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Daz69

GROWTH HORMONE, INSULIN, AND TESTOSTERONE - AND WHY THEY ARE SYNERGISTIC

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Things Insulin is Great for:


- Increases whole body protein synthesis rates
- Reduces rates of whole body protein breakdown (however the rate of protein degradation in skeletal muscle may not be affected)
- It requires intracellular amino pools to have amino acid concentrations maintained at levels higher than normal for increased MPS rates (this is key to understand - very important - hint: think GH synergy here)
- Directly activates sodium/potassium ATPase pump in skeletal muscles cells (CR note: could increased sodium/potassium be beneficial to those using insulin in supraphysiological doses?) - this allows certain aminos to be more easily taken into muscle cells (think lysine and alanine)
- Unlike lysine and alanine, leucine transport rates are not affected (hint: think GH synergy here)
- Insulin increases total and intracellular GHRs, stimulates receptor biosynthesis, and inhibits translocation of intracellular receptors to the cell surface, but does not affect receptor internalization. 
- Stimulates mitochondrial oxidative phosphorylation in skeletal muscle along with synthesis of gene transcripts and mitochondrial protein
- Enhances GH-induced activation of the ERK1/2 / MEK1/2 pathways via post-GHR mechanisms - these pathways have a direct role in the promotion of growth
- Helps resensitize GH pathways (ERK1/2 and MEK1/2)

 

Things GH is Great for:

 

- Decreases rate of amino acid oxidation and specifically leucine (recall from above this is what insulin requires for anabolism so adequate amino intake plus GH's limiting of oxidation equals greater anabolism properties)
- Increases whole body protein synthesis rates (just like insulin - double WIN)
- Increases transport rates for leucine and phenylalanine (these were not increased by insulin so again another reason these are synergistic when used as you recall insulin requires all aminos readily available and usealble for maximized anabolism - in addition the rate at which aminos can be transported in/out of muscle cells is vital when discussing theoretical rates of anabolism, although this is vastly oversimplified of course)
- Increases hepatic IGF-1 production which appears to be critical component of insulin's action within skeletal muscle tissue
- Increases systemic IGF-1 leading to increased insulin sensitivity 

 

Things AAS are Great for:


- Increases mRNA levels of myosin heavy chain, IGF-1, and IGF-2 receptors in skeletal muscle tissue
- Increases intramuscular IGF-1 mRNA expression and decreased IGFBP4 implying an increased level of free IGF-1

 

Now, with that out of the way, you can see why insulin used without GH can be a fool's errand. Essentially you acquire all the risks associated with supraphysiological insulin administration with but a small fraction of its potential benefits.

Growth hormone ultimately leads to two main types of IGF-1...the first is called endocrine but most of us just call it systemic...if you go to the doctor, these are normally what gets measured. It happens in the liver and circulates throughout the body...it should be stated that there isn't much evidence that this type of IGF-1 has a direct relationship with hypertrophy though - surprisingly enough. The second type, and this is the cool one, is called autocrine/paracrine or as is often called "local IGF". This is the stuff that has local effects and when created by muscle cells it is very likely this has a direct result on rates of hypertrophy!

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Fair point.

 

Guys, Daz has gone to the trouble of writing a pretty comprehensive post (much of which I didn't understand, but I'm sure some of you will...) Let's show him the respect of not derailing this topic with rubbish.

 

Now, we were talking about growth whore moans hormones. ;-)

 

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52 minutes ago, Pseudonym said:

Fair point.

 

Guys, Daz has gone to the trouble of writing a pretty comprehensive post (much of which I didn't understand, but I'm sure some of you will...) Let's show him the respect of not derailing this topic with rubbish.

 

Now, we were talking about growth whore moans hormones. ;-)

 

 

Read it again... Basically hGH, or insulin are no good on their own.. AAS + hGH are synergistic as explained above..

hGH increases IGF-1.. Systemic IGF-1 doesn't appear to do much for hypertrophy, but autocrine/paracrine IGF-1 does..

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1 minute ago, Slinwarrior said:

Good post Daz, apologies for the prostie comments. I've run GH and slin together and definitely felt they worked better together than GH alone 

 

If you look at the data from the considerable research done, there seems to be little (if any) increase in skeletal muscle hypertrophy... Just intracellular water retention..

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Dang that's a lot of post...

 

What do you mean insulin increases MPS?

 

Do you mean it is increased in a dose-responsive manner?

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On 02/06/2018 at 10:41 AM, Kalidane said:

Dang that's a lot of post...

 

What do you mean insulin increases MPS?

 

Do you mean it is increased in a dose-responsive manner?

 

It's one of insulin's mechanism of actions, to increase muscle protein synthesis..

 

Along with Growth/gene expression, glycogen synthesis, fat synthesis, and glucose transport..

 

Effect of insulin on human skeletal muscle protein synthesis is modulated by insulin-induced changes in muscle blood flow and amino acid availability:

 In conclusion, physiological hyperinsulinemia promotes muscle protein synthesis as long as it concomitantly increases muscle blood flow, amino acid delivery and availability.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2804964/

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Cool, it's dose responsive.

 

I bet moderate hyperinsulinemia would enable the uptake of a shit ton of whey protein.  Wouldn't even need carbs in the mix.  Assuming test isn't rate limiting MPS.

 

Reduced leucine oxidation thanks to hGH doesn't seem interesting when there is an abundance of that amino acid from whey protein.

 

What about the combined effects of insulin, AAS and hGH on reducing the anabolic refractory period?  Never been able to find info on this.  It must be modulable.

 

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23 hours ago, Kalidane said:

Cool, it's dose responsive.

 

I bet moderate hyperinsulinemia would enable the uptake of a shit ton of whey protein.  Wouldn't even need carbs in the mix.  Assuming test isn't rate limiting MPS.

 

Reduced leucine oxidation thanks to hGH doesn't seem interesting when there is an abundance of that amino acid from whey protein.

 

What about the combined effects of insulin, AAS and hGH on reducing the anabolic refractory period?  Never been able to find info on this.  It must be modulable.

 

 

Of course you would need carbs, it's the response to insulin that opens GLUT4 transporter allowing glucose to enter cells..

 

What do you mean by anabolic refractory period..???

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So I pin a bunch of insulin then need endogenous insulin to get a result?  Doubt it.  Let the exogenous slin keep busy shuttling amino acids.   Though I can see that carb intake would be needed to avoid trashing blood sugars.

 

By refractory period, I'm talking about muscle protein synthesis having a refractory period.  

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