some great set of pictures there, thanks for sharing bro
I think the pic of Lee at 13 is the most insane, you could believe other at 17-18 being that developed but at 13 when puberty is really only just kicking in is unbelievable!
These are examples of people and animals that suffer from it.Originally Posted by tim290280
Many of you have seen or heard about Wendy the whippet - a dog with a rare genetic mutation that has led to her being called the Arnold Schwarzenegger of dogs.
The genetic mutation is a deficiency in myostatin, which is a growth factor that limits muscle tissue growth.
But that rare genetic defect does not occur only in the whippet breed. In fact, it can and has occurred in other animals… even in humans themselves!
Behold! The ultimate collection of myostatin deficient monstrosities!
Recently part of a genetics study done in the U.S. on mutation in the myostatin gene in whippets, people mistake her for a pitbull with a pinhead.
The uber-muscled whippets are called “bullies,” not because of their nature — Wendy likes nothing better than a good back scratch and isn’t shy about sitting in your lap to ask for one — but because of their size.
She’s about twice the weight of an average whippet, but with the same height and small narrow head — and the same size heart and lungs, which means she probably won’t live as long as normal whippets.
Here some more pics of lab rats with the condition.
And now for Humans.
Richard Sandrak Also known as Little Hercules, is renowned for his physique at an extremely young age. He started training at two years of age and by the time he was six was pressing 4 times more than his own weight. His father only allowed him to eat according to a strict diet, consisting of liquid nutrients and vegetables.
A 21 month old toddler from Michigan with myostatin deficiency, he has 40 percent more muscle mass than normal, jaw-dropping strength, breathtaking quickness, a speedy metabolism and almost no body fat. Liam came into the world with many birth defects. He had a small hole in his heart, enlarged kidneys, frequently vomited and was born four weeks premature. Medical records indicated that his biological father was “unusually strong.”
“He could do the iron cross when he was 5 months old,” said his adoptive mother, Dana Hoekstra of Roosevelt Park. She was referring to a difficult gymnastics move in which a male athlete suspends himself by his arms between two hanging rings, forming the shape of a cross.
Two days after birth, he was able to fully stand-up and support his own weight. Months later, he began developing ripped abs, naturally doing pull-ups, inverted sit-ups, Olympic styled iron crosses, thigh muscles compared to that of Lance Armstrong and even punching holes into walls during tantrums (he accidentally gave his Mom a black eye once as well).
One famous bodybuilder who allegedly has a myostatin deficiency was Kenneth “Flex” Wheeler.
Unfortunately, Flex Wheeler’s career was cut short in 2000 after he suffered kidney failure and had to retire from professional body building.
that is the most bad ass looking dog i have ever seen in my life. it looks totally unreal.
partial myostatin gene inhibition=blessing, full inhibition=curse
Great Post Samoan Z!
True, myostatin inhibition on an animal or human can lead to astounding muscle mass but not necessarily leading to a good thing.
A study I had to read and present recently presented myostatin inhibited mice compared to a wild type (or control group). The results were very surprising. One would expect having a gene that regulates muscle growth would be not only bigger but stronger as well. That was not the case.
The myostatin inhibited mice had a drastic fiber switch to Type IIb muscle fibers. These fibers have a very fast contraction time, low resistance to fatigue, very high force production, low mitochondrial density and very large motor neuron size.
The study showed that the myostatin inhibited mice generated only 53% of the force developed by the wild type. More muscle but only 53% of the strength!?
We delved further and found that despite the fiber type change, using Succinate Dehydrogenase staining (SDH) there was a significantly lower mitochondrial/myonucleus ratio in not only the Type IIb fibers than normal but all fibers (more significantly in the Fast Muscle).
What does this mean?
A blockade of mitochondrial respiration in skeletal muscle results in decreased titanic force generation, independent of fiber change.
Also, there was a greater formation of tubular formation that are responsible for a more rapid release and reuptake of calcium, accounting for differences in twitch kinetics (contraction and relaxation time)
All this means that myostatin inhibition does not seem to benefit from the high tetanic force generation to be expected of glycolytic fibers, and the mitochondrial depletion would suggest increased fatigability and exercise intolerance.
There is a long way to go in the research of myostatin inhibitors, natural and slight myostatin inhibition seems to carry some beneficial side effects as seen in some of today's bodybuilders but can lead to many problems. Unnatural inhibition as explained above is not beneficial for the extra muscle gained. I do not think we will be seeing the use of myostatin inhibitors for a long time or ever.
Sorry for the long post, this is just an area I have been researching and find fascinating.
If I were to attempt gene doping I would stick to GH or IGF-1. But I am looking forward to SARMs (nonsteroidal selective androgen receptor modulators) more than anything. They effect only skeletal muscle, meaning less/no side effects.