A GH and fat loss protocol (rhGH lipolysis) that is science-based

Estrogen does lower GH response resulting in reduced serum IGF-I levels, while aromatizable androgen (e.g., Test, Deca, EQ, Dbol) increases GH response resulting in increased serum IGF-I levels.

While the process of in situ aromatization positively regulates IGF-I a la rhGH, the aromatase product (e.g., E2) negatively regulates IGF-I a la rhGH.

Notably, trienes like trenbolone dramatically reduce IGF-I but increase muscle (satellite) cell responsiveness to it. That is, despite low absolute serum IGF-I levels with tren & rhGH, there will be better local tissue utilization of the IGF-I isoforms that GH increases the activity of.
So the process of aromatization is helpful to improve the production of IGF-1 from HGH, but the product of aromatization negatively influences the same conversion? Or have I misunderstood something?
 
I am sure it’s here but my eyes are smoked. Is it consensus to dose IM or SQ for the fasted cardio fat loss protocol
 
I am sure it’s here but my eyes are smoked. Is it consensus to dose IM or SQ for the fasted cardio fat loss protocol

I’ve read this whole thread but it’s so much to take in, I’d be lying if I said I remembered it all. From what I believe I’ve gathered, IM injections tend to peak and diminish quicker than injecting SubQ.
 
Thanks @Type-IIx for this piece. I would also be interested on the book...

I am still digesting all the info shared but I would like to get your feedback if I got it correctly. Considering that:
1) Meal 3 at 12am
2) Meal 4 (pre-workout) at 3pm
3) Training at ~5pm
4) Meal 5 (post workout) at 8pm

What would be the best time to inject the GH? 1hr after meal 4? It shall be IV right?

What about pre-fasted cardio? Do you think that the lipolytic effect is diminished by eating 2hr after the injection (wake up >inj > 30m later cardio> breakfast after cardio)?

Thanks.

By this protocol, you'd administer the bolus at 4 pm.

Pre-fasted cardio is fine, it's just unnecessary with rhGH use. The belief in this practice seems to have arisen from the early view of GH as a protein sparing hormone secreted during starvation. I believe you should eat 4-4.5 hr post-bolus (and post-training; cardio at the end of a session would make more sense to me, but you can incorporate your fasted cardio early AM or wherever).

I started doing this yesterday with an 11iu injection 1 hour after my preworkout Meal and beginning training 1 hour after the 11iu is administered. Do you know when it's optimal to take 50mg of anadrol around this? I've been taking it with the pre-workout meal, so 2 hours before training

So I'm taking 11iu GH daily in one bolus preworkout shot, but if I were to take more would you start split dosing in some way at some point, like leaving a bolus shot pre-workout and taking some amount either postworkout, before bed, or both?
 
I started doing this yesterday with an 11iu injection 1 hour after my preworkout Meal and beginning training 1 hour after the 11iu is administered. Do you know when it's optimal to take 50mg of anadrol around this? I've been taking it with the pre-workout meal, so 2 hours before training
What you're doing is great, taking it with some fat/lipid (doesn't have to be much) in the preworkout meal.
So I'm taking 11iu GH daily in one bolus preworkout shot, but if I were to take more would you start split dosing in some way at some point, like leaving a bolus shot pre-workout and taking some amount either postworkout, before bed, or both?
Good question. Yes, this protocol calls for a single large bolus to tolerability but if intolerable, then split it by taking your second (lesser) dose at nighttime (pre-bed) on training days.
 
Ok ya, pre bed makes way more sense than postworkout because the bolus shot will still have my levels high postworkout, but at bedtime my levels are bottomed out. Thank you.
 
Estrogen does lower GH response resulting in reduced serum IGF-I levels, while aromatizable androgen (e.g., Test, Deca, EQ, Dbol) increases GH response resulting in increased serum IGF-I levels.

While the process of in situ aromatization positively regulates IGF-I a la rhGH, the aromatase product (e.g., E2) negatively regulates IGF-I a la rhGH.

Notably, trienes like trenbolone dramatically reduce IGF-I but increase muscle (satellite) cell responsiveness to it. That is, despite low absolute serum IGF-I levels with tren & rhGH, there will be better local tissue utilization of the IGF-I isoforms that GH increases the activity of.
Do you believe that lower serum igf-1 on tren yields better gains or higher serum igf-1 with a bunch of test? Or does the tren and HGH work better than the high test and HGH just because tren is that much more powerful on AR's?
 
Do you believe that lower serum igf-1 on tren yields better gains or higher serum igf-1 with a bunch of test? Or does the tren and HGH work better than the high test and HGH just because tren is that much more powerful on AR's?
Tren & lower serum IGF-I increases muscle size greater than (>) Test & higher serum IGF-I†.

Test & higher serum IGF-I increases total body size > Tren & lower serum IGF-I.

On an equimolar basis (equivalent per-mg), of course.

Serum IGF-I is a measure of the liver-secreted circulating IGF-I in the blood compartment. This mitogen increases cell division leading to, e.g., growth of the bones, connective tissues, basically all tissues. It makes us larger humans.

Tren increases the activity of autocrine/paracrine IGF-I isoforms (IGF-IEa; IGF-IEc, also known as MGF) in the muscle compartment. This means that the satellite cell response (reflecting the process of hypertrophy) to these isoforms is greatly increased, "doing more with less."

In the muscular compartment, autocrine/paracrine IGF-IEa is increased by rhGH, and IGF-IEc by lifting weights.

†: Note that muscle size here refers to the myofibril diameter, the contractile units, rather than, e.g., the circumference or volume of the upper arms. The former refers specifically to myofibrilar hypertrophy of muscle fibers, that it can be argued, is overly myopic, because we also care about cell swelling and sarcoplasmic hypertrophy, glycogen, etc.
 
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Tren & lower serum IGF-I increases muscle size greater than (>) Test & higher serum IGF-I†.

Test & higher serum IGF-I increases total body size > Tren & lower serum IGF-I.

On an equimolar basis (equivalent per-mg), of course.

Serum IGF-I is a measure of the liver-secreted circulating IGF-I in the blood compartment. This mitogen increases cell division leading to, e.g., growth of the bones, connective tissues, basically all tissues. It makes us larger humans.

Tren increases the activity of autocrine/paracrine IGF-I isoforms (IGF-IEa; IGF-IEc, also known as MGF) in the muscle compartment. This means that the satellite cell response (reflecting the process of hypertrophy) to these isoforms is greatly increased, "doing more with less."

In the muscular compartment, autocrine/paracrine IGF-IEa is increased by rhGH, and IGF-IEc by lifting weights.

†: Note that muscle size here refers to the myofibril diameter, the contractile units, rather than, e.g., the circumference or volume of the upper arms. The former refers specifically to myofibrilar hypertrophy of muscle fibers, that it can be argued, is overly myopic, because we also care about cell swelling and sarcoplasmic hypertrophy, glycogen, etc.
@LSDPowerlifting if you read this and think, "I just wanted to know practically which is better, Test & rhGH vs. Tren & rhGH," note that this is a false dilemma that we'll never have to deal with in practice - because we should never run Tren without Test. We don't care so much about how the two differ, but rather, how the two combine.

Compound selection is always the first step after defining the goal of a cycle/blast. Compound selection decisionmaking should never be a matter of whether we add more a) Test or b) Tren because this means that our decisionmaking is constrained merely by availability of compounds; a hopefully artificial case that you never deal with in practice (implies insufficient planning, lack of funds, lack of access to an efficient market - which we know cannot be true because you are here, etc.)
 
@LSDPowerlifting if you read this and think, "I just wanted to know practically which is better, Test & rhGH vs. Tren & rhGH," note that this is a false dilemma that we'll never have to deal with in practice - because we should never run Tren without Test. We don't care so much about how the two differ, but rather, how the two combine.

Compound selection is always the first step after defining the goal of a cycle/blast. Compound selection decisionmaking should never be a matter of whether we add more a) Test or b) Tren because this means that our decisionmaking is constrained merely by availability of compounds; a hopefully artificial case that you never deal with in practice (implies insufficient planning, lack of funds, lack of access to an efficient market - which we know cannot be true because you are here, etc.)
So I take it there is an optimal test/tren ratio? or is it completely individual based?
 
I guess what I was trying to ask was would low test/high tren/high GH build more fibrous muscle tissue than high test/high GH? I guess high test/high GH would build more bone/tendon/ligament because of way higher serum igf-1?
 
incredible thread @Type-IIx. Have you covered GH use for hypertrophy in this thread or will you be dropping that gem in your book?

Currently experimenting with bolus dose pre-bed or post-workout. Wondering what your preferred approach would be
 
So I take it there is an optimal test/tren ratio? or is it completely individual based?
Individualized (depends on body weight, past compound use, etc.) and dependent on the objective or goal of the blast, other compounds used, etc.

As a rule, there is no such thing as an "optimal ratio."

When people talk about apparent dosing that seem to work well in terms of "optimal" (maximal utility) and/or "ratios," (dose proportions) they're just trying to describe what worked for somebody else (n=1 or n=many); but doing so without appreciating the individual factors that shaped that particular cycle/blast, and that change even within the same individual over time.
 
I guess what I was trying to ask was would low test/high tren/high GH build more fibrous muscle tissue than high test/high GH? I guess high test/high GH would build more bone/tendon/ligament because of way higher serum igf-1?
Low Test/High Tren/High GH would build more fibrous muscle tissue than high test/high GH if these are the only two independent variables (drug selection & dose). That's right, high test/high GH would be less potent and selective in growth of myofibrils. You'd achieve a significantly different "look" if all you ever ran over the course of 10 years was one versus the other.

The former (low T/hi Tren/hi GH) would characteristically lead to a dense, sinewy, striated muscle whereas the latter would characteristically lead to an increase in volume without density (a more "watery" look).

Assuming everything else was perfect, nutrition, training, recovery, and genetic endowment, the former might look more in line with the 90s era bodybuilders whereas the latter might look more in line with the modern era.
 
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incredible thread @Type-IIx. Have you covered GH use for hypertrophy in this thread or will you be dropping that gem in your book?

Currently experimenting with bolus dose pre-bed or post-workout. Wondering what your preferred approach would be
Thank you for the kind words! RhGH for hypertrophy is detailed in the Practical section of the book.

Are you asking about my preferred approach for rhGH for hypertrophy? If so I am afraid I must demur because of that fact, its being a prized section of the book that I don't intend to divulge.
 
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