ok, we all know that TEST increases the bonding of type 2 muscle fibers to create a type 2c muscle fiber, hence Hypertrophy. BUT, what I just found out is that the “BOND” between the satallite cell AND the Type 2 fiber is VERY WEAK and UNSTABBLE. Meaning that it is very difficult to maintain, or should I say, easy to break. ( the bodies use it or lose it principal).
So, what my thinking is, is that using TEST may be a non-benficial or rather high maintence situation. Say you do a cycle with test…after the cycle, to maintain that EXTRA 15 lbs you just put on would be rather difficult ( because of your bodies NATURAL anabolic environment returning to normal) to maintain. Also from all the guys I’ve seen use TEST, they lose ALOT of their size. I’ll admit, they were not the most dedicated, but they weren’t idoits either.
What am I saying? Well maybe Test’s bads out weight its goods. I know it is the foundation of cycles, but I don’t beleive that is written in stone. I’m just spittting out a thought for some feedback. keep in mind I have not juiced…YET!!!
how was their post cycle recovery? I know alot of people who lose size post cycle. the reason, simple, no clomid, bad diet, less training. dumb people in general, with the mentality of juice it up now, get big do it again next summer. I for one, keep most of my gains, and people are amazed usually. oh, and test is always my base.
hahah - horse…soon, when i get cash, and im still reading, collecting real world info.
type 2c muscle fiber is the “bodybuilding fiber” It is when satalite cells mend with a type 2b fiber
Im just saying that from studies, in general, keeping that type 2c fiber is difficult already ( which can be done by eating and working it out consistantly). Test is shown to INCREASE this “bond” more than other steriods. I’m just saying, that what it takes to maintain the TEST gains ( maybe compared to other AAS) is harder due to gains made to an already unstable bond.
Well, what you are saying is irrelivant because most other compounds other than test don’t have much effect on the formation or distribution of satelite cells. Therefore, you should just be happy with what you get and what you keep with test. If you form new fibers, sweet a bonus. Not to mention, the word hypertrophy refers to the growth of existing muscle fibers, not the formation of new ones which satelite cells are responsible for, so youre not really dealing with the proper nomenclature here. And by the way, what the hell are you reading dude? I think you might have some other shit to learn before you start dealing with this material.
this falls under the topic of overanalyzed to say the least. what studies are you discussing here? i seriously doubt these type of studies are being performed by certified individuals. as cy recently said, actual studies involving steroids and there response to the human body in reguards to body building are very few and far between. you need to stop reading so much bro. just get yourself jacked up on a nice test/tren cycle and tell us about muscle fibers as you bench press the weight room! lets not try and reinvent the wheel here. test puts meat on my bones and it stays there. thats all i am worried about at the end of the day. not various types of muscle fibers and how test does or doesnt do anything to build or keep them. not trying to be harsh. just trying to bring you back to reality.
squatty…this words come from Dr. Fred Hatfield, “THE” Dr. Squat, 1988 record holder…look him up. He is supplying the info regarding “hypertrophy” , which he describes as white muscle fiber BONDING with satelite cells, not creating new cells papa.
What I posted was in regards to my OWN thinking with this science. Dr. Squat says the BOND is very easily broken ( if the right eating and training isn’t consistant). Then I applied this to the " Test/satellite cell" recent scientific findings to ask for an opinion on a theory I posted. So to everyone out there who thinks I am retarded…read this again before you post something stupid…and before you post…read it again just in case. I can see this might turn into a dead thread.
Hatfield is a smart man… however, the word hypertrophy does not describe the formation of new muscle. Hypertrophy is the growth of existing muscle. I don’t mean to rain on your parade, shit I wish I could be reading what you are reading, however… the fact that test causes these new satelite formations at all is a strong positive, whether they are broken down or not. You can never say that the bad’s of test outweigh the goods.
SQUATTY,
“Not to mention, the word hypertrophy refers to the growth of existing muscle fibers, not the formation of new ones which satelite cells are responsible for…”
How’d you get the impression that sat. cells form new fibres? This simply isn’t the case. They fuse with existing fibres to repair/hypertrophy.
“I think you might have some other shit to learn before you start dealing with this material.”
lats2dope,
whoever coined the term “bodybuilding fiber” to describe a IIc needs to have their butt kicked. All practicallity aside, satellite cell fusion (aka bonding) wouldn’t be any different when induced by test than it would induced by training.
if you are interested in the sattelite cell activation, why not take creatine year round.It has been shown in studies it also activates satellite cells, and is much easier to maintain all year round, then the 20 week test protocol used to show sattelite cell activation.
Don’t tell me about irony… ass. Learn the destinction between hypertrophy and satellite cell activation.
Satellite Cells and Brand Spanking New Muscle
In the first study, researchers found an increase in satellite cell and myonuclear number in normal men receiving Testosterone enanthate. Just so we’re clear, this study essentially shows that varying doses of exogenous Testosterone causes satellite cells to fuse to existing muscle tissue, thereby creating new and permanent muscle
Anecdotal evidence somewhat supports this idea as well. Androgens like methandrostenolone (D-bol) and oxymetholone (Anadrol) are well known for having awesome effects in terms of increasing muscle size, but more often than not, they have more of a reputation for “leaving you with little” upon cessation of use. As I stated in my Steroids for Health 2003 article, this seems to account, at least partially, for the differences in terms of retention of gains.
What does all this mean in the real world? It means androgens like Testosterone, nandrolone, boldenone, oxandrolone, trenbolone, A1E and methenolone may also be useful in that regard. On the other hand, androgens like methandrostenolone, oxymetholone and 4-AD-EC may be better suited for hypertrophy of existing muscle cells.
This isn’t to say that those latter androgens don’t bind to the AR at all, just that the previously mentioned androgens (trenbolone, Test, etc.) are better suited, as they appear to bind more avidly to the AR. Neither am I implying that those androgens which bind avidly to the AR won’t induce hypertrophy of existing muscle tissue, just that they’re better suited for activation of satellite cells and the subsequent effects leading to the formation of new muscle cells. (1-5)
As you can see… satellite cells respoonsible for new muscle… other mechanisms are responsible for the growth of existing muscle… AKA HYPERTROPHY!!!
Oh Jeebus…
I enjoy writing for this magazine, but this is one side effect I loathe: people taking the information as dogma. While I appreciate your showing where you got the info, it’s quite simply incorrect (according to the model we currently have). The very part of the article you quoted stated that the satellite cells fuse with existing fibres to result in hypertrophy (although this article should not be the basis for our understanding of the underlying principles). It’s no secret, that’s just how muscles grow (intracellular water issues aside). This seems to be a fundamental misunderstanding that needs to be cleared up. I’m not sure how the concept of “satellite cells= new fibres” came about, but it needs to be put to rest. There are a ton of reviews on the topic which are often free and online (Booth had a good one in JAP last year). Read the literature, then we’ll chat some more.
More importantly, there’s no need to be a dick just because you’re wrong and someone calls you on it (whether or not you believe your limited information to be correct). I refrained from writing anything derogatory even though you exhibit little understanding of the topic at hand, and were both condescending and hypocritical in your original post. We’re all on the same side and we’re all here to learn. You were wrong (twice), hypocritical (twice), and a dick (twice), but it won’t help anyone for me to go on some inane rant about your penis size (or the like). Just take what’s presented here and learn from the experience (as well as the information). That’s probably the most important thing anyone can take away from any board.
Having said all that, I’d love to have a scientific discussion with anyone about satellite cells, because even the literature is “limited” and should never be taken as dogma.
Cheers!
This is where I get pissed off. I don’t like it when people take my word and use it in an argument. When I answer column questions, they’re meant to be used in a certain context, not as an argument which I’ve never made. Anyhow, I often simplify things so as not to confuse people. As a result, when people post things like this, I then have to debate with people for the next 3 weeks explaining why I did and didn’t say such things. It’s really ridiculous and I’m sick of it.
With this particular stem cell fusing with existing muscle, I suppose yes, that technically is considered “hypertrophy” but at the same time, not the hypertrophy we’ve come to know and people commonly think of when it comes to such. Rather than confusing people and saying that both are forms of hypertrophy, I thought it best to differentiate between the two, as they are not the same. As for me saying it’s new muscle, well it technically is as those cells weren’t fused with existing muscle previously (existing as undifferentiated stem cells) and to my knowledge, those differentiated cells are there to stay. As common sense would tell you, if you didn’t have something before, and do now, you can say you now have something which is newly added. I’d be happy to debate with you. I don’t check on the forum much, but you can e-mail me at cw@t-mag.com if you have some questions regarding this.
This really isn’t an area I specialize in but I’ve taken grad courses in molecular genetics, cellular biology and of course molecular bio so I have a decent base of knowledge from previous schooling.
Hey guys I think latstodope was right. Ya’ll might owe him an apology or an atta boy or something like that.
Clin Exp Pharmacol Physiol. 2002 Mar;29(3):209-13
Skeletal muscle is a complex and heterogenous tissue capable of remarkable adaptation in response to exercise training. The role of gene transcription, as an initial target to control protein synthesis, is poorly understood. 2. Mature myofibres contain several hundred nuclei, all of which maintain transcriptional competency, although the localized responsiveness of nuclei is not well known. Myofibres are capable of hypertrophy. These processes require the activation and myogenic differentiation of mononuclear satellite cells that fuse with the enlarging or repairing myofibre. 3. A single bout of exercise in human subjects is capable of activating the expression of many diverse groups of genes. 4. The impact of repeated exercise bouts, typical of exercise training, on gene expression has yet to receive systematic investigation. 5. The molecular programme elicited by resistance exercise and endurance exercise differs markedly. Muscular hypertrophy following resistance exercise is dependent on the activation of satellite cells and their subsequent myogenic maturation. Endurance exercise requires the simultaneous activation of mitochondrial and nuclear genes to enable mitochondrial biogenesis. 6. Future analysis of the regulation of genes by exercise may combine high-throughput technologies, such as gene-chips, enabling the rapid detection and analysis of changes in the expression of many thousands of genes.
