Pct/intensity

[H8duke]

I know this topic has been discussed in depth in the past,but I'm looking for new experiences or opinions concerning workout regimens while on PCT. Should you keep at it hard/heavy or lower the intensity? Also what are the reccomendations concerning either lean x or retain? I'm going to run rebound reloaded an activate after a 4 week solo SD run. I've also read its best to start lean x 2.5 -3 weeks into pct. any feedback would be greatly appreciated.

[dinoiii]

dinoiii's feedback:

(1) Intensity is dependent upon a number of factors. If you are asking whether you should essentially ramp down intensity to compensate for metabolic change, this holds some truth, but dietary modification would cover better here. What I am saying is that Intensity (% of 1RM with resistance training) should in effect remain as high as "on" cycle, however caloric tallies will be altered as PCT progresses. There is a rep/set relationship as well as intensity/set relationship that exist. These are critical factors to consider at this time as well.

(2) Lean Xtreme: Quotes from other posts

Cortisol Blocking agents --> should be started about 2 --> 2.5 weeks into post-cycle or you could worsen adrenal function, possibly shutting it down and offering a rebound effect that you were not planning for. For the said reasons, it is both bost efficient and of sound rationale to hold off on it in the immediate post-cycle realm.


In brief:
Post cycle, you are actually in a hypOadrenalism (inclusive of cortisol and other adrenal corticosteroids) state. Rendering further suppression of cortisol not in your best interest at that time. Furthermore, it could actually offer a nasty rebound when cortisol does kick in via route of various feedback systems. Universally, it appears independent of type of cycle 2-3 weeks = appropriate timing of incorporation of such agents...mind you, provided caloric tallies remain adequate. I mean you have to keep your calories appropriately up when you come off cycle initially and gradually reduce. Make sense?


PCT:ACV III article

ANTI-CATABOLICS

7-oxo DHEA (3-acetoxyandrostat-5-ene-7,17-dione) / 7-ketoDHEA

DHEA finds conversion into some 150 metabolites (that we are currently aware of), each with unique actions within the body. One of the reasons my aforementioned comments about the mother-compound DHEA on how I think it is a prohormone that should in fact be banned are worrisome is due to the likely subsequent banning of potentially-useful metabolites. In the early get-go, 7-oxo, TM’d as 7-keto products seem to hold the most promise supported by the literature. I like its seemingly absent conversion to estrogen or testosterone and its anti-catabolic properties (which are purported to control and/or reduce body fat.

The rationale supplied for use of this compound in the post-cycle era, however, through cortisol suppression, I have never understood effectively as stated in Part II and in various posts. Exogenous androgen introduction tends to universally suppress the adrenal gland via feedback inhibition of ACTH. Recall that ACTH subsequently imparts action on production of various adrenal hormones, in this case cortisol being one. For how this effect is seen here, I offer the following “simplified” model:

Step 1: “On” cycle = exogenous androgen introduction, not only leading to subsequent endogenous shutdown of the Leydig cell production of testosterone through feedback inhibition of the pituitary’s production of LH, but also a negative feedback that mimics adrenal cortical (zona reticularis) overproduction of androgenic outflow offering negative feedback tie-in to ACTH pathways.

Step 2: “Off” cycle (PCT) = cessation of exogenous androgen introduction in a still suppressed ACTH (albeit partial) environment (hypOadrenalism) and subsequent low-level cortisol production, amongst other adrenal byproducts.

Step 3: ACTH regeneration BEFORE LH regeneration (due to partial vs. complete negative feedback mechanisms). The question we set out to answer was when this becomes clinically significant. The answer appears to be more complex than the time I would like to offer here, however, I will summarize a few key points:

(1) Half-life of the exogenous compound seems to play a role on ACTH regeneration (which may seem “common sensical”, but how many automatically have assumed immediate catabolism?).
(2) Many factors (dietary as well as other) seem to impart a role on anti-catabolic nature of post-cycle time frame (again, perhaps another “common-sensical” point, but how often is it seen that people go from a hypERcaloric state while “on” cycle into a state of immediate hypOcalorism?).
(3) Another in-house study has given us some answers into regeneration-time frames. Oveall, the 3-week mark post-cycle appears preliminarily to be a time of universal cortisol up-regulation. The first two weeks are assumed to remain in suppression almost independent of the type of agent used. Use of substances such as 7-oxo / 7-keto compounds seems better left out of post-cycle planning for that immediate 2-week time frame.



In PCT, we have compared various post-cyclers and people that have gone with AND without (same individual) and the differences on a hormonal homeostatic basis are sound and verified. I think it dangerous to get into continuing realms of hypOadrenalism, because if you do NOT let the feedback on cortisol die out, you have the potential for one of two things:

(1) While you will remain suppressed from a cortisol standpoint, you risk crossover feedback and a risk of a very modest adrenal insufficiency state

-why should I care? this particular state will dictate fat deposition. It is funny because just as people bastardize cortisol and its "evil" catabolic effects...the essence of catabolism also surrounds adipose catabolism. post-cycle is a time when you are already going through metabolic changes for the negative...there is no reason to promote (even potentially) the realm of weight gain, etc... You would see physique enhancement if done properly. If not done properly on the other hand, you risk a post-cycle crash (but in a different sense) just as if you had gone it alone.

(2) Alternatively, an administration at this time has direct effects on corticosteroid-binding globulin (CBG - also called transcortin). To meet cortisol demands in a hypOadrenal state, the level of CBG DECREASES allowing the activity level of cortisol to take over (so to speak)...This will prove itself to also be contradictory to the state we are trying to promote.

[dinoiii]

I have spoken at length about the other items in the other products you mention in this very forum, so I will direct you there.

[H8duke]

Very helpful info....thanks bro!