Calculated Blast w/ Testosterone

GrymReefer

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Summary: My main goal is to solidify the idea of a proper preparation that can be followed prior to running an extremely short cycle for maximum results with minimal impact. The idea is that a slow depletion followed by exogenous hormone administration and massive surge in caloric intake (carbs, protein) will produce a glycogen supercompensation effect that can be exacerbated and prolonged due to the variables of the equation. (AAS-increase protein synthesis, increase nitrogen retention, increase nutrient utilization and storage, increase angiogenesis....) If this does work then it would personally replace my standard cycle time (12-16 weeks). I have no real scientific data to back up anything I'm thinking.
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NOTE! to whoever reads this and is more knowledgeable. Please please please correct whatever I got wrong. I tried to proof read it a few times to fix anything I previously was incorrect on.


WOOOHH I'm down to a 162 pounds! I have been slowly depleting and depleting and depleting. Then some jogging and jogging and jogging.

My goal? I have no clue. Waiting for a gym in town to get done with construction and I have had this idea about a little jumpstart.

A short blast of testosterone maybe 250-300mg/wk for 6 weeks. However, I'll be starting the cycle from complete glycogen depletion and then within that week immediately increase my carbohydrate intake astronomically and lower my fat intake.

I would obviously experience a brief moment of glycogen supercompensation, but in conjunction with AAS and meticulous supplemental intake... I'm thinking I may be able to conjure some quality muscle without too much effect on the HPTA due to the brief stint. I would also maintain my cardiovascular activities, but only to hopefully control any attempt to store away energy as adipose tissue.

I'm fairly familiar with glycogen compensation because of my usual diet of teetering on the edge of a ketogenic environment only to overwhelm the body once a week during my refeed stage and nullify any possible processes associated with a catabolic environment. Seeing how AAS increase the ability at which the body can utilize nutrients and increase the body's ability to retain certain nutrients in larger quantities than normal...I believe I may actually be slightly successful.

I have absolutely no real scientific data to back up any of this, but only personal experiences with how I interpreted my body's response on cycle and with dieting.

I was reading through this study one night while I was pondering my random ideas that led up to this experiment. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612416/

Any input, thoughts on improvement, or scoldings are welcome!

EDIT: I have had thoughts about using trenabolone and having the testosterone solely in place to maintain natural physiological processes that would go to hell if someone were to just use tren alone. My reactions to tren isn't exactly satisfactory though...

I plan on using propionate for my testosterone ester. I have no problem pinning myself every 5 minutes for the rest of my life. Sero understands it with the needle fetish. Now.... I was thinking that if I were to use a longer acting ester such as enanthate, but I split the dosage up between 3-4 injection sites.... theoretically I would be able to achieve a higher serum concentration than following the standard protocol of using it all at one injection site. What I need to figure out is how much would that alter the dosage intervals due to separation of the initial dosage to multiple sites and the rate at which the ester is cleaved off from the testosterone considering multiple contact points..

An accelerated rate of testosterone absorption while also using a esterification that generally allows larger volume per injection without compromising the stability (reference to the acetate ester).............still thinking
 
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WOOOHH I'm down to a 162 pounds! I have been slowly depleting and depleting and depleting. Then some jogging and jogging and jogging.

My goal? I have no clue. Waiting for a gym in town to get done with construction and I have had this idea about a little jumpstart.

Get back to the gym, back to the gym, back to the gym ;)

A short blast of testosterone maybe 250-300mg/wk for 6 weeks. However, I'll be starting the cycle from complete glycogen depletion and then within that week immediately increase my carbohydrate intake astronomically and lower my fat intake.

I would obviously experience a brief moment of glycogen supercompensation, but in conjunction with AAS and meticulous supplemental intake... I'm thinking I may be able to conjure some quality muscle without too much effect on the HPTA due to the brief stint. I would also maintain my cardiovascular activities, but only to hopefully control any attempt to store away energy as adipose tissue.

I'm fairly familiar with glycogen compensation because of my usual diet of teetering on the edge of a ketogenic environment only to overwhelm the body once a week during my refeed stage and nullify any possible processes associated with a catabolic environment. Seeing how AAS increase the ability at which the body can utilize nutrients and increase the body's ability to retain certain nutrients in larger quantities than normal...I believe I may actually be slightly successful.

I have absolutely no real scientific data to back up any of this, but only personal experiences with how I interpreted my body's response on cycle and with dieting.

So, you're going to do a 6 week cycle when you finally get back to the weights? I can't see why you wouldn't successfully gain some quality LBM (quite a lot in fact, given you've not trained for a while). And periodising your carb intake seems pretty sound too.

I was reading through this study one night while I was pondering my random ideas that led up to this experiment. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612416/

Any input, thoughts on improvement, or scoldings are welcome!

Nice study you found there Grym. How did it prompt your ideas though?

EDIT: I have had thoughts about using trenabolone and having the testosterone solely in place to maintain natural physiological processes that would go to hell if someone were to just use tren alone. My reactions to tren isn't exactly satisfactory though...

I plan on using propionate for my testosterone ester. I have no problem pinning myself every 5 minutes for the rest of my life. Sero understands it with the needle fetish. Now.... I was thinking that if I were to use a longer acting ester such as enanthate, but I split the dosage up between 3-4 injection sites.... theoretically I would be able to achieve a higher serum concentration than following the standard protocol of using it all at one injection site. What I need to figure out is how much would that alter the dosage intervals due to separation of the initial dosage to multiple sites and the rate at which the ester is cleaved off from the test...


Are you asking which ester would give you a higher serium concentration of testosterone?
 
ahhh I'm terrible with using the quotes sytem...

1. The gym and I are in a "complicated relationship"

2. I would assume that going from a depletion stage that is carefully balanced from nutrient manipulation to.. an all out refeed session except this session lasts for 6 weeks straight. Still working out the numbers but I was going to go from an average of 2100 calories per day to 4700 calories per day. My workout routine however would be focused solely on negative lifts and drop sets. It would allow me to work with lighter weight to help prevent a possible injury, but still overload my system.

3. I noticed a lot of studies, not just this one, have the test animals running very short periods of administration. Also thinking about your myostatin reference...why not attempt to maximize that little window of peak anabolic activity while also minimizing any possible suppression that could lead to a net loss during the recovery and reestablishment of homeostasis in reference to the HPTA. And whatever mechanics myostatin focuses on. I still can't fully comprehend that little world...yet Really this idea was slightly off the wall and I didn't really want to even post the madness, but I'm sure someone else can learn from me. What you shouldn't think about doing. The study just happen to feed a few key words into my brain. It is an interesting one though nonetheless.

In reference to glycogen reuptake following the massive 6 week refeed... the body was in a sponge like state and introducing all the crucial nutrients while also introducing hormones that increase the utilization drastically is putting your chances of harboring an overwhelming anabolic state very likely. CFC, I know that YOU know that after contests when they go back to the gym, that environment their body is in allows for some very substantial development to take place.

EDITEDIT: 4. Using testosterone with a long acting ester, but dividing the location of the injections (500mg/wk injected every 7 days - besides a single 500mg injection to have one active depot - you separate the dosage to 2 250mg injections in separate locations - 2 active depots possessing 250mg/ ea vs. 1 active depot possessing 500mg) though it is a hypothetical situation having 2 active absorption sites would produce a higher peak serum level in regards to testosterone.

Now... hypothetically speaking if the single 500mg injection took 14 days to successfully cleave the ester from the testosterone, then would splitting the dosage also split the rate at which it is absorbed? So the 250mg injections would last 7 days. If that held true then an injection that was originally recommended at 14 day intervals would require more frequent pins.

Why use a long acting ester vs a short acting ester? From my interpretation...a shorter ester has a higher probability to crash out of the solution especially when an abnormal quantity per ml is created such seen in many UGL's... while a long acting ester may not be as susceptible due to their solubility. Sooo... would it be possible to split the dosage of a long acting ester and have comparable rates of absorption to a short/middle acting ester?

example... 500mg/wk of testosterone propionate injected at 250mg dosages every 3 days - 500mg/wk of testosterone cypionate split between 5 injection sites in one day at 100mg/ea. injection interval done every 7 days...

Due to the adjustments in rationing the weekly dosage between multiple depots, it allows a faster rate of absorption vs. a single depot injection containing the whole weekly dosage.

Would this protocol produce a peak serum level comparable to a faster acting ester? If so, then would having a slower acting ester also prevent the roller coaster effect that is seen with short acting esters?
^^^Ignore majority of the ideas about multiple injection sites. after learning a little more later on in the research process I didn't understand the absorption process completely. Will fix when I get back from work.

EDITEDITEDITEDITEDIT.....

so after further research I have come to learn that I am trying to find what falls in the category of pharmacodynamics...

So I understand finding concentration and volume of distribution...

X= amount of drug in body V= volume of distribution C= concentration in the plasma...

X=VC - C=X/V - V=X/C

But...I have a feeling this doesn't cover the cleavage rate for the esters via hydrolysis...or I am in the completely wrong ball park.

Source for equations and general understanding: http://www.ashp.org/DocLibrary/Bookstore/P2418-Chapter1.aspx

here is my 162 lb corpse on the left...and the estimated outcome from this cycle protocol :)


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Supercompensated glycogen loads persist 5 days in resting trained cyclists.

Abstract

Research data indicates a persistence of elevated muscle glycogen concentration 3 days post-supercompensation in resting athletes. This study expands our earlier findings by determining whether muscle glycogen remains elevated 3, 5, or 7 days post-supercompensation. Seventeen trained male cyclists underwent one bout of exhaustive exercise to deplete muscle glycogen. This was followed by a 3-day consumption of a high carbohydrate/low protein/low fat diet (85:08:07%). Three post-loading phases followed with subjects randomly assigned to either a 3-day, 5-day, or 7-day post-loading maintenance diet of 60% carbohydrate and limited physical activity. Biopsies (50-150 mg) of the vastus lateralis were obtained pre-load (BASELINE), at peak-load (PEAK), and either at 3-day, 5-day, or 7-day post-load (POST). On average, PEAK to POST muscle glycogen concentrations decreased 34, 20 and 46% respectively for the 3-, 5-, and 7-day POST groups. Only the 7-day post-load group's PEAK to POST mean muscle glycogen concentration decreased significantly. In addition, multi-regression analysis indicated that the PEAK glycogen level was the main determinant of the number of days that glycogen levels remained significantly greater than BASELINE. Thus, trained athletes' supercompensated glycogen levels can remain higher than normal for up to 5 days post-loading. The amount of carbohydrate consumed, the level of physical activity, and the magnitude of the glycogen supercompensation determine the interval for which the glycogen levels are elevated.


Source: http://www.ncbi.nlm.nih.gov/pubmed/17120016

So reflecting on that little bit of information... The glycogen levels were still within a super compensated state even though the original introduction of carbs while depleted happened days earlier. Now this study had the athletes undergoing a strenuous exercise to achieve glycogen depletion.

However, I have slowly depleted myself over the last few months minus some random cake binges. I can honestly say that I have been functioning on 50G or less of carbohydrates. Only time I would consume any carbohydrates is in the morning via my morning fruit and before running. The amount was so miniscule that I've generally considered the pre-workout glucose consumption is readily burnt up due to the demand for fast energy and the state my body has been maintaining for weeks on end.

My refeeds haven't even been that large either due to the simple equation of dieting.. I try to maintain a balance between calories in-calories out..

Consider this statement from the abstract above, "The amount of carbohydrate consumed, the level of physical activity, and the magnitude of the glycogen supercompensation determine the interval for which the glycogen levels are elevated."

So combine an extended depletion state, with a massive surge of carbohydrate intake (excess of 600-800G) and exogenous administration of hormones. The possibility of creating a post glycogen compensated period that lasts longer than the original study described seems possible. If it would be possible to incorporate one day every 7-10 days to drastically lower carbohydrate intake and do a depletion activity, it could be possible to exacerbate the supraphysiological storage of glycogen and prolong the mechanics associated with this anabolic window.

Referencing a study I used before in a different conversation about glycogen: http://ajpendo.physiology.org/content/278/1/E177

Glycogenin activity in human skeletal muscle is proportional to muscle glycogen concentration

Abstract

The de novo biosynthesis of glycogen is catalyzed by glycogenin, a self-glucosylating protein primer. To date, the role of glycogenin in regulating glycogen metabolism and the attainment of maximal glycogen levels in skeletal muscle are unknown. We measured glycogenin activity after enzymatic removal of glucose by α-amylase, an indirect measure of glycogenin amount. Seven male subjects performed an exercise and dietary protocol that resulted in one high-carbohydrate leg (HL) and one low-carbohydrate leg (LL) before testing. Resting muscle biopsies were obtained and analyzed for total glycogen, proglycogen (PG), macroglycogen (MG), and glycogenin activity. Results showed differences (P < 0.05) between HL and LL for total glycogen (438.0 ± 69.5 vs. 305.7 ± 57.4 mmol glucosyl units/kg dry wt) and PG (311.4 ± 38.1 vs. 227.3 ± 33.1 mmol glucosyl units/kg dry wt). A positive correlation between total muscle glycogen content and glycogenin activity (r = 0.84, P < 0.001) was observed. Similar positive correlations (P < 0.05) were also evident between both PG and MG concentration and glycogenin activity (PG, r = 0.82; MG, r = 0.84). It can be concluded that glycogenin does display activity in human skeletal muscle and is proportional to glycogen concentration. Thus it must be considered as a potential regulator of glycogen synthesis in human skeletal muscle.

Stll working on this....
 
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Personally I like the idea. For ester of choice I'd say opt for phenyl prop. It's short but stays in solution easily. This is essentially how I kicked off my blast. Depleted and flat as a board. Then went back to maintenence calories and transformed. I'd personally go for tpp for your test though as a longer ester woukd be just peaking towards the end, allowing your body to not fully reap the benefits of that 6 weeks. It'd allow eod dosing too. Or go with acetate if you don't mind daily injects, it's fast, painless, though does crash somewhat easily.
 
Personally I like the idea. For ester of choice I'd say opt for phenyl prop. It's short but stays in solution easily. This is essentially how I kicked off my blast. Depleted and flat as a board. Then went back to maintenence calories and transformed. I'd personally go for tpp for your test though as a longer ester woukd be just peaking towards the end, allowing your body to not fully reap the benefits of that 6 weeks. It'd allow eod dosing too. Or go with acetate if you don't mind daily injects, it's fast, painless, though does crash somewhat easily.

The thing I was getting at is using a long ester testosterone, but besides injecting hypothetically 500mg into one site. I'd seperate the dosages into 250mg shots and use two different locations that day.

This would allow two different access points for delivery, distribution and expulsion. another hypothetical statement... the 250mg shot, once the ester is cleaved it allows 190mg of testosterone into the body over 7 days. Having 2 locations simultaneously breaking down the ester would result in 380mg being delivered into the blood stream. If that shot was kept at the volume of 500mg, the weekly absorption rate would be half due to the process of hydrolysis.

This theory could be wrong, though. I'm still having some difficulty comprehending such a complex process.

I DO know that the active depot can only come into contact with so much tissue and that contact would be a factor in rate of absorption. Like pinning insulin subcutaneously, if you split your humalog dosage between 2 sites you put yourself in a situation of increased rate of absorption and most likely have to immediately eat to compensate for the hasted delivery or you go into a coma.

I could be screwing this all up because I can't really clarify in my mind the comparisons of an aqueous suspension of a compound vs an esterification in regards to the pharmacokinetics.

If I remember an ester (for steroids) is a chain attached to the peptide to protect the 17th carbon position..? (esters are made up of carbon and hydrogen atoms..carbon atoms-17th carbon chain that is my logic) I'm sure they exist on other positions as well.


EDITEDITEDITEDIT

May have been going about it wrong the whole entire time. I have to head into work soon, but I discovered this study in the cataclysmic abyss that is the internet.

http://www.usrf.org/news/TRT/Dobs and Mazer, '99, JCEM copy.pdf - Pharmacokinetics comparison between transdermal test (boo) and testosterone enanthate (yay) I'll have to read into it later and further confuse myself. Whoever had the patience to read through all these posts...I hope some of the studies were helpful or at least entertaining.

If you know how to get ahold of a comprehensive study that talks about the popular esters associated with testosterone and the respective pharmacokinetics please post it!
 
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I plan on using propionate for my testosterone ester. I have no problem pinning myself every 5 minutes for the rest of my life. Sero understands it with the needle fetish. Now.... I was thinking that if I were to use a longer acting ester such as enanthate, but I split the dosage up between 3-4 injection sites.... theoretically I would be able to achieve a higher serum concentration than following the standard protocol of using it all at one injection site. What I need to figure out is how much would that alter the dosage intervals due to separation of the initial dosage to multiple sites and the rate at which the ester is cleaved off from the testosterone considering multiple contact points..

An accelerated rate of testosterone absorption while also using a esterification that generally allows larger volume per injection without compromising the stability (reference to the acetate ester).............still thinking



Martyesters_zps47cdbb39.gif


See the above reaction, it's an equilibrium reaction. Esters spontaneously react with water. The blood within your body is a water based solution, hence testosterone esters break down naturally to some extent once they hit the blood stream, but this process is also facilitated via enzymes known as esterases (also present in the blood stream).

When you inject your oil it creates a depot with a specific surface area exposed to the blood plasma within your muscles. The oil containing testosterone ester at the exposed surface area interface leaches out slowly into your body's blood stream.

Lower volume injects have a larger surface area to volume ratio to begin with than larger injects, therefore injecting small volumes of gear decreases the half life of testosterone ester within your body.

Remember minto et al. showed greater bioavailability to glutes 72%, as opposed to delts 56%.... Where were you thinking of injecting..?
 
^^^I remember you explaining this to me when I asked if there was a way to use a bunch of smaller depots to accelerate the break down of long esters.
I gotta ask, what happens to the rest of the gear that isn't absorbed? Such as delts it's 56%, so what happens to the remaining 44%?
 
See the above reaction, it's an equilibrium reaction. Esters spontaneously react with water. The blood within your body is a water based solution, hence testosterone esters break down naturally to some extent once they hit the blood stream, but this process is also facilitated via enzymes known as esterases (also present in the blood stream).

When you inject your oil it creates a depot with a specific surface area exposed to the blood plasma within your muscles. The oil containing testosterone ester at the exposed surface area interface leaches out slowly into your body's blood stream.

Lower volume injects have a larger surface area to volume ratio to begin with than larger injects, therefore injecting small volumes of gear decreases the half life of testosterone ester within your body.

Remember minto et al. showed greater bioavailability to glutes 72%, as opposed to delts 56%.... Where were you thinking of injecting..?

Thank you Thank you Thank you! I've always done it on my glutes. I probably should switch it up considering i got some scar tissue there.

So I'm assuming you understand what I'm trying to do for the most part? I still don't understand fully what I'm doing, but I got some hunches. I'm on lunch right now and I definitely got some more questions to bombard you with when I get back!
 
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^^^I remember you explaining this to me when I asked if there was a way to use a bunch of smaller depots to accelerate the break down of long esters.
I gotta ask, what happens to the rest of the gear that isn't absorbed? Such as delts it's 56%, so what happens to the remaining 44%?

Piss it out I think
 
I think I'm missing a link here Grym. Why are you so interested in glycogen supercompensation? I could understand if you were a marathon runner, or if you're getting ready for a show. But how does this converge with the short cycle you're planning? Are you trying to link supercompensation with elevated MPS?
 
^^^I remember you explaining this to me when I asked if there was a way to use a bunch of smaller depots to accelerate the break down of long esters.
I gotta ask, what happens to the rest of the gear that isn't absorbed? Such as delts it's 56%, so what happens to the remaining 44%?

Many esterified substances are metabolised (broken down) and excreted before they are able to reach target sites. So large depots and different muscles with varying blood supplies are likely to modify bioavailability. Generally speaking we might assume that if you can get a drug into the bloodstream as quickly as possible, it's less likely to suffer degradation. The longer it sits away from a capillary and remains uncleaved, the greater the chance it won't make it intact.
 
I think I'm missing a link here Grym. Why are you so interested in glycogen supercompensation? I could understand if you were a marathon runner, or if you're getting ready for a show. But how does this converge with the short cycle you're planning? Are you trying to link supercompensation with elevated MPS?

I've used carb cycling for 2-3 years and I recognized that on the days of my refeeds I more often than not increased moderately in whatever lift I was doing either with the total volume or increase in weight. Now that could just be contributed to me seldom having my glycogen storage properly filled ( I feel nausea all the time when I lift especially legs and back)

Later on I began noticing I responded extremely well to over emphasizing the negative portion of all my lifts and I began dropping the my total weight I used in exchange for the best mind-muscle connection I could achieve. People always say you need the mind muscle connection and I always had the belief I was already there, but in actuality I just began to achieve that real connection last year or so.

Soo....if I can maintain an overzealous amount of fuel for my workouts and come in with extreme intensity that is generally hard for me to consistently replicate for each workout I do AND I come back with the knowledge I got from getting rid of the egotistical aspect of the lift and focus on the real mechanics and really feel those sets... I believe I can give myself some pretty substantial development in regards to my LBM.

Now....this is something I need to dig around on. Sarcoplasmic muscle development results in a larger glycogen storage. Having a larger glycogen storage allows me to increase my intensity for longer periods of time before I start getting light headed/throwing up at the gym :) This allows me to really stress my muscle fibers and force the body to recover and overcome.

If your acronym MPS stands for muscle protein synthesis then yes I kind of had that idea. I know I read a study while typing some of this stuff up and it was in regards to the total availability of glycogen in correlation to overall skeletal muscle development. Introduce AAS into the system and you got yourself a well oiled machine as long as you keep all the working parts functioning in harmony.

And sorry I am extremely disorganized in structuring my thoughts accordingly. I'm surprised some of you had the patience to finish the whole thing!
 
Many esterified substances are metabolised (broken down) and excreted before they are able to reach target sites. So large depots and different muscles with varying blood supplies are likely to modify bioavailability. Generally speaking we might assume that if you can get a drug into the bloodstream as quickly as possible, it's less likely to suffer degradation. The longer it sits away from a capillary and remains uncleaved, the greater the chance it won't make it intact.

Also, thanks for this explanation. I kind of did my usual habit of focusing way too much on very tedious biological processes and started to derail my own research process. I just like to know how everything works all the way down to a single cell when it comes to me being a mad scientist on my own body.
 
I've used carb cycling for 2-3 years and I recognized that on the days of my refeeds I more often than not increased moderately in whatever lift I was doing either with the total volume or increase in weight. Now that could just be contributed to me seldom having my glycogen storage properly filled ( I feel nausea all the time when I lift especially legs and back)

Later on I began noticing I responded extremely well to over emphasizing the negative portion of all my lifts and I began dropping the my total weight I used in exchange for the best mind-muscle connection I could achieve. People always say you need the mind muscle connection and I always had the belief I was already there, but in actuality I just began to achieve that real connection last year or so.

Soo....if I can maintain an overzealous amount of fuel for my workouts and come in with extreme intensity that is generally hard for me to consistently replicate for each workout I do AND I come back with the knowledge I got from getting rid of the egotistical aspect of the lift and focus on the real mechanics and really feel those sets... I believe I can give myself some pretty substantial development in regards to my LBM.

Now....this is something I need to dig around on. Sarcoplasmic muscle development results in a larger glycogen storage. Having a larger glycogen storage allows me to increase my intensity for longer periods of time before I start getting light headed/throwing up at the gym :) This allows me to really stress my muscle fibers and force the body to recover and overcome.

If your acronym MPS stands for muscle protein synthesis then yes I kind of had that idea. I know I read a study while typing some of this stuff up and it was in regards to the total availability of glycogen in correlation to overall skeletal muscle development. Introduce AAS into the system and you got yourself a well oiled machine as long as you keep all the working parts functioning in harmony.

And sorry I am extremely disorganized in structuring my thoughts accordingly. I'm surprised some of you had the patience to finish the whole thing!

No, I managed to follow that ok :)

I agree, you can train more intensely and for longer when your glycogen stores are high. I don't believe your aim should be to remain supercompensated for prolonged periods though - once saturation has been achieved, insulin sensitivity falls off a cliff, which will result in diminished MPS (muscle protein synthesis) and increased (visceral) fat gain.

Typically, this is why lots of guys tend to cycle carbs through the day (I know you already carb cycle quite a bit). If you're relatively depleted before a session, then boost glycogen before the workout (and/or drink a carb-enriched amino drink during workout), getting a nice insulin surge, you should get a good training boost. Assuming levels decline by the end of the workout, the body will supercompensate to some extent with the following meals, and gradually deplete through the next day.

Allowing these natural peaks and troughs, just as between growth hormone and insulin, ghrelin, leptic etc, enhances the body's own anabolic processes. It's difficult (and sometimes impossible) to be in two states at the same time (eg being fasted and being fed). You can play with hormones to some degree - eg injecting insulin and GH - but it's a pretty blunt tool and soon results in negatives (eg diminished insulin sensitivity). Thus again you need to periodise any such protocol, or use specific tools like (fasted) cardio etc to flip the reset switch on things like mTOR and AMPK signalling.
 
This is definitely going to be postponed, but I will continue to add to this thread. Idk if anyone was actually interested in this idea, but I appreciate you guys for taking the time to chime in and help me out. Much appreciated.

There is way more than meets the eye right now and I need to read and read and read and read. I might try to pick up a weight in between my reading. I think you guys workout enough though to cover my lack of working.
 
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Many esterified substances are metabolised (broken down) and excreted before they are able to reach target sites. So large depots and different muscles with varying blood supplies are likely to modify bioavailability. Generally speaking we might assume that if you can get a drug into the bloodstream as quickly as possible, it's less likely to suffer degradation. The longer it sits away from a capillary and remains uncleaved, the greater the chance it won't make it intact.

Also an appreciable amount of testosterone would get metabolised to DHT via 5-alpha reductase, and E2 via CYP19A1 (aromatase)..
 
Also an appreciable amount of testosterone would get metabolised to DHT via 5-alpha reductase, and E2 via CYP19A1 (aromatase)..

Thankfully I have absolutely no response to DHT in the field of hair loss. I use AI's on any cycle no matter what. Some people use them only on an as needed basis when they become aware of estrogenic side effects.

A lot of people would disagree with me on that one so I just kinda keep my AI on cycle required hooblaa to myself as to not cause confusion. The moderators and veteran members of this board got wayyyy more experience than I do and thus I would consider their input/ideologies a sound guideline for safe AAS usage.
 
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Why are you postponing your plan? You're just getting started :)

It would probably help if you were able to think more about precisely what goal you are attempting to attain with any given protocol, because then it will be easier for others on here to try to interject some ideas of their own.

Reading between the lines, my understanding of your goals was two-fold:

(1) Preserve HPTA function as much as possible for easy recovery
(2) Maximally anabolic strategy for quickest gains over short cycle

So the 6 week duration was predominantly to not overly tax the HPTA. And you were going to maximise the short time by rebounding into it from a depleted, detrained state.

Ideas for part (1) might include:- taurine at 5g per day for testes preservation, and potentially HCG at 100iu E3D or so; an AI every day to hold oestrogen to physiological levels. All if which may improve recovery and lessen the damage caused by excessive aromatase (oestrogenic) activity.

Ideas for part (2) might include:- increasing the dose of AAS every week up to week 6 to counter myostatin/potential AR adaptation; gradual inclusion or increased dose of supplements (creatine, leucine/EAAs etc) and ramping up of calorie/carb/protein intake; possible use of peptides (eg GHRPs) to boost GH in natural patterns, improving insulin sensitivity, cell proliferation, and reducing fat gain; regular cardio to also boost insulin sensitivity; potentially a 1-2 day fast per 1-2 weeks with use of fat burners, FRAG, and as much low intensity cardio as possible to reduce bodyfat without slowing gains at all.

Out of these various ideas, you might then focus in on certain areas with more research to improve your (and our!) understanding of it and how it might be optimised to suit your own personal protocol?

Just a thought...
 
Definitely agree on the taurine. Helps with not only atrophy of the testes, but also osmotic regulation for water retention, has been shown to lower blood pressure and a I remember a study pointing to mega dosing (10G+) and increase in resting GH levels. Thankfully it is very soluble in water unlike quite a few things I choke down, but I think 3-5G is usually my dosing range. As with the other supplements I think I'm covered in that department. If I went the route of taking pills rather than creating my own blends of complimentary compounds, my belly would probably jingle around from so much capsules.

Only fat burner I've ever experimented with is clenbuterol in conjunction with cytomel. I'm always a little hesitant to use clen/t3 or anything that has a major interaction with my thyroid due to my mother taking cytomel and synthroid. I remember seeing that in the medicine cabinet since I was 13. Assuming it was hypothyroidism.


Now on the basis of going into this from a moderately sedentary lifestyle in reference to heavy weightlifting...
I have been keeping my cardio at an alright pace and with carb cycling I believe this is has been the number one reason why I haven't gained a bit of body fat and actually have been leaner than usual. Would the the cardio off and on since I originally went into hibernation 5 months ago be sufficient to keep the rust off on my body overall? I don't want to jump into the training too crazy and just strain something. I'm planning on focusing solely on dropsets, to failure, and large volume vs. my old methods of 6-8 rep range low volume/high intensity w/ minimal rest periods.

Staying with a lighter weight will help me get the groove back for proper form and get the mind-muscle connection going again and I always did enjoy the different feeling I got from working out during deload stages in my training protocol. (8 weeks on w/ 4 week deload periods)

On the topic of HCG, I was thinking of cutting it out or taper it down for the last week. I know we've had this discussion before and this is definitely something I gotta dive into deeper, but because HCG mimics LH and theoretically that would be suppressive, theoretically of course. And seeing how the HPTA is a douche bag, gets butt hurt when it recognizes your body is getting a fix from somewhere else and cuts you out. I need to figure out if possibly using a very miniscule dosage lets say 75-100iu/wk would still give the leydig cells enough reason to continue production of endogenous testosterone, but in a lower T state. Partial testicular atrophy is 100x better than full blown shut down.

Thanks for your thoughts on this. Always nice to have a second opinion on the matter with more experience backing it. I got a couple days off coming up at the end of the week. I'll probably spend that getting the rest of my school crap finalized and heavy research time! I also found a gym in town that is catered towards the "bodybuilder" persona. My dentist owns it so I guess I should check it out and he'll cut me a deal. I really don't care how terrible a gym is because I can't get creative, but if you don't have a squat rack or at least some barbaric creation for squatting..... don't even ask me to check it out.
 
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