Plan for (possible) 2nd cycle

[DriverDan]

Right now I can't decide what I want to do, but that doesn't keep me from planning. I wanted to do my first shows in April, 2 weekends in a row (4/5 & 4/12). After being out of the gym for 2 months from a broken collarbone I'm not sure I'll be ready. I lost some quality mass and put on fat. I'm 95% sure I can lose the fat but now I'm not happy with my size. I'm 12 weeks out right now.

I'm figuring out my options. No matter what I decide to do I want to cut. Even if I don't compete I want to lose at least 15 lbs of fat and get down to single digit body fat %. Right now I'm contemplating cutting to the end of January. This will give me a chance to get back into it and hopefully get close to where I was. Then run a cycle for 4 weeks, recomp or light cut depending on how the fat loss is going. A week into PCT go to keto and lose the remaining fat for the shows.

I have a few products in stock to choose from. 1 bottle of Prop, more Tren than I'll ever use, 2 bottles of EST's Epi clone, 2 bottles of Jungle Warfare (possibly a PH) and one of Pro-Anabol (not a PH). Right now I'm leaning towards Epi + one of the others. PA gave me excellent muscle fullness and pumps so I'm thinking of using it just before the contest during keto as it should be fine during/after PCT.

Possible 4 week cycles:
30mg epi + 60mg tren
30mg epi + 60mg prop

I would have to keep a VERY close watch on my fat loss to make sure I'm meeting deadlines. The last thing I want to do is get behind. I can't afford to risk crash dieting at the end and losing more muscle.

Input?

[FrankZane]

and this ??

1. week epis 30mg + prop 30
2. week epis 30mg + prop 30
3. week epis 30mg + prop 30 + tren
4. week epis 30mg + prop 30 + tren
5. week epis 30mg + tren
6. week epis 30mg + tren

[DriverDan]

I was thinking of something like that too. Not sure I want to use 3 compounds though.

[solomon1979]

Just use Methyl E and Trenadrol. Try and work up to 40mg of Methyl E. Something like this seems like a good option.

Day 1 10mg Methyl E/60mg Trenadrol
Day 2 20mg Methyl E/60mg Trenadrol
Days 3-30 30mg Methyl E/60mg Trenadrol
Days 31-42 40mg Methyl E

[DriverDan]

Update: Lifting is going well, I'm getting back into it. Weights are still way down but pain isn't restricting my lifts as much. Pump is back in a big way. I expect the pain to be almost, if not all gone by the end of this month. Speaking of the end of this month, here's what I've come up with for a cycle:

Day 1: 10mg Methyl E/30mg Trenadrol
Day 2: 20mg Methyl E/30mg Trenadrol
Days 3-7: 30mg Methyl E/30mg Trenadrol
Days 8-30: 30mg Methyl E/60mg Trenadrol
Days 31-42: POSSIBLY 40mg Methyl E/60mg Trenadrol

(very close to solomon's suggestion)

Bump to 40mg will depend on how I feel. Tren may end earlier than 6 weeks, again depending how I feel. I used Tren @ 60mg briefly during my Bold cycle but stopped it when prolactin sides occurred. I'm going to be much more prepared for that this time around. If it happens again I may keep it at 30mg or drop it all together. I'm really hoping it doesn't happen though because I have 3+ bottles of it still.

My goal will be recomp. I'd LOVE to be the same weight at the end with a loss of 10 lbs of fat, that would be AMAZING but doubtful. I'm going to come up with a complete supplement plan for the cycle. I need to go through my stash and see what I need to order.

For the rest of January (10 days) I'm going to be doing some serious dieting. <2000 kcal per day Sunday through Friday. Saturday is 3000+ kcal refeed, mostly clean. Diet isn't keto but focuses on getting 1.25+g protein/lb and 40-50+ g of fat with the rest from carbs. I'm using a combo of stims (Amp and N-Cinerate) and ALRI ThyrogenX along with the regular sups. Goal is at ~2lbs fat loss per week.

[mw1111]

I like Sol's plan w/ Epi and Tren. I pretty sure that is about what Bmoremade26 is running right now. I on week 3 of Methyl e at 50mgs and i have to say its is exceding my expectations.

[bmoremade26]

sol's idea sounds good he gave me the idea on the dosing for the methyl e :D im running trenadrol for a little over 5 weeks and methyl e for 6 weeks im probably going to up tren to 90 though for last three weeks ... solomon also suggested running dermacrine with epi ... maybe u could look into that .. from his log on it seems to be a quality product and im definately gonna try it out later on

[B-natural]

Well, tren and epi are both class I's, I've heard of ppl having great results, but is it the combo or the fact that both are good products when ran solo, I would run one or the other, not both....

[solomon1979]

Well, tren and epi are both class I's, I've heard of ppl having great results, but is it the combo or the fact that both are good products when ran solo, I would run one or the other, not both....

Here's an interesting piece of information about those classifications-
December 29, 2000
Issue #27

Q&A WITH PAT ARNOLD

Q: I hear that there are two classes of steroids. Class I bind to the androgen receptor to impart their activity and they include nandrolone and testosterone. Class II do not bind to the androgen receptor but impart their actions by as yet undetermined means. Class II steroids include d-bol and 4-AD and these are supposed to stack awesomely with Class I. Do I have this right?

A: There are not two classes of anabolic steroids. This theory has no acceptance, let alone mention, in the scientific literature, but is instead the belief of the exceptionally outspoken dudes over at Testosterone.net.

This theory can be blown out of the water by one simple fact. D-bol, 4-AD, anadrol and the other so called“Class II” steroids have very high androgenic activity. Androgenic activity is manifested through the classic androgen receptor and there is no argument about that. Therefore these “Class II” compounds, like the “Class I”, are exerting at least some part of their effects through the androgen receptor.

You want proof? Consider the following article:


--------------------------------------------------------------------------------

Effect of steroids with antiandrogenic properties on androgenic and myotrophic activity of testosterone and some of its derivatives. Neurosci Behav Physiol.,1980

May-Jun;10(3):227-31.

In this article they use an anti-androgen (receptor antagonist) to test
effects on various tissues when taken along with a variety of
anabolic steroids. The effect with dianabol is described as follows:
"The results obtained upon joint administration of dianabol and the
antagonist were somewhat unexpected. The latter in doses of 2.5 and
7.5mg/rat/day caused a decrease in the response to dianabol only on the
part of the muscle and inhibited the stimulatory effect of dianabol on
the mass of the accessory (androgen sensitive) organs only in the
maximum dose."


--------------------------------------------------------------------------------

Dianabol is described by the T-Mag theorists as being a classic "Class
2" (acts anabolically not by the androgen receptor). This study
completely contradicts their theory because when administered with an
androgen receptor antagonist, dianabol's anabolic activity was vastly
reduced. Reduced even more so than it was with testosterone (a
purported "Class 1" steroid). I mean, these results are the total opposite of what
would be expected from the “Class Theory” of steroids!!

There is a very simple explanation why some steroids do not bind much to the androgen receptor in-vitro, yet exert strong anabolic / androgenic effects in-vivo. Hey, I did not make up this explanation, it is the one accepted by the scientists themselves. You see, many drugs do not exert their effects in their original form but are instead metabolized into the active compounds. Such drugs are termed “prodrugs”. So even though these Class II compounds have negligible binding to the androgen receptor in their parent form, they have metabolites that do bind very well. For instance, oxymetholone (anadrol) metabolizes into 17alpha methyl-DHT (mestanolone) which binds very strongly to the AR. Furthermore, 4-AD metabolizes into testosterone doesn’t it? Well duh!!

No, there are not two classes of anabolic steroids. The evidence does not suggest this at all. So why did such a theory get proclaimed with such confidence? Why did it get accepted by the lame ass public just because “they said so”? I dunno!


--------------------------------------------------------------------------------

[B-natural]

interesting, if only I had a science background I could have a rebutal, guess I'll go curl up in the corner and call in my superhero DINOIII....

(as I side note, I know this gets annoying to reference dinoiii and some of us don't have the spine to stand up for things, but if I don't have the knowledge I'll pull someone in who does, and I don't wanna be that dude in the background goin "ya, see, f****n told you so dude" but jus to see what another knowledgeable fella thinks, I reference the Doc)

[mw1111]

Here's an interesting piece of information about those classifications-

SOLMON= PA's PUPPET:eek: :D JK!! LOL!

[solomon1979]

SOLMON= PA's PUPPET:eek: :D JK!! LOL!

Nah, but I seriously don't like how things are being stacked based on classifications. There's plenty of evidence that this system has some inconsistancies.

[DriverDan]

Using two classifications is probably valid to a certain degree. There will always be overlap but it only makes sense that some sterosoidal compounds act through different means.

[MAD DOG]

Valid Point!

[DriverDan]

I made a nice spreadsheet of each day from now until the end of PCT and all supplement dosing. Way too large to post. It was very helpful in showing what I have left for support sups, what I need to buy, and the timetable for everything. Cycle will start Sat Feb 2nd and end Fri March 14th (6 weeks). PCT will then run for 30 days to Sun April 13th.

Planning out my support sups now. Dosing isn't certain yet but I'll be taking Vitex and L-Dopa for prolactin support along with the usuals (hawthorn, saw palmetto, silymarin, coq10, SAMe). PCT will be at minimum ALRI Restore and I3C.

Of course everything is subject to change. If I don't feel like I'm ready to start I'll put it off for another week. I don't want to start if my body isn't ready.

[MAD DOG]

Epi/tren with thyro cuts 2 by san should do the trick.

[dinoiii]

This is actually a really nice thread! Some joint cycle planning, a little theory, some PA, etc...

Dan,
I wish you well in your recovery process and look forward to your chroniclization of your return (whether you opt to compete or not).


Just use Methyl E and Trenadrol. Try and work up to 40mg of Methyl E. Something like this seems like a good option.

Day 1 10mg Methyl E/60mg Trenadrol
Day 2 20mg Methyl E/60mg Trenadrol
Days 3-30 30mg Methyl E/60mg Trenadrol
Days 31-42 40mg Methyl E

Day 1: 10mg Methyl E/30mg Trenadrol
Day 2: 20mg Methyl E/30mg Trenadrol
Days 3-7: 30mg Methyl E/30mg Trenadrol
Days 8-30: 30mg Methyl E/60mg Trenadrol
Days 31-42: POSSIBLY 40mg Methyl E/60mg Trenadrol

To Sol and Driver,

Do you really find the necessity of 10-20mg of epitho products? I see that you only incorporate them for a few single days (which is better than most); are you merely assessing tolerance with that protocol?


Nah, but I seriously don't like how things are being stacked based on classifications. There's plenty of evidence that this system has some inconsistancies.

"Evidence" in the world of AAS is hard to come by. There are two "class systems" that have been hypothesized:

[1] The first is as suggested and gives basic recommendations of cycles; sure its not clear-cut, but to disregard that actions occuring primarily through systems other than the AR is funny - especially when we have data for AR-displacement. The reason it has been protested is because there is cross-talk (if you will) between receptors. I encourage checking out oxandrolone research for more. To suggest it doesn't work - perhaps (maybe more accurately though, it has not been applied correctly, because our knowledge is lacking in this area and you could likely call the system what you will...there are always exceptions to the "rules" of generalization; but I certainly wouldn't suggest data has been convincing to show the contrary).

I won't get into the article posted because PA vs. BR is simply NOT something I care to discuss.


[2] The more generic system divides class systems into administration routes: I (injectable), II (oral), III (oral + injectable). The application here does nothing to aid cycle designations for most - so why use it?


D_

[solomon1979]

To Sol and Driver,

Do you really find the necessity of 10-20mg of epitho products? I see that you only incorporate them for a few single days (which is better than most); are you merely assessing tolerance with that protocol?




"Evidence" in the world of AAS is hard to come by. There are two "class systems" that have been hypothesized:

[1] The first is as suggested and gives basic recommendations of cycles; sure its not clear-cut, but to disregard that actions occuring primarily through systems other than the AR is funny - especially when we have data for AR-displacement. The reason it has been protested is because there is cross-talk (if you will) between receptors. I encourage checking out oxandrolone research for more. To suggest it doesn't work - perhaps (maybe more accurately though, it has not been applied correctly, because our knowledge is lacking in this area and you could likely call the system what you will...there are always exceptions to the "rules" of generalization; but I certainly wouldn't suggest data has been convincing to show the contrary).

I won't get into the article posted because PA vs. BR is simply NOT something I care to discuss.


[2] The more generic system divides class systems into administration routes: I (injectable), II (oral), III (oral + injectable). The application here does nothing to aid cycle designations for most - so why use it?


D_

Its to assess tolerance. I've jumped the gun on an Epithio cycle and used a high amount at the onset and just noticed increased sides(back pumps). I've also gradually upped the dosages on another cycle and it alleviated this substantially. My point of including the article was to keep people from automatically dismissing stack options based on the classification system. Some of the hormonal products available today, don't necessarily follow the same androgen receptor pathways. There are a few products that are marketed(in name and product write up claims) as being related to certain well known androgens, but are actually not even related to them at all. Then, there are the mystery products like Trenadrol and Methoxy-TST, which have even left formulators confused.

[neonhypoxia]

First off I'de like to say that I could have been a better student in my endo class. Also while my job does happen to be doing research on hormones it isn't with androgens. (actually its with prostaglandins and we are way better at killing lab rats then at being successful) So feel free to disagree with me, I'm just giving my view. I think the big problem here is that both sides are trying to over simplify the issue. One saying that there are two classes so just pick one from each, and the other saying that they are all basicly the same class. The general rule is that if it doesn't seem extremely complicated, then your biology probably isn't right.

It is very possible that they all work via the AR, but it is just as likely that some work by other means. Some could be influencing gene expression or protein synthesis by other methods. Its even very possible that some might work by a method that no one has proposed yet. To further complicate things while only one type of AR has been discovered, it is still extremely possibly that there are other classes and subclasses of ARs. I'm sure that someone is going to tell me that (insert name of study) said that only one AR has been found when they looked, so there must only be one AR. I'm highly doubtful of that considering that almost everytime the same thing was said, later on it was found out that indeed there were different classes of the receptor. 5ht (seratonin) and dopamine are good examples of this.

Also simply adding a steroid that is suppose to be a nonAR mediated one, and then adding an AR antagonist and seeing what happens is an awful way to go about looking at the issue. An AR antaganist blocking its action does not say that it the drug in question must work by the AR. It could be that it doesn't work by the AR, but that the AR antagonist caused a feed back mechinism which blocked it from working by other means. There is also a good chance that at least some of the class IIs work by mediating something that happens after the AR is activated.

Personaly if feel that there is probably more than on class of AR, which would explain why some class Is stack well. I also think that many of the class IIs work not just by a different means from the AR, but that there are several different ways they can work. So think of the class IIs not as really being a class, but as a collection of several different classes that are still poorly understood.

In short, its complicated and all of the science is no where near being in.

[dinoiii]

Its to assess tolerance. I've jumped the gun on an Epithio cycle and used a high amount at the onset and just noticed increased sides(back pumps). I've also gradually upped the dosages on another cycle and it alleviated this substantially. My point of including the article was to keep people from automatically dismissing stack options based on the classification system. Some of the hormonal products available today, don't necessarily follow the same androgen receptor pathways. There are a few products that are marketed(in name and product write up claims) as being related to certain well known androgens, but are actually not even related to them at all. Then, there are the mystery products like Trenadrol and Methoxy-TST, which have even left formulators confused.

Good feedback.

And I can certainly appreciate your issues with the class system. I think one of the unfortunate things is that it was taken and applied to supplements when you do have all of these discrepencies and things being mislabeled which makes it a hard sell.

I still would approach some cycles with a class system of sort in mind, but there are some things it leaves to be desired like something being 5-alpha-reduced and other things not being. Think to an Epi + Bold offering; is it really a clean suggestion by the class system? No way and this is one of those times where it may come down to things like 5-alpha-reduction, etc... structural components that are just not given appropriate thought when thinking about AR binding.


D_

[dinoiii]

First off I'de like to say that I could have been a better student in my endo class. Also while my job does happen to be doing research on hormones it isn't with androgens. (actually its with prostaglandins and we are way better at killing lab rats then at being successful) So feel free to disagree with me, I'm just giving my view. I think the big problem here is that both sides are trying to over simplify the issue. One saying that there are two classes so just pick one from each, and the other saying that they are all basicly the same class. The general rule is that if it doesn't seem extremely complicated, then your biology probably isn't right.

It is very possible that they all work via the AR, but it is just as likely that some work by other means. Some could be influencing gene expression or protein synthesis by other methods. Its even very possible that some might work by a method that no one has proposed yet. To further complicate things while only one type of AR has been discovered, it is still extremely possibly that there are other classes and subclasses of ARs. I'm sure that someone is going to tell me that (insert name of study) said that only one AR has been found when they looked, so there must only be one AR. I'm highly doubtful of that considering that almost everytime the same thing was said, later on it was found out that indeed there were different classes of the receptor. 5ht (seratonin) and dopamine are good examples of this.

Also simply adding a steroid that is suppose to be a nonAR mediated one, and then adding an AR antagonist and seeing what happens is an awful way to go about looking at the issue. An AR antaganist blocking its action does not say that it the drug in question must work by the AR. It could be that it doesn't work by the AR, but that the AR antagonist caused a feed back mechinism which blocked it from working by other means. There is also a good chance that at least some of the class IIs work by mediating something that happens after the AR is activated.

Personaly if feel that there is probably more than on class of AR, which would explain why some class Is stack well. I also think that many of the class IIs work not just by a different means from the AR, but that there are several different ways they can work. So think of the class IIs not as really being a class, but as a collection of several different classes that are still poorly understood.

In short, its complicated and all of the science is no where near being in.

Nice post.

I think Llewelyn has suggested a similar offering.



D_

[DriverDan]

Epi/tren with thyro cuts 2 by san should do the trick.
I did some searching on T2 and didn't find a lot of info. There is limited research on it. Some have speculated it causes negative feedback and requires a thyroid PCT which isn't something I don't care to deal with. My metabolism is pretty good so for now I'll just stick to a calorie restricted diet and stim based fat burners. Thanks for the suggestion though.

The only reason I'm using ThyrogenX is because I got a bottle for free as a result of an ALRI log I ran. I wouldn't have bought it otherwise.

This is actually a really nice thread! Some joint cycle planning, a little theory, some PA, etc...

Dan,
I wish you well in your recovery process and look forward to your chroniclization of your return (whether you opt to compete or not).
Yeah, some good discussion going on. I'm 98% sure I'm going to compete. This week's workouts have been going great. Strength is starting to return.

To Sol and Driver,

Do you really find the necessity of 10-20mg of epitho products? I see that you only incorporate them for a few single days (which is better than most); are you merely assessing tolerance with that protocol?
My reasoning was tolerance assessment. The first week of tren at 30mg is to assess prolactin sides this time around. Jumping straight into 60mg half way through Bold didn't work out well for me.

First off I'de like to say that I could have been a better student in my endo class. Also while my job does happen to be doing research on hormones it isn't with androgens. (actually its with prostaglandins and we are way better at killing lab rats then at being successful) So feel free to disagree with me, I'm just giving my view. I think the big problem here is that both sides are trying to over simplify the issue. One saying that there are two classes so just pick one from each, and the other saying that they are all basicly the same class. The general rule is that if it doesn't seem extremely complicated, then your biology probably isn't right.

It is very possible that they all work via the AR, but it is just as likely that some work by other means. Some could be influencing gene expression or protein synthesis by other methods. Its even very possible that some might work by a method that no one has proposed yet. To further complicate things while only one type of AR has been discovered, it is still extremely possibly that there are other classes and subclasses of ARs. I'm sure that someone is going to tell me that (insert name of study) said that only one AR has been found when they looked, so there must only be one AR. I'm highly doubtful of that considering that almost everytime the same thing was said, later on it was found out that indeed there were different classes of the receptor. 5ht (seratonin) and dopamine are good examples of this.

Also simply adding a steroid that is suppose to be a nonAR mediated one, and then adding an AR antagonist and seeing what happens is an awful way to go about looking at the issue. An AR antaganist blocking its action does not say that it the drug in question must work by the AR. It could be that it doesn't work by the AR, but that the AR antagonist caused a feed back mechinism which blocked it from working by other means. There is also a good chance that at least some of the class IIs work by mediating something that happens after the AR is activated.

Personaly if feel that there is probably more than on class of AR, which would explain why some class Is stack well. I also think that many of the class IIs work not just by a different means from the AR, but that there are several different ways they can work. So think of the class IIs not as really being a class, but as a collection of several different classes that are still poorly understood.

In short, its complicated and all of the science is no where near being in.
Less than 10 posts and already contributing content like this? :eek: Keep it up and you'll be a great addition to the board.

Your point was a more scientifically founded explanation of what I said. Despite being an autodidact I haven't learned that much about organisms/bio, so uh yeah, much better than what I could post ;)

[MAD DOG]

I Have Used It Numerous Times And Am Using It Now With Great
Results. If Problems Arise Most People Use Blaze By San. My
Metabolic Rate Has Slowed Over The Years.;)

[DriverDan]

Here's an interesting discussion point. Ignoring possible side effects (such as potential gyno and prolactin), would increasing estrogen help combat dry joints?

[DriverDan]

I'm contemplating using adrenosterone (11-oxo) instead of epi + tren. There's a 6 month recomp contest on another board I'd like to enter but non-DSHEA compliant PHs aren't allowed (11-oxo is). I'd be looking at 30g bulk run for 6 weeks (~715mg per day). Not sure if I can afford it though unless I sell off some of my stash.

[MAD DOG]

I'm contemplating using adrenosterone (11-oxo) instead of epi + tren. There's a 6 month recomp contest on another board I'd like to enter but non-DSHEA compliant PHs aren't allowed (11-oxo is). I'd be looking at 30g bulk run for 6 weeks (~715mg per day). Not sure if I can afford it though unless I sell off some of my stash.


What kind of results are u expecting?

[MAD DOG]

Thinking about the 11 oxo also, what are your views and exp w it?

[DriverDan]

I've decided to keep my original plan in place. Epi + Tren for 6 weeks. I'm going to start a contest prep log this week. The cycle will start next weekend.