Thread: Looking for cycle advice.

Gonna bump this, am I missing any info that you need for some advice? I also wanted to ask if there is any problems taking ephedra while on a cycle. really interested in knowing if I should start off heavy: 2 vials a week...or slow 1 vial a week....should I stagger the deca in the middle or take it continuously....any help would be appreciated.

I am ofcoarse surfing for answers, but I have read enough posts on this board to see many of you are knowledgeable. Nowhere I look though does it ever address my age or weight and height, it's always smaller dudes.

no ephedra wont do any harm , how much r u taking ,r u taking it for joint and bone pains??

ur cycle is explosive , like an anti tank MISSILE

IT WILL ROCK U

UR CYCLE IS PERFECT , JUST INCREASE DECA TO 200MG / WEEK FOR WHOLE CYLE , THEN UR GOOD TO GO

+ 200MG OF DECA WILL LUBRICATE UR JOINT AND GIVE U LES PAINFULL WORKOUTS

WHAT ABOUT UR PCT , DID U PLANNED IT ??

I have not....whatwould you reccommend? Should I being doing that during my cycle? I thought that I would just do that post cycle...not sure how much to get though.

You said the cycle was explosive..but I was actually asking in what order I should take it...I was thinking of a 13 week cycle:
week 1: 250 sust
week 2: 250 sust
week 3: 500 sust 100 deca
week 4: 500 sust 100 deca
week 5: 500 sust 250 test 100 deca
week 6: 500 sust 250 test 200 deca
week 7: 500 sust 250 test 200 deca
week 8: 250 sust 500 test 100 deca
week 9: 250 sust 500 test 200 deca
week 10: 500 sust 250 test
week 11: 500 sust 250 test
week 12: 250 sust
week 13: 250 sust

Like I said before, this is my first cycle and just wanted to check it out.....I was asking how you guys might structure it...I was thinking of something like above.

Any advice be great!!!

SIMPLE CYCLE FOR U MY MAN

WEEK 1-10 DECA 200/200/200/200/400/400/400/200/200/200

WEEK 1-12 SUS 250/250/250/500/500/500/250/250/250/250/250/250

WEEK 8-12 TEST 200/200/200/200

I WONT RECOMND THE 3rd ONE TEST , sustanon is already 4 test blend

any additional test wont do no good , it would be better IF YOU to stick with DECA AND SUS ONLY .

NOW PCT is POST CYCLE THERAPY is done aftr the cycle .

during aas cycle ur natural test production shuts down and body stops producing test.

so when ur off the steroids , ur HPTA , or hypothalamus function shuts down .

DURING THIS TIME , THE CORTISOL WHICH WAS BLOCKED DURING UR CYCLE COMES TO PLAY

and starts eating up ur muscles , so to avoid catabolic state and revive natural test production we

do a pct and protect ur muscles from being lost .

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At the age of puberty, Gonadatropin Releasing Hormone (GnRH) is increasingly released from the Hypothalamus, in turn causing the secretion of Follicle Stimulating Hormone (FSH) and Luetenizing Hormone (LH) from the pituitary, and finally the male gonads (testes) are then stimulated by those pituitary hormones (LH and FSH). (1). FSH, although generally thought to only have a role in production of sperm, actually aids the in regulation of Leydig Cell function (2), while LH directly causes the Leydig Cells in the testes to secrete androgenic hormones such as testosterone (which is causes a surge in other anabolic hormones: Insulin Like Growth Factor, Growth Hormone, etc…). Androgens do this by then targeting other tissues inside the body, either by attaching to the Androgen Receptors (AR), which are found primarily in the cytoplasm of specific cells, or by what’s known as non-receptor mediated effects. When an androgen (your own natural testosterone or an anabolic steroid you’ve injected or ingested) binds to a receptor inside the cell, it activates the transcription of specific genes. What does this mean? Don’t worry, it just means that the steroid molecule gives the cell a message to do something. In the case of testosterone, for example, one of the messages it sends to the cell is to increase nitrogen retention in your body, thus allowing you to use more of the protein you take in, and build more muscle. In the case of testosterone (or anabolic steroids in general), this transcription causes a lot of different anabolic effects to take place: an increase in IGF, a decrease in cortisol, an increase in Red Blood Cell count, and the increased protein synthesis I already told you about. This is not to say that AR binding is the only thing that causes anabolic or androgenic effects, however. Oxymetholone and Methandrostenolone (Anadrol and Dianabol) both bind very weakly to the AR yet are both highly anabolic and androgenic. The diagram below is an example of an androgen’s entry into a target cell, where it (in this case) stimulates protein synthesis, which is a major anabolic effect:

Under the control of this heightened state of androgens, you also go through androgenic development as well as anabolic development. This can be seen in puberty when males grow body hair experience voice changes, as experience genital development and growth.
Another characteristic of androgens in the body is that they are subject to what’s known as a “negative feedback loop”. Lets review one of the first things I mentioned, ok? Your Hypothalamus secretes GnRH, thus making the pituitary secrete LH & FSH, finally in turn causing the testes to stimulate the Leydig cells to produce testosterone (by conversion of cholesterol), remember? Ok, now, once testosterone is created however, it has the ability to in turn to undergo various metabolic processes that will inhibit GnRH, which in turn inhibits the secretion of LH and FSH, and that brings a halt to natural testosterone production. Once testosterone has stopped being produced, it no longer sends this negative signal, and GnRH eventually begins to do its job again. In this way, your body prevents excess hormones from being secreted and thus maintaining homeostasis (the status quo… in this case a state where you are neither gaining nor losing muscle) (1). This negative feedback loop is partially why we use anabolic steroids…we want more testosterone for anabolic purposes (or more Anavar or whatever) than our body will let us produce (not that our bodies produce Anavar, but you get the idea). When we use that injectable testosterone, it sends the message to our body to begin the negative feedback loop and discontinue producing/secreting the hormones that cause our natural testosterone production. The chart below clearly shows this process, displaying both the negative and positive feedback system(s):

So what I’m saying is that anabolic steroids increase androgen levels in the blood, bringing a halt to GnRH, making the pituitary gland (eventually) responds by reducing the release of LH; this loss of LH has the effect of shutting down testosterone, of course, which you know is produced by the Leydig cells in the testes after they are stimulated by LH. Am I being repetitive? Yes. Do you need to understand all of this in order to understand the PCT protocol I’m about to outline? Yes. Remember, the negative feedback loop is, of course, no problem while we are on a cycle. Want more testosterone (or androgens) in your body? Fill up a few more syringes!
But all good things come to an end, and most of us choose to end our cycles at some point. At this point, while there is still some androgens floating around in us, our natural production won’t begin, and even once they are out, there may be some lag time before your body figures out that it needs to start producing its own androgens again. As I said before, this lag time is severely catabolic and it’s where you lose a lot of your gains. SO what we need to do is coax the body into quickly producing its own androgens.
One of the first drugs we’ll consider for this purpose is what is typically called a SERM. Nolvadex
Estrogen is also important for a properly functioning immune system, and not only that, but your lipid profile (both HDL and LDL) should also show marked improvement with administration of tamoxifen (34). (Tamoxifen) is a SERM (Selective Estrogen Receptor Modulator, which means that it has the ability to act as an anti-estrogen with regard to certain genes, yet also acting as an estrogen with respect to others. That’s the “selective” part I guess. It does this by blocking gene transcription in some cases, and initiating gene transcription in others (3). Luckily for us, it has estrogenic effects on bones (meaning it increases their density), and blood lipids -meaning it lowers cholesterol-, (4)(5)as well as preventing gynocomastia by preventing estrogen gene transcription in breast tissue. However, it acts as an anti-estrogen in the pituitary, thus increasing LH and FSH, which results in an increase in testosterone. 20mgs of Nolvadex will raise your testosterone levels about 150% (6)...Nolvadex actually has quite a few applications for the steroid using athlete. First and foremost, it’s most common use is for the prevention of gynocomastia. Nolvadex does this by actually competing for the receptor site in breast tissue, and binding to it. Thus, we can safely say that the effect of tamoxifen is through estrogen receptor blockade of breast tissue (7).
Nolvadex also has some important features for the steroid using athlete. In hypogonadic and infertile men given nolvadex, increases in the serum levels of LH, FSH, and most importantly, testosterone were all observed (35)It can also block a bit of estrogen in the pituitary, which is a great benefit when used with HCG (more on that later) (36)(37). The increase in testosterone Nolvadex can give someone with a dysfunctional is basically that 20mgs of Nolvadex will raise your testosterone levels about 150% (6)...Why don’t we use Clomid, another SERM? Well, basically because it takes much more to do the same thing. In comparison, it would require 150mgs of Clomid to accomplish that type of elevation in testosterone, but Nolvadex also has the added benefit of significantly increasing the LH (Leutenizing Hormone) response to LHRH (LH-releasing hormone) (6). This most likely indicates some kind of upregulation of the LH-receptors due to the anti-estrogenic effect Nolvadex has at the pituitary. Although both Nolvadex and Clomid are both SERMs, they are actually quite different. As you already know, Nolvadex is highly anti-estrogenic at the hypothalamus and pituitary, while Clomid exhibits weak estrogenic activity at the pituitary (7), which as you can guess, is less than ideal. It should be avoided for the PCT I’m suggesting…and in fact, avoided in general…it’s simply not as good as Nolvadex.
Need I even add that the 150mgs of Clomid you need to get the hormonal increase experienced with 20mgs of Nolvadex is much more expensive? So lets dump the Clomid…and no, using it along with Nolvadex will provide no “synergy” that I’ve ever seen in any relevant study.
SO how much Nolvadex should you use during PCT? I favor using 20mgs.day, although to be totally honest, you can probably even get away with far less than that. Doses as low as 5mgs/day have proven to be as effective as 20mgs/day for certain areas of gonadal stimulation. (8) 20mgs/day, however, is a dose that myself and others have used with great success, and the research I’ve done in this area typically uses this milligram amount. SO lets stick with 20mgs/day for now.
So that effectively suggests Nolvadex can not be used at Mega-doses to get a mega-increase in your natural hormones. We can’t use huge doses of any Anti-Estrogen, actually, and expect huge increases in our natural hormones, actually. Arimidex (an Aromatase Inhibitor –which means it stops the conversion of testosterone into estrogen-another drug used to fight breast cancer like Nolvadex) exhibits basically the same effects when .5mgs or a full 1mg is used (9) and I have even read studies where up to 10mgs/day of Arimidex is studied with no clear benefit over 1mg/day. Letrozole (another Aromatase Inhibitor) is capable of inhibiting Aromatase maximally at a mere 100mcg/day (10.). So clearly we need to add in other compounds to our PCT, because Mega-Doses of one compound will not I think it’s absurdly funny to see people recommending upwards 40-80mgs/day of Nolvadex, or a full milligram (or two!) of Arimidex, in their post-cycle or on-cycle suggestions. I’d steer very clear of listening to anyone who makes those types of recommendations…
All of this tells me that you can’t simply use mega-doses of Anti-Estrogens or SERMS to do anything more than reasonable doses. It must be, therefore, that your body can only respond with so much vigor to any one drug in those families. So lets add in another drug or two, ok? This way we can use reasonable doses of a few drugs and produce some synergy…hopefully decreasing our recovery time.
We’ll need something to go with Nolvadex, which acts in a different manner, and Human Chorionic Gonadatropin (HCG) is the clear choice here. Here’s where things get a bit controversial (no, really…I know you , because I’m pretty much the only person around (currently) who recommends HCG for Post-Cycle Therapy. Although I’m seen as Old School in this respect, really, this is a totally new paradigm for HCG use, made possible only by the inclusion of the other compounds I am introducing to you for PCT. HCG is the natural choice, as it has been used successfully to cure AAS induced (11), and this alone warrants its inclusion to our cycle.
HCG is a peptide hormone manufactured by the embryo in the early stages of pregnancy and later by the placenta to help control a pregnant woman’s hormones (can anything really be said to control a pregnant woman’s hormones except ice-cream and chocolate?). Obviously, as you can guess from the name, it is a substance that stimulates the gonads (hence: gonadotropin). It does this by initiating gene transcription that is identical to that of Luetenizing Hormone, thereby causing the Leydig Cells to produce testosterone. Sounds great right? We can stimulate LH and FSH production with our Nolvadex, and then directly stimulate the Leydig Cells as well, to produce tons of testosterone by different routes! Well...it’s not all that simple.
Unfortunately, while HCG increases Testosterone, it increases estrogen as well(12). As you probably know, estrogen acts directly on the Leydig cells to effect changes in the activities of enzymes important for testosterone synthesis (13) and may actually be considered an important part of that negative feedback loop I mentioned earlier. In addition, an increase in circulating levels of LH have been shown to induce down-regulation of LH-receptors in both rodent studies (14), as well as in human studies (15); since HCG mimics LH, you can expect it to do the same. This LH downregulation can cause an increase in steroidogenic cholesterol (the cholesterol earmarked by your body for conversion into testosterone). (16). Thus, after the initial HCG induced surge in testosterone is over, if you have used enough to downregulate your LH-receptors and increase estrogen too much, then more steroidogenic cholesterol is available. This is telling me that less is being converted to testosterone. In fact, rodent models suggest that if you take a dose large enough to cause a sharp increase of plasma testosterone, you will actually desensitize your Leydig cells to your next shot, and will possibly not experience any rise in testosterone from the second dose at all, or may only experience a very slight one at best (17.). Since this is due to LH-Receptor downregulation, and that occurs in human models too, it is pretty fair to assume that if your first dose of HCG is too large, your second won’t be very effective. Unfortunately, this lack of an increase in testosterone doesn’t necessarily mean that the HCG may be unable to increase circulating levels of Estrogen (18) And remember that increase in Estrogen will (most likely) cause your body ultimately to produce less testosterone. Low LH post-cycle is not the primary cause of slow recovery, because LH generally rises to levels above baseline after a cycle much sooner than testosterone production does. This is probably because the pituitary is working very hard to get your atrophied Leydig cells to start producing testosterone again. HCG should also bring back testicular volume; I feel the need to mention this because it’s important to me and I suspect most men as well. It would also appear that HCG works very well when it’s used on men who have low levels of LH to begin with (as you would be after a cycle), as many studies on pre-pubertal boys and Hypogonadotropic Hypogonadal men would suggest (19)
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for u PCT

START 18 DAYS AFTR UR LAST SUSTANON SHOT

WEEK 1-4 CLOMID 100/100/50/50

WEEK 1-4 AROMASIN .25 ( TAKE AROMASIN .25 MG EVERYOTHER DAY DURING THE CYCLE FROM WEEK 6 ONWARDS ) .

WEEK 1-2 HCG 500 IU ONCE A WEEK ( OPTIONAL )

dont ever use NOLVA WITH DECA .

THIS WOULD BRING UR "" HAMMER AND BALLZ TO WORK AGAIN ""

HOPW THIS HELPS .

Thank you for the advice. I will put the deca on the front of the cycle starting at 200.

Yeah I know what PCT is...was just wondering if you take clomid during a cycle at all or just stick to the clomid and tamoxifen post (for the cycle above).

NO NLOVA DURING OR AFTR A DECA CYCLE

DECA + NOLVA = RECIPE FOR GYNO

ACTALLY MANY PPL TOOK CLOMID DURING CYCLE , BUT IT WLD FUCK UP

THE SYSTEM because during cycle androgen levels r still pretty high so

clomid is recomnded when androgen levels drop down to low

DURING THE CYCLE USE , AROMASIN OR FEMARA , THESE R AIs , they will

block the ar5 and wont allow the aromatization , u will hv good lean gains.

take aromasin like this .25 mg every other day during cycle from week 6

dont use nolva during or even aftr cycle .

do this for pct

clomid 100/100/50/50

aromasin .25/.25/.25/.25

this is enough .

the truth is that it will only kick start ur HPTA to work .

the complete HPTA recovery takes months to cover up fully.

stay away from nolva , if ur CYCLE has deca in it .

do this for pct

clomid 100/100/50/50

aromasin .25/.25/.25/.25

this is enough .

This a daily, bi daily. or just weekly intake?

THIS I DAILY INTAKE FOR BOTH THE products

i will start the same pct in a few days .

i would recommend that you dont oversaturate your fresh receptors and do this as a first time cycle i know i have used gear for 20yrs and training for 32 yrs. now.
1) test cyp or test E 500mg a wk for testE or 400mg a wk test cyp.
2)oral steroid---20mg d-bol to kick start the cycle do it first 4 weeks of cycle, so take the 20mg d-bol in the 1st 4 wks of cycle then drop the d-bol
3)keep nolva on hand for gyno or estrogen sides, dont use unless absolutely necesarry.
4) 12wk cycle of 400mg cyp or 500mg testE after last shot, start your pct with clomid 100mg first 3-5 days then for next 9 days clomid, at 50mg ed. use hcg throughout your cycle, 12 wks then after last shot and wait 5 days give yourself a subq shot in the lower belly a 1,500ius of hcg and wait again another 7 days and give your last subq shot of hcg 1,500ius, nolva only if needed. thats your smart pct then get your blood work done from your dr. more is not better when your first cycle and older at that. imho

Originally Posted by unclem

i would recommend that you dont oversaturate your fresh receptors and do this as a first time cycle i know i have used gear for 20yrs and training for 32 yrs. now.
1) test cyp or test E 500mg a wk for testE or 400mg a wk test cyp.
2)oral steroid---20mg d-bol to kick start the cycle do it first 4 weeks of cycle, so take the 20mg d-bol in the 1st 4 wks of cycle then drop the d-bol
3)keep nolva on hand for gyno or estrogen sides, dont use unless absolutely necesarry.
4) 12wk cycle of 400mg cyp or 500mg testE after last shot, start your pct with clomid 100mg first 3-5 days then for next 9 days clomid, at 50mg ed. use hcg throughout your cycle, 12 wks then after last shot and wait 5 days give yourself a subq shot in the lower belly a 1,500ius of hcg and wait again another 7 days and give your last subq shot of hcg 1,500ius, nolva only if needed. thats your smart pct then get your blood work done from your dr. more is not better when your first cycle and older at that. imho

yes very true , i told u tht cycle on basis of what u wanted to USE FOR UR CYCLE

THE ABOVE WRITTEN INFO IS VERY TRUE , RECEPTOR SITES ARE FRESH

DONT LOAD THM FROM EVERY DIRECTION.

WLD X2222222 , THE ABOVE GIVEN ADVICE .