hcg help bros
- 03-01-2010, 04:41 PM
- 03-01-2010, 09:53 PM
week 1-6: tbol, 50mg/day
week 1-15: test e, 500mg/week
hCG: 1500iu e4d, 3 doses total, starting week 16
arimidex: .5mg mon/thurs, week 12-17
nolvadex: week 17-20 (40/20/20/10)
it looks kind of confusing, and might be just downright wrong, but from what i've gathered this should work. the hcg doses are taken from the power pct protocol, the only change i made is using adex instead of nolva/clomid with the hcg (i'm assuming the purpose of this is to prevent aromatization from such high doses of hcg?). what i'm thinking of doing is running adex for the last 4 weeks of my cycle + the 2 weeks the ester clears, and then doing the hcg the 2 weeks while the ester clears--which is right up until pct. i would just run nolva but i don't have enough and i have a lot of adex. i've heard adex takes 5 weeks to start working so thats why i'm starting it well before hcg. the purpose of this is to prevent gyno while using the larger doses of hcg. depending on how much i bloat, i may start adex earlier in the cycle. how stupid/good does the above look? is running the adex with hcg pointless?
03-01-2010, 10:07 PM
The HCG i highly suggest u get more, its probably the cheapest thing u have listed up there and is really not hard to get.
The adex is very low for a cycle like this most people run .5mg EOD depending on how much bloat/estro related sides. and most people run the adex from the point at which they need it cause of bloat till the ester clearing period or 3 days prior to PCT.
Im assuming u have read nolva vs clomid. I personally prefer clomid on such long cycles but to each his own.
Adex is generally used to prevent the armoatization of the test while on cycle. It has very little/nothing to do with the HCG. The bloat and estro related sides are from the aromitization of testosterone not HCG.
You need to do a bit more research ur on the right path though.
03-01-2010, 10:46 PM
as for the hcg, i'm taking this dosing directly from the poWer pct protocol, which requires 4500ius. i might run it throughout the cycle instead but its rather expensive for me to get that much for some reason. the poWer pct protocol seems to be a highly-regarded means of using hcg so i figure why spend the extra cash?
03-01-2010, 10:51 PM
You are injecting 500mg of testosterone a week. The aromatase activity from injecting such a higher amount than the body can will result in more aromatase activity. HCG will help you stay somewhat less suppressed however it will never produce more testosterone than testoterone injections.
What i am saying is that an AI will help with excess aromatase activity, however the cause is not going to be from the HCG.
If thats what u read about adex and u believe it go ahead and run it, it may be enough for you it may not be.
03-01-2010, 11:21 PM
what do you think of the poWer pct protocol vs running low doses of hcg throughout the cycle? i figure the latter would work better but probably not leaps and bounds... and might even be a greater risk for desensitizing the leydig cells-- 2 250iu shots a week, 32 shots total sounds like a bad idea to me (then again what do i know).
03-01-2010, 11:48 PM
I honestly have only run a low dose of HCG throughout my test cycles. I have run from week 3 to week 14 on a test e cycle at 500IU''s per injection twice a week (totally 1000IU''s a week). I can tell you my natty test is actually higher after i got my blood work done than when i started (retested blood work 1 month after pct was finished). I like running hcg throughout my cycle and feel it helped a lot. To fully answer your question i would have to run both ways and let you know how its goes and honestly i cannot tell you which way (for sure) is better.
What it basicly comes down to is would u rather run a low dose longer or run a very high dose for a short period of time? I perosnally think its better to run the low dose for the extended period of time.
And not knowing is what this forum is for. Go look around do ur research and figure out how you want to run it. The most important thing about ancillaries and PCT doseages are that once you make a plan stick to it, switching doseages and protocols mid cycle or mid pct will cause a lot of problems.
Honestly it really is up to you to do the appropriate research get a good understanding of what is going on and to make the decision based on what you think.
03-02-2010, 12:03 AM
03-02-2010, 03:47 PM
03-02-2010, 04:09 PM
Swale's HCG Advice
by Swale (MD / HRT Specailist). originally posted at steroidology
I advise my AAS patients to use small amounts of HCG (250IU to 500IU) two days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.
Any more than 500IU of HCG per day causes too much aromatase activity. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).
If 250IU or 500IU on two days each week isn?t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn?t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.
The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERM?s at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of AAS (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.
I want my patients to stop taking HCG within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a ?bridge?. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can?t ?fool? the body?it is smarter than you are.
I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground?and we don?t want that, do we?).
All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other
JC: Dr. John has updated the original paper you published. Here it is:
My New HCG Protocol Paper
This paper is about to be published in The American Academy of Anti-Aging Medicine 2004 Clinical Updates:
AN UPDATE TO THE CRISLER HCG PROTOCOL
By John Crisler, DO
In my paper “My Current Best Thoughts on How to Administer TRT for Men”, published in A4M’s 2004/5 Anti-Aging Clinical Protocols, I introduced a new protocol where small doses of Human Chorionic Gonadotrophin (HCG) are regularly added to traditional TRT (either weekly IM testosterone cypionate or daily cream/gel). The reasons and benefits of this protocol are as follows, along with a new improvement I wish to share:
Any physician who administers TRT will, within the first few months of doing so, field complaints from their patients because they are now experiencing troubling testicular atrophy. Irrespective of the numerous and abundant benefits of TRT, men never enjoy seeing their genitals shrinking! Testicular atrophy occurs because the depressed LH level, secondary to the HPTA suppression TRT induces, no longer supports them. It is well known that HCG—a Luteinizing Hormone (LH) analog—will effectively, and dramatically, restore the testicles to previous form and function. It accomplishes this due to shared moiety between the alpha subunits of both hormones.
So, that satisfies an aesthetic consideration which should not be ignored. Now let’s delve into the pharmacodynamics of the TRT medications. For those employing injectable
testosterone cypionate, the cypionate ester provides a 5-8 day half-life, depending upon the specific metabolism, activity level, and overall health of the patient. It is now well-established that appropriate TRT using IM injections must be dosed at weekly intervals, in order to avoid seating the patient on a hormonal, and emotional, roller coaster. Adding in some HCG toward the end of the weekly “cycle” compensates for the drop in serum androgen levels by the half-life of the cypionate ester. Certainly the body thrives on regularity, and supplementing the TRT with endogenous testosterone production at just the right time—without inappropriately raising androgen OR estrogen (more on that later)—approximates the excellent performance stability of transdermal testosterone delivery systems for those who, for whatever reason or reasons, prefer test cyp.
But there’s another metabolic reason to employ this protocol. The P450 Side Chain Cleavage enzyme, which converts CHOL into pregnenolone at the initiation of all three metabolic pathways CHOL serves as precursor (the sex hormones, glucocorticoids and mineralcorticoids), is actively stimulated, or depressed, by LH concentrations. It is intuitively consistent that during conditions of lowered testosterone levels, commensurate increases in LH production would serve to stimulate this conversion from CHOL into these pathways, thereby feeding more raw material for increased hormone production. And vice versa. Thus the addition of HCG (which also stimulates the P450scc enzyme) helps restore a more natural balance of the hormones within this pathway in patients who are entirely, or even partially, HPTA-suppressed.
It is important that no more than 500IU of HCG be administered on any given day. There is only just so much stimulation possible, and exceeding that not only is wasteful, doing so has important negative consequences. Higher doses overly stimulate testicular aromatase, which inappropriately raises estrogen levels, and brings on the detrimental effects of same. It also causes Leydig cell desentization to LH, and we are therefore inducing primary hypogonadism while perhaps treating secondary hypogonadism. 250IU QD is an effective, and safe, dose. After all, we are merely replacing that which is lost to inhibition.
In my previous report I recommended 250IU of HCG twice per week for all TRT patients, taken the day of, along with the day before, the weekly test cyp injection. After looking at countless lab printouts, listening to subjective reports from patients, and learning more about HCG, I am now shifting that regimen forward one day. In other words, my test cyp TRT patients now take their HCG at 250IU two days before, as well as the day immediately previous to, their IM shot. All administer their HCG subcutaneously, and dosage may be adjusted as necessary (I have yet to see more than 350IU per dose required).
I made this change after realizing that the previous HCG protocol was boosting serum testosterone levels too much, as the test cyp serum concentrations rise, approaching its peak at roughly the 72 hour mark. The original goal of supporting serum androgen levels with HCG had overshot its mark.
Those TRT patients who prefer a transdermal testosterone, or even testosterone pellets (although I am not in favor of same), take their HCG every third day. They needn’t concern themselves with diminishing serum androgen levels from their testosterone delivery system. These patients will, of course, notice an increase in serum androgen levels above baseline.
While HCG, as sole TRT, is still considered treatment of choice for hypogonadotrophic hypogonadism by many , my experience is that it just does not bring the same subjective benefits as pure testosterone delivery systems do—even when similar serum androgen levels are produced from comparable baseline values. However, supplementing the more “traditional” TRT of transdermal, or injected, testosterone with HCG stabilizes serum levels, prevents testicular atrophy, helps rebalance expression of other hormones, and brings reports of greatly increased sense of well-being and libido. My patients absolutely love it. As time goes on, we are coming to appreciate HCG as a much more powerful--and wonderful--hormone than previously given credit.
Copyright John Crisler, DO 2004. This article may, in its entirety or in part, be reprinted and republished without permission, provided that credit is given to its author, with copyright notice and 2. All Things Male - Center for Men's Health clearly displayed as source. Written permission from Dr. Crisler is required for all other uses.
03-02-2010, 04:19 PM
I do a full metabolic panel All testosterone tests, estradiol, LH FSH t3 and t4. nothing has come back worry some.
Did a quick search of Power PCT protocol cant find any medical journals supporting this do u have a link? cause maybe im just missing something.
03-02-2010, 04:25 PM
03-02-2010, 04:28 PM
here is a study as to why HCG is better on cycle than in PCT
By Eric M. Potratz (Email)
Eric M. Potratz has developed his education in the field of endocrinology and performance enhancement through years of research, counseling, and real world experience. Over the past five years he has been a private consultant for hundreds of athletes and bodybuilders alike, and is the founder & president of Primordial Performance.
Post-Cycle-Therapy is a must upon cessation of steroid use. Many great Post Cycle Therapy protocols have been outlined over the years, and many individuals have had success with following such protocols. Nevertheless, what works can always work better, and I intend to show you the most effective way to recover from AAS. This is especially the case for those that have had a lack of success following popular advice. In this article I will address the misunderstanding and misuse of Human Chorionic Gonadotropin (hCG) and show you the most efficient way to use hCG for the fastest and most complete recovery.
HCG unraveled –
Human Chorionic Gonadotropin (hCG) is a peptide hormone that mimics the action of luteinizing hormone (LH). LH is the hormone that stimulates the testes to increase testosterone levels. (1) More specifically LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone.
When steroids are administered, LH levels rapidly decline. The absence of an LH signal from the pituitary causes the testes to stop producing testosterone, which causes rapid onset of testicular degeneration. The testicular degeneration begins with a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin-like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production. (2-6,19) However, this degeneration can be prevented by a small maintenance dose of hCG ran throughout the cycle. Unfortunately, most steroid users have been engrained to believe that hCG should be used after a cycle, during Post-Cycle-Therapy. Upon reviewing the science and basic endocrinology you will see that a faster and more complete recovery is possible if hCG is ran during a cycle.
Firstly, we must understand the clinical history of hCG to understand its purpose and its most efficient application. Many popular “steroid profiles” advocate using hCG at a dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical (1960’s) hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency. (21,22) A prolonged LH deficiency causes the testes to desensitize, requiring a higher hCG dose for ample stimulation. In men with normal LH levels and normal testicular sensitivity, the maximum increase of testosterone is seen from a dose of only 250iu, with minimal increases obtained from 500iu or even 5000iu. (2,11) (It appears the testes maximum secretion of testosterone is about 140% above their normal capacity.) (12-18) If you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.
One term that is critical to understand is testosterone secretion capacity which is synonymous to testicular sensitivity. This is the amount of testosterone your testes can produce from any given level of LH or hCG stimulation. Therefore, if you have reduced testosterone secretion capacity (reduced testicular sensitivity), it will take more LH or hCG stimulation to produce the same result as if you had normal testosterone secretion capacity. If you reduce your testosterone secretion capacity too much, then no amount of LH or hCG stimulation will trigger natural testosterone production – and this leads to permanently reduced testosterone production. (recovering full testosterone production is a topic for another article)
To get an idea of how quickly you can reduce your testosterone secretion capacity from your average steroid cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration. (2,9,10) By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%. (2-6)
Note: visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone. (4) This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, when the testes may only appear 5-10% smaller, the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly reduced to 98% of their normal production. (3-5) So do not judge how "shutdown" you are by testicular size!
The decreased testosterone secretion capacity caused by steroid use was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu hCG post cycle. It was found that the steroid users were about 20 times less responsive to hCG, when compared to normal men who did not use steroids. (8) In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with hCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size. (7) Another study with men using low dose steroids for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks (6) (INSL3 is an important biomarker for testosterone production potential and sperm production) 20
In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. We must protect our testicular sensitivity. Besides, with hCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle.
Based on studies with normal men using steroids, 100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of hCG. (2) It is important that low-dose hCG is started before testicular sensitivity is reduced, which appears to rapidly manifest within the first 2-3 weeks of steroid use. Also, it’s important to discontinue the hCG before you start Post-Cycle-Therapy so your leydig cells are given a chance to re-sensitize to your body’s own LH production. (To help further enhance testicular sensitivity, the dietary supplement Toco-8 may be used)
Based off the above information, an optimal dose of hCG during the cycle would be 250iu every 4 days, or as a less desirable alternative, once a week shot of 500iu. Keep in mind, that the half-life of hCG is 3-4 days, while the half-life of LH is only 1-2 hours. Considering this difference in excretion time, it is best to space each dose of hCG at least 4 days apart for the optimal "peak and valley" replication. However, going more than 7 days between each hCG shot may promote increase the rate of desensitization from lack of LH or hCG stimulation.
If you are starting hCG late in the cycle, one could calculate a rough estimate for their required hCG "kick starting" dosage by multiplying 40iu x days of LH absence. (ie. 40iu x 60 days = 2400iu HCG dose) Remember, since the testes will be desensitized later in a cycle, you will require a higher dose. Also, the maximum daily dose of hCG should not exceed 5000iu, and 4-7 days must be taken off between each shot. Generally, a higher dose will require a longer off period between each shot. (eg., 2500iu = 7 days between each shot)
Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.
For preservation of testicular sensitivity, use 250iu every 4 day starting 14 days after your first AAS dose. At the end of the cycle, drop the hCG two weeks before the AAS clear the system. For example, you would drop hCG about the same time as your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG about 10 days before your last oral dose. This will allow for a sudden and even clearance in hormone levels. This will initiate a strong LH and FSH surge from the pituitary, to begin stimulating your testes to produce testosterone. Remember, recovery doesn’t begin until you are off hCG since your body will not release its own LH until the hCG has cleared the system.
In conclusion, we have learned that utilizing hCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from “on cycle” to “off cycle” thus avoiding the post cycle crash.
1. Glycoprotein hormones: structure and function.
Pierce JG, Parsons TF 1981
Annu Rev Biochem 50:466–495
2. Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression
Andrea D. Coviello, et al
J. Clin. Endocrinol. Metab., May 2005; 90: 2595 - 2602.
3. Luteinizing hormone on Leydig cell structure and function.
Histol Histopathol 12:869–882 (1997)
4. Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing hormone-deprived rats
SM Mendis-Handagama, et al.
Endocrinology, Dec 1992; 131: 2839.
5. Effect of long term deprivation of luteinizing hormone on Leydig cell volume, Leydig cell number, and steroidogenic capacity of the rat testis.
Keeney DS, et al.
Endocrinology 1988; 123:2906–2915.
6.The Effects of Gonadotropin Suppression and Selective Replacement on Insulin-Like Factor 3 Secretion in Normal Adult Men
Katrine Bay, et al
J. Clin. Endocrinol. Metab., Mar 2006; 91: 1108 - 1111.
7. Successful treatment of anabolic steroid–induced azoospermia with human
chorionic gonadotropin and human menopausal gonadotropin
Dev Kumar Menon, et al.
FERTILITY AND STERILITY VOL. 79, SUPPL. 3, JUNE 2003
8. Testicular responsiveness to human chorionic godadotrophin during transient hypogonadotrophic hypogonadism induced by androgenic/anabolic steroids in power athletes
Hannu et al.
J. Steroid Biochem. Vol. 25, No. 1 pp. 109-112 (1986)
9. Comparison of testosterone, dihydrotestosterone, luteinizing hormone, and follicle-stimulating hormone in serum after injection of testosterone enanthate of testosterone cypionate.
Schulte-Beerbuhl M, et al 1980
Fertil Steril 33:201–203
10. Effects of chronic testosterone administration in normal men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production.
Matsumoto AM, et al 1990
J Clin Endocrinol Metab 70:282–287
11. Effect of human chorionic gonadotropin on plasma steroid levels in young and old men.
Longcope C et al
Steroids 21:583–590 (1973)
12. Regulation of peptide hormone receptors and gonadal steroidogenesis.
Catt KJ, et al
Rec Prog Horm Res 1980; 36:557–622
13. Effect of human chorionic gonadotropin on the endocrine function of Papio testes
GV Katsiia, et al
Probl Endokrinol (Mosk), Sep 1984; 30(5): 68-71.
14. Reproductive function in young fathers and grandfathers.
Nieschlag E, et al.
J Clin Endocrinol Metab 55:676–681 (1982)
15. The aging Leydig cell III Gonadotropin stimulation in men.
Nankin HR, et al. 1981
J Androl 2:181–189
16. Reproductive hormones in aging men. I. Measurement of sex steroids, basal luteinizing hormone, and Leydig cell response to human chorionic gonadotropin.
Harman SM, et al. 1980
J Clin Endocrinol Metab 51:35–40
17. Prolonged biphasic response of plasma testosterone to single intramuscular injections of human chorionic gonadotropin.
Padron RS, et al. 1980
J Clin Endocrinol Metab 50:1100–1104
18. Gonadotrophins and plasma testosterone in senescence. In: James VHT, Serio M, Martini L, eds. The endocrine function of the human testis.
Mazzi C, et al. 1974
New York: Academic Press, Inc.; 51–66
19. Androgen biosynthesis in Leydig cells after testicular desensitization by luteinizing hormone-releasing hormone and human chorionic gonadotropin.
Dufau ML, et al.
Endocrinology 105 1314–1321 (1979)
20. Insulin-Like Factor 3 Serum Levels in 135 Normal Men and 85 Men with Testicular Disorders: Relationship to the Luteinizing Hormone-Testosterone Axis
K. Bay, S. et al
J. Clin. Endocrinol. Metab., Jun 2005; 90: 3410 - 3418.
21. Stimulation of sperm production by human chorionic gonadotropin after prolonged gonadotropin suppression in normal men.
Matsumoto AM, et al 1985
J Androl 6:137–143
22. Human chorionic gonadotropin and testicular function: stimulation of testosterone, testosterone precursors, and sperm production despite high estradiol levels.
Matsumoto AM, et al. 1983
J Clin Endocrinol Metab 56:720–728
03-02-2010, 04:29 PM
03-03-2010, 11:20 AM
The only link I have on my new computer is the abstract from the power PCT study, I'll try to find the full write up after work.
03-09-2010, 05:02 AM
I kno about the whole "You know your body more than anyone" bit, but I was wondering if hCG would be needed for, say a 8-10 wk cycle of test-e?
I could definitely do w/o hCG, so if 8 or 10 wks is good w/o it, I'll be a happy camper =]
03-09-2010, 12:23 PM
03-09-2010, 01:21 PM
Dosage is 500mg a wk, 250 Mon and Thurs. I'll kickstart w/ some Mdrol or run Epi for the first 3-4 wks depending on what I run. That's it
EDIT: First real juice cycle. Yea, first injection of test of my life! Kinda excited actually...
03-09-2010, 02:19 PM
I suggest u strt ur own thread about what ur running and ask for advice cause you will get lot more responses that way.
As far as teh HCG goes it probably isnt required for your cycle, your cycle is at a decent amount of test per week and isnt very long. The reason i asked amount is that i personally notice that when running 500-750mg/week my testes dont shrink terribly but once i get to over a gram a week they atrophe a lot. (maybe just my personal experience).
So could u use hcg? yes u could (if ur cycle is 10+ weeks) do u need to? no probably not. And i am defining need as in restoring natty test post cycle back to normal given a certain amount of time and PCT drugs, not as to how fast you will be recovered post cycle.
Just a quick suggestion if you are running test e/c/sustanon use it for at least 10 weeks to get the most out of the effects.
03-09-2010, 08:27 PM
Also, would I need something like adex or aromasin or any AI during cycle at my length?
I will make a thread later (probably start of my first log), but need advice on my questions before.
03-09-2010, 08:31 PM
03-10-2010, 02:40 PM
03-10-2010, 06:21 PM
ur going to be pretty surpressed from a long cycle like that. If i where running that i would dose
03-15-2010, 03:01 AM
03-22-2010, 07:00 PM
Similar Forum Threads
- By BigDro in forum General ChatReplies: 8Last Post: 09-21-2010, 10:57 PM
- By BigDro in forum Cycle InfoReplies: 2Last Post: 09-17-2010, 11:02 PM
- By WATERLOGGED in forum 35 and OlderReplies: 16Last Post: 12-18-2006, 11:27 PM
- By Blatalian in forum AnabolicsReplies: 10Last Post: 12-14-2004, 04:46 PM
- By RippedUp in forum General ChatReplies: 1Last Post: 03-27-2003, 04:46 PM