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Two New and Very Powerful Substances

Peter Bond wrote a highly pertinent article here: Where are the myostatin inhibitors?

I would mention that good ol' testosterone attenuates Myostatin (decreases Mst expression and enhances β-catenin signaling, thereby ↑Fst expression, thereby inhibiting Mst) and functions via myriad other anabolic pathways.

Attenuation of myostatin has also been highlighted as an important factor by which β2-agonists (e.g., Clen) elicit hypertophy.

Myostatin does seem an interesting target, to induce hypertrophy & hyperplasia, as it is pluripotent.
 
It could possibly be done
But unsure if the raws would be expensive
You need mice/rabbits and some basic laboratory equipment/knowledge to raise antibodies.

The issue would be getting the antigen you want to raise them against.
 
Peter Bond wrote a highly pertinent article here: Where are the myostatin inhibitors?

I would mention that good ol' testosterone attenuates Myostatin (decreases Mst expression and enhances β-catenin signaling, thereby ↑Fst expression, thereby inhibiting Mst) and functions via myriad other anabolic pathways.

Attenuation of myostatin has also been highlighted as an important factor by which β2-agonists (e.g., Clen) elicit hypertophy.

Myostatin does seem an interesting target, to induce hypertrophy & hyperplasia, as it is pluripotent.
I've often wondered how the myostatin inhibition could be isolated to just skeletal muscle tissue.
 
I've often wondered how the myostatin inhibition could be isolated to just skeletal muscle tissue.
I won't be able to provide any references or anything as I am going off memory. However the few kids that were born with no myostatin expression had pretty normal hearts and the concerns that their cardiac tissue would be adversely affected had proven mostly unwarranted. Also some people had noted that myostatin inhibitors would kind of automatically target skeletal muscle and not really impact the heart. Why and through what mechanism? No idea really....

But at the very least one can assume that the scientists at Big Pharma did not look at these and say "this will hit the cardiac tissue right away and make people's hearts blow up". Had that been the case they'd not have bothered investing into these in the first place.
 
I've often wondered how the myostatin inhibition could be isolated to just skeletal muscle tissue.
Myostatin is only expressed in skeletal muscle. I swear I'm having déjà vu because I thought we had this conversation before.
 
Myostatin is only expressed in skeletal muscle. I swear I'm having déjà vu because I thought we had this conversation before.
I've never looked into myostatin to any great degree. I'm not sure if we ever discussed myostatin although it wouldn't surprise me. It's very odd this TGF-β factor. Cardiac patients show a large amount of myostatin suggesting the heart is causing heart and skeletal muscle atrophy while inhibition of myostatin does not produce the same result in both types of muscle tissue. Leads me to conclude that myostatin has varying degrees of action on specific muscle cell types and in atrophy or hypertrophy.
 
I've never looked into myostatin to any great degree. I'm not sure if we ever discussed myostatin although it wouldn't surprise me. It's very odd this TGF-β factor. Cardiac patients show a large amount of myostatin suggesting the heart is causing heart and skeletal muscle atrophy while inhibition of myostatin does not produce the same result in both types of muscle tissue. Leads me to conclude that myostatin has varying degrees of action on specific muscle cell types and in atrophy or hypertrophy.
I have seen something along the lines of decreasing Mst being associated with decreased GDF11 (which may be related to cardiomyopathy/cardiac hypertrophy). But MSTN (gene) is expressed in type I & II fibers in human skeletal muscle exclusively. I can send you my notes on Myostatin (as it relates to androgens) if you're interested, let me know. It's interesting IMO.
 
Myostatin is only expressed in skeletal muscle. I swear I'm having déjà vu because I thought we had this conversation before.
Lots of doctors say that it can “ it can negatively influence cardiac muscle hypertrophy.”
 
Lots of doctors say that it can “ it can negatively influence cardiac muscle hypertrophy.”
The confusion arises from the high sequence homology between MSTN (GDF8) & GDF11, and the difficulty in producing viable recombinant GDF11 (that is in fact pure; rather than containing fragments of MSTN & vice versa). The upshot of this difficulty resulted in confusion in the reported outcomes in the study of MSTN & GDF11. See the attached image for an illustration of the high sequence homology between the two.

Both MSTN & GDF11 are members of the TGFβ superfamily but serve distinct functions (see Suh, J., & Lee, Y.-S. (2020). Similar sequences but dissimilar biological functions of GDF11 and myostatin. Experimental & Molecular Medicine. doi:10.1038/s12276-020-00516-4).

Whereas loss of MSTN results in hypermuscularity, GDF11 deletion results in abnormal organ development (e.g., myocardium/heart) & skeletal patterning. The GDF11-null phenotype results as well in perinatal lethality (early death), whereas the MSTN-null phenotype results in long term viability. Consider as well the clinical trial data and reported side effects in humans: cardiac hypertrophy/myocardial or other organ growth are not a consequence of the trialled MSTN inhibitors.

Sequence homology between MSTN & GDF11:
Sequence-homology-Myostatin-vs-GDF11.ProM.jpg
 
I have seen something along the lines of decreasing Mst being associated with decreased GDF11 (which may be related to cardiomyopathy/cardiac hypertrophy). But MSTN (gene) is expressed in type I & II fibers in human skeletal muscle exclusively. I can send you my notes on Myostatin (as it relates to androgens) if you're interested, let me know. It's interesting IMO.
Sure. Send anything. You have my email. Oh and OT: I'm still researching the Venn diagram that is the HPTA and the HPA axis. Whoa. Quite a lot there. The thing is that while we have a shortage of studies regarding AAS and their use, the adrenal axis and glucocorticoids/adrenaline are the exact opposite - studied to death! Thousands of available studies and published articles.
 
Sure. Send anything. You have my email. Oh and OT: I'm still researching the Venn diagram that is the HPTA and the HPA axis. Whoa. Quite a lot there. The thing is that while we have a shortage of studies regarding AAS and their use, the adrenal axis and glucocorticoids/adrenaline are the exact opposite - studied to death! Thousands of available studies and published articles.
I'll send you over what I have. That is greatly appreciated wrt OT - I'd love to wrap my mind around that. I'll tie in with your product/conclusion as best as I can what I know about AAS and glucocorticoids also (i.e., it is my working hypothesis that AAS myotrophy is principally a result of increasing intramuscular IGF-I activity & glucocorticoid modulation [naturally most effects are turned on by AR activation; but not all]; and the effects of AAS on glucocorticoids vary dramatically on a per- compound basis). I think we can even work towards a model of understanding different compounds better than currently understood (i.e., through the myopic lens of testosterone).
 
I'll send you over what I have. That is greatly appreciated wrt OT - I'd love to wrap my mind around that. I'll tie in with your product/conclusion as best as I can what I know about AAS and glucocorticoids also (i.e., it is my working hypothesis that AAS myotrophy is principally a result of increasing intramuscular IGF-I activity & glucocorticoid modulation [naturally most effects are turned on by AR activation; but not all]; and the effects of AAS on glucocorticoids vary dramatically on a per- compound basis). I think we can even work towards a model of understanding different compounds better than currently understood (i.e., through the myopic lens of testosterone).
That's my goal as well. Glucocorticoid modulation is without a doubt an indispensable attribute compound per compound as underactive HPAA means inflammation and poor immune system ("test flu", et al) while overactive HPAA means increased epinephrine (anxiety/depression common with AAS) and hyperglycemia right up to glucocorticoid-induced diabetes mellitus (GIDM). Then you add that the adrenal cortex also produces testosterone while the medulla and reticulum produce other chems and you have quite a crossover. Additionally, the GR and the AR both activate a common set of genes but not entirely. There's an overlap. Much to distill and in the process now.
 

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