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napsgeargenezapharmateuticals domestic-supplypuritysourcelabsResearch Chemical SciencesUGFREAKeudomestic

Proof of A/S far reaching genetic potential...

Alright, I didn't read the paper - but I can think of a few points of criticism:

1. How long and how much did these guys take AS. Also how long have they been off? All of these variables could profoundly influence the development, activation, and/or maturation of satellite cells into myonuclei.

2. What endocrinological factors influence myonuclei development and maintainance? You may undergo hyperplasia but once you go off steroids, do you have the hormonal strength to activate the growth of that new fiber? These may be "inactive" in that natual levels of test, etc. may only be able to support a limited number of myonuclei.

3. Technical flaws. Biopsy sampling variation has plagued in vivo hyperplasia studies for decades. It's really not that easy (or accurate) to determine muscle fiber count without excising the entire muscle.
 
Technical flaws. Biopsy sampling variation has plagued in vivo hyperplasia studies for decades. It's really not that easy (or accurate) to determine muscle fiber count without excising the entire muscle.

Although anabolic steroids were not involved, the classic study demonstrating that exercise induces muscle hyperlasia looked at muscle cross sections rather than biopsy samples

Anat Rec 1992 Jun;233(2):178-95
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Morphological observations supporting muscle fiber hyperplasia following weight-lifting exercise in cats.

Giddings CJ, Gonyea WJ.

Department of Cell Biology and Neuroscience, University of Texas Southwestern Medical Center, Dallas 75235-9039.

Although exercise-induced muscle fiber hyperplasia has been demonstrated through direct fiber counts following nitric-acid digestion of muscle, morphological studies to determine the mechanism of hyperplasia have not been performed previously. In this study, light and electron microscopy were used to evaluate evidence of muscle fiber splitting or de novo formation of new muscle fibers. Since both fiber hypertrophy and hyperplasia may result in alterations in the muscle nuclear populations, myonuclear number and satellite cell frequency were assessed quantitatively to determine their role in regulating muscle fiber size. Ten adult cats performed weight-lifting exercise, and the right (exercised) and left (control) forelimbs were fixed by vascular perfusion. Spaced serial sections were used to evaluate muscle fiber morphology along the length of fibers, and muscle fiber areas were measured. Myonuclei and satellite cells were
counted using electron microscopy. Morphological evidence supporting muscle fiber hyperplasia was observed in exercised muscles. These observations included the presence of small fibers which may signify de novo fiber formation. Myonuclear counts indicate that myonuclear density is not a primary regulator of fiber size. Satellite cell frequency was unchanged following exercise. Autoradiographic studies revealed satellite cell activation by uptake of tritiated thymidine in exercised muscles. Satellite cell activation appears to result from increased activity in exercised muscles. These findings confirm previous studies demonstrating muscle fiber hyperplasia following weight-lifting exercise, and suggest that de novo fiber formation is the major mechanism contributing to muscle fiber hyperplasia in this model.
 
Totally agree!

Hello, Im new here but old to the game. Four years ago I was 195 lbs and started juicing, heavily. I wont like, I was using a shitload. I did this for two years, two years later I weighed over 300 lbs. Remember, my natural weight was only around 185 lbs if I didn't train. Now after two years of no juice, im 240 at about seven percent bodyfat. The only way to justify this is a modification in my genetics. I know for a fact they changed my genetics.

Cage
 
dankduke said:
great info...love reading shit like this!!!

Me too! I consider myself to be pretty sharp but I still have to read them like 3 times!
 
Yea, but Nandi - you can only take large cross-sections of muscle in animal models, not living humans, unless they don't mind you removing their biceps, etc. Also, cats (the traditional model for hyperplasia) are a weak argument for hyperplasia in humans during normal muscle loading conditions. Most of the hyperplasia models are based on stretch compensation where they remove an agonist muscle like the gastroc to investigate hyperplasia in the soleus.

I'm not saying it doesn't occur in humans. In fact, I think it does but only over a long period of time under repeated musculoskeletal stress. We're talking years here.
 
I agree with you Dr.X, that it can often be a leap of faith to extrapolate from animals to humans. I think that's one reason the relative importance of hyperplasia v. hypertrophy is still so hotly debated in the sports physiology world. As far as I know there is not a human study that would be considered the "smoking gun".
 
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