Myostatin - any future potential?

[Peter LeDrew]

Originally Posted by Trans_Isomer

The only one I remember was from Champion nutrition and Biotest

Pinnacle Juiced Protein with Myo-Zap!!!

http://www.nic************/juiced-pr...ozap-79837.htm
I was swindled many years back buying a couple tubs when I was 20, but at least I got them very cheap.

I think there was a study done by Dr. Ziegenfuss... oh wait, here is an interview with the Biotest clan and him on their newest product back then which, you guessed it, contained Myostat or CSP-3... some lofty promises eh!
http://figureathlete.tmuscle.com/fre...tin_roundtable

Not sure we should trust anyone in this industry!

[Dr.Dave1]

leptin plays a role in myostatin regulation

PLoS One. 2009 Sep 4;4(9):e6808.
Leptin administration favors muscle mass accretion by decreasing FoxO3a and increasing PGC-1alpha in ob/ob mice.
S?inz N, Rodr?guez A, Catal?n V, Becerril S, Ram?rez B, G?mez-Ambrosi J, Fr?hbeck G.

Absence of leptin has been associated with reduced skeletal muscle mass in leptin-deficient ob/ob mice. The aim of our study was to examine the effect of leptin on the catabolic and anabolic pathways regulating muscle mass. Gastrocnemius, extensor digitorum longus and soleus muscle mass as well as fiber size were significantly lower in ob/ob mice compared to wild type littermates, being significantly increased by leptin administration (P<0.001). This effect was associated with an inactivation of the muscle atrophy-related transcription factor forkhead box class O3 (FoxO3a) (P<0.05), and with a decrease in the protein expression levels of the E3 ubiquitin-ligases muscle atrophy F-box (MAFbx) (P<0.05) and muscle RING finger 1 (MuRF1) (P<0.05). Moreover, leptin increased (P<0.01) protein expression levels of peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha), a regulator of muscle fiber type, and decreased (P<0.05) myostatin protein, a negative regulator of muscle growth. Leptin administration also activated (P<0.01) the regulators of cell cycle progression proliferating cell nuclear antigen (PCNA) and cyclin D1, and increased (P<0.01) myofibrillar protein troponin T. The present study provides evidence that leptin treatment may increase muscle mass of ob/ob mice by inhibiting myofibrillar protein degradation as well as enhancing muscle cell proliferation.

effect of modulating myostatin in old mice - beneficial cardiac effects in addition to increase in muscularity

Aging Cell. 2009 Aug 6.
Effects of myostatin deletion in aging mice.
Morissette MR, Stricker JC, Rosenberg MA, Buranasombati C, Levitan EB, Mittleman MA, Rosenzweig A.
Summary Inhibitors of myostatin, a negative regulator of skeletal muscle mass, are being developed to mitigate aging-related muscle loss. Knock-out (KO) mouse studies suggest myostatin also affects adiposity, glucose handling and cardiac growth. However, the cardiac consequences of inhibiting myostatin remain unclear. Myostatin inhibition can potentiate cardiac growth in specific settings (Morissette et al., 2006), a concern because of cardiac hypertrophy is associated with adverse clinical outcomes. Therefore, we examined the systemic and cardiac effects of myostatin deletion in aged mice (27-30 months old). Heart mass increased comparably in both wild-type (WT) and KO mice. Aged KO mice maintained twice as much quadriceps mass as aged WT; however, both groups lost the same percentage (36%) of adult muscle mass. Dual-energy X-ray absorptiometry revealed increased bone density, mineral content, and area in aged KO vs. aged WT mice. Serum insulin and glucose levels were lower in KO mice. Echocardiography showed preserved cardiac function with better fractional shortening (58.1% vs. 49.4%, P = 0.002) and smaller left ventricular diastolic diameters (3.41 vs. 2.71, P = 0.012) in KO vs. WT mice. Phospholamban phosphorylation was increased 3.3-fold in KO hearts (P < 0.05), without changes in total phospholamban, sarco(endo)plasmic reticulum calcium ATPase 2a or calsequestrin. Aged KO hearts showed less fibrosis by Masson's Trichrome staining. Thus, myostatin deletion does not affect aging-related increases in cardiac mass and appears beneficial for bone density, insulin sensitivity and heart function in senescent mice. These results suggest that clinical interventions designed to inhibit skeletal muscle mass loss with aging could have beneficial effects on other organ systems as well.

[Robboe]

Originally Posted by Dr.Dave1

leptin plays a role in myostatin regulation

This seems logical. If energy state is low the body has no interest in building energy-costly muscle.

[neuron]

Originally Posted by Robboe

This seems logical. If energy state is low the body has no interest in building energy-costly muscle.

The leptin receptor mediates numerous growth cascades:

http://www.jci.org/articles/view/30453/figure/1

[Robboe]

Originally Posted by neuron

The leptin receptor mediates numerous growth cascades:

http://www.jci.org/articles/view/30453/figure/1

Already saw this and saved it for reading from teh other thread.

[neuron]

Originally Posted by Robboe

Already saw this and saved it for reading from teh other thread.

Leptins predominant role in the brain is to signal satiety - which means the body has met its energetic needs and is in a state of anabolism.

[GeneGnomeX]

Originally Posted by Dr.Dave1

leptin plays a role in myostatin regulation



effect of modulating myostatin in old mice - beneficial cardiac effects in addition to increase in muscularity

This probably wouldn't happen in a healthy model though. With obesity and immobilization basal atrophic gene expressions are increased and all muscle fibers are decreased, so increasing mitochondrial gene expressions also increases type I fibers, but in normal models I wouldn't expect a further increase in mass. I recall obese humans also have increased myostatin expression. So leptin may not have much of an effect when these atrophic pathways are not as active.

[Robboe]

Originally Posted by neuron

Leptins predominant role in the brain is to signal satiety - which means the body has met its energetic needs and is in a state of anabolism.

That makes total sense, especially during periods of scarcity when energy levels are low.

[illilian]

www.novoseek.com

do a myostatin search and it goes to several recent research documents

[illilian]

and this document is a study on the relationship between myostatin and tendons.

http://www.informaworld.com/smpp/con...77190903052539


i wonder if there's a way to "re-program" the function of myostatin.

[Robboe]

Originally Posted by illilian

i wonder if there's a way to "re-program" the function of myostatin.

Affordably during your lifetime? Unlikely.

[JeffD729]

What I would like to know is after discontinuance of the myostatin peptide will there be a negative feedback loop like there is with every other pharmaceutical after use when discontinued, due to the fact that your body will take countermeasures when it notices a surplus of any hormone to maintain homeostasis. So after you stop using this drug or are taking it past the point of realizing results, won't your body elevate myostatin binding protein when it notices there is an elevation of myostatin inhibition. Like when you use AAS longer thank 4-6 weeks, or you come off, your body elevates catibolic hormones or estrogen when aromitizing AAS is used to maintain homeostasis. This creates a kind of dependence on the drug or a lag period while off. If this applicable to this peptide, which only seems to make sense, how long does the lag period last. That would suck to have elevated myostatin once I get off. So, won't you have to continue the drug after an off period to continually see results and not diminish the results you gained from the previous cycle? There are established ways to come off other drugs such ass AAS-clomid, HCG, and Letrozole. For IGF-1 and HGH. GHRP-6, Hexarelin, and CJC-1295. There are no protocols for the myostatin peptide. This frightens me and anyone who's going to be the guinea pig.

[dallasmsl]

Good points. Never thought of that. Of course, it hasn't been tested yet so know one knows. At the age of 50, I still have no problems being the guinea pig.

[Patrick Arnold]

Originally Posted by JeffD729

What I would like to know is after discontinuance of the myostatin peptide will there be a negative feedback loop like there is with every other pharmaceutical after use when discontinued, due to the fact that your body will take countermeasures when it notices a surplus of any hormone to maintain homeostasis. So after you stop using this drug or are taking it past the point of realizing results, won't your body elevate myostatin binding protein when it notices there is an elevation of myostatin inhibition. Like when you use AAS longer thank 4-6 weeks, or you come off, your body elevates catibolic hormones or estrogen when aromitizing AAS is used to maintain homeostasis. This creates a kind of dependence on the drug or a lag period while off. If this applicable to this peptide, which only seems to make sense, how long does the lag period last. That would suck to have elevated myostatin once I get off. So, won't you have to continue the drug after an off period to continually see results and not diminish the results you gained from the previous cycle? There are established ways to come off other drugs such ass AAS-clomid, HCG, and Letrozole. For IGF-1 and HGH. GHRP-6, Hexarelin, and CJC-1295. There are no protocols for the myostatin peptide. This frightens me and anyone who's going to be the guinea pig.

you would have to keep taking it. thats why the option of gene therapy is much more practical. the insertion of genes that control myostatin levels in muscles results in an ongoing effect without having to take continued regular dosing of a drug

[nobodyhome]

Originally Posted by Patrick Arnold

you would have to keep taking it. thats why the option of gene therapy is much more practical. the insertion of genes that control myostatin levels in muscles results in an ongoing effect without having to take continued regular dosing of a drug

The idea is that reducing myostatin levels would supposedly lead to significant muscle hyperplasia, right? So what would happen if you stopped taking it? All of those new cells would just die?

****, on the other hand, if you stopped taking it, what would happen if your myostatin levels rose sky high on the rebound? Would you go through a period where you had less muscle tissue than you started with?

[Patrick Arnold]

Originally Posted by nobodyhome

The idea is that reducing myostatin levels would supposedly lead to significant muscle hyperplasia, right? So what would happen if you stopped taking it? All of those new cells would just die?

****, on the other hand, if you stopped taking it, what would happen if your myostatin levels rose sky high on the rebound? Would you go through a period where you had less muscle tissue than you started with?

most of the research i have read about myostatin in adults indicate increased muscle hypertrophy, not hyperplasia. But even if there was hyperplasia there is evidence that these cells have the ability to revert back to quiescent satellite cells (sort of the hyperplasia in reverse).

simply put, your body always attempts to return to homeostasis. But this does necessarily mean a compensatory rebound below baseline is inevitable

[benny.sohr]

Originally Posted by Patrick Arnold

you seem to trust retailers made up science

patrick,

what do you think about prosoucrce's myo-t12 product? And what about the clinical studies are they bs? and is the other guy talking about shooting up (IM) this supplement???

[JeffD729]

Yes, Intramuscular. I'm talking about the myostatin propeptide. Check it out on purepeptides.

[Patrick Arnold]

Originally Posted by benny.sohr

patrick,

what do you think about prosoucrce's myo-t12 product? And what about the clinical studies are they bs? and is the other guy talking about shooting up (IM) this supplement???

as far as i know there was only one study showing myostatin changes in blood of one person

the stuff is certainly not purified enough to inject

i would never count anything out but i think its a longshot that this stuff will do anything

[mrbeverage]

there has been a substance out for years now called Humanofort, it is also made from fertilized egg yolk, but its purpose was to raise IGF1, amongst other things. is this the same substance as the myo T12?, unlike the ********* product Humanofort is cheap.

Dietary Supplement. Naturally boosts testosterone levels! Helps reduce recovery time! Humanofort is a powerful, pharmaceutically standardized extract from fertilized chicken eggs containing naturally occurring IGF-1, IGF-2, FGF (fibroblast growth factors), NGF (nerve growth factors), EGF (epidermal growth factors), and CTGF (connective tissue growth factors) with unique cell stimulating properties. (Notice: This statement has not been evaluated by the FDA. This product is not intended to diagnose, treat, cure or prevent any disease.) Humanofort is formulated to: Naturally increase testosterone and growth hormone levels. Naturally decrease cortisol levels, oxidative stress, and decrease recovery time. Balance adrenal functions. Due to active growth factors, many users report a boost in sexual drive, improved mood and sleep, and improved fat loss after using Humanofort for at least 3 weeks

Nutrition Facts
Serving Size 1 capsule
Servings Per Container 60

Amount Per Serving

% Daily Value


Humanofort 100 mg


*percent Daily Values are based on a 2,000 calorie diet.

Ingredients: Humanofort: Embryonic Peptide Matrix Yielding Naturally Occurring IGF-1, IGF-2, FGF (Fibroblast Growth Factors), NGF (Nerve Growth Factors), EGF (Epidermal Growth Factors), CTGF (Connective Tissue Growth Factors).

[JeffD729]

Bros, anything like this taken orally is gonna be greatly deactivated. Same with HGH. You see all of the countless oral HGH supplements OTC that don't do crap. I'm pretty sure all growth factors need to be injected.I took that celldyne folstaxan crap and it didn't do anything for me. I order two jugs, payed 200 bucks, and was only sent one. I don't even know the story on that product or that little scammer Rick Greene anymore. On his website it shows a study conducted to prove its efectiveness. Notice how it only states a decrease in serum myostatin by 34% or whatever. Nowhere does it state that as a result there was an increase in muscle growth.

[Screwtape]

The reason that fertilized egg yolk products are being sold is that they contain follistatin, which reduces myostatin expression. I still have no idea how follistatin can be orally active.

[Patrick Arnold]

Originally Posted by Screwtape

The reason that fertilized egg yolk products are being sold is that they contain follistatin, which reduces myostatin expression. I still have no idea how follistatin can be orally active.

scant little will be absorbed intact in the gut. maybe some fragments that retain some activity may be absorbed too, but once again a miniscule amount

there are things you can take to increase the pral bioavailablity of peptides though, such as proteolytic inhibitors like aprotinin, and surfactants like the bile acid sodium glycocholate

[bloodsimple1234]

Originally Posted by Patrick Arnold

scant little will be absorbed intact in the gut. maybe some fragments that retain some activity may be absorbed too, but once again a miniscule amount

there are things you can take to increase the pral bioavailablity of peptides though, such as proteolytic inhibitors like aprotinin, and surfactants like the bile acid sodium glycocholate

right,they do not tell you that in the advertising though.I do not know why a Doctor would not "know" this yet someone who is not even a doctor yet like myself would,then again when your selling something some hide things.... believe it or not!

[Patrick Arnold]

Originally Posted by bloodsimple1234

right,they do not tell you that in the advertising though.I do not know why a Doctor would not "know" this yet someone who is not even a doctor yet like myself would,then again when your selling something some hide things.... believe it or not!

can you imagine what ads would be like if no one hid anything and told the truth? actually that would make a funny skit

[neuron]

Originally Posted by Patrick Arnold

there are things you can take to increase the pral bioavailablity of peptides though, such as proteolytic inhibitors like aprotinin, and surfactants like the bile acid sodium glycocholate

How would they help it get across the gut? The proteolytic inhibitor would make it especially impossible to be absorbed and the detergent would.....?

[Bane]

Originally Posted by Patrick Arnold

scant little will be absorbed intact in the gut. maybe some fragments that retain some activity may be absorbed too, but once again a miniscule amount

there are things you can take to increase the pral bioavailablity of peptides though, such as proteolytic inhibitors like aprotinin, and surfactants like the bile acid sodium glycocholate

Or NO donors.

[JeffD729]

Face it, anything in supplement form claiming to reduce myostatin is not going to be effective in building muscle. Same rule for 90% of all the other supplements. You are going to have to buy the injectable pharmaceutical peptide. That's why the pros are so damn jacked. They take very few supplements and a whole lot of pharmaceuticals that the general public does not have access to, the money to afford them, or even the knowledge on how to implement them into a drug protocol. Right now this peptide is being sold is at $770 per mg. If the 100-200 mcg/day dose is accurate, you're gonna need anywhere from 3-5 mgs. just to do a 4-5 week cycle. And is 4-5 weeks a long enough duration? I was training with Marcus Haley and he personally knows a guy distributing this peptide and from what he said it is really effective but no one has really tried it yet. He said this guy was giving it to his dog, which is a chow, and it put on 40 lbs. I don't know if this is true because he is a big bull****ter.

[illilian]

why would ya waste it on a dog??

[TaoistWarrior]

Is this teh dog? I'm getting deja vu, brahs.