HGH Peak - Subcutaneously/ Intramuscularly

Sure it’s normal but less is best you’ll see by mirror and bodyfat responds too food etc currently on 12iu gh too and just prefer lower than normal blood sugars personally

But 80s is good
I guess if I would add some metformin I could get my fasted blood glucose levels down to 70 in the morning but I honestly don't see the point in adding it. Considering that I am bulking and "only" on 0.5mg semaglutide per week my fasted numbers are actually pretty good.
 
Sure it’s normal but less is best you’ll see by mirror and bodyfat responds too food etc currently on 12iu gh too and just prefer lower than normal blood sugars personally

But 80s is good
No, fasting hypoglycemia is a bad thing and it's a myth that hypoglycemia enhances fat loss or body composition.
 
I guess if I would add some metformin I could get my fasted blood glucose levels down to 70 in the morning but I honestly don't see the point in adding it. Considering that I am bulking and "only" on 0.5mg semaglutide per week my fasted numbers are actually pretty good.
Yeah especially for bulking it’s amazing most are high 90 hitting 100 lol
 
just go with hcb1c ?
Why are us bodybuilders all about insulin sensitivity why do you think this
Insulin sensitivity and blood glucose levels are associated, but are not on in the same. We want high insulin sensitivity in skeletal muscle, but insulin resistance in fat cells. Insulin sensitivity is a complex phenomenon with central, peripheral, and endocrine factors beyond merely blood glucose.

HbA1C is indeed more useful a proxy for long-term health monitoring than blood glucose readings. As a practical matter, I generally adjust rhGH dose by nadir values and HbA1C (to avoid hypoglycemia, and to refer to chronic blood glucose stability within a healthy range)
 
Insulin sensitivity and blood glucose levels are associated, but are not on in the same. We want high insulin sensitivity in skeletal muscle, but insulin resistance in fat cells. Insulin sensitivity is a complex phenomenon with central, peripheral, and endocrine factors beyond merely blood glucose.
The great Matt Porter had a theory that rhgh makes fat cells resistant then we combine metformin other insulin sensitive substance that specifically targets purely muscle tissue going by study’s then fat burning (clen) metabolism boosting substance (t4) (t3) high protein hot peppers capsaicin (Carolina Reaper) and you’ll be a fat burner protein synthesis nitrogen Retention machine
 
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The great Matt Porter had a theory that rhgh makes fat cells resistant then we combine metformin other insulin sensitive substance that specifically targets purely muscle tissue going by study’s then fat burning (clen) metabolism boosting substance (t4) (t3) high protein hot peppers capsaicin (Carolina Reaper) and you’ll be a fat burner protein synthesis nitrogen Retention machine
Metformin is a biguanide, its mechanisms of action are not completely understood, but rather than specifically targeting purely muscle tissue, its primary sites of action for insulin sensitizing effects (a somewhat minor mechanism besides its primary glucose disposal actions) are actually the liver & gut (primarily by AMPK activation). Metformin reduces hepatic lipid stores & increases intestinal GLP-1 activity.

Its effects on skeletal muscle are generally unfavorable, as AMPK activation inhibits mTORC1/P70S6K1 phophorylation, thereby preventing the adaptive preferential shift from type I to type IIA fibers (resulting in a tendency towards reduced strength gains) & abrogates the endurance training enhancement of insulin sensitivity.

Metformin is generally beneficial in combination with rhGH, but requires some balancing of tradeoffs/risks. The incretins (e.g., GIP & GLP-1 agonists) are generally better.
 
Metformin is a biguanide, its mechanisms of action are not completely understood, but rather than specifically targeting purely muscle tissue, its primary sites of action for insulin sensitizing effects (a somewhat minor mechanism besides its primary glucose disposal actions) are actually the liver & gut (primarily by AMPK activation). Metformin reduces hepatic lipid stores & increases intestinal GLP-1 activity.

Its effects on skeletal muscle are generally unfavorable, as AMPK activation inhibits mTORC1/P70S6K1 phophorylation, thereby preventing the adaptive preferential shift from type I to type IIA fibers (resulting in a tendency towards reduced strength gains) & abrogates the endurance training enhancement of insulin sensitivity.
But on hgh insulin 3-5gram gear I don’t think the mtor issue or reduced binding androgen defects would matter as we know metformin hgh the igf1 is higher and as a bodybuilder who’d built his strength base it means nothing to me and it won’t over shadow tren anadrol halo in and 2g test in a stack.
 
But on hgh insulin 3-5gram gear I don’t think the mtor issue or reduced binding androgen defects would matter as we know metformin hgh the igf1 is higher and others have had 400-500 igf1 score on 1500mg metformin
With slin in the mix, Metformin is like pissing into the wind. Indeed, 3 - 5 g of AAS would call for greater care in avoiding hypoglycemia, as well.
 
Does it? How?

I agree that insulin is bad for insulin sensitivity, I wrote about this here: MesoRx Article

How would Metformin ameliorate exogenous insulin's effects on insulin sensitivity?
It won’t completely you’d need to cycle off inuslin at least but semaglutide and metformin gave me hba1c of 3.3 and that’s on 12iu hgh so it’s definitely working for me

And I pin gh 5 times around meals so frequent Shots and not resistant I’ve read where you’ve said pin all at once
 
It won’t completely you’d need to cycle off inuslin at least but semaglutide and metformin gave me hba1c of 3.3 and that’s on 12iu hgh so it’s definitely working for me

And I pin gh 5 times around meals so frequent Shots and not resistant I’ve read where you’ve said pin all at once
You've got things figured out it would seem. Get back to me when you can elaborate on how and why Metformin prevents insulin resistance a la insulin toxicity, and how your use of drugs demonstrates this with particularity. I think there may also be an additional claim made that 5X daily rhGH administration is superior or equal to 1X for insulin sensitivity, if you wouldn't mind walking me through that in a case where insulin is not used.
 
You've got things figured out it would seem. Get back to me when you can elaborate on how and why Metformin prevents insulin resistance a la insulin toxicity, and how your use of drugs demonstrates this with particularity.
also type2 this was a good read that you put on deca finished that off today. Nandrolone Data (including joint pain relief mechanisms [by Type-IIx])

to the metformin
sorry you are correct lol apologies so why the hell am I using it lol should I just stop since semaglutide is better

Study here

Results:​

A total of 11 trials with a total of 865 participants met the inclusion criteria. Participants were between 4 and 18 years old. The time span of these studies ranged from 2001 to 2017. The daily dose of metformin was from 1000 mg to 2000 mg and the duration of intervention was 8 weeks to 18 months. Compared with placebo, metformin with lifestyle intervention reduced the level of LDL-C (P = 008, MD = - 4.29, 95% confidence interval [CI]: -7.45, -1.12). However, there was no obvious differences in improving insulin resistance, fasting glucose, and HDL-C.

Conclusion:​

Metformin may improve the level of LDL-C, but it has no significant effect on insulin resistance. The use of metformin may be a new approach to lipid metabolism management in overweight or obese children and adolescents.
 
I guess if I would add some metformin I could get my fasted blood glucose levels down to 70 in the morning but I honestly don't see the point in adding it. Considering that I am bulking and "only" on 0.5mg semaglutide per week my fasted numbers are actually pretty good.
Semaglutide, according to my information, should inhibit appetite or rather even increase satiety and also slow down stomach emptying. Do you feel these effects? If so, would you recommend semaglutide at all if you plan to eat a lot of food?
 
Semaglutide, according to my information, should inhibit appetite or rather even increase satiety and also slow down stomach emptying. Do you feel these effects? If so, would you recommend semaglutide at all if you plan to eat a lot of food?
I would not recommend it while bulking or eating a lot of food for another reason. Every time I eat a big meal or even eat too many smaller meals I get sick.
 
I would not recommend it while bulking or eating a lot of food for another reason. Every time I eat a big meal or even eat too many smaller meals I get sick.
I am a big supporter of optimizing insulin sensitivity. However, these effects on hunger/ stomach are useless to me both in a build up and during the diet.
 
I am a big supporter of optimizing insulin sensitivity. However, these effects on hunger/ stomach are useless to me both in a build up and during the diet.
Appetite suppression is only a side effect of GLP-1 receptor agonists like semaglutide and these sides fade away over time. So if you slowly work you way up to 0.5mg and stay there for a couple weeks it will get better and better quickly.
 
How slowly would you work your way up here? Start with 0.1mg - increase by 0.1mg every week until you reach 0.5mg? And would you say your appetite is back to almost the same state as before you started?
 
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