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Is it normal to loose strength on heavy lifts like the bench press during pct, im 4 weeks in just finished pct and my strength as went down somewhat from a couple of weeks ago .Will i experience some sort of "come back" or "rebound" in the next couple of weeks when test levels get back to normal?.. say 8 -10 weeks after cycle taking that pct is done correctly.
Some people experience PCT differently. Some dont lose any muscle gain, some continue to gain. Do a solid PCT, keep eating to feed the new muscles, and you will be as straight as mother nature will allow.
Post cycle you will probably lose some of the aggression from the higher test levels during the cycle. This can also contribute to a loss of strength mainly from less aggressive training and less confidence. As Capebuffalo said complete your PCT, eat and rest and you'll lose less gains.
It happens. As mentioned, you need to keep those calories high and continue to train as hard as you can.
If that's the case, then why cycle in the first place? Some people on the fence might be encouraged to cycle based on your comment, which is dead wrong. You loose size and strength after cycling. The goal is keep what you can but you will inevitably loose both size AND strength when you stop. Anyone claiming different is a liar. The truth of the matter is some people lose ALL their gains and then some when they stop depending on how long they're shutdown. A prime example is Kevin Levrone. That guy has incredible genetics and he's half the man he used to be.Quote:
Originally Posted by Capebuffalo
That's awful tough talk for a one eyed fat man. After a cycle, the muscles are in need of a stimulation that is at a level close to what they had been given while “on.” Unfortunately many times trainees become paranoid afterwards and continue to keep the level of intensity high. Big mistake! This causes a couple of things. For starters, it opens up the body to burn out in the form of neural fatigue. This in part, is primarily because the body can no longer cope with the demands that are being placed upon it. The hormonal system is in a state of recovery and the body cannot withstand the same amount of stress anymore. Two, injury can and often does occur as the loads used can no longer be supported by the body due to the rapid increase of muscle tissue and the lag in development of the supporting soft tissues. As a result you have a strong muscle but your tendons and ligaments cannot support the muscles that are being used to lift the loads.
Instead of sucking it up and kissing 40% or more of that hard earned muscle away post cycle, a training program needs to be structured in such a way that it allows for the body to adapt back to it’s regular state and still allows for a stimulus to be received.
Look man, you're wrong. Suck it up and just admit it. I've been wrong many times over the past 12+ years on the boards. Stop pedaling nonsense too. Giving people the idea that they'll keep 100% of their gains AND "continue" gaining post-cycle is absolutely moronic and ludicrous.
Where in the hell do I say you will keep 100% of your gains. People are different. You will be as straight as mother nature will allow i.e your individual body and how you train afterward. But you can prove unequivocally no one in the history of steroids has gained on pct. I will bow to the knowledgable member.Quote:
Originally Posted by Capebuffalo
It's actually a real simple concept. I'll break it down for you. You cannot avoid supressing your HPTA when using exogenous test. Impossible. The only difference is how long it takes to recover, if you can recover 100% (not everyone does). During the recovery time, gains will be lost along with strength. In order words, you deflate and get weaker. This is an indisputable fact.Quote:
Originally Posted by Capebuffalo
Opioid Modulation for Preventing AAS Induced HPTA Suppression.
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.
Suppression of the HPTA (Hypothalamus, Pituitary, Testicular Axis) is seemingly unavoidable during a steroid cycle. What I will be presenting in this article is a new idea to the world of AAS users. This exciting new concept addresses the possibility of limiting and possibly preventing suppression of the (HPTA) during cycle. More specifically, I will show you how to actively modulate the hypothalamus & pituitary pulse generator during cycle and how this can prime our endocrine system for a quicker, smarter, and healthier recovery from anabolic androgenic steroids (AAS).
For a moment, let’s forget the concept of “post cycle therapy”, and embrace the idea of “on cycle therapy” – active therapy throughout a steroid cycle. The HPTA involves a constant biological interplay of responses and feedback loops that can ultimately become shutdown and degraded during AAS administration. However, research suggests suppression of the hypothalamus and pituitary may be preventable during steroid use. Before we delve into the details, lets first take a quick recap on the HTPA and how it responses to AAS.
HPTA – The basics
When the hypothalamus senses low hormone levels, it secretes gonandotropin releasing hormone (GnRH). This GnRH then travels a short distance to the nearby pituitary gland to stimulate the release of the gonadotrophins -- luteinizing hormone (LH) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testes, to activate their respective leydig and seritoli cells. LH initiates testosterone production by stimulating the leydig cell receptor (steroidogenesis), while FSH initiates sperm production by stimulating the sertoli cell receptor (spermatogenesis).
AAS’s inhibit hormone production just as your body’s own hormones do. Testosterone interacts with the androgen receptor (AR) and estrogen interacts with the estrogen receptor (ER). When these hormones are in high concentration, they cause the hypothalamus to decrease its release of GnRH, which decreases LH and FSH production from the pituitary. (1) This cuts off the signal to the testis and halts all hormone production. This process is a daily event for the rhythmic endocrine system. Spikes in LH & FSH are followed by spikes in testosterone, and spikes in testosterone result in a reduction of LH & FSH release until testosterone levels decline and LH & FSH is released again. The caveat with most steroids, is that hormone levels remain chronically high (24/7) and do not allow release of LH or FSH, thus leaving the pituitary and testis in a dormant state for as long as the steroids are administered.
While low-dose on-cycle hCG is a good protocol to mimic LH and keep the testes from atrophy, (discussed here) it won’t help prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testes. That is, when the GnRH secretion from the hypothalamus stops (during a steroid cycle), the pituitary reduces its number of GnRH receptors and becomes less and less responsive to GnRH stimulation as time goes on. (11) This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the other hand, both the pituitary and testis will decrease receptor concentration during over stimulation as well, as its been found from too much hCG use or too much GnRH stimulation.(12,13) The point here, is that only minor stimulus is required for the preservation of sensitivity in the endocrine organs. Perhaps a completely neglected and suppressed pituitary (or testes) may explain the lack of full and prompt recovery for many steroid users, despite adherence to a “tried and true” PCT regimen. So the question is – How can we prevent suppression of the testes, and better yet, how can we prevent suppression of the pituitary?
A closer look –
There are several ways that steroids can inhibit LH & FSH release from the pituitary based on the receptors they occupy, and this is important to understand if you plan on blocking AAS induced suppression. For instance, it appears that AAS which bind strictly to the AR only inhibit LH & FSH release by suppressing GnRH release from the hypothalamus (ie Primobolan, Proviron, Anavar or Masteron). (34,37,39) However, AAS which possess estrogenic (ER) or progestogenic (PR) activity inhibit LH & FSH by directly down-regulating the GnRH receptors on the pituitary, while also reducing GnRH release from the hypothalamus. (35,38) Therefore, progestin based AAS such as trenbolone and nandrolone are “double suppressive” because they are binding to the AR and PR and suppressing LH & FSH by two different mechanisms. (36) The same can be said for steroids that aromatize, such as testosterone or methandrostenolone since they can activate both AR and ER receptors.
Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis (37), and that administration of Arimidex can greatly reduce testosterone’s suppression of LH release. (42) However, since progesterone based AAS’s such as nandrolone and trenbolone are inherently progestogenic based on their hormone structure, there is no way to prevent them from activating the PR. Therefore, it’s virtually pointless to try to block the suppression from progestin based anabolics. However, we can block suppression from the ER by using either non-aromatizing AAS’s or aromatase inhibitors. So this now leaves us with suppression of LH & FSH via the AR, but this suppression can be blocked, and that’s exactly what I’m going to show you.
When it comes to suppression of the hypothalamus, there is more than a simple on/off switch for the hypothalamus control center. Evidence suggests that there isn’t even a direct AR or ER receptor on GnRH secreting neurons. (2-6) Meaning, steroid hormones do not directly influence GnRH release from the hypothalamus, but actually communicate through an intermediary. (7)
It was well summarized here by A. J Tilbrook et al,
“It follows, that the actions of testicular steroids on GnRH neurons must be mediated via neuronal systems that are responsive to steroids and influence the activity of GnRH neurons.”
And again here by FJ Hayes et al,
“It was thus postulated that estrogen-receptive neurons were acting as intermediaries in the non-genomic regulation of GnRH by estrogen”
There is a network of neurogenic intermediaries in the hypothalamus governing GnRH release from steroid hormone influence. More specifically, it is the combined efforts of neuro-active peptides and catecholamines which send the message of “suppression” to the GnRH neurons once activated by steroid hormones. (16) These primary messengers are known as a group of neuro-active peptides called endogenous opioid peptides (EOP’s). (7,16) The EOP’s consist of the three main peptides -- b-endorphin, dynorphin, and enkephalins, which act upon their respective u-opioid, k-opioid, and s-opioid receptors. It appears that the most influential EOP in GnRH modulation is b-endorphin, acting upon the u-opioid receptor. (8-10) For this reason, b-endorphin will be the main focus of the article (although there are other minor intermediates involved.)
When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH and consequently suppress LH & FSH. We know that steroid hormones must communicate with these opioid receptors in order for them to inhibit the release of GnRH from the GnRH neurons, since the GnRH neurons do not have their own AR or ER receptors. What’s most interesting here is that the suppression on GnRH neurons can actually be intercepted by a u-opioid receptor antagonist – such as naloxone, and the orally active congers naltrexone, and nalmefene.
This is accomplished by blocking the u-opioid receptor and preventing the inhibitory effects of b-endorphin upon the GnRH releasing neuron. It should be noted that this “antagonism” of suppression is not due to antagonism of the AR or ER itself, since u-opioid antagonists to not bind to hormone receptors. (15,32)
The effect of a u-opioid receptor antagonist on the HPTA is demonstrated here --
Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present. (17) Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone, DHT, and estrogen administration in both animals and humans. (18-25) It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH. (26,27)
U-opioid antagonists have long been used for treatment of opioid dependence; not only to control cravings of narcotics, but to restore a suppressed endocrine system. (28,29) It’s well known that strong opioid based drugs such as methadone, cocaine, heroin and alcohol can suppress GnRH and therefore suppress LH & FSH. It seems that this decease of GnRH, LH & FSH is due to the same EOP mechanisms seen with AAS induced suppression. (33) In alcoholics, cocaine and heroin users, naltrexone and naloxone have been used to restore LH and testosterone levels. (28,29) Naltrexone has even been proposed as a treatment for male impotence and erectile dysfunction. (30,31)
Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to block b-endorphin, respectively. (14,18) Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with BA water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male. (18) While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit. (20,24) Increasing the dose of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. A twice a week dosing protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shutdown – Just enough to keep them in the “ball game” so to speak. Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.
A word of caution: The opioid antagonists mentioned in this article are recognized as safe and non-toxic at the given dosages; however they can cause severe withdrawal symptoms in opiate users (methadone, morphine, cocaine, and heroin addicts.) Caution is also advised when using opioid antagonists prior to sedation or surgery as they can reduce effectiveness of anesthetics. Temporary nausea, headache or fatigue, are occasional side-effects associated with the use of these drugs. Naltrexone has been reported to heighten liver enzymes, while naloxone and nalmefene do not appear to have this issue. At any rate, a twice a week protocol for 4-16 weeks is unlikely to cause any liver issues that may be associated with naltrexone. Contrary to popular believe, opioid antagonists do NOT have any addictive properties.
A few point to consider -
For those who choose to embark on an opioid antagonist protocol several things should be considered.
Remember, progestin based anabolics such as trenbolone and nandrolone are “double suppressive” because they desensitize the pituitary directly by PR activation. It also appears that no opioid receptor antagonist or aromatase inhibitor can prevent suppression via the PR. Therefore, trenbolone or nandrolone are going to cause unavoidable inhibition of HTPA function by causing suppression via the ER, AR and PR. (40,41) If one hopes for a prompt and full recovery post cycle, perhaps progestin based anabolics are better avoided, or at least limited in duration of use.
As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogen suppresses the hypothalamus and pituitary. Usage of an AI such as anastrozole, letrozole, or exemestane (Aromasin) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary GnRH receptors. (35,37,38) Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these AI’s. (43-47)
References
1. Hypothalamic Gonadotropin-Releasing Hormone: Basic and Clinical Aspects.
Yen SSC
Raven Press, New York, pp 245–280 (1991)
2. Absence of androgen receptors in LHRH immunoreactive neurons.
Huang X, Harlan RE.
Brain Res 1993; 624:309–311
3. Augmented hypothalamic proopiomelanocortin gene expression with pubertal development in the male rat: evidence for an androgen receptor-independent action.
Kerrigan JR, et al.
Endocrinology.128:1029-1035. (1991)
4. Distribution of estrogen receptorimmunoreactive cells in the preoptic area of the ewe: co-localisation with glutamic acid decarboxylase but not luteinizing hormone-releasing hormone.
Herbison AE, et al.
Neuroendocrinology 1993; 57:751–759.
5. Unmasking the neural progesterone receptor in the preoptic area and hypothalamus of the ewe: no colocalization with gonadotropin-releasing neurons.
Skinner DC, at el.
Endocrinology 2001; 142:573–579.
6. Multimodal influences of estrogen upon gonadotropin releasing
hormone neurons.
Herbison AE.
Endocrine Reviews 1998; 19:302–330.
7. Negative Feedback Regulation of the Secretion and Actions of Gonadotropin-Releasing Hormone in Males
A.J. Tilbrook and I.J. Clarke
Biol Reprod, Mar 2001; 64: 735
8. Steroid Control of Gonadotropin-Releasing Hormone Secretion: Associated Changes in Pro-Opiomelanocortin and Preproenkephalin Messenger RNA Expression in the Ovine Hypothalamus
James A. Taylor, et al.
Biol Reprod, Mar 2007; 76: 524
9. Do gonadotropin-releasing hormone, tyrosine hydroxylase-, and ß-endorphin-immunoreactive neurons contain oestrogen receptors? A double-label immunocytochemical study in the Suffolk ewe
Lehman MN, Karsch FJ.
Endocrinology 1993; 133:887–895
10. α-Endorphin blocks luteinizing hormone-releasing hormone release by inhibiting the nitricoxidergic pathway controlling its release
I actually know Eric. I've talked to him many times. You think Eric will tell you that you don't lose gains post-cycle, lol? Yeah, let's load up on opiate agonists to speed up the recovery process. btw, you have to inject this stuff but I'm sure you knew that.
Whats an opiate agonist? Sounds fun! I am thinking of a PCT that actually might work to keep the best gains. What if you Dr tested your test after a cycle, when they are low. Then prescribes you Axiron or another topical testosterone? I am prescribed Axiron 90mgs daily that I plan to go back on after the cycle to see if that works. Heck, it might not, but I am going to try it. Maybe the topical stuff stacked with A-HD or similar Test booster would work great. Ill post about it when I start. Just an idea.
they're not fun. They're used to get block the opiate receptors so you don't get high when you shoot up heroin. You want to take that? If you can recover naturally try that route first. If all measures fail (I ran 3 PCTs before going on TRT) then look into TRT, but understand TRT is a lifetime commitment.Quote:
Originally Posted by warmouth
So you did run the PCT before going on TRT? Do you think that would be the best route to take? I figured if I come of cycling, I would jump righ back on to see if it held gains a little better. I was also going to use the A-HD because it is an estrogen blocker and a strong test booster. Not sure yet. I got Nolva when I ordered the gear, but since the TRT thing, I think it would be a wste for my to use the Nolva. Dont know. Oh yeah, I have been on TRT for 7 months. I stopped it when I went on the Prop, but plan the jump back soon.Quote:
Originally Posted by Juice Authority
So their is no "come back" effect a couple of weeks after pct where test rises back to normal?
When is the best time to judge if i lost strength during pct or a little while after pct?
What's your age and cycling history? That matters. I'll have to respond tomorrow morning.Quote:
Originally Posted by warmouth
I am 30 years old. Ran one cycle so far and in the middle of it now. It is Prop Test 100mgs EOD. Thank you.Quote:
Originally Posted by Juice Authority
Not necessarily.Quote:
Originally Posted by Juice Authority
Naltrexone is orally available in the form of film-coated tablet, namely ETHYLEX.
28 tablets per box, each tablet is 50mg.
Produced & distributed by DEM Pharmaceuticals.
I will make you a deal Juice Authority. If anyone I respect on here such as Gix Bon Swifto TR StPete or Matt looks at this thread and calls me a liar as you did and tells me there is no way it has ever happened or could ever happen. And my post are worthless, I will walk away and you wont have to worry about seeing my advice given anymore. Fair enough? But if they don't, I myself would like an apology. And for the record I have been wrong before on here. Hell Gixxer has corrected on a few occasions. However it was done with tact, not in a belittling manner. I tend to only give advise I have practical knowledge of , or know someone personally. I will await my fate. Cape
"Naloxone lacks oral bioavailability therefore injection is required."Quote:
Originally Posted by Turkish Juicer
Dude, really? Come on. I was strongly disagreeing with your comments, and still do. It wasn't a personal attack. Relax. Deep breath in and out.Quote:
Originally Posted by Capebuffalo
I can accept this. Differing ideas is what makes this board great. Differing ideas are what founded this great country. I am a grown man with a family and pride myself on honesty and integrity. That is how I want my son to be raised. But your statement "Anyone claiming different is a liar." is a slap in my face that i won't tolerate. You don't know me or my character, but if you look at my post, I may give some a hard time (usually the under -aged who won't listen) but the majority is honest advice. If I get in over my head with someone I ask for someone with more knowledge to step in, so at no time am I giving totally bad advice. If you are fine with this I would like to stay around and help where I can and learn where I can. Sorry about the one eyed fat man remark, but I do love Rooster Cogburn.Quote:
Originally Posted by Juice Authority
I didn't start TRT until I was 36 after many years of cycling use and abuse under my belt. Prior to starting TRT, I would generally recover within the normal range. The problems started when I didn't allow the body to completely recover before started the next cycle. All it took was one time of making that mistake. I ran 3 PCTs over 8 months and total test was still under 300ng. The doc first gave me Androgel. The absorption rate of the gel is low plus insurance wouldn't cover it because there is no generic equivalent. I talked to the pharmacist and she sent a prescription change request to the doctor for Test Cyp. They started me off at 200mgs/e10days. Bloodwork later showed that wasn't enough so he bumped it up to 200mgs/wk. Now that's me. Testosterone starts to decline at 30 and by age 35 it drops off a cliff. Short story long, I would wait if were you. At least give PCT an honest and patient effort before making a lifetime commitment to TRT.Quote:
Originally Posted by warmouth
Fair enough. Wrong choice of words.Quote:
Originally Posted by Capebuffalo
I will. Ill give the PCT a try. My natural Test levels are under the 400 mark and that is why he put me on TRT in the first place. I hate it, and it really doesnt work that well for me, but I guess that is part of life. My libido went from through the roof, to literally nothing withing 1 year. Since I got married, it just hasnt been where it needs to be. I can still get in the mood, just at the wrong times (3am, church, dinner, etc) but once the mood wears off, I cant get back to it. I was hoping the Prop would throw my libido way back like it was a few years ago, but not much yet.Quote:
Originally Posted by Juice Authority
What is this, a joke?Quote:
Originally Posted by Juice Authority
I just gave you full info on Naltrexone, which is an is an opioid receptor antagonist used primarily in the management of alcohol dependence and opioid dependence, just like its cousin Naloxone, another opiate agonists with the difference of being an injectable.
Read the posts through before responding.
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I was responding to the previous post. Perhaps you should read the entire thread before responding. What was being discussed is an obvious off-label use of the drug.Quote:
Originally Posted by Turkish Juicer
Naloxone, naltrexone and nalmefene seem progressively more powerful in their potency to block b-endorphin, respectively. (14,18) Naloxone lacks oral bioavailability therefore injection is required. An injectable preparation could easily be made with BA water due to the water solubility of the compound. A 40mg subcutaneous injection would be a typical dose of naloxone. Naltrexone is orally active, with a safe and effective oral dose being about 100mg for a 220lb male. (18) While a lower dose of about 25-50mg of nalmefene would seemingly have the same benefit. (20,24) Increasing the dose of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. A twice a week dosing protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shutdown – Just enough to keep them in the “ball game” so to speak. Also, a twice a week dosing protocol would most likely limit the increased opioid sensitivity induced by the long-term use of the drugs.
What were you using before you got blood work? Getting blood work done after completing PCT is not always a good indicator. PCT may artificially boost total test only for it to drop again once you complete PCT. PCT is mainly to kickstart HPTA recovery. The body needs to reach its own homeostasis point on its own. That's where the only cure, or not, is time.Quote:
Originally Posted by warmouth
good thread
All the bickering aside:
I have ended my cycle 3 weeks ago and gained possibly a few % in strength and lost no weight/size at all.
I am following a sticky I seen on here somewhere by Marcus which said to pound down Vitamin C along with cholesterol rich foods.
So far so good. But, this seems like it varies so much from person to person. Most likely about your genetic potential, it's all about what your body really wants to do.
We'll see if I keep everything, I don't know if I will - But it would be nice.
Best advice: Keep the calories high and mostly from rich heavy foods like liver and eggs, take a about 3k mg's of Vitamin C per day and stay on your workouts. I cut my workouts to under 45 minutes, but now I workout every other day.
Keep me posted. I would like to know if it happens and how long after cycle and pct if you start to lose anything. Who knows maybe liver is a wonder food. I however won't know. Like the saying goes"Sewer rat might taste like pumpkin pie. But I ain't going to eat the nasty mother f-er"Quote:
Originally Posted by samson_420
I agree with what you said about the post cycle loss of gains but you are wrong about the Naloxone.... It is available as an oral. I have used it.Quote:
Originally Posted by Juice Authority
I doubt it. More like genetics at play. . .People do good with different shit. Seeing others losing gains sucks.Quote:
Originally Posted by Capebuffalo
I wasnt on anything at all. I just had been struggling with a lack of libido and low energy and he tested my Test levels and said they were "normal". The paperwork said the normal range was 400-1100 and I was at like 402. He said I was good to go, but I knew I wasnt because I had a 2 week honeymoon and had sex 3 times. Couldnt sleep at night but was sleepy all day. The Axiron he gave me sucks bad, and the Prop hasnt been the greatest either, but it is better than the Axiron. So I was naturally fairly low without taking anything. And I thought that spread from 400-1100 was ridiculous being at 29 I was 2 points over being considered "low" and he said I was fine.Quote:
Originally Posted by Juice Authority
Naltrexone is oral. Naloxone is by injection.Quote:
Originally Posted by tboney
What was your free test level? That's the number that matters. Either way, if total test is above 300ng they can't put you on TRT. You could run the Prop with Mast P or Proviron. That should make a big difference.Quote:
Originally Posted by warmouth
I was on suboxone for a long time.. It is a oral, sublingual tab. It contains buprenorphine and naloxone.Quote:
Originally Posted by Juice Authority
So u guys are saying u cannot keep the gains once pct and after pct?? I mean even on pro hormones IV kept a lot of it and haven't dome it for 6 months..
No, that's not what they are saying.Quote:
Originally Posted by bdw1269
Read the thread over dude, don't be so lazy.