T Nation

Var and ATP/PCr


I recently was asked about the relationship of Var and PCr in one of the stickies. It reminded me to look it up as it was something that piqued my interest a whileback now.. i have read up on it a little and i will document that here for anyone else who knows more to add to and help me/us learn about this benefit.
I'll start with what i know about the energy system in question and how it relates to that..

Adenosine Triphosphate is the primary anaerobic fuel source used by our bodies cells. It is burnt in the mitochondria (the 'power factory' of a cell).
The mitochondria are part of our cells now, but once were seperate organisms in the 'pond of life' - both becoming symbiotic(sp?) organisms and creating the beginning of life as we know it IIRC.

I digress..
When we use ATP we 'burn' a phosphate molecule - this turns the Adenosine TRI-phosphate into Adenosine DI-phosphate.
This is where Phosphocreatine comes in.
Phosphocreatine is used to replenish the phosphate molecule in the ADP to turn it back into ATP. Easy.

You can see that this is why supplementing Creatine (in its now many forms) can help with force production in fast, powerful muscle contraction - the type of exercise that uses this energy system (explosive movement upto 10-15 seconds use the ATP/PCr system).
The other energy systems are the Lactate (Glycogen) and Aerobic (Oxygen) - the energy source is in brackets.

Now, according to the wonderweb sites i visited in a quick look into the anavar/PCr relationship it seems that oxandrolone stimulates the formation of Phosphocreatine - and this is how it supports that energy system and is also how it gives it's increase in strength (supplementing creatine commonly gives a 10% increase in strength - this has been noticed by myself and has been widely reported too), especially the strength we use in bodybuilding and powerlifting - short, explosive 'events'.
However with higher increases in var dose you have the increased formation of PCr (and Androgen Receptor[AR] mediated anabolism) while with Creatine supplementation there is only so much you can utilise..

I believe that Var DOES have this effect on PCr formation but what i want to know is if the other AAS do also - or if the other Class I steroids do at least?
Bill Roberts brushed on this recently - or something similar (IIRC) in which he suggested that many AAS drug profiles are 'beefed up' to make each drug sound more different than the next - when really they work by 2 different pathways only, the AR mediated and Non-AR mediated.. with his classification of the two into strong affinity for the Androgen Receptor - Class I, and weak affinity - Class II.

I read that Anavar

however i am pretty sure this is the case for (at least) all Class I steroids. I wonder if the same can be said for it's PCr effects?



I personally do not believe that Anavar possesses any special properties which other forms of AAS do not. I think Bill is correct and the authors of these AAS books simply try as hard as they can to make their book seem special, and a "must have" reference. Everything you need to know about AAS, could more than likely fit on one, maybe two sheets of paper.

I'm so sick of people glorifying certain compounds. Equipoise is one that stands out and truly puzzles me. I have never used this compound, as every first hand account I read states, the user did not see any results until they approached 600 or more mg/week. Even the profiles that I have read do not paint such a great picture for it. You also always hear about how it raises RBC and makes you more vascular. Well, I have yet to use an AAS that didn't perform well in both of those areas. I just don't understand the appeal of EQ.

It just doesn't make sense to me , with all the information out there, why these ignorant observations continue to flood message boards and gyms. Especially since there really isn't anything new under the sun in regards to AAS...so isn't it time we started to recognize and address all of the fallacies that so many continue to perpetuate.

Anyway...back to the Anavar. I notice increases in strength endurance with creatine even when only using Testosterone. I have also used a touch over 200mg/day of Anavar for approximately four weeks. I noticed nothing special about this compound. All of the effects I experienced were certainly comparable to what I experience with Trenbolone of Masteron. The effects on my hairline were directly comparable to Masteron, which is to say, it ate away a good bit off of my hairline. I think at the dose I was using, I would have noticed anything that could have been interpreted as proprietary to that compound. I frankly was not impressed, considering all of the hype I have read on the internet.


Perhaps you're correct wrt anavar. I certainly don't disagree with the fact that purported differences between compounds are discussed and written about in a manner that far exceeds our scientific knowledge. Maybe sometimes this is done to pad books. Llewellyn.

At the same time - and I hope that I'm not misinterpreting the scope of your excellent post, WHB - I see no a priori reason why small structural differences shouldn't be expected to lead to different binding properties and hence, functional differences between AASs. I'm speaking generally, not specifically about anavar. If most of the benefits from a "type I" AAS result from a simple interaction with the AR, it doesn't mean that there aren't other actions occuring, and that there are differences in the rates / levels of these other activities. Likewise I'd expect the same with "type II" AAS, where non-AR actions would be playing an even bigger role in the net benefits to the user. Additionally, structural differences in the parent compound will result in different activities of metabolites.

Consider briefly testosterone. In addition to AR binding and the activities of DHT, we know that it binds to other receptors, as well as many sites on the genome. It binds to promoter regions of many genes (eg. 3a-HSD) presumably acting as a transcription factor (and probably to other sites, but acting as an inhibitor) as well as to key proteins (eg. P450). How many heterodimers does it form? I have no idea, but I imagine the addition of a carbonyl group or methyl sure could change many of these interactions.

When one considers secondary, or lesser modes of action of AAS's, in vivo studies get harder to design. They're bad enough as it is... largely filled with ailing, rather than healthy patients for obvious reasons, and rarely do they comprehensively analyze markers or compare multiple compounds. Anavar is ironically, perhaps the second-most studied AAS, though I doubt there have been more than a handful of studies using healthy, athletic patients.


While not unreasonable to imagine that the androgen receptor might act subtly differently -- tend to promote different genes -- according to the exact shape of whatever is binding it, I know of no evidence that such is the case.

The estrogen receptor does have properties along those lines, hence the SERMs which are estrogenic in some tissues and antiestrogenic (that is to say, occupying the ER but accomplishing nothing except blocking effective ligands from binding) in others.

But it doesn't seem that the AR activates different genes according to what binds it, nor does a given compound binding it wind up being an activator in some tissues and a blocker in others.


Interesting points. I've got to say that it's far, far easier for me to rely on your knowledge wrt the absence of definitive examples of differential transcriptional regulation (activation or inhibition) than it is for me to spend the next 8 hours scouring papers for possible counter-evidence. Still, that absence of evidence doesn't mean that I'm convinced, just that the right experiments haven't been done :slight_smile: JMO.

If you don't mind a follow up question, Bill, what are your thoughts wrt AAS effects on corticosteroid signalling and activity? Is this a minor, secondary path of action by all AAS? Anavar seems to have a "reputation" for lowering cort levels. I don't know if that reputation is simply brolore... Apparently it effectuates this through AR binding, not direct GR binding, too. The infamous "The Clear" is a very strong GR binder and even knocks down TAT activity. I *assume that this is done via its GR binding, but obviously it might also be the result of AR binding.


But why would you consider it likely, without evidence?

Is there a practical reason such as your noting behaviors of differing steroids that seems to require such a theory?

Really don't know on that one.


No, I'm not working backwards from observed differences.

I simply consider heterogeneity likely due to the complex nature of most transcriptional binding complexes, and the general variety with which even the simplest of pathways seem to be regulated.

AR dimerization, for example, would be one point at which I wouldn't be at all surprised to find differential phosphorylation, perhaps mediated either directly or indirectly by the AAS itself, and resulting differences in transcriptional activation efficiency.

But I never meant to suggest that all variation would need to be wrt the AR-mediated effects, as some might be due to other things contemplated in this thread, such as some mechanisms by which cort expression might be altered, & possibly even PCr upregulation.


Actually, it's a lot more complex for a receptor to have a different genomic response to different ligands than it is for it to be on/off.

Assuming it isn't on/off, at least with regards to genomic activity, while having no evidence for that assumption, despite years of research that ought to have found evidence, and having no observational basis either seems an odd philosophy.



I don't want to hijack Brooks thread, but I think he might like to hear this too. So instead of PMing the both of you, I'll just try and make my point and move on...

As bodybuilders, powerlifters, strength enthusiast, or whatever each of us individual AAS users label ourselves, there exist a limited number of outcomes we expect from the use of them. Lets say there are three expected outcomes, all of which may or may not be expected all at the same time, though the majority of us know this is not always a realistic expectation. One, increased anabolism, two, increased strength, and three, decreased catabolism (catabolism typically being due to severe calorie restriction or wasting diseases). I think the majority of users would agree with this, no?

What else do we know? We need to keep estrogen levels in the normal range. We are also certain that AAS work via at least two mechanisms, AR mediated and Non-AR mediated. I am sure some will say, "Well, we don't know jack shit about the Non-AR mediated effects of AAS." That's fine, I'm not worried about what we don't know right now, only about what we do know. We also know, that to maximize the effect(s) of AAS, in turn satisfying the desired outcome(s) we expect from the use of AAS, we should come as close as we can to saturating these two mechanisms via a combination of compounds that we know will excel in covering our bases in both of those regards.

So, in essence we have the algorithm we need for achieving our goals, with regards to AAS use. Estrogen in normal range + AAS to saturate AR mediated effects + AAS to saturate Non-AR mediated effects = Increased anabolism and/or Increased strength and/or Decreased Catabolism.

We are aware of what AAS are appropriate for satisfying the criteria listed above. So, why do we debate the minutiae surrounding these compounds. I simply believe, that for the majority of people using these drugs, there is little need for debate about what compound is 5% more efficient in aiding the replenishment of ATP or whatever is being discussed. I don't find it particularly useful in any sort of practical sense. And frankly, 99 out of 100 discussions I see on the boards about these sort of things lead absolutely nowhere, as there is no one who is even remotely qualified to speak about the subject involved in the discussion. It's like watching two Forrest Gumps debate The validity of the Kirchhoff approximation for rough surface scattering using a Gaussian roughness spectrum! (BTW that's just a subject I stumbled upon in a Google search, of which I know nothing) This is where these mythical attributes become forever associated with certain compounds.

I'm not saying that you shouldn't ask these questions and I'm not not saying you shouldn't search for the answers. I find the subject endlessly entertaining and love to hear about new information and discoveries. I think for medicinal purposes, these sorts of discussions are more appropriate. So, I will leave these discussions for those that are far more educated in the subject than I.


I love it! When the Kid drops phrases like that I know I'm defeated.

Fwiw, I agree with you 100% on the practical uselessness of any purported differences in secondary characteristics of the compounds. I think virtually all goals can be met through the use of only a handful of AAS.


You love Gaussian roughness spectrums.

I agree with your point (pointless debate) if there is no-one qualified to answer in full, but i hoped there would at least be someone more knowledgeable than me (and two of the posters who's opinions i value most here replied, which is nice..:stuck_out_tongue_winking_eye:) who may know a little more on the subject than me, and have a theory based on information that i didnt know and would find interesting - plus i just find the detailed intracacies of such drugs and their modes of action very interesting.

I did get 2 opinions that i am happy with, but i am a little on the fence and will convey that in the future on the subject.
WTMN has a point i think, and this was my hesitation to simply jump on BR's thought process on the subject.
I wondered that IF Var has this property - would it extend to other Class I AAS or other Class I steroids that are not DHT based - say Turinabol.

I think it is entirely possible, although i do believe that profiles are written with more differences than they deserve, just because this PCr formation has been discovered to be a benefit of var supplementation, doesnt mean it doesnt occur in others similar, but less researched drugs and with the limited amount i know about the drugs in question, it very well could do.

One point of interest - Var is described to have little to no effect on the HPTA in low dosages - ~10mg/day, however with higher dosages PCT will be needed as it will still suppress the HPTA as the body will think it has enough Test already - the negative feedback loop in action.
Well THIS is nothing special is it - as it is supposed to be with var. Many AAS dont suppress in low dosages - as long as the dose is less than the endogenous androgen amount, suppression will not occur. Think Test at <25mg/wk.
It doesnt necessarily mean it is effective at the dosages that are non-suppressive, as it most certainly is not at 10mg/day - but it is just a recorded fact that seems to have been misread and misguided.

Lastly WTMN and WHB, i also agree with the full effects of AAS being easily attained with a handful of possibilities - when people come here asking what can they possibly cut with if they have no winstrol or methyltren or add strength with without halo or cheque drops, it is often frustrating that people think only one product is suitable for their goals - when many a physique was built on a whole lot less different types of steroid.

My regulars include Test, Dbol, Tren and Deca. Recently i have even been considering dropping the Deca, as tren gives the same quality gains but more comfortably for me. Little else is needed until my actual competition cycle where i will have less estrogen and more androgens. Simple yet effective.



woah woah woah, there, hold your horses muscle marys :stuck_out_tongue:

Brook started this thread due to a question i posed in the newbie cycle planning thread (cheers Brook!)

I asked because i am not a bodybuilder or a strenght athlete. I'm a combat athlete fighting MMA. I wanted to plan a cycle appropriate to my discipline which would give appropriate strength/endurance/recovery/catabolism prevention etc. gains without piling on the mass. So these questions are particularly pertinent.

WHB - You mentioned that you found nothing particular about Equip (or var) in terms of performance the test didn't provide. You mentioned endurance and EPO.

But what sort of endurance work did you do to make this assumption? I presume your talking about endurance in lifting weights, say 5 sets of 5, minute breaks in between, or whatever other strenght protocol you got going on.

However, this is a WORLD apart from doing 2hours of Muay Thai, with conditioning, shadow boxing, sparring, 3-4 times a week - 4mile runs (with hill sprints) every morning 3-4 times a week and strength training 3 times a week on top of that.

The anaerobic (and aerobic) endurance required for that as well as other gauges of fitness are worlds apart from bodybuilding training that the majority of AAS users are on.

What i wanted to know was the sport specific effects of AAS. I mean, trenbolone is notorious for adversely effecting anaerobic performance (and i've been told this by many guys at my gym who used it - i don't know if this is true).

What i'm saying is, from a bodybuilding 45min-1hour workout session lifting weights perspective, all the drug may be a much of a muchness. But from a different training protocol, do these individual factors become more pronounced and more significant?

I've never used AAS's, but people in all sorts of sports use them. Even cricketers - tho i don't know why the fuck Shane Warne would need to use Nandrolone, the chubby fat bastard that he is/was. Still tho, test may be the ultimate for bodybuilders - but is it what a tennis player needs for his training regime? Wouldn't he, in that instance, prefer a drug that delivers the same strength gains without the mass - or effects EPO/ATP etc without the other qualities of test.

Would be good to see some peer-reviewed work into this, tho im' sure its few and far between.

Sorry for any ignorant questions, i'm totally new to this.


Wyldflower - Here's a recent abstract that has some relevance only in the fact that it shows Test to have the same sort of magic properties that are associated with EQ commonly (I realize that Test = bulk, for the most part, which you don't want). Elsewhere, it's been shown that the strength of Test's effects on blood are increase with dose. Perhaps the problem with using anavar for this purpose is simply its relative weakness, thus some of these blood effects aren't noticed at standard doses.

J Steroid Biochem Mol Biol. 2009 Feb; 113(3-5):189-94.

Testosterone action on erythropoiesis does not require its aromatization to estrogen: Insights from the testosterone and estrogen treatment of two aromatase-deficient men.

Rochira V, Zirilli L, Madeo B, Maffei L, Carani C.

Dept of Medicine, Endocrinology and Metabolism, and Geriatrics, Univ. of Modena and Reggio Emilia, Argentina.

Androgens act on erythropoiesis, but the relative role of testosterone (T) and estradiol (E(2)) on erythropoietic parameters in men is a poorly investigated issue.

In order to evaluate separately the effects on erythropoiesis of high-dose T administration alone and of physiological dose of E(2) administration alone two adult men with aromatase deficiency were assessed before and during each treatment. Blood cell count, hemoglobin (Hb), hematocrit (Hct), erythrocyte mean cell volume (MCV), erythrocyte mean corpuscular hemoglobin (MCH), erythrocyte mean corpuscular hemoglobin concentration (MCHC), serum ferritin, iron and total iron-binding capacity (TIBC), serum erythropoietin, serum total testosterone and estradiol were evaluated.

Hb, Hct and red cell count rose during testosterone treatment, consistently with the increase in circulating testosterone, but failed to increase during estradiol treatment. A decrease in Hb, Hct and red cell count was recorded in one of the two subjects during estradiol treatment, with a concomitant decrease in serum testosterone.

Circulating T alone is capable of and sufficient to influence erythropoiesis, especially at supraphysiological dosage, while circulating E(2) have not the same effect on erythropoietic parameters, suggesting the hypothesis that the erythropoietic changes induced by androgens are not mediated via its aromatization to estrogens.


What I wrote doesn't only apply to bodybuilders and powerlifters. I believe I was sufficiently clear on that. You may apply the same algorithm, as it will suit your desires just fine. It seems you might be limiting your choice of compounds simple because of internet rhetoric. You have no experience with any of these compounds, correct?

Careful now...I stated that I have never used EQ, and I compared Anavar's effects to the effects of Masteron and Trenbolone. Though, if you can find any scientific evidence that shows EQ to produce a higher RBC count than Testosteone, or for that matter any AAS, with comparable dosages, I would love to see it.

I'm not sure what assumptions you are referring to exactly.

Your logic doesn't seem very sound here. You're saying, if an increase in anaerobic and aerobic capacity is seen at the lower end of the spectrum, then an increase will not be seen at the higher end of the spectrum? I'm not sure exactly what you are getting at with this.

It's not set in stone that Trenbolone will hinder your aerobic and/or anaerobic capacity.

I'm not sure exactly what you are trying to say here. You would not want to use any more AAS than is necessary in any given situation, whether it be bodybuilding or athletics. What individual factors are you referring to?

I'm not sure why you are pigeonholing Testosterone in this way. More than a few cyclist have tested positive for Testosterone, are they massive? I'm sure many other athletes are also using Testosterone, and you would never know by the looks of them. Absolutely, you have plenty of options other than Testosterone, but you don't really need me to tell you that, it should be obvious.

Its not that your questions are ignorant, they just lack specificity. You need to distill your thoughts a bit and make yourself and your questions a bit more clear.


eh... yeah... we got an internet arguer on our hands...

Anyways, "whotookmyname" - thansk for the snippet of the study. Very illuminating.

Any studies comparing the different anabolic compounds tho? That's what would be of most illumination in this situation.


Excuse me? I addressed each of your points/questions in a calm, polite manner. You seem like an arrogant prick with some unjustified sense of entitlement. You need to earn respect around here. As far as I'm concerned from this point, you can fuck off. I'm done trying to help you.


Roid rage!

Brother WHB, to address your post directly would require me to laboriously take apart each one of your sentences invidually as you did mine, adding counter-arguments concerning semantics, turn of phrases and irrelevant digressions.

It would be more productive to keep this discussion focused rather than "he said" "she said" "i meant" etc.

I've found most of the responses so far very informative. Including yours. Especially yours. But especially whotookmyname.

Anyway, back to the discussion. I'm sure all of us here would be very interested to hear from anyone else who has anythign else to add.

I'm beginning to wonder - why bother with anything else except Test? I mean, if for some instances the "mass" that test gives you is undesired - then its a simple case of using less right?

I heard on the rumour mill that Anderson Silva uses an exclusive 600mg per week Equip cycle.

But i can't get my head round this - will an equivalent or less amount of Test affect the EPO in your blood the same as Equip? Will it have the SAME effect on ATP?

So why chose one over the other?

Halotestin makes you more aggressive - but then so does test - so why favour halotestin for aggression over test? For that matter, why favour ANYTHIGN over test? Is it purely a choice regarding side effects?

I think this is a poorly studied area and there's little information i can find on this.


Hello. I'm obsessively obsessed with this topic. I just came across this thought i'd share:


"Alkylated [anabolic steroids] are more effectively absorbed when given PO and are MORE EFFECTIVE STIMULANTS OF BONE MARROW. Alkylated anabolic steroids include oxymetholone (dogs and cats: 1-5 mg/kg, PO, every 18-24 hr) and stanozolol (dogs: 1-4 mg, PO, bid; 25-50 mg, IM/wk; cats: 1 mg, PO, bid; 25 mg, IM/wk; horses: 0.55 mg/kg, IM, weekly for up to 4 wk). Nonalkylated anabolic steroids include nandrolone decanoate (dogs: 1-1.5 mg/kg, IM/wk; cats: 1 mg/kg, IM/wk; horse: 1 mg/kg, IM, once every 4 wk). Boldenone undecylenate is approved for horses at 1.1 mg/kg, IM, every 3 wk"

AAS effect on RBC is because they stimulant bone marrow, and bone marrow is what produces RBC. Is Boldenone Undecylenate an alkylated or a nonalkylated steroid? This text doesn't seem to make it clear as Boldenone is in a sentence of its own at the end, not sure what they mean by that.



However, when coming across this sort of thing it's necessary to look at the doses used before saying one compound or group of compounds is "more effective" than the other.

While I didn't read the study, in the quote above, note that same doses are not being compared.

And further it's not as simple as "same doses": for example let's say that in some measured result that seemed desirable, 400 mg/week nandrolone decanoate somewhat outperformed 400 mg/week testosterone decanoate.

Well does that mean in practice nandrolone must be more effective?

No, because many will be side-effect-limited to the 400 mg/week nandrolone dose but could readily go higher with the testosterone, in which case the testosterone would be the more effective.

Except where there is drastic outperforming, or the thing that is definitely the more tolerable at higher doses is also the one that is more effective per milligram, it's not even so simple as "same doses."

But when it's totally apples and oranges such as comparing (above) injectables at a small fraction of the weekly dose used for the orals, then general conclusions really should not be drawn. At least not without going deeper into the data than the abstract does.


Hi Bill,

As you are a man of learning. Do you think it's true what that veterinary article says? That alkylated steroids have more of an effect on RBC than non-alkylated? If so, what's with the fuss about Boldenone?