2 On 2 Off Experiment

Pharma
81

I’m pretty happy with my recovery in between cycles at this point. My sex drive is fine in between cycles, I still make gains in between cycles… In fact, I think I look better off cycle, as some of the “water softness” goes away. Yes I’m aware I could do that by avoiding sodium, but I’m a strength guy, training for a specific strength competition. I don’t give a hoot. I’ll get healthy after my meet. In addition, I feel that this is MUCH better psychologically… there’s not the ups and downs of “OH MY G-D, I’M A SUPERMAN”, followed by “Oh noes! ZOD TOOK ALL MY SUPERPOWERS”. I get a nice boost during the hardest part of my training, and when the cycle ends, the next boost isn’t so far away.

After I finish my upcoming meet, I’m going to do a “get healthy and athletic” block, and start doing some steady state cardio, and I’ll throw in some tabata work as well. Possibly some yoga to work on mobility, but only if I can find a yoga class thats about mobility, and not centering my chakras. I will take 4-6 weeks off of AAS while I do this, and at that point, depending on what I decide to do with training, I’ll probably make a run at this 2 on 2 off again with just TP or TNE, but at a substantial dose.

Something that alarms me at my relatively hardcore gym: the absolutely ignorant use of AAS. I mean… UNbeLEIVABLE. I was recently told that unless I’m running 800g/week of test for at least 6 months, its hardly worth it.

82

[quote]IKIMURA wrote:
From what I have read the new trend is two on two off for three cycles then 4 weeks off[/quote]

So the idea is that after that 4 weeks off at the end, you should reach full recovery?

83

“I was recently told that unless I’m running 800g/week of test for at least 6 months, its hardly worth it.”

Actually, it’s not a bad cycle. Pretty basic and effective. What I expect from a “hardcore” gym. I have been to gyms in the UAE, that everyone was on heft amount of juice + GH. I would get questions like "you look small, are you running enough test? " “You should really get on some GH, it’s really good stacked with test”.

People that total 1000kg @ 100kg bodyweight probably need to “cruise” on that.

84

UAE, ha… shoulda just asked them if the wanted to come over for beers and discuss AAS. If they say no, accuse them of being homosexual for having looked at your body so much.

That’ll win you friends.

86

Can the ability to recovery quickly from a 2-week cycle be hindered depending on the compounds/dosages that are ran? In Bill Robert’s case study, it looked like his trainee recovered fine from running Tren and D-Bol at 50g/day each, but what if the cycle was “heavier”? For example, what if another compound where thrown in there, or if the dosages were increased?

How much would those factors matter when it comes to recovering within 4 weeks? Or, does the rule still apply that so long as you are off within 14 days recovery will be quick and painless? I ask because I’m curious about a stack consisting of Tren A, Test P, and maybe methyldrostanolone.

87

Compared to the test susp/halo cycle, the tren/dbol cycle has seemed to be an easier recovery for me. I cannot say why. I ran the suspension through day 14. I ran the tren through day 12. The key is 14 days of suppression, not 14 days of injections. I think I may run a higher dose of Tren on my next cycle. I may decrease the Dbol. I’ve gotten greasy and zitty on the dbol, as I experienced in the past.

88

[quote]OTS1 wrote:
Anyone know of any safe/effective appetite stimulants… mine is gone[/quote]

Marijuana.

89

[quote]Nazario wrote:
OTS1 wrote:
Anyone know of any safe/effective appetite stimulants… mine is gone

Marijuana. [/quote]

That stuff makes me silly. I don’t like it.

91

Ditto, there is a finite amount both of growth possible and of AR activation.

You can only get so much, which is why (IMO) GH, slin, IGF, MGF all work so well in those who are pushing the boundaries of their AAS use - they allow one to further ‘enhance’ themselves lifting another genetic barrier with each drug.

92

I don’t know if this was being relied on, in questioning the dose because it showed androgenic activity in skin, but there used to be (maybe still is) a theory of “receptor spillover” which had it that somehow when androgen receptors were full, now the excess steroid winds up in other places.

This isn’t the case whatsoever – “spillover” does not exist. There are also, conservatively (I haven’t done the calculation in more than 10 years) at least a million molecules of steroid for every androgen receptor in the body.

93

Is this fact because only free steroid molecules attach to the androgen receptor?

The spill-over theory, would that be an alternative to the theory that i believe which is the theory that you cannot have 100% binding of the AR.

(as we have spoken about before; x achieving 60% saturation of the AR, x2 achieving 75%, x3=81%, x4=87%, etc.)

94

Excellent thread, loving the info.

Keep the updates and discussions up :wink:

95

[quote] Brook wrote:
at least a million molecules of steroid for every androgen receptor in the body

Is this fact because only free steroid molecules attach to the androgen receptor?

The spill-over theory, would that be an alternative to the theory that i believe which is the theory that you cannot have 100% binding of the AR.

(as we have spoken about before; x achieving 60% saturation of the AR, x2 achieving 75%, x3=81%, x4=87%, etc.)[/quote]

It’s a fact because of how huge Avogadro’s number is. (This number describes how many molecules are present per gram of material, according to the molecular weight of the substance.)

Doing a calculation using this constant, 288 grams (the mw of testosterone is about 288) of testosterone comprises about 6 x 10^23 molecules.

Let’s say you inject an amount of ester containing about 288 mg of testosterone.

So that would be about 6 x 10^20 molecules, or about 600 million trillion, if I’ve figured correctly.

This dwarfs the number of androgen receptors in the body. (Which I once calculated an estimate for based on findings in the literature, but I don’t recall what it was now. But it’s lots less.)

So the ideas, for example, that blocking receptors increases the amount of steroid available – a commonly claimed thing – or that there is “receptor spillover” are not right. It’s kind of like thinking that dunking your beach ball into the water on the East Coast of the US will result in high tides in the UK.

96

So what does this mean for dosages?

I was not relying on an idea of spillover effect when thinking about lowering dbol dosage. I was thinking much simpler: that a lower dose would result in less profound effects. Perhaps this will yield less desired result as well, but I’m playing with dosages IOT find the best cost/benefit for this mix. Maybe 30/day dbol with 75/day TA will be better for me. I won’t know until I try. I do think that based on what I’ve experienced with this cycles, I seem to like:

  1. Test
  2. Strong “androgens” like halo and tren.

Also, I find it interesting, that 40mg/day dbol produced more estrogenic sides (nipple tingling) than 100mg/day test susp.

97

Well, you want to find what for you is a well-liked balance between desired effects and undesired side effects. Only you can make that call on things like what is happening with your skin. Both because at the other end of the computer screen, another person really can’t know how minor or how bad that may be, and also another person cannot know how much it matters to you.

The meaning of what I was saying was that it can’t and shouldn’t be assumed from the presence of such side effects that maximal anabolic effect for that individual occurs at a lower dose than that.

On the nipple-tingling: I would recommend not putting up with that. An AI or SERM should be used.

98

Agreed. I was running 1mg/day adex. I will up the dose on that, since I have it, and next time around try some letro.

99

[quote]Bill Roberts wrote:
Brook wrote:
at least a million molecules of steroid for every androgen receptor in the body

Is this fact because only free steroid molecules attach to the androgen receptor?

The spill-over theory, would that be an alternative to the theory that i believe which is the theory that you cannot have 100% binding of the AR.

(as we have spoken about before; x achieving 60% saturation of the AR, x2 achieving 75%, x3=81%, x4=87%, etc.)

It’s a fact because of how huge Avogadro’s number is. (This number describes how many molecules are present per gram of material, according to the molecular weight of the substance.)

Doing a calculation using this constant, 288 grams (the mw of testosterone is about 288) of testosterone comprises about 6 x 10^23 molecules.

Let’s say you inject an amount of ester containing about 288 mg of testosterone.

So that would be about 6 x 10^20 molecules, or about 600 million trillion, if I’ve figured correctly.

This dwarfs the number of androgen receptors in the body. (Which I once calculated an estimate for based on findings in the literature, but I don’t recall what it was now. But it’s lots less.)

So the ideas, for example, that blocking receptors increases the amount of steroid available – a commonly claimed thing – or that there is “receptor spillover” are not right. It’s kind of like thinking that dunking your beach ball into the water on the East Coast of the US will result in high tides in the UK.
[/quote]

I didn’t mean why are there so many molecules per se, as i have an understanding of the scale there… but more why do we dose in a manner that allows so many more molecules per receptor?

To illustrate where my mind is going with this, here are the only reasons i can think of for such a unbalanced ratio of molecule:receptor -

  1. That only the non-bound (free) androgen molecules can attach to the AR, and this is only a very small percentage of total androgen levels,
  2. That many of the molecules are involved in non-AR mediated activity, and/or
  3. More than one steroid molecule is active at a receptor at any one time.

JJ

100
  1. Because the molecules are not confined to a tiny volume around the receptor.

Thus, it takes a vast number in the body to have a quite low concentration of free testosterone in the vicinity of the receptor, such as in the picomolar range. (In the millionths of a micromolar.)