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Discussion in 'Steroid Forum' started by pauladrive, Aug 27, 2010.
I wish I could afford GH, but I might give the EQ/deca a try
I've learnt how to quote.. Jim can you explain this again s little more simplified.
The positive studies are almost ALWAYS performed on an external cell/subject outside of its normal environment (hence in vitro). So taking connective tissue and examining the effects of a compound on the tissue in a lab.
In terms of the last statement. Very simple. When it comes to AAS, the muscle gets stronger faster than the connective tissue so the tissue can not sustain the muscular effort any longer. If your connective tissue are accustomed to you benching 315 and you would naturally be able to progress to 335 in 6 months but through the use of PEDs you can now bench 495 in that time, your connective tissue does not reap the benefits of your AAS usage. Those connective tissue now have a much greater chance of suffering injury, even if using a "healing" steroid.
Thank you. So you are saying that aas do help heal or strengthen tendons, ligaments and that alike but since muscle strength improves at a faster rate it can be counter productive?
Keeping this in mind, if true, over a few years muscles go back to their natural size and ligaments or tendons keep healing, with careful consideration to exercise this is a good thing..
No not really. I'm saying that the gains to muscle development are too fast for the connective tissue so they eventually run into trouble. The more dramatic "dem gainz" the more potential for injury.
I fail to see the fundamental difference in what you just compared to what I said other then not mentioning whether aas do or don't assist in healing tendons or ligament.
Your choice of words here in the former comment is open to interpretation:
a) Connective tissue does get stronger faster on aas but not at the even faster rate of which muscle is built OR
b) Muscle is built faster on aas while the connective tissue continues to grow or heal at a normal rate.
Sorry you fail to see what I am explaining to you. There's Google.
" Ok Google" .. "A or B" ..
I understood the rest, I think it's more so what Dr Jim is not saying I'm interested in, I see he is more literal than you which is what I want to poke at. I see you interpreted his last statement as connective tissue when he only said tendons, and while I'm on that he said IME.
Do you have experience with all types of connective tissue being impaired by muscle growing at a more accelerated rate than the tissue? Can you provide sources or examples, I'm genuinely interested if you do.
Since AAS improve the conditions in someway, whether it be a higher RBC or more nutrients traveling around with it, is it not arguable that conditions are improved (even if only a little).
I'm not asking about tendons and to the best of my knowledge, muscles growing faster then my ligaments heal will not be an issue. I'm just trying to create the best results for my own recovery, which is not because I lifted to big chasing "dem gainz".
You're very wrong and I explained to you what Dr. Jim very clearly explained to you. In all AAS, the "SKM" I.e. Skeletal muscle strengthens at a rate faster than connective tissue, including both ligament and tendon. This can be found with a very very simple 1st grade Google search. I don't see why you cannot grasp this. No your bro science is not accurate in terms of RBCs, even with EQ and Deca, and Dr. Jim has been very explicit in this subject. Now just think for one second about this.
Would EQ have more potential for tearing of CONNECTIVE TISSUE than say Trenbolone? No, not even close because tren is a stronger anabolic compound. Would a Tennis player be more prone to injury than say a power lifter? Probably not because the power lifted is gaining much more strength than the tennis player. Would person "A" who uses 600 mg of EQ and squats moderately in each component of "FITT" be less prone to a tear than person B who employs a more intense "FITT" approach and all other variables are identical? YES. The results are subjective. Each situation is different. But if 2 subjects are very similar in all variables other than the dosage of steroids and/or intensity of FITT, the one who pushes the boundaries of dosage, type of training, and type of compound is going to be more prone to CONNECTIVE TISSUE damage. This is biology 101 and actually is one of the few things the mainstream medical and education community addresses in finite detail.
In regards to sources? I don't see how you need Dr. Jim or any member to provide you with sources that you could easily locate yourself. That's the point "Give a man a fish and he'll eat for a day, teach a man to fish and he'll eat for a lifetime."
Have you ever used advanced search In Google? Very simple. You type "advanced search" in Google and then you click on it. Under the option for file type, you change it to ".pdf." In your search you Google "steroids side effects," or you can google "anabolic steroids and tendons," or "anabolic steroids and ligament." Or "anabolic steroids effects on ligament." You want to sift through and rely on medical journals.
You could even type in "Google scholar" in "the Google" and click on it. This will give you more scientific information.
This is something where it actually is not difficult to find peer reviewed data. I found 20 different documents that backed up my point that I made. I was going to link them but I'm trying to help you fish for yourself young man. In regards to finding peer reviewed in vivo HUMAN studies proving that steroids aid in recovery of ligament or damage? Good luck finding that.
Sorry for being so short tempered in my post. But to summarize:
-intensity of training
-duration of use
-power of the actual steroid itself
-dose of the steroid
-use/abuse of the steroid
All play a factor. Again, the peer reviewed data available on steroids in a rehabilitation role is extremely limited in terms of in vivo human studies proving AAS as a means to expedite the recovery process of connective tissue. Most of that data would be bro science my friend.
Thank you, I didn't consider searching this way.
In regards to running test with EQ or Primo or something similar that is going to positively affect collagen production, does it matter which ester of Test is run? I would guess you'd want to use Test C or E do to longer half life that is similar to half life of EQ?
First of all, to save the veterans here time, I will tell you that the article that you quoted, even though well circulated around the internet and forums alike, has no evidence to back up the things it claims. The author provided no sources when writing this and in reference to collagen synthesis, nobody has been able to find evidence to support his percentages or even proof that collagen synthesis occurs. (this is discussed earlier in this very thread).
It is 'bro science'; it has not been through the controlled tests to be scientically proven. Further to that from what I can find, it stands almost alone, other then some comments of "yeah it worked for me" here and there (which may be considered enough for some), there are few if any at all other reports of 'bro science' to back it up.
If you have more sources of bro science on collagen synthesis please post or even private message me because I'm interested as well.
Now the answer to your question:
No, the ester you use would not matter.
Thanks for clarification. The thread is 15 pages long so I didn't read every comment
So overall, do you guys think that EQ would help me recover from a severely torn labrum in my shoulder and torn peroneal tendons in my ankle? or would surgery on the shoulder be the option?
Are u fucking kidding me! Go read Gerber boy and return with an informed question!
[OA] [Sheep] Genomic and Lipidomic Actions of Nandrolone On Detached Rotator Cuff Muscle
Early nandrolone application mitigates muscle-to-fat conversion with tendon release
Nandrolone down-regulates the muscle lipidome, independent of the transcriptome
Fatty, atrophied muscle looses responsiveness to nandrolone
The transcript response to nandrolone is down-regulated in detached muscle
Responsiveness to nandrolone is related to androgen receptor protein levels
Reversal of fatty infiltration of pennate rotator cuff muscle after tendon release is hitherto impossible. The administration of nandrolone starting at the time of tendon release prevents the increase in fat content, but does not revert established fatty infiltration.
We hypothesised that tendon release and myotendinous retraction cause alterations in lipid related gene expression leading to fatty muscle infiltration, which can be suppressed by nandrolone through its genomic actions if applied immediately after tendon release.
The effects of infraspinatus tendon release and subsequent tendon repair at 16 weeks were studied in six Swiss Alpine sheep. In the interventional groups, 150mg nandrolone was administered weekly after tendon release until sacrifice (N22W, n=6) or starting at the time of repair (N6W, n=6). Infraspinatus volume, composition, expressed transcripts, lipids, and selected proteins were analyzed at baseline, 16 and 22 weeks.
Tendon release reduced infraspinatus volume by 22% and increased fat content from 11% to 38%. These changes were not affected by repair. Fatty infiltration was associated with up-regulation of 227 lipid species, and increased levels of the adipocyte differentiation marker PPARG2 (peroxisome proliferator-activated receptor gamma 2). Nandrolone abrogated lipid accumulation, halved the loss in fiber area percentage, and up-regulated androgen receptor levels and transcript expression in the N22W but not the N6W group.
The results document that nandrolone mitigates muscle-to-fat transformation after tendon release via a general down-regulation of lipid accumulation concomitantly with up-regulated expression of its nuclear receptor and downstream transcripts in skeletal muscle. Reduced responsiveness of retracted muscle to nandrolone as observed in the N6W group is reflected by a down-regulated transcript response.
Fluck M, Ruoss S, Mohl CB, et al. Genomic and lipidomic actions of nandrolone on detached rotator cuff muscle in sheep. J Steroid Biochem Mol Biol. Genomic and lipidomic actions of nandrolone on detached rotator cuff muscle in sheep
Yang X, Wang Y, Yan S, et al. Effect of testosterone on the proliferation and collagen synthesis of cardiac fibroblasts induced by angiotensin II in neonatal rat. Bioengineered. http://www.tandfonline.com/doi/full/10.1080/21655979.2016.1227141
The objective is to explore the effect of testosterone on the proliferation and collagen synthesis of neonatal rat cardiac fibroblasts (CF) induced by Angiotensin II (Ang II) and the underlying mechanisms. Derived from neonatal rats, the CFs were divided into 4 groups: the control group, Ang II group, testosterone group, and testosterone + Ang II group in vitro. Cell cycle distribution, collagen counts, and phosphorylated extracellular signal-regulated kinase (ERK1/2) (p - ERK1/2) expression were assessed by flow cytometry, VG staining, and immunocytochemistry, respectively. The Ang II group had a much higher proportion of cells in the S-phase, higher collagen contents, and a higher p - ERK1/2 expression level than either the control or testosterone group. However, these factors were significantly reduced in the testosterone + Ang II group as compared to the Ang II group. In terms of cells in the S-phase and the collagen contents, there was not a significant difference between the testosterone group and the control. However, the protein expression of p-ERK1/2 was significantly increased in the testosterone group as compared to the control. Testosterone inhibits the proliferation and collagen synthesis of CF induced by Ang II. The underlying mechanism may involve the ERK1/2 signaling pathway.
Dr. Scally would using the "Pauling Method" of supplementation be of any benefit to us? I apologize if I sound ignorant and I realize Pauling's method supposedly assists with heart disease, but their premise is promoting arterial repair via collagen synthesis. My question is if while on cycle, one were to supplement the diet with the lysine,proline,vitamin c etc. could the addition of these "raw materials" or building blocks possibly assist in the process of the collagen synthesis we are trying to ensure? I've read through the thread but if this has been asked already I missed it. Actually I guess I should have started by asking what you think/know of the Pauling Williams Therapy? Do you think its legit or junk science? I rarely post and am sorry if this is a stupid question guys. I usually just lurk, thank you all for the info you share.
Pharmacological Inhibition of Myostatin Protects Against Skeletal Muscle Atrophy and Weakness After Anterior Cruciate Ligament Tear
Anterior cruciate ligament (ACL) tears are among the most frequent knee injuries in sports medicine, with tear rates in the US up to 250,000 per year. Many patients who suffer from ACL tears have persistent atrophy and weakness even after considerable rehabilitation.
Myostatin is a cytokine that directly induces muscle atrophy, and previous studies rodent models and patients have demonstrated an upregulation of myostatin after ACL tear.
Using a preclinical rat model, our objective was to determine if the use of a bioneutralizing antibody against myostatin could prevent muscle atrophy and weakness after ACL tear. Rats underwent a surgically induced ACL tear and were treated with either a bioneutralizing antibody against myostatin (10B3, GlaxoSmithKline) or a sham antibody (E1-82.15, GlaxoSmithKline).
Muscles were harvested at either 7 or 21 days after induction of a tear to measure changes in contractile function, fiber size and genes involved in muscle atrophy and hypertrophy. These time points were selected to evaluate early and later changes in muscle structure and function.
Compared to the sham antibody group, seven days after ACL tear, myostatin inhibition reduced the expression of proteolytic genes and induced the expression of hypertrophy genes.
These early changes in gene expression lead to a 22% increase in muscle fiber cross-sectional area and a 10% improvement in maximum isometric force production that were observed 21 days after ACL tear.
Overall, myostatin inhibition lead to several favorable, although modest, changes in molecular biomarkers of muscle regeneration and reduced muscle atrophy and weakness following ACL tear. This article is protected by copyright.
Wurtzel CN, Gumucio JP, Grekin JA, et al. Pharmacological inhibition of myostatin protects against skeletal muscle atrophy and weakness after anterior cruciate ligament tear. J Orthop Res. Pharmacological inhibition of myostatin protects against skeletal muscle atrophy and weakness after anterior cruciate ligament tear