with some of the smartest minds ive seen on this board how is everybody not understanding the action of this drug. It makes you sensitive to insulin, hmm what others things do that , low carbs, cardio, yep you figured it out dieting. Which for building mass is counter productive. I get everyone wants to do two things at once believe me if I could I would surf the net while im driving, or get work done while my gf is talking to me but we all know that you will miss some shit. But yea you can still do it lol and if your girl has an attitude like mine you better be hoping you paid attention.
with some of the smartest minds ive seen on this board how is everybody not understanding the action of this drug. It makes you sensitive to insulin, hmm what others things do that , low carbs, cardio, yep you figured it out dieting. Which for building mass is counter productive. I get everyone wants to do two things at once believe me if I could I would surf the net while im driving, or get work done while my gf is talking to me but we all know that you will miss some shit. But yea you can still do it lol and if your girl has an attitude like mine you better be hoping you paid attention.
metformin decreases carbohydrate absorption to a degree. this could also be the reason for having stomach issues.
i always get the shits and cant stop farting when i use metformin WHILE EATING HIGH CARBS. low carbs = much less problems
this also makes metformin a suboptimal choice for bulking imo.
look into berberine, it has none of the sides but all the benefits and then some.
maybe you could rotate metformin and berberine for dieting/bulking too.
Okay guys, so do we know if it inhibits gluconeogenesis completely or only partially? Any more info regarding IGF-1 blunt?
If we could know the answer for these questions I'd say this drug is freakin wonderful year round...
with some of the smartest minds ive seen on this board how is everybody not understanding the action of this drug. It makes you sensitive to insulin, hmm what others things do that , low carbs, cardio, yep you figured it out dieting. Which for building mass is counter productive. I get everyone wants to do two things at once believe me if I could I would surf the net while im driving, or get work done while my gf is talking to me but we all know that you will miss some shit. But yea you can still do it lol and if your girl has an attitude like mine you better be hoping you paid attention.
metformin decreases carbohydrate absorption to a degree. this could also be the reason for having stomach issues.
i always get the shits and cant stop farting when i use metformin WHILE EATING HIGH CARBS. low carbs = much less problems
this also makes metformin a suboptimal choice for bulking imo.
look into berberine, it has none of the sides but all the benefits and then some.
maybe you could rotate metformin and berberine for dieting/bulking too.
If you are using insulin sensitizers during bulking you are using things that are just like metformin.
This goes to SMA as well. Why do people like JM keep saying insulin sensitizing agents are great during bulks? Then why would metformin be a poor choice?
Curious
If you are using insulin sensitizers during bulking you are using things that are just like metformin.
This goes to SMA as well. Why do people like JM keep saying insulin sensitizing agents are great during bulks? Then why would metformin be a poor choice?
Curious
If you are using insulin sensitizers during bulking you are using things that are just like metformin.
This goes to SMA as well. Why do people like JM keep saying insulin sensitizing agents are great during bulks? Then why would metformin be a poor choice?
Curious
TBH tho although I know my anatomy, physiology i am not very knowledgeable with. here are some cliffs maybe you can cypher some of this.
The molecular mechanism of metformin is incompletely understood: inhibition of the mitochondrial respiratory chain (complex I), activation of AMP-activated protein kinase (AMPK), inhibition of glucagon-induced elevation of cyclic adenosine monophosphate (cAMP), and consequent activation of protein kinase A (PKA), inhibition of mitochondrial glycerophosphate dehydrogenase, and an effect on gut microbiota have been proposed as potential mechanisms.Activation of AMPK, an enzyme that plays an important role in insulin signaling, whole body energy balance, and the metabolism of glucose and fats,[93] was required for metformin's inhibitory effect on the production of glucose by liver cells.
The mechanism by which biguanides increase the activity of AMPK remains uncertain; however, metformin increases the concentration of cytosolic adenosine monophosphate (AMP) (as opposed to a change in total AMP or total AMP/adenosine triphosphate).[96] Increased cellular AMP has also been proposed to explain the inhibition of glucagon-induced increase in cAMP and activation of PKA.[90] Metformin and other biguanides may antagonize the action of glucagon, thus reducing fasting glucose levels.[97] Metformin also induces a profound shift in the faecal microbial community profile in diabetic mice and this may contribute to its mode of action possibly through an effect on glucagon-like peptide-1 secretion.[91]
In addition to suppressing hepatic glucose production, metformin increases insulin sensitivity, enhances peripheral glucose uptake (by inducing the phosphorylation of GLUT4 enhancer factor), decreases insulin-induced suppression of fatty acid oxidation,[98] and decreases absorption of glucose from the gastrointestinal tract.The increase in insulin binding after metformin treatment has also been demonstrated in patients with NIDDM [100]. AMPK probably also plays a role, as metformin administration increases AMPK activity in skeletal muscle.[101] AMPK is known to cause GLUT4 deployment to the plasma membrane, resulting in insulin-independent glucose uptake.
Some more benefits of using Metformin: it reduces cholesterol while raise HDL, also it only increase insulin sensitivity in skeletal muscle not adipocytes.
This is great during AAS, GH, Insulin cycle.
I'm gonna keep using it year round, will post results...
If you are using insulin sensitizers during bulking you are using things that are just like metformin.
This goes to SMA as well. Why do people like JM keep saying insulin sensitizing agents are great during bulks? Then why would metformin be a poor choice?
Curious
TBH tho although I know my anatomy, physiology i am not very knowledgeable with. here are some cliffs maybe you can cypher some of this.
The molecular mechanism of metformin is incompletely understood: inhibition of the mitochondrial respiratory chain (complex I), activation of AMP-activated protein kinase (AMPK), inhibition of glucagon-induced elevation of cyclic adenosine monophosphate (cAMP), and consequent activation of protein kinase A (PKA), inhibition of mitochondrial glycerophosphate dehydrogenase, and an effect on gut microbiota have been proposed as potential mechanisms.Activation of AMPK, an enzyme that plays an important role in insulin signaling, whole body energy balance, and the metabolism of glucose and fats,[93] was required for metformin's inhibitory effect on the production of glucose by liver cells.
The mechanism by which biguanides increase the activity of AMPK remains uncertain; however, metformin increases the concentration of cytosolic adenosine monophosphate (AMP) (as opposed to a change in total AMP or total AMP/adenosine triphosphate).[96] Increased cellular AMP has also been proposed to explain the inhibition of glucagon-induced increase in cAMP and activation of PKA.[90] Metformin and other biguanides may antagonize the action of glucagon, thus reducing fasting glucose levels.[97] Metformin also induces a profound shift in the faecal microbial community profile in diabetic mice and this may contribute to its mode of action possibly through an effect on glucagon-like peptide-1 secretion.[91]
In addition to suppressing hepatic glucose production, metformin increases insulin sensitivity, enhances peripheral glucose uptake (by inducing the phosphorylation of GLUT4 enhancer factor), decreases insulin-induced suppression of fatty acid oxidation,[98] and decreases absorption of glucose from the gastrointestinal tract.The increase in insulin binding after metformin treatment has also been demonstrated in patients with NIDDM [100]. AMPK probably also plays a role, as metformin administration increases AMPK activity in skeletal muscle.[101] AMPK is known to cause GLUT4 deployment to the plasma membrane, resulting in insulin-independent glucose uptake.