Guest viewing limit reached
  • You have reached the maximum number of guest views allowed
  • Please register below to remove this limitation

a lie article about myostatin blockers

G3NEiol_lwS

New member
www .ergo-log .com/myostatintendons.html
this article tries to say that having myostatin blocked somehow weakens tendons. and the proof thats bs is the fact ppl born with myostatin gene mutations dont have tendon problems.
 
Invalid Link Removed
Invalid Link Removed Invalid Link Removed

  • Invalid Link Removed
  • Invalid Link Removed
  • Invalid Link Removed
  • Invalid Link Removed
  • Invalid Link Removed
  • Invalid Link Removed
  • Invalid Link Removed
  • Invalid Link Removed

  • Invalid Link Removed
  • Invalid Link Removed
  • Invalid Link Removed




[h=1]Tendons of myostatin-deficient mice are small, brittle, and hypocellular[/h]
  • Invalid Link Removed,
  • Invalid Link Removed, and
  • Invalid Link Removed Invalid Link Removed
Invalid Link Removed Author Affiliations

  • Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109

  • Edited by Kevin P. Campbell, University of Iowa College of Medicine, Iowa City, IA, and approved November 15, 2007 (received for review July 29, 2007)

[h=2]Abstract[/h] Tendons play a significant role in the modulation of forces transmitted between bones and skeletal muscles and consequently protect muscle fibers from contraction-induced, or high-strain, injuries. Myostatin (GDF-8) is a negative regulator of muscle mass. Inhibition of myostatin not only increases the mass and maximum isometric force of muscles, but also increases the susceptibility of muscle fibers to contraction-induced injury. We hypothesized that myostatin would regulate the morphology and mechanical properties of tendons. The expression of myostatin and the myostatin receptors ACVR2B and ACVRB was detectable in tendons. Surprisingly, compared with wild type (MSTN [SUP]+/+[/SUP]) mice, the tendons of myostatin-null mice (MSTN [SUP]−/−[/SUP]) were smaller and had a decrease in fibroblast density and a decrease in the expression of type I collagen. Tendons of MSTN [SUP]−/−[/SUP] mice also had a decrease in the expression of two genes that promote tendon fibroblast proliferation: scleraxis and tenomodulin. Treatment of tendon fibroblasts with myostatin activated the p38 MAPK and Smad2/3 signaling cascades, increased cell proliferation, and increased the expression of type I collagen, scleraxis, and tenomodulin. Compared with the tendons of MSTN [SUP]+/+[/SUP] mice, the mechanical properties of tibialis anterior tendons from MSTN [SUP]−/−[/SUP] mice had a greater peak stress, a lower peak strain, and increased stiffness. We conclude that, in addition to the regulation of muscle mass and force, myostatin regulates the structure and function of tendon tissues.
Click to expand...

[h=3]Tendons May Need Myostatin to Stay Supple[/h] Blocking the protein myostatin as a possible way of increasing muscle mass and strength has been a goal of clinical and laboratory research in the muscular dystrophies for several years. However, new results from the University of Michigan reveal a previously unrecognized downside of myostatin blocking.
John Faulkner and colleagues, who published their results Jan. 8 in Proceedings of the National Academy of Sciences, have found that mice bred to lack myostatin from birth have tendons that are 14 times stiffer than tendons in mice that produce myostatin.
Tendons attach muscles to bone, and their flexibility plays a role in protecting muscle fibers from contraction-associated injuries. Muscle fibers in boys with Invalid Link Removed are particularly susceptible to this type of injury.
It isn’t yet known whether myostatin blocking has the same effect on human tendons as it does on mouse tendons, or whether blocking myostatin months to years after birth would be different from stopping its production before birth. However, the findings are a caveat about strategies to block myostatin as a treatment for muscular dystrophy.
Click to expand...


[h=1]Myostatin in tendon maintenance and repair.[/h]Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
[h=3]Source[/h]Division of Orthopaedics, AIM/IKE, Faculty of Health Sciences, Linkoping University, Linkoping, Sweden. [email protected]

[h=3]Abstract[/h]Myostatin, a negative regulator of muscle growth, has recently been found to be expressed in tendons. Myostatin-deficient mice have weak and brittle tendons, which suggest that myostatin could be important for tendon maintenance. Follistatin expression in the callus tissue after tendon transection is influenced by loading. We found that follistatin antagonises myostatin, but not GDF-5 or OP-1 in vitro. To study if myostatin might play a physiological role in soft tissue, we transected 64 rat Achilles tendons and studied the gene expression for myostatin and its receptors at four different time-points during healing. Intact tendons were also studied. All samples were studied with or without mechanical loading. Unloading was achieved with botulinum toxin injections in the calf muscles. The expression of the myostatin gene was more than 40 times higher in intact tendons than in the callus tissue during tendon healing. The expression of myostatin was also influenced by loading status in both intact and healing tendons. Thereafter, we measured the mechanical properties of healing tendons after local myostatin administration. This treatment increased the volume and the contraction of the callus after 8 days, but did not improve its strength. Our results indicate that myostatin plays a positive role in tendon maintenance and that exogenous protein administration stimulates proliferation and growth of early repair tissue. However, no effect on further development towards connective tissue formation was found.
Click to expand...



you were saying?
 
those studies are not correct because people are born without myostatin functioning at all and their tendons are fine.
 
theres lies about steroids and supplements its not really new
 
I wrote about this and in general its true. Myostatin inhibition seems to cause a chain of events including the reduction of factors (tgf-beta) that contribute to fibrosis and cartilage /tendon repair. If I were injured i certainly would not use a myostatin inhibitor during the healing process.
 
yeah im sure all the ppl born with myostatin 100% disabled would agree that their tendons cant support their heaps of extra muscle
 
G3NEiol_lwS said:
yeah im sure all the ppl born with myostatin 100% disabled would agree that their tendons cant support their heaps of extra muscle
Click to expand...

so you don't think for a minute that perhaps the persons body is compensating somehow? Its a bit different to be born one way, than to take a drug for an effect.


also, why would ANYONE lie about this?
 
VaughnTrue said:
so you don't think for a minute that perhaps the persons body is compensating somehow? Its a bit different to be born one way, than to take a drug for an effect.
Click to expand...
yeah but the studies are saying molecularly tendons become weak. and if mysotatin made tendons weak like that then ppl born with myostatin mutations would be just like ppl born with connective tissue weakness(prone to injury). and myostatin mutations wouldnt be a beneficial genetic mutation.
VaughnTrue said:
also, why would ANYONE lie about this?
Click to expand...
probably for the same reasons ppl lie about steroids
 
there are currently no drugs available either OTC or available by RX that significantly reduce myostatin.


there is no conspiracy. Please take off your tin foil hat and relax.
 
its unlikely but possable that these biologists and scientists ignored certain stuff on accident.unlikely because its their job to pay attention to key facts. its more likely that their emotions and morals in regards to performance enhancing drugs played factor in their conclusions that myostatin blockers somehow cause tendon weakness. bottom line though is if a lack of myostatin resulted in significantly weaker tendons then people with myostatin mutations would have more tendon injuries. which they dont.
1+1=2. this is how obvious it is that the first study you posted is full of ****. so believe it or not lies exist about p.e.d.s. and you calling me a tinfoil hatter for thats like insulting anybody who thinks lies exist about p.e.d.s so theres no reason for disrespect.
 
Isn't creatine a (mild?) myostatin blocker? There were always myths around about how creatine could increase injuries in athletes... But I never had a problem with creatine... And keep in mind, only because mice/rats got weak tendons, thats not a 1:1 translation to human physiology. A hint maybe. So I would say the jury is still open on that one... unless anyone got human studies / case studies?

Makes me think if I should cycle off creatine once in a while though.
 
G3NEiol_lwS said:
yeah but the studies are saying molecularly tendons become weak. and if mysotatin made tendons weak like that then ppl born with myostatin mutations would be just like ppl born with connective tissue weakness(prone to injury). and myostatin mutations wouldnt be a beneficial genetic mutation.
probably for the same reasons ppl lie about steroids
Click to expand...

myostatin deficiency certainly is not a beneficial genetic mutation. to survive in a inhospitable world it is important to conserve energy, especially in times of famine. wasting all your bodies resources on more muscle than is necessary is not good

and i dont think anyone has studied the functional properties of tendons from people born with myostatin deficiency. You are acting quite ignorantly. You have no data to support your position, just some belief about imaginary people with myostatin deficiency and their health
 
WTF's a myostatin blocker? Example? Is this something else that they're saying is contained in CRAZE?!!
 
You must log in or register to reply here.
Back
Top