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A new look at dieting "gene activation"

Ask the modified question as:

"what does the body do when you consume excess calories with anabolic steroids, thyroid hormones, growth hormone, beta-adrenergic agonists, caffeine GLP-1RA-GIP with weight training"

Isn't that what most, not all, here are incorporating with excessive calories?
I doubt most are taking thyroid when trying to gain ?
 
.
 
How does that work exactly? I thought once you have muscle mass you can get away with less protein and still maintain
That is less it's under 1 gram per pound of lean body mass. Right now at my level of protein i won't get much bigger than 190, im happy with that. To add extra muscle i will have to up the protein as the body will be building new tissue not just maintaining existing muscle. You ever hear of John Medows famous trainer 260lbs he was maintaining that on 150 grams of protein. In his own words it takes less to maintain it that it does to build it
 
I doubt most are taking thyroid when trying to gain ?
I do believe I've read both @Beef_Stu_97 takes T4 year round, and @luki7788 takes T4 and T3 year round. I'd suspect neither are pushing factitious hyperthyroidism. And as @Sectør mentioned, a majority of individuals pushing higher doses of GH are tossing in T4.

My point was to the OP. He's asked some AI a very rudimentary query about excessive caloric intake and what it does to the human body. That question doesn't factor in reality. Such as if a person is sedentary, obese, active, or any sort of medication(s) -very small example of my premise to reask a realistic modified question.

Be more complex with questions to answers you so seek, you'll see the dynamics change immensely.
 
No this is demonstrably false

Look I agree that bulking is slow and takes forever and feels like you aren’t making progress

And I agree that dieting feels like you are getting more muscular every day and making awesome progress

But that’s because dieting you are stripping the fat, revealing the muscle, and feeling better about yourself

But you will never grow to your full potential on restricted calories
Theres no way to know for sure what i do know is in a low calorie state there is more hgh and igf1 in the blood stream and it stays active longer. When you bulk you lose insulin sensitivity and high amounts of circulating insulin blunt hgh before the liver can convert it to igf 1. Im done defending my theories ill let my progress pics speak for me. Im just trying to convince one guy on here because seeing is believing. Don't believe me so I gave the name and pics of one of my clients that turned pro...not good enough. So eventually someone will get tired of taking baby steps and shoot me a DM. Then everyone can see an impartial demonstration of the RSD
 
Theres no way to know for sure what i do know is in a low calorie state there is more hgh and igf1 in the blood stream and it stays active longer. When you bulk you lose insulin sensitivity and high amounts of circulating insulin blunt hgh before the liver can convert it to igf 1. Im done defending my theories ill let my progress pics speak for me. Im just trying to convince one guy on here because seeing is believing. Don't believe me so I gave the name and pics of one of my clients that turned pro...not good enough. So eventually someone will get tired of taking baby steps and shoot me a DM. Then everyone can see an impartial demonstration of the RSD

@luki7788 Is this true?
 
Theres no way to know for sure what i do know is in a low calorie state there is more hgh and igf1 in the blood stream and it stays active longer. When you bulk you lose insulin sensitivity and high amounts of circulating insulin blunt hgh before the liver can convert it to igf 1. Im done defending my theories ill let my progress pics speak for me. Im just trying to convince one guy on here because seeing is believing. Don't believe me so I gave the name and pics of one of my clients that turned pro...not good enough. So eventually someone will get tired of taking baby steps and shoot me a DM. Then everyone can see an impartial demonstration of the RSD
We do have a way of knowing

Not only does the personal experience of every bodybuilder who has ever lived overwhelmingly support this

But there are a plethora of studies showing it

 
We do have a way of knowing

Not only does the personal experience of every bodybuilder who has ever lived overwhelmingly support this

But there are a plethora of studies showing it

Yes, high insulin levels can blunt the effects of growth hormone (GH). Insulin and GH have complex, often opposing interactions in metabolic regulation. Elevated insulin levels, such as in hyperinsulinemia or insulin resistance, can interfere with GH signaling and its downstream effects, particularly on fat metabolism and insulin-like growth factor-1 (IGF-1) production. Here’s a concise breakdown:GH Signaling Inhibition: High insulin can suppress GH receptor expression and impair GH-induced JAK2-STAT5 signaling in the liver, reducing IGF-1 production, which mediates many of GH’s anabolic effects.Lipolysis Suppression: GH promotes fat breakdown (lipolysis), but insulin is a potent inhibitor of lipolysis. High insulin levels can override GH’s fat-mobilizing effects, limiting its ability to reduce fat mass.Metabolic Crosstalk: Chronic hyperinsulinemia, as seen in conditions like obesity or type 2 diabetes, can disrupt GH’s role in protein synthesis and glucose metabolism, further blunting its efficacy.
 
Yes, high insulin levels can blunt the effects of growth hormone (GH). Insulin and GH have complex, often opposing interactions in metabolic regulation. Elevated insulin levels, such as in hyperinsulinemia or insulin resistance, can interfere with GH signaling and its downstream effects, particularly on fat metabolism and insulin-like growth factor-1 (IGF-1) production. Here’s a concise breakdown:GH Signaling Inhibition: High insulin can suppress GH receptor expression and impair GH-induced JAK2-STAT5 signaling in the liver, reducing IGF-1 production, which mediates many of GH’s anabolic effects.Lipolysis Suppression: GH promotes fat breakdown (lipolysis), but insulin is a potent inhibitor of lipolysis. High insulin levels can override GH’s fat-mobilizing effects, limiting its ability to reduce fat mass.Metabolic Crosstalk: Chronic hyperinsulinemia, as seen in conditions like obesity or type 2 diabetes, can disrupt GH’s role in protein synthesis and glucose metabolism, further blunting its efficacy.
Right there in black and white. Every statement I've made I've backed with actual scientific studies
 
I disagree.

1. "In a low-calorie state, there is more HGH and IGF-1 in the blood and it remains active longer" - FALSE

how it looks in reality:
In a low-calorie state, pulsatile GH secretion does indeed increase, but IGF-1 decreases, it does not grow. This is due to a deficiency of energy substrates and a decrease in hepatic stimulation, because IGF-1 synthesis requires calories, protein and insulin.
In studies in people on a low-calorie diet (especially low-carbohydrate), IGF-1 levels drop significantly, despite increased GH.

there is even scientific evidence confirming this:
"Fasting increases GH secretion but reduces serum IGF-1 due to hepatic GH resistance."
→ (e.g., Ho et al., Endocrine Reviews, 1988)

2. "Insulin blunts HGH before the liver converts it to IGF-1" — FALSE AND CONTRARY TO PHYSIOLOGY
Reality:
Insulin is synergistic with GH in the context of IGF-1 production.
GH and insulin act together on hepatocytes and stimulate IGF-1 expression — insulin does not "block" GH action, but is required for proper GH → IGF-1 conversion.
Insulin may reduce endogenous GH secretion during acute spikes (e.g. after a meal), but this is quite different from blunting the action of GH in the circulation

Science:
"Hepatic IGF-1 synthesis is dependent not only on GH but also on sufficient insulin availability."
→ (Clemmons et al., J Clin Endocrinol Metab, 1998)

3. "Large amounts of insulin blunt hGH before the liver can convert it to IGF-1" — NON-PHYSIOLOGICAL

GH has a half-life of about 15–25 minutes, IGF-1 ~12–15 hours.
GH binds to the GH receptor on liver cells and there activates IGF-1 transcription. This process is not blocked by circulating insulin.
So on the contrary, insulin increases GH activity in the liver because it increases the sensitivity of liver cells to GH.

Moreover, GH in the context of excess insulin becomes more lipolytic and anti-insulin, which leads to a shift of energy substrates toward fat utilization — this is precisely the desired effect in the reduction or recomposition phases.

4. Argumentation style: "I will not defend my theories anymore, look at my photos" - SUBJECTIVE AND NOT SUBSTANTIVE

In bodybuilding, photos are important, but they cannot replace biology and the mechanisms of hormone action.
This approach is a typical example of the argument: "it works for me, so I'm right".
In reality, these effects can be due to many other factors (genetics, androgen doses, training period, diet, rest, etc.), and not to a single theory about IGF-1 or insulin.
 
You are all arguing with someone who thinks that 1400 calories is the “best method to gain muscle and stay lean”.

Keep that in mind… this may not be worth the effort here at this point lol

Right...and at the same time I think that is where we and him are talking around each other. This thread went from that is the best way to build muscle to "you can maintain a very lean (contest ready essentially) look with a good amount of muscle once you've built a lot of muscle because it doesn't take much to maintain".

At this point, I don't actually know what he is even arguing for or against.
 
Right...and at the same time I think that is where we and him are talking around each other. This thread went from that is the best way to build muscle to "you can maintain a very lean (contest ready essentially) look with a good amount of muscle once you've built a lot of muscle because it doesn't take much to maintain".

At this point, I don't actually know what he is even arguing for or against.
Because he has no clue either…
 
Started off as an interesting debate for me then it turned 💩 run arounds….
At this point wtf are we even trying to discuss. 🤦🏻‍♂️
 

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