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what is the main reason for an off cycle?
- Thread starter jbowen260
- Start date
Just what OMEGA posted.
solidspine
New member
I seriously think once every 10-15 years, you should take a break, If you are on a cruise or out of the county on vacation, just do pct and take a break and then go back on.
Although, it is important to take a break from training, now and then, gear, well like I said, I have no idea why you would take a break.
Although, it is important to take a break from training, now and then, gear, well like I said, I have no idea why you would take a break.
T
thegoodfoods
Guest
Solid, Your opinion intrigues me and gets questions stirring in my head. Now this is what I've done over the past 6 months... Ran a test-only cycle for 8 weeks, took 6 weeks off with PCT, Ran Test E 500mg/ew Deca 400mg/ew for 11 weeks, took 6 weeks off. And NOW I started another cycle consisting of Sustanon 750mg/wk wks 1-12 Tren Ace 100mg/ed wks 1-10. I'm in week 3 of my current cycle and am wondering if I will get signifiacant gains. My first time with Tren, I'm wondering if I will get much benefit out of it. I got a few reps on my bench and squat and almost all the sides. Could you add input?solidspine said:
How do you plan out your cycles? Do you replace PCT with baseline amount of Test? Please give me an example of a year's worth if cycle(s) if you don't mind.
T
thegoodfoods
Guest
well the only reason to opt to get off that would bother me is the decreased benefit (muscle growth/strength) you might get from running these compounds back to back.
Please correct me if I'm wrong. I would like to know
Please correct me if I'm wrong. I would like to know
airsmith2k
New member
people say they come off for 6-8 weeks but i wonder if they realize the stuff is usually still in you for 3 weeks after your last shot so ur really only off for like 2 weeks lol
T
thegoodfoods
Guest
I think that, even after a long cycle ie 20 weeks, your receptors will repair themselves after 2-3 months.
solidspine
New member
I have been on for 10 years,
Initially did cycles and maintained with the time on, time off theory,
Changed significantly 3 years ago, and I am still gaining, I experiment occasionally. Like at present I am on a high dosage cycle, have no idea just yet if it is a good idea.
For you and any one else, gear is a major part of any cycle, but DIET, TRAINING AND REST are more then equal. So with out enough protein you will not grow, I am of the position your protein should come from fish, meat, chicken, etc, not just shakes, and you need clean calories, every day, It is hard to eat a lot.
I use to keep detailed records of everything, what gear, when, where, how much, what anti e, and what body part I injected. In addition I kept detailed training logs.
But in 10 years I have gained about 45lb of muscle, and kept it all, have weighted more, but it was fat.
The second part of your question, I use to like a lot of different gears, anabolic, androgenic, now I can keep it to 3 or 4, always using test.
My gear usage for the last year looks like this with no real breaks. I have done one HGC cycle in the last year, but my nuts don’t shrink that much, and when they do, I don’t care.
1) 500mg Test E per week for about 2 months
2) Cycle of
Test E 500mg per week
D-bol 50mg per day,
Tren ace 100mg per day
Winny 50mg per day
Only 2 compounds per week, the cycle lasted about 18 weeks.
3) Then I went up to 1000 mg per week of test E for a good 2-3 months, got pretty bloated was surprised.
4) Next addition was 100mg Tren Ace for 50 days, and then back down to 1000mg of Test alone, after the tren, I added some d-bol at 50mg per day, again for 50 days.
5) now I am in week 2 of a high dosage experiment, 2grams Test E,
800mg of Deca, and will be adding 100mg tren ace per day for 50 days.
If I missed something, I was simply on 1 gram of test e.
It is incredibly hard to workout, eat, rest and keep this up, I also have some IGF-1, and more d-bol on order. My plan is to stay on this high dose cycle for 12 weeks, eat at least 4000 calories, and train like a mad man, which is the easy part.
I am older so the critical aspect I did not mention is minimize/eliminate or work around injuries or you should just stay home. That is specifically why I am on deca and not EQ or even Primo.
I have always maintained adequate anti-e, never have had and never want gyno.
Calbaser, Liquidex, Nolvedex and AIFM
I am 5’5”
196 lbs
57 years old
Bf is 10 percent
Goal is 215lbs with bf below 8 percent. With the calories you can see why I need the fina.
I Additionally I take some prescription medications, specifically diovan which keeps my blood pressure at about 120/ 68 and my resting pulse never climbs above 65.
I would never check my pulse or BP on amply 02, need to wait about 12 hours
needtogetaas
New member
Post Cycle Therapy (PCT) is a key component in a steroid cycle, as suppression of the Hypothalamus, Pituitary, Testicular Axis (HPTA) is seemingly unavoidable to a steroid user. 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, we will learn how we can 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).jbowen260 said:
For a moment, let’s forget the concept of "post cycle therapy", and embrace the idea of "constant 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 exogenous hormone 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 gonadotrope receptors. These, in turn, secrete the gonadotrophins, luteinizing hormone (LH) and follicle stimulating hormone (FSH). These gonadotrophins travel all the way down to the testis, to activate their respective leydig and seritoli cells. LH initiates testosterone production via the leydig cell receptor (steroidogenesis), while FSH initiates sperm production via the sertoli cell receptor (spermatogenesis).
AAS’s inhibit hormone production just as endogenous 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 testis from atrophy, (to be covered in a future article) it does nothing to prevent pituitary atrophy. We forget that the pituitary is susceptible to the same degradation and atrophy as the testis. 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 weeks pass.11 This is analogous to atrophy of the testis, during absence of an LH or FSH signal. On the same accord, 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 preservation of function and sensitivity. Perhaps a completely neglected and suppressed pituitary may explain the lack of full and prompt recovery for many steroid users, despite adherence to a "tried and true" hCG, clomid/nolva regimen. So the question is – How can we prevent suppression of the pituitary, and better yet, how can we prevent suppression of the hypothalamus?
A closer look –
In should be mentioned that another mechanism in which AAS inhibit LH and FSH release from the pituitary is by direct suppression upon the pituitary GnRH receptors and consequent quenching of LH & FSH secretion.35,38 However its appears that AAS which bind strictly to the AR, do not exert a direct negative effect on pituitary function or sensitivity.34,37,39 This agrees with the theory that non-aromatizing steroids such as Primobolan, Proviron or Masteron are not nearly as suppressive as an aromatizing AAS’s such as testosterone or Dianabol. Evidence suggests that estradiol is about 200x more suppressive than testosterone on a molar basis37, and that administration of arimidex can greatly reduce testosterones suppression on GnRH and LH release.42 So, we know anti-estrogens can limit suppression of AAS, but this only solves half the problem.
When it comes to suppression of the hypothalamus, and what seems to be basic endocrinology, we find it is not so simple upon closer examination. There is more than a simple on-off switch for the hypothalamus control center, a lot more. Evidence suggests that there isn’t even a direct AR or ER action upon GnRH release.2-6 That is, steroid hormones do not directly influence GnRH release from the GnRH neurons.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 for GnRH release that communicate the inhibitory effects of steroid hormones. 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 intermediates involved.
When steroid hormones reach the hypophysial portal, they activate the EOP’s, which suppress GnRH. 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 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 these hormone receptors.15,32
The effect of a u-opioid receptor antagonist on the HPTA can be seen 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 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 dis-inhibit LH release, respectively14,18 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 with either of these drugs will surely increase the likelihood of side-effects without notably increasing the benefit. An every 3rd day protocol would seem appropriate with these drugs, as only to increase GnRH and LH release enough to prevent pituitary and testicular shrinkage – Just enough to keep them in the "ball game". 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 opioids 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.
A few point to consider -
For those who choose to embark on a every 3rd day protocol of an opioid antagonist several things should be considered. First, total prevention of HPTA suppression is unlikely in a cycle of 1gm or more per week of AAS. However, by following smart cycling guidelines, suppression will at least be minimized to the point where normal HPTA function could be regained within days of AAS clearance, rather than months. The protocol suggested in this article would at least allow steroid users to limit the usage of classic SERM’s for PCT, as these drugs can have obvious undesired effects. Several things shall be considered when planning an AAS protocol designed to limit suppression.
It appears that progestin based AAS such as trenbolone and nandrolone which bind not only to the AR, but also to the progesterone receptor (PR) also have a directly suppressive effect on pituitary sensitivity36 (similar to estrogens). It also appears that no opioid receptor antagonist or anti-aromatase can prevent suppression via the PR. Therefore, a multiple gram stack of testosterones and nandrolones is no doubtingly going to completely suppress 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 nandrolones are better avoided, or at least not stacked with heavily aromatizing AAS without the concurrent use of a strong AI.
As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogens 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 gonadotropes. 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
solidspine
New member
Needto where did you copy that from?
needtogetaas
New member
solidspine said:
I find all the info.I like to read read read research research research all day long.
T
thegoodfoods
Guest
Thank you so much, Solid! I'm going to put this thread on my favorites list for future use.solidspine said:
Do you take or have you ever taken HGH?
BTW You're JACKED at 5'5"! Pics??
needtogetaas
New member
I run a restaurant and have a good staff so I dont have to work much.in the summer I work a lot more but even then I have plenty of time to be on a comp.ironclaw said:
I make good money but I am far from rich thats for shore.lol
Brad.
Last edited:
Sweetsrcool
New member
solidspine did u seriously say it has taken you 10 years to put on 45 pounds of muscle
HOLY CRAP i think your gear is bogus bro
HOLY CRAP i think your gear is bogus bro
mr.nitro
Banned
45lbs of muscle only, and on a 5'5" guy, thats significant. I would have to gain 80lbs to get the same look being that im 6' . I look skinny at 200.
so back on topic, do you think gear loses its effectiveness after being used long term? I thought that was one reason for comming off.
so back on topic, do you think gear loses its effectiveness after being used long term? I thought that was one reason for comming off.
First of all, it's not really accurate to say you've "kept" any amount of muscle if it's being maintain in an artificially enhanced anabolic environment. It's how much you keep when you come off that counts.
Coming off alows the HPTA to repair. When it does, your receptors regenerate and you produce more natural T, which in turn makes the next cycle more productive. Even those on HRT may take mini breaks in an effort to get the body to at least attempt working on its own. This prevents total shutdown. It's a kind of holistic, natural approach. Going off solififies the gains. If you can carry the extra muscle naturally, it's there to stay.
Of course, if you've decided to do heavy, long duration cycles, it's kinda pointless to come off. Accept that you will relying on the gear for the rest of your life, and that's it. But common sense tells you that adding that carrying too much extra weight, even if it's muscle, is not particually healthy. And there are BP and cholesterol issues that may eventually will require drugs to control. And there's no way that 100 mgs of orals a day isn't damaging to the liver. No one with any knowledge will argue that -- doctors, athletes, pharmacologists, pro bodybuilders, no one. It's not debatable. To some it doesn't matter. I had a friend who was told his liver was giving out from years of abuse and he ignored the warning. He's dead now.
Coming off alows the HPTA to repair. When it does, your receptors regenerate and you produce more natural T, which in turn makes the next cycle more productive. Even those on HRT may take mini breaks in an effort to get the body to at least attempt working on its own. This prevents total shutdown. It's a kind of holistic, natural approach. Going off solififies the gains. If you can carry the extra muscle naturally, it's there to stay.
Of course, if you've decided to do heavy, long duration cycles, it's kinda pointless to come off. Accept that you will relying on the gear for the rest of your life, and that's it. But common sense tells you that adding that carrying too much extra weight, even if it's muscle, is not particually healthy. And there are BP and cholesterol issues that may eventually will require drugs to control. And there's no way that 100 mgs of orals a day isn't damaging to the liver. No one with any knowledge will argue that -- doctors, athletes, pharmacologists, pro bodybuilders, no one. It's not debatable. To some it doesn't matter. I had a friend who was told his liver was giving out from years of abuse and he ignored the warning. He's dead now.
solidspine
New member
On most of three years simply not impressed at that time for the price, that was over 4 or 5 years ago, so maybe growth has improved.
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