Pct on test only

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ackrug

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So i have all i need to do the pct off the first cycle sticky iam doing 400mg a week at the moment. Is the pct in that stucky really necessary for the ammount in taking?
 
ackrug said:
So i have all i need to do the pct off the first cycle sticky iam doing 400mg a week at the moment. Is the pct in that sticky really necessary for the ammount in taking?[/QUOTE]

No.... At 400mg/week you might be better off tapering off in the last few weeks, no PCT..!!
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I agree with Daz. It's a gentle cycle. Taper down if you have enough test left - eg 50mg twice a week for 2 weeks at the end of your cycle should be adequate.
 
In your opinion this being my first cycle how soon can i jump on the next one? Also should be taking any arimidex during this cycle?
 
ackrug said:
In your opinion this being my first cycle how soon can i jump on the next one? Also should be taking any arimidex during this cycle?
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Anything over 3 months, the longer the better... At 400mg/week, if splitting the dose to 2 X/week, its unlikely you should require an AI...
 
Daz and CFC are correct - with such a low dose you're better off just tapering off the testosterone. Also, as Daz stated - minimum of 3 months inbetween cycles. Due to the supraphysiological dose of testosterone you were taking, your androgen receptors (AR) down-regulate over the course of your cycle (your body is always trying to maintain homeostasis). The longer you are off, the more time you are giving your body to return to normal and up-regulate your testosterone receptors. This way, when you decide to cycle on again your body will be able to actually utilize the anabolic hormones you're taking.

IF you start experiencing estrogen related side effects (gynocomastia, a large amount of bloat, decreased (drastically) libido etc.) THEN you can consider using an aromatase inhibitor (AI) such as arimidex. However, if you don't have these side effects then it's better that you reduce your potential level of polypharmacy. IF you decide to use an AI, do not use aromasin. This is a suicide inhibitor which means it binds irreversibly to aromatase (the enzyme that converts testosterone to estrogen). You DO NOT want this as you're tyring to restore your hormone levels (the ratio between estrogen and testosterone) to normal. You need some estrogen for this to be accomplished.
 
pharmbiak said:
Daz and CFC are correct - with such a low dose you're better off just tapering off the testosterone. Also, as Daz stated - minimum of 3 months inbetween cycles. Due to the supraphysiological dose of testosterone you were taking, your androgen receptors (AR) down-regulate over the course of your cycle (your body is always trying to maintain homeostasis). The longer you are off, the more time you are giving your body to return to normal and up-regulate your testosterone receptors. This way, when you decide to cycle on again your body will be able to actually utilize the anabolic hormones you're taking.
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That's interesting pharmbiak you mention AR down-regulation, I was of the opinion AR can upregulate to accommodate supraphysiological doses of hormones at least up to the 6 month mark...?

Your thoughts pls...
 
Sorry GF, I misspoke and oversimplified. Initially, yes, there is an up-regulation of the AR but after sustained elevated testosterone levels some desensitization occurs which leads to a decrease in mRNA levels acting as a negative feedback loop. In several cases it was found that the AR content increased but the binding affinity for androgens decreased resulting in a net loss of testosterone utiilization. Essentially, after sucha long period of exposure the extra testosterone (above a certain point) became useless, whereas initially when first starting a cycle the extra free testosterone resulted in an almost linear dose-dependent effect curve. So, there's still benefit to an extended cycle (longer than 12 weeks) but the growth experienced isn't near what one expects an the beginning of a cycle... almost a sort of plateau effect. Leaving a 3 month gap or so between cycles resulted in a stronger initial resopnse to the androgens. I can't find the citations at the moment and it's been awhile since I've read up on this but I'll try to go through my citation list when I get the chance and find some articles as this is still oversimplified and I'm sure that I'm missing some information somewhere; my apologies.

-Pharm
 
^^^ that's interesting. Any idea if there's ways to combat the desensitization other than increasing dose or cruising? Would explain why blasts seem to stall out after a while, not in my case as my blasts are usually 16 weeks or so.
 
i) There is an up-regulation of the AR but after sustained elevated testosterone levels some desensitization occurs which leads to a decrease in mRNA levels acting as a negative feedback loop..

ii) AR content increased but the binding affinity for androgens decreased resulting in a net loss of testosterone utilization...

iii) After sucha long period of exposure the extra testosterone (above a certain point) became useless...

iv) There's still benefit to an extended cycle (longer than 12 weeks) but the growth experienced isn't near what one expects an the beginning of a cycle... almost a sort of plateau effect...

v) Leaving a 3 month gap or so between cycles resulted in a stronger initial response to the androgens...

These are very interesting points you mention pharmbiak, over the years I have experienced similar effects, especially the plateau you speak of at about 12 weeks..

a) Increasing the dose after 12 weeks seems necessary to hold onto gains, but not increase them..

b) 5 years of cruise/blast inclusive of blast up to 26 weeks results in no greater gains over the long term..

c) The first 3-6 years accounted for the majority of gains, the last 2 decades has been a battle to retain results gained in the first 10 years..

I am interested in your thoughts:

Can a cruise/blast work effectively if the dose on cruise is low enough, and long enough to obtain the stronger initial response when returning to the blast..?
 
^^^also I wonder if binding affinity to AR affects this as well. Would something like tren, or even methyl tren which bind strongly and provide strong effects cause this desensitization at a faster pace compared to more mild compounds like primo and boldenone or even the low strength Masteron.
 
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