utilize short courses that will cause less disturbance in the system, less "dead cars" in the receptor spaces and therefore less time needed for the body to remove them and free up the spaces. This has been claimed repeatedly in many books and articles, and it is claimed constantly on bulletin boards and the like. If it were just being stated as an abstruse hypothesis, with no practical implications, with no decisions being based on it, that might be of little importance.

Unfortunately, this claim is used to support all kinds of arguments and bad advice concerning practical steroid usage. Thus, the error is no small one. We will look at this matter fairly closely in this article.

However, in brief the conclusions may be summed up as follows: There is no scientific evidence whatsoever that AR downregulation occurs in human muscle, or in any tissue, in response to above normal supraphysiological levels of AAS. Where AR downregulation in response to AAS has been seen in cell culture, these results do not apply because the downregulation is either not relative to normal androgen levels but to zero androgen, or estrogen may have been the causative factor, or assay methods inaccurate for this purpose were used, or often a combination of these problems make the results inapplicable to the issue of supraphysiological use of androgens by athletes.

AR upregulation in response to supraphysiological levels of androgen in cell culture has repeatedly been observed in experiments using accurate assay methods and devoid of the above problems.

AR downregulation in response to AAS does not agree with real world results obtained by bodybuilders, whereas upregulation does agree with real world results. A neutral position, where levels in human muscle might be thought not to change in response to high levels of androgen, is not disproven however.

The "theoretical" arguments advanced by proponents of AR downregulation are invariably without merit. The belief that androgen receptors downregulate in response to androgen is one of the most unfounded and absurd concepts in bodybuilding.

While this may seem perhaps an overly strong condemnation of that view, please consider that the claims for downregulation seen in books such as Anabolic Reference Guide 6th Issue , World Anabolic Review, Underground Steroid Handbook, etc. The authors merely assert downregulation. They have done it so many times that by now many people assume it is gospel.

In this paper you will be provided with evidence, and the evidence does not support their claim. Overview of Regulation Meaning of regulation "Regulation" of a receptor refers to control over the number of receptors per cell. It is a possible in many cases for the receptors of a cell to be sensitized or desensitized to a drug or hormone, independently of the number of receptors.

Similarly, it is possible for the receptors to upregulate or downregulate, to increase or decrease in number, independently of any changes in sensitivity. If sensitivity remains the same, then upregulation will yield higher response to the same amount of drug or hormone, and downregulation will result in less response.

So if we are discussing androgen receptor regulation, we are discussing how many ARs are present per cell, and how this may change. Changes in regulation must, of necessity, be between two different states, for example, levels of hormone. In the case of bodybuilding, we are interested in supraphysiological levels vs. In most research that is done, the comparison is often between normal levels and zero levels, or the castrated state. We may describe regulation with the two levels being in either order.

Upregulation as levels decrease from normal to zero is the same thing, but in the reverse direction, as downregulation as levels increase from zero to normal. The term which would be used will depend on context, but does not change meaning, so long as the direction of change in level of hormone is understood. If upregulation occurs as levels decrease from normal to zero, as is probably the case in some tissues, this would imply nothing about what may happen as levels increase beyond normal.

It does not prove that downregulation would occur. It would be a serious error to take a study comparing normal levels and zero levels and use that study to argue the effect of supraphysiological levels. Unfortunately, such mistakes are commonly made by authors in bodybuilding. Forms of regulation Broadly speaking, there are three things that control the number of receptors. The rate frequency of this process can be either increased promoted or decreased repressed depending on what other proteins are bound to the DNA at the time.

Increase or decrease of this rate can be a form of regulation: However, all else rarely is equal. The process of making protein from the mRNA code is called translation. Changes in efficiency of translation can also be a form of regulation. The third contributing factor to regulation is the rate of loss of ARs. If the cell produces x ARs per hour, and their half life is say 7. Thus, control of rate of turnover, or change in half-life, can be another means of regulation.

The Arguments for Downregulation Arguments from the popular literature I am indebted to one of my former colleagues at Dirty Dieting for contributing these first several arguments, which are from one of his published articles.

I could never have thought of them myself: The above statement is an assertion only, and therefore cannot be accepted as evidence that AAS use in athletes downregulates the AR.

Users of anabolics find value in the increased doses of androgen, and advanced users may well need all that they are using simply to maintain their far-above-normal mass, let alone gain further mass. The reference to "re-opening" the testosterone receptors is dubious at best, since the receptors are not closed, nor is their any indication in any scientific literature that such could possibly be the case, or that some given style of training will remedy any such nonexistent condition.

Each group needs what the other has-which is the very reason that the first cycle of anabolics has the most effect. More accurately, the cycle starting at the lowest muscular bodyweight will have the most effect. This may be because the closer you are to your untrained starting point, the easier it is to gain.

Let us look at the example of a person who achieved excellent development with several years of natural training and then has gained yet more size with several steroid cycles. He then quits training for a year and shrinks back almost to his original untrained state.

If he resumes training and uses steroids, will his gains be less than in his first cycle? So what that it may be his fifth or tenth cycle, not the first? There is no counter inside muscle cells counting off how many cycles one has done. In examples that I know of, the gains in such a cycle have been greater than in the first cycle. No, that does not prove upregulation, but it is strong evidence against the permanent-downregulation-after-first cycle "theory.

This is true under any conditions, regardless of whether AAS are involved or not. Thus the "first cycle" argument proves nothing with regards to AR regulation. In any case, regulation is a short term phenomenon, operating on the time scale of hours and days.

But if it were permanent or long-lasting as this writer believes, then if steroid use were ceased for a long time, one ought to shrink back to a smaller state than was previously achieved naturally, despite continuing training. After all, one would have fewer receptors working, having damaged them forever supposedly with the first cycle.

That is, of course, not the case. Which is not surprising, because the "theory" is medically ridiculous. In other words, testosterone is said to be able to upregulate its receptors in 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 a11 sorts of excesses. 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.

This is a strawman argument. Resistance training is demonstrated to upregulate the androgen receptor, for example, and also stimulates growth by other means. Therefore it is not surprising that those who do not train do not gain nearly as much muscle as those who do. The argument that AAS use alone, without training, will not produce a championship physique proves nothing with respect to how the androgen receptor is regulated.

It does not even suggest anything, to any person with judgment. And the concept that upregulation could only exist as an uncontrollable upwards spiral is entirely incorrect. Rather, for any given hormone level, there will be a given AR level. There is no feedback mechanism, not even a postulated one, where this would then lead to yet higher hormone level, leading to yet higher AR level, etc.

While I do not know if these subjects did experience AR upregulation in their skeletal muscle tissue, if their receptor numbers had let us say increased by some percentage, there would come some point in increased muscle mass where catabolism again matched anabolism, and further growth would not occur. No runaway spiral of muscle growth would be expected either. Thus, my colleague is arguing against non-issues. In those heaviest users there should be upregulation of androgen receptors.

If that were true, here's what would happen. The androgens would cause their receptors to multiply and get increasingly more potent as time went on. If androgen receptors were truly upregulated that way, steroid users would get their best gains at the end of a cycle, not the beginning, and professional bodybuilders would get far more out of their cycles than first-timers.

The concept that AR activity is measured by "gains" is simply ridiculous. The function of the activated AR is not to produce gains per se, but to increase protein synthesis.

That will only result in gains if muscle catabolism is less than the anabolism. As muscle mass becomes greater, so does catabolism. At some point under any hormonal and training stimulus, equilibrium is reached, and there are no further gains. With high dose AAS use, that point is at a far higher muscle mass than if androgen levels are at only normal values.

The concept that the steroids are "not working" for the bodybuilder who is maintaining 40 lb more muscular weight than he ever could achieve naturally, and who might even still be gaining slowly but not as fast as in his first cycle is, at best,an example of poor reasoning..

The difference cannot be substantially increased percentage of occupied receptors, since almost all are occupied in either case.

What does that leave as the possibilities? More receptors, or non-receptor-mediated activity.

Iamges: anabolic reference guide 6th issue

anabolic reference guide 6th issue

And he may need more than this.

anabolic reference guide 6th issue

AR levels were not measured. If many mRNA molecules are produced, then, generally, they will cause many corresponding protein molecules to be produced. Scientific Evidence Apparently Favoring Downregulation While there are no studies showing downregulation in human skeletal muscle resulting from high-dose AAS use, there are some studies in cell culture, and sometimes in vivo, which seem to indicate that downregulation can occur, though not as a result of increase in androgen from normal to supraphysiological.

anabolic reference guide 6th issue

In male rats, differential activities are also seen. Now with this in mind, how can we help get the cars out of there? Biochemistry is usually much broader than any one specific cell being studied. There is a range where there is still some anabolic support yet there is fairly little inhibitory effect, but past this range, there still is not great anabolic effect, but there is substantial inhibition. Thus, my colleague is arguing against non-issues. We may also speculate that different AAS have different effects on nerves, and these anabolic reference guide 6th issue being rapid anabolic reference guide 6th issue not mediated by the AR. They also affect the activation rate of enzyme systems involved in protein metabolism, thus enhancing protein synthesis and inhibiting protein degradation called an anti-catabolic effect.