Test & Winny- Are They Synergistic???

since they bind to the same receptor, they wont be synergetic...but they may activate the transcription of different proteins, so its pretty hard to answer compleatly. But i wouldnt expect not to see a difference between test/win and a higher dose of test on muscle metabolism.

Personally I have noticed far greater gains stacking winstrol and test than I would have achieved using test alone at a higher dose. Here is a nice little read by Huck. Stacking opposing classes of anabolics for maximum efficiency By Huck Finn For all my brotha's getting ready to put together those winter bulking regimens,thought this might come in handy for you... Anabolic Steroids achieve their effects on hypertrophy through different mechanisms,and as such are classified into two different categories,class-I and class-II compounds.I will explain which ones work through which pathway,and how to effectively combine opposing groups to maximize potentiation of one another for explosive growth.... Class-I-These are steroids who's *****ry influence on anabolism is achieved through aggressive binding and activation of the androgen receptor...Examples of potent class-I's are-Deca-durabolin,primobolan,equipoise,oxandrolone... Class-II-These are compounds with potent activity independent of A/R binding/activation,and their activity has been monitored in neuron's,microsomes,mitochondria,etc...Examples of potent class-II's are-Anadrol,Dianabol,winstrol,Fluoxymesterone... Then we have steroids that are potent combination steroids all by themselves(meaning they display influences on growth through both class-I and II activity,and thus are very effective as'stand-alone'anabolic agents as well as forming the 'base' of most steroid stacks)....Two compounds possess this unique characteristic-Trenbelone and Testosterone.Either of these two steroids should form the base of most users stacks,as the cover both A/R and non-A/R mediated mechanisms,and adding to them with either a class-I or II will only potentiate that particular mechanism towards muscular hypertrophy... Now that we're aware of which compounds work through which mechanism,how do we combine them effectively to maximize each one's potential?As explained above,Testosterone and trenbelone should form the base of any serious steroid stack,but great effects can be had by combining single mechanism steroids from opposing classes....Examples of this type of synergistic combining could be(but are not limited to) *CUTTING* Winstrol & Equipoise Winstrol & primobolan Fluoxymesterone & Equipoise or Primobolan *BULKING* deca& Dianabol Anadrol & Equipoise or Primobolan Winstrol & deca And of course,using test or tren as the base compound for either cutting or bulking will only make results that much more explosive.If using test for cutting,an anti-aromitase should be incorporated... __________________

Side by side comparison:Testosterone Vs.winstrol by Huck Finn Hey fella's.Digging through my archives and came across this jewel of an abstract-Test and winstrol going head to head as anabolics.Some interesting results to say the least...Test blew away the winstrol in GH/IGF-1 stimulatory capabilities,but winstrol outshined test in nitrogen retention activities.Awesome study...Enjoy. Short-term modulation of the androgen milieu alters pulsatile, but not exercise- or growth hormone (GH)-releasing hormone-stimulated GH secretion in healthy men: impact of gonadal steroid and GH secretory changes on metabolic outcomes. Fryburg DA, Weltman A, Jahn LA, Weltman JY, Samojlik E, Hintz RL, Veldhuis JD J Clin Endocrinol Metab 1997 Nov 82:3710-9 J Clin Endocrinol Metab . Volume 82 . Issue 11 Abstract Gonadal steroids are known to alter GH secretion as well as tissue metabolism. The present study was designed to examine the effects of short term (2- to 3-week) alterations in gonadal steroids on basal pulsatile (nonstimulated) and exercise- and GH-releasing hormone-stimulated GH secretion, urinary nitrogen excretion, and basal and exercise-stimulated oxygen consumption. Two protocols were conducted, which reflect a total of 18 separate studies. In the first paradigm, 5 healthy young men were each studied in a double blind, ran***ized manner during 3 different gonadal hormone manipulations, in which serum testosterone was varied from hypogonadal (induced by leuprolide) to eugonadal (saline injections) to high levels (Testosterone Enanthate, 3 mg/kg.week, i.m.). There was a washout period of 8 weeks between treatments. In the second protocol, 3 of the original subjects were studied after 2 weeks of treatment with Stanozolol (0.1 mg/kg.day). Two to 3 weeks after the desired changes in serum testosterone, each subject was admitted to the General Clinical Research Center for study. The hypogonadal state (serum testosterone, 33 ng/dL) increased urinary nitrogen loss (by 34%; P < 0.005) and decreased basal metabolic rate (by 12%; P < 0.02) compared with the eugonadal state (testosterone, 796 ng/dL). High dose testosterone (1609 ng/dL) further decreased urinary nitrogen loss over the eugonadal state (by 16%; P < 0.05). Stanozolol yielded the lowest urinary nitrogen excretion of all (P < 0.03). Like urinary nitrogen, the basal metabolic rate showed the greatest change between the hypogonadal and eugonadal states (12%; P < 0.02), with a lesser change during high dose testosterone treatment (4%). Analogously, end-exercise oxygen consumption rose by 11% between the hypogonadal and eugonadal states (P < 0.05). Between the hypogonadal and eugonadal states, no significant changes in pulsatile (nonstimulated), exercise-stimulated, or GRF-stimulated GH secretion or serum insulin-like growth factor I concentrations were observed. Raising testosterone to supraphysiological levels increased pulsatile GH secretion by 62% over that with leuprolide and by 22% over that with saline (P < 0.05). High dose testosterone treatment also increased serum insulin-like growth factor I concentrations by 21% and 34% over those during the eugonadal and hypogonadal states, respectively (P < 0.01). Testosterone did not affect either exercise- or GRF-stimulated GH secretion. In protocol 2, stanozolol did not affect any parameter of GH secretion. To examine the interaction between GH secretion and testosterone on urinary nitrogen excretion and basal metabolic rate, a one-way analysis of covariance was undertaken. Statistical examination of GH production as the covariate and testosterone (by tertile) as the interactive factor demonstrated significant relationships between serum testosterone levels and either urinary nitrogen (P < 0.02) or basal metabolic rate (P < 0.01), but not GH secretion (P = NS). In summary, these results demonstrate that short term modulation of the androgen milieu affects metabolic outcome without necessitating changes in GH secretion. These results have significance for both normal physiology and for the treatment of hypogonadal GH-deficient patients

Thanks for the info, Liftsiron!

Any personal experiences, guys??

Posted by: Texas Ranger

Any personal experiences, guys??

Not yet, but planning this next:
1000 mg Test enth/wk
600 mg deca/wk
100 mg winny ED

Can't wait for March!

Nice posts liftsiron. I would have loved to see how tren would have stacked up, in that study. Since tren is notorious for increasing nitrogen retention while dieting, increases GH and igf-1 and has a high affinity for AR's.

Bill Roberts has written some good articles on classifying steriods into two catagories also. Anadrol falls into the either/or catagory for some ppl. If you aren't subject to the estrogenic/progestic sides, anadrol is a very potent cutting drug.

I wonder how test/Tren A and Anavar would work on a cutting cycle, it would have to be an awesome combo. Of course when cutting diet is the most important factor. Test and winny also make a good cutting combo much more effective imo when EQ is added. I have seen bros cut whlle on androl provided a powerful anti-e like letro was used.

Posted by: liftsiron

I wonder how test/tren and anavar would work on a cutting cycle, it would have to be an awesome combo. Of course when cutting diet is the most important factor. Test and winny also make a good cutting combo much more effective imo when EQ is added. I have seen bros cut whlle on androl provided a powerful anti-e like letro was used.

That's the stack I would really like to try. I've never used anavar and have been kinda anxious to try it every since jguns posted that study. Since both tren and var give good strength gains, I think low rep trainig might be best. Throw in some cardio and get cut and strong! What do you think about using letro, T3 and a beta agonist with this stack?

Testosterone and winny MAY act synergistically on a multitude of levels. They most certainly do not work in the same manner, I believe Winny binds muich stronger to microsomal AR, that it activates different transcriptional mechanisms etc. And that is just in their AR mediated effects.

Apart from that winny also blocks the low affinity GR, in concert with testosterone which blocks the high affinity GR. So they may act together to reduce catabolism. I say may, because of course 17AA steroids also increase GR density.

And apart from that it works in a variety of ways quite different to testosterone. They have different effects on GABA metabolism, on insulin, on FGF's, on calcium levels.

Whether they really are synergistic to an extent that makes a difference is beyond me. But certainly the possibility is there that they could be synergistic, and one should not discard the possibility "because they bind to the same receptor".

Nice post BC.

Thanx, i'd be careful about posting those huck finn cut and paste's, I see a lot of stuff in there that is not only entirely incorrect, but that was disproven some time ago. Especially in the first post with that class I and class II bull Bill Roberts concocted in some drunken fashion one night. It was never accepted, and frankly its far too simplistic to explain anything.

The best example perhaps is Testosterone itself. One of the best drugs as far as AR binding and transcription goes, and definitely the drug with the most known non-AR mediated mechanisms of growth as well. So which is it ? Class I or Class II ? Fact is, all known AAS bind the AR (class I) and all of them have at least some form on non-AR mediated effect (Class II).

Big Cat, thanks for replying! My goal with this cycle is to achieve a dense, hard look to my physique and not so much a big weight gain(ie.20-25lbs)like a Test/Dbol or Test/Drol cycle would. I'm going to get down to 6'3" 225lbs 7-8% bodyfat naturally before starting the cycle. Here's what I had in mind.

test enanthate@500mgs for 12 weeks
Winstrol@50mgs ED for weeks 8-14 weeks
Liv-52 & R-Ala for Liver Protection.

Sounds good?? If not, what would you change??

Posted by: Big Cat

Thanx, i'd be careful about posting those huck finn cut and paste's, I see a lot of stuff in there that is not only entirely incorrect, but that was disproven some time ago. Especially in the first post with that class I and class II bull Bill Roberts concocted in some drunken fashion one night. It was never accepted, and frankly its far too simplistic to explain anything.

The best example perhaps is testosterone itself. One of the best drugs as far as AR binding and transcription goes, and definitely the drug with the most known non-AR mediated mechanisms of growth as well. So which is it ? Class I or Class II ? Fact is, all known AAS bind the AR (class I) and all of them have at least some form on non-AR mediated effect (Class II).

I know what your saying, my intention was to show what drugs work well together rather that bring the class I and II aspect into play which I should have clarified. The same can be said when people try to class anabolic aas as either an androgen or anabolic when all have properities of both, altough some have greater androgenic charcterisitics than others.