New 'Mighty Mouse' Formula Found

mystyc writes to tell us that scientists at Johns Hopkins have improved upon their original "mighty mice" discovery. Teamed with the biotech firm MetaMorphix and pharmaceutical company Wyeth, they have found a new agent that interacts with the muscle-limiting protein myostatin that was able to trigger a 60% increase in muscle size after just two weekly injections.

Comments

Abstract / free full paper link

[Frangible]

ABSTRACT: Myostatin is a secreted protein that normally functions as a negative regulator of muscle growth. Agents capable of blocking the myostatin signaling pathway could have important applications for treating human muscle degenerative diseases as well as for enhancing livestock production. Here we describe a potent myostatin inhibitor, a soluble form of the activin type IIB receptor (ACVR2B), which can cause dramatic increases in muscle mass (up to 60% in 2 weeks) when injected into wild-type mice. Furthermore, we show that the effect of the soluble receptor is attenuated but not eliminated in Mstn(-/-) mice, suggesting that at least one other ligand in addition to myostatin normally functions to limit muscle growth. Finally, we provide genetic evidence that these ligands signal through both activin type II receptors, ACVR2 and ACVR2B, to regulate muscle growth in vivo.

Full journal article (PDF)

No miracle pill here

[Valdrax]

Well the number one through three issues I can think of is whether or not it increases tendon and ligament strength. I'm pretty sure if all it does is block myostatin that it doesn't do either. If not, then you run the risk of having muscles way too strong for your joints.

Of course you run this same risk if you leap right into weight lifting with low-rep, heavy-weight work without spending the time to strengthen these joints with high-rep, low-weight work first.

On the other hand, since this almost certainly does nothing for neuromuscular response, you'll also end up with a lot of large but mostly useless muscle mass that's untappable for you.

In other words, don't expect this to substitute for working out for anyone who's not trying to stave off the decay of their existing muscles.

Re:What happened to the heart?

[inputsprocket]

It only affects striated muscle. Heart muscle is smooth and so is unaffected.

Wrong

[Seoulstriker]

Heart muscle is also striated. However, the cardiac myocytes are not multi-nucleated and the pattern is more zig-zaggy. Nevertheless, if the cardiac myocytes were not striated, the muscle just wouldn't have enough force to contract and propel blood through the chambers and the peripheral vasculature.

I'm still waiting on the published research...

Superficial vs practical

[UnclePow2223]

Aside from the obvious jokes that can be made of this news and the military applications of a super soldier or sports being taken to a new (and unnecesary level) it's stories like this that give some hope to families like mine that have a loved one diagnosed with muscular dystrophy. My nephew, only 2 years old, has already been diagnosed with this dibilitating disorder. People with MD usually don't live far past their 20s or 30s. So I for one am anxious to see what human testing would yeild and the side effects. But that doesn't mean I wouldn't laugh at some more superficial suggestions for its application....

"Enlarged" heart - depends...

[jpellino]

Ventricular Hypertrophy - in a sedentary person - is an indication of the (usually left) vetricle working too hard to overcome narrowed atreries, and increasing its mass for that reason only.

Many athletes have "enlarged" hearts - simply because the heart is working harder for the right reasons. For years world class athletes were being denied decent health insurance rates, because a chest x-ray would show a larger than normal heart, and MDs knew of only one reason for it - the bad one. It was in large part Kenneth Cooper's study of aerobic exercises for the Air Force that started the large school of info on the actual effects of exercise on the cardiovascular system.