Oral AAS before a workout.

[Andy13]

On cortisol and gains.......


Here's a discussion between Bill Roberts and myself on the issue.



(Bill) GR 'blockking' AAS
Andy 2002-05-20 21:25:15
Does you have any info on different AAS and their affinity for the glucocorticoid receptor? How much do you think this property contributes to the over-all effectiveness of the AAS? Andy


Bill Roberts 2002-05-21 13:54:54
I would have to go look stuff up again to give you much of an answer on details of different androgens. (And you'd probably be as quick as me in doing so.) On the question of whether I think it's important to effectiveness, I don't think so. After all, if you want to, you can drive cortisol levels as low as you might like with Cytadren, and this does not improve efficacy of a cycle though it certainly does give you joint pains. So I don't see why an androgen being a glucocorticoid receptor antagonist would be of any more value in increasing gains.

Andy 2002-05-21 20:02:27
I meant to say while dieting, to possibly decrease the expression of gluconeogenic and proteolytic genes. This may shift metabolism a little more toward fatty acid oxidation and maybe slight ketone body production-- neither of which would make a measurable difference in fat loss, but MAY make a difference as far as muscle preservation. Andy

Bill Roberts 2002-05-22 13:45:13
To test this out, try taking Cytadren at doses like 500-1000 mg/day. This will reduce your cortisol. Not to your benefit, I think, but it's something you can try and determine for yourself. This I think would much more clearly answer the question of whether reducing cortisol effect is of value in whatever situation you wish to apply it to, than would trying an androgen which also has some anti-glucocorticoid effect: because in the latter case, you have another factor confounding estimatation of the effect of the antiglucocorticoid activity.

Andy 2002-05-23 14:02:36
Eeewwwwww.... I know of too many benefits from cortisol to be willing to take cytadren (is that the side-chain cleaving enzyme inhibitor?).. The reason why I asked this question in the first place was because I have read a number of papers that suggest that GR antagonization MAY lead to some kind of over-all greater effect from the AAS.. However, these claims were from studies using HRT doses of androgen-- nothing like what would be considered 'effective' for a BBer... I began to wonder if muscle loss while dieting (the kind of diet that lowers the electro-chemical gradient in a certain inner membrane, if you know what I mean) was predominantly due to increased gluconeogenesis. I don't remember the specifics, but there's this so-called pyruvate-alanine cycle works with the liver and muscle and supplies the 3-carbon skeleton's needed for glucose generation in the liver. Not sure about this (I have NO access to any resources right now) but I believe that t3 and cortisol are the main players in the manufacture of protein degrading enzymes for the eventual liberation of alanine... I think fatty acid oxidation enzymes are synthesized in response to other hormones besides cortisol such as epi' and maybe glucagon (last time I checked, the latter was a potent activator of lipase activity IN VITRO, although this had not been demonstrated in vivo). Anyway.. I think t3 is less of a concern as far as muscle loss since it increases protein synthesis (although, apparently not as much as it does degredation). What's YOUR opinion? I trust any gut feeling you have over what some dude who took cytadren has to say. (you know that) Most BBer's analytical methods aren't even logical, let alone experimentally meaningful Andy

Bill Roberts 2002-05-23 21:46:25
The "side effects" from Cytadren are due to the usually-intended effect of decreasing cortisol. If the hypothesis is that reducing effects produced as a consequence of cortisol receptors binding cortisol (by providing an antagonist) will have some desired effect, but the antagonist confounds the issue by having other agonist properties of its own, then this can readily be tested by simply reducing the amount of cortisol and seeing if this gives the desired effect.
But instead, the effect is more or less as you described for higher doses of Cytadren, namely, Eeewwwwww....

"So it does not seem reasonable to attribute benefits of anabolic steroids to reducing cortisol receptor activity, since a known means of reducing this activity does not give the claimed benefit in individuals with normal cortisol levels in the first place." (Bill Roberts)

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[superchicken]

Ok.. do you have any rational reasoning for why you believe this or is this just your un-tested, gut feeling?

no, the only thinking behind it is that muscles are in a prime state for recovery right after a workout. but i dont know how much proetien synthesis occurs during this time, maybe a lot, maybe a little. im asking.

but who knows, there may be other systems which become overloaded, and maybe this wouldnt show much benefit.

also the pump, means more blood in the muscle, possibly aiding more nutrient uptake.

im just pondering, im not arguing you, im asking for an opinion.

to clarify a little, im referring to taking say 1/3 of the daily dose before a workout, then space the rest evenly.

 

[athlete03]

Andy, I know some disagree with some of what Bill Roberts sez. Would you say you completely agree with him?

 

[Andy13]

Absolutely.. Bill knows more about AAS than (for starters) anyone on this board. I'll put it this way- I do not know of ANYONE who could rival his knowledge.

It's really hard to prove Bill wrong at anything.. He's writes in a VERY objective style and does not use 'absolutes' for things which have not been 100% proven to be true. I see guys posts 'absolutes' all the time for things they know NOTHING about. It irritates the hell out of me to see someone post (for instance) "t-prop causes less water retention than TE." I would say to this person.. "how do you know this to be true?" And I will get some illogical, idiotic response such as "I looked leaner while on TP." (which is absolute dogshit as far as any kind of logical or reasonable rationalization.. let alone PROOF enough to state, as an absolute certainty, that TP causes less water retention than TE).


And these are the guys that 'don't agree' with what Bill says. This too irritates me.. Probably because Bill knows 100x more than the idiots who try to attack what he states... Some average joe disagreeing with what BIll says is a lot like some common folks who think that evolution did not happen.. Now.. How is it that these folks somehow know more than people with PhD's in evolutionary biology? Can you imagine a group of 'creation' people versus a group of biology PhDer's in a formal debate? Those folks would get smoked.. Same thing with the average joe juicer versus Bill Roberts..

Andy

 

[BigAndy69]

Absolutely.. Bill knows more about AAS than (for starters) anyone on this board. I'll put it this way- I do not know of ANYONE who could rival his knowledge.

It's really hard to prove Bill wrong at anything.. He's writes in a VERY objective style and does not use 'absolutes' for things which have not been 100% proven to be true. I see guys posts 'absolutes' all the time for things they know NOTHING about. It irritates the hell out of me to see someone post (for instance) "t-prop causes less water retention than TE." I would say to this person.. "how do you know this to be true?" And I will get some illogical, idiotic response such as "I looked leaner while on TP." (which is absolute dogshit as far as any kind of logical or reasonable rationalization.. let alone PROOF enough to state, as an absolute certainty, that TP causes less water retention than TE).


And these are the guys that 'don't agree' with what Bill says. This too irritates me.. Probably because Bill knows 100x more than the idiots who try to attack what he states... Some average joe disagreeing with what BIll says is a lot like some common folks who think that evolution did not happen.. Now.. How is it that these folks somehow know more than people with PhD's in evolutionary biology? Can you imagine a group of 'creation' people versus a group of biology PhDer's in a formal debate? Those folks would get smoked.. Same thing with the average joe juicer versus Bill Roberts..

Andy

I don't agree with this at all. Bill Roberts is most likely the top guy when it comes to THEORETICAL knowledge of steroids but what about real world experience?

Theoretical knowledge is only part of the puzzle, what looks good on paper doesn't always translate to the real world and vice versa

 

[Andy13]

I don't agree with this at all. Bill Roberts is most likely the top guy when it comes to THEORETICAL knowledge of steroids but what about real world experience?

Theoretical knowledge is only part of the puzzle, what looks good on paper doesn't always translate to the real world and vice versa

Do you understand that "theoretical" knowledge (as you call it) is the ONLY logical and reasonable information we have to go on???


I mean, give me a break... You can't say that some dude saying "I did test prop and looked leaner" is EVEN in the ballpark as what is ALREADY known???

If you haven't realized yet, BBing is SO incredibly dominated by psychology... so much that what "some dude" says doesn't mean shit.

 

[Zyglamail]

Do you understand that "theoretical" knowledge (as you call it) is the ONLY logical and reasonable information we have to go on???


I mean, give me a break... You can't say that some dude saying "I did test prop and looked leaner" is EVEN in the ballpark as what is ALREADY known???

If you haven't realized yet, BBing is SO incredibly dominated by psychology... so much that what "some dude" says doesn't mean shit.

I have to agree with Andy13 here. There are some big dudes in the gyms with years of cycling under there belt who really dont have the slightest idea of whats going on within thier bodies or what makes this "stuff" work. They have listened to thier friends and experimented but that doesn make them smart or educated.

Im not trying to discount real world experience but lets face it the real world experience done cant really be quantified or qualified since the data, as Andy has pointed out, is usually nothing more than anecdotal at best.

 

[BigAndy69]

You guys are way off; we are not talking about Big Joe and Big Pete who have been juicing for 10 years and who think Deca a good finishing drug and Clomid is not necessary. We are talking about guys who know there bodies and can see how different compounds affect them. Smart guys like Dan Duchaine.

I consider myself an expert on Clen and T3. Before using either drug, I read all I could; medline, physician desk reference, popular books, websites...

I found that a lot of the theory was off.

A lot of what people are taught is wrong such as T3 will strip you of all your muscle. Theoretically, it makes sense, but in real life it doesn't happen.

I used up to 50mcg with no STEROIDS and I did not lose any muscle or strength. I did look extremely tiny and my muscle were softer than they had ever been. I had trouble "feeling" my muscles because there was such a lack of pump. I looked about 20lbs lighter, yet I haden't lost an ounce. This can easily be thought of as muscle lost but I know my body so I was able to really zoom in on what was going on.

The point is that theory is extremely important, but real world experience is just as important. That's why Duchaine was the man(unlike Roberts), he talked the talk and he walked the walk...

 

[panerai]

Br J Pharmacol 1999 Mar;126(6):1301-6

Increased dopaminergic and 5-hydroxytryptaminergic activities in male rat brain following long-term treatment with anabolic androgenic steroids.

Thiblin I, Finn A, Ross SB, Stenfors C.

Department of Forensic Medicine, Karolinska Institute, Stockholm, Sweden.

1. The effects of treating groups of rats with four different anabolic androgenic steroids (AAS) (testosterone, nandrolone, methandrostenolone, and oxymetholone) on 5-hydroxytryptamine (5-HT) and dopamine (DA) neurones in different brain regions were examined. The AAS was injected six times with 1 week's interval and the rats were sacrificed 2 days after the final injection. 5-HT and its metabolite 5-hydroxyindoleacetic acid (5-HIAA), DA and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured. The effect on DA and 5-HT synthesis rate was analysed as the accumulation of 3,4-dihydroxyphenyl-alanine (DOPA) and 5-hydroxytryptophan (5-HTP), respectively, after inhibition of the amino acid decarboxylase with NSD-1015 (3-hydroxy-benzylhydrazine dihydrochloride). Additionally, the monoamine oxidase (MAO) activity was analysed in the hypothalamus. 2. The DOPAC + HVA/DA ratio was increased in the striatum in all treatment groups. However, the synthesis rate of DA was significantly increased only in the methandrostenolone treated group. 3. The 5-HIAA/5-HT ratio was increased in all treatment groups in the hippocampus, in the frontal cortex in the methandrostenolone-treated animals and in the hypothalamus in the testosterone- and oxymetholone-treated rats, while the 5-HT synthesis rate was not affected by the AAS-treatments. 4. The MAO-A activity was increased in the oxymetholone-treated rats while the other treatment groups were unaffected. The MAO-B activity was not changed. 5. The results indicate that relatively high doses of AAS increase dopaminergic and 5-hydroxytryptaminergic metabolism in male rat brain, probably due to enhanced turnover in these monaminergic systems.

PMID: 10217522 [PubMed - indexed for MEDLINE]
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Dianabol and corisol production....
Why higher dose right before and right after workout? Obviously, before, to stimulate CNS, and both before and after to prevent anti-catabolism, to which hard workout will lead.
Dan Duchaine was saying that as little as 10mg of dbol will decrease endogenous cortisone level by 50-70%.
This method of using dbol russian and east germans were using for years, and nobody knows their dbol better then them. Check all the studies on dbol, half of them come from former eastern block.
While I was not able to locate studies on dbol and contisol, still there are good amount on AAS in general and glucocorticoids.
First of all, what is mechanism of action of AAS regarding catabolism?
Supraphysiological doses may evoke anabolic effects via a separate mechanism independent of the androgen receptor. Indirect evidence has shown this could be an anticatabolic effect based on an antiglucocorticoid action:
AAS can displace glucocorticoids from their glucocorticoid receptor,
Antagonists of glucocorticoids can prevent muscle atrophy,
Large doses of AAS increase the amount of urinary free cortisol. (Wu F C W. Endocrine Aspects of Anabolic Steroids. Clin Chem. 1997. 43 (7): p. 1289 - 1292)
Cortisol enhances glucagon stimulated glycogenolysis and also enhances enzyme activity in mobilising protein from muscle sources ready for conversion to produce glucose. If this activity is inhibited by AAS displacing cortisol for its receptor then catabolism of muscle is prevented and there will be an increase in glycogen retention, increasing endurance.(
Berne R M, Levy M N. Principles of Physiology. 2nd ed. Mosby. 1996. p. 678 - 681)


Taken from
http://www.mesomorphosis.com/articles/bahrke/bahrke10.htm

Hevery et al. (1976) reported that one benefit of taking anabolic-androgenic steroids, as expressed by some athletes, lay in the reduction of fatigue during the training season, which allows for more training to be done. Freed et al. (1975) provide anecdotal and self-report information that athletes using anabolic-androgenic steroids are generally less easily fatigued, allowing for longer, more frequent and/or intense training sessions. This could be related to the fact that anabolic-androgenic steroids can block and reverse the anticatabolic effects of glucocorticosteroids that are released during periods of stress including physical exertion (Kochakian 1976; Kruskemper 1968; Williams 1981). Work with rats has also demonstrated reduced alkaline protease activity (Dahlmann et al. 1981) and increased glycogen supercompensation (Gillepsie & Edgerton 1970) in androgen-related animals

Some more studies:

1. Br J Nutr 1986 Jul;56(1):289-304 Related Articles, Books, LinkOut


The effect of manipulating growth in sheep by diet or anabolic agents on plasma cortisol and muscle glucocorticoid receptors.

Sharpe PM, Buttery PJ, Haynes NB.

University of Nottingham School of Agriculture, Loughborough, Leics.

1. The cortisol status (total plasma cortisol concentration, free cortisol concentration, transcortin capacity) and the characteristics of skeletal muscle binding for cortisol and dexamethasone were examined in female lambs either implanted with Zeranol or trenbolone acetate or whose dietary intake was restricted. 2. The skeletal muscle glucocorticoid receptor had a high affinity for the glucocorticoid triamcinolone (relative binding affinity 0.85) and cortisol (relative binding affinity 0.51) with virtually no affinity for trenbolone. 3. Trenbolone acetate treatment reduced the binding capacity of sheep skeletal muscle for cortisol within 2 d of implantation. The other treatments had little effect except a small reduction in the animals where food intake was restricted. Similarly, binding capacity for dexamethasone was reduced by trenbolone acetate treatment but was not affected by the other treatments. This reduction in trenbolone acetate-treated animals is, at least in part, due to a reduction in glucocorticoid receptors. 4. Transcortin capacity was elevated by Zeranol treatment but reduced with diet restriction or trenbolone treatment. 5. No support for the suggestion of free cortisol concentration being important in the growth-promoting mechanism of trenbolone or Zeranol was obtained. 6. Although insulin concentrations were not significantly altered by treatment (P greater than 0.05), when combining all the animals there was evidence of a negative correlation between total cortisol/insulin value (P less than 0.05) or free cortisol:insulin value and growth rate (P less than 0.001). Free cortisol was negatively correlated to growth rate (P less than 0.05) and transcortin capacity positively correlated (P less than 0.01).

PMID: 3314981 [PubMed - indexed for MEDLINE]
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1. Am J Physiol 1975 Nov;229(5):1381-6 Related Articles, Books, LinkOut


Interaction of anabolic steroids with glucocorticoid receptor sites in rat muscle cytosol.

Mayer M, Rosen F.

While glucocorticoid hormones act catabolically on skeletal muscle through their binding to glucocorticoid-specific receptors in the cytosol, androgens exert anabolic responses but no androgen-specific binding proteins could be detected in this responsive tissue. However, various nonradioactive androgens were effective in displacing labeled dexamethasone or cortisol from their respective cytoplasmic receptors in muscle, both in vitro and in vivo. The inhibition of glucocorticoid binding by androgens is competitive, and could be observed following a single or repeated administration of the androgens to adrenalectomized-castrated animals. The synthetic androgen fluoxymesterone and the hormone testosterone displayed Ki values of 7.5 X 10(-6) M and 1 X 10(-5) M, respectively, for the inhibition of [3H]dexamethasone binding in muscle cytosol. On the basis of competition experiments it is postulated that interaction of androgens with glucocorticoid receptors prevents the binding of glucocorticoids and might be responsible in part for the anabolic effects of pharmacologic doses of androgens in muscle.

PMID: 173192 [PubMed - indexed for MEDLINE]
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Now, even I read numerous times that 17-alpha methyl group stimulate liver to produce growth factors, I couldn't find any studies that would prove it. Still, it doesn't mean, it's not true, just some more research should be done.
Nevertherless, due fast acting of methandienone, first pass through liver will spike activity in aromatise enzyme, and spike in estrogen level will in turn stimulate IGF-1.

Now, why slightly higher dose right before workout? Simply for the spikes reason in CNS stimulation, dopamine production, IGF-1 release and anti-catabolic effect postworkout.

 

[jsn]

are you crazy !? you believe in evolution ??!

jsn