Joints/Tendons/Bone

[miamifunk]

I wish I could afford GH, but I might give the EQ/deca a try

 

[Thatshitcray]

Looking at this case I wonder what other mechanisms were contributory such as; how long was this patient "lifting heavy", his lifting mechanics, the number, type, and/or duration of AAS use, etc.

I mean how often do we see cyclists begin some thread asking which AAS are best to "support collagen" growth?

The confusion seems to arise from a few select in-vitro PETRI DISH studies on FIBROBLASTS, that noted AAS tended to accelerate the synthesis of collagen PRECURSORS.

A few other studies assayed the effects of AAS on the SERUM concentration of once again collagen PRECURSORS.

Guys this type of data should NOT be extrapolated to the synthesis of ARTICULAR collagen (tendons, ligaments, hyaline cartilage, fascia, etc) where blood flow is more likely the rate limiting step.

What is KNOWN, AAS associated SKM hypertrophy occurs at disproportionate pace compared to articular collagen and this effect alone predisposes a select group of cyclist to tendon disruption, IME.

I've learnt how to quote.. Jim can you explain this again s little more simplified.

Ok I found this more then just a little bit confusing.. sooo nor Deca or eq help the body produce the collagen required to heal ligaments (or tendons) BUT the increased blood flow assists with healing them? Did I get that right? If not then somebody please tell me what I can take to heal a knee ligament, I'll probably do a cycle anyway to strengthen the muscles surrounding the area but if I could tailer that cycle for ligament repair it would be ace. Cheers.

 

[antipcman]

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.

 

[Thatshitcray]

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..

 

[antipcman]

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.

 

[Thatshitcray]

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.

When it comes to AAS, the muscle gets stronger faster than the connective tissue

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.

 

[antipcman]

Sorry you fail to see what I am explaining to you. There's Google.

 

[Thatshitcray]

" 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.

Guys this type of data should NOT be extrapolated to the synthesis of ARTICULAR collagen (tendons, ligaments, hyaline cartilage, fascia, etc) where blood flow is more likely the rate limiting step.

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).

What is KNOWN, AAS associated SKM hypertrophy occurs at disproportionate pace compared to articular collagen and this effect alone predisposes a select group of cyclist to tendon disruption, IME.

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".

 

[antipcman]

" 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.

 

[antipcman]

Sorry for being so short tempered in my post. But to summarize:
-intensity of training
-stretching
-diet
-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.

 

[Thatshitcray]

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.

Thank you, I didn't consider searching this way.

 

[new to the game]

i've heard that EQ actually increases tendon strength and can be stacked with test to sort of counter-act the test from impairing the tendons. was planning on including it in my next cycle when winter gets here , wanted to try a lower dose of test (500mg of Enanthate), 600mg of deca/ and a low dose of EQ to keep the tendons strong. the deca is awesome for collagen synthesis and helps with joint pain which is crucial for powerlifting ---- i found an article in my research file ..

While injecting test increases protein synthesis by roughly 50 times, depending on dose and time, most bodybuilders forget that it will reduce collagen synthesis by more than 50% -- more like 80%, giving you the collagen synthesis rate of a senior citizen. Since collagen makes up tendons, bros are very prone to injury if they continue to lift very heavy, unless they cycle off T and let their collagen synthesis get back to normal. It's like having the skeletal muscle of a gorilla with the tendons of a very old man.

Winstrol increases collagen synthesis. It will give you bigger tendons. However, your body compensates for this by making them more brittle, weaker, and more prone to injury. I can't tell you how many bros work out anaerobically and become injured while on winstrol. Guys who lift in the 1-5 rep range while on winstrol, to baseball players who sprint all out from a stationary position -- winstrol should be the LAST drug they choose. Most of them like winstrol because they don't get the weight gain from it but it is very detrimental to bros who train for any sport anaerobically. Tendons tear easily on it.

Also, the drugs I mention increase collagen synthesis while also increasing collagen cross-linking integrity, making for a much stronger tendon.

Winstrol, on the other hand, will dramatically increase collagen syn, but ironically it decreases collagen cross-linking integrity, thus making a much weaker tendon.

You can plan a cycle of AAS which will increase collagen synthesis and skeletal muscle growth at the same time. The key is the drug(s) you choose.

Deca, Equipoise, Anavar, and Primobolan will ALL increase skeletal muscle while at the same time dramatically increase collagen syn and bone mass and density, leaving you with a substantially reduced chance of becoming injured than if you choose to use AAS like sus, cyp, or enth.

While testosterone will increase bone mass and density, even at supra-physiological levels, the result is weaker tendons due to inhibition of collagen syn.

To plan a cycle where the goal is to increase skeletal muscle mass/strength while at the same time increase joint/tendon/ligament strength, enough to keep up with the dramatic increase in skeletal muscle, you must choose drugs like Eq, Deca, Anavar, or Primo as the base of your cycle. Testosterone and its esters can be added to your cycle to keep levels within a 'normal' physiological range (ie, 100-200 mg/wk) but must not go above this. Since drugs like eq, deca, anavar and primo will reduce endogenous, natural levels of test, these levels may be maintained with exogenous test in the 100-200 mg/wk range. Test at this dose will not inhibit collagen syn, but paradoxically, will help increase it. It is when exogenous testosterone is used > 200 mg/wk that collagen syn is inhibited.

Deca @ 3 mg/kg a week(about 270 mg/wk for a 200 lb male) will increase procollagen III levels by 270% by week 2. Procollagen III is a primary indicator used to determine the rate of collagen syn. As you can see, deca is a very good drug at giving you everything you want -- an increase in collagen syn, an increase in skeletal muscle, and increases in bone mass and density. The one thing it does not give you is wood.

Primobolan, @ 5 mg/kg, will increase collagen synthesis by roughly 180% -- less than deca and equipoise but still substantial.

Equipoise @ 3 mg/kg will increase procollagen III by approximately 340% -- slightly better than deca.

Oxandrolone has over a hundred studies documenting its effectiveness at treating patients needing rapid increases in collagen syn to enhance healing.

These drugs have longer half-lives than most other AAS, so this should be considered when timing your post cycle clomid use. Here they are:

Deca: 15 days Equipoise: 14 days Primobolan: 10.5 days

Anavar has a half-life of only 8 hours so it should not pose a problem.

GH is probably the most remarkable drug at increasing collagen synthesis. It increases collagen syn in a dose dependant manner -- the more you use, the more you will increase collagen syn. It has also demonstrated this ability in short and long term studies. From what I've read, hGH at 6 iu/day increased the collagen deposition rate by around 250% in damaged collagen structures. This result indicates that the increased biomechanical strength of wounds to collagen structures treated with biosynthetic human growth hormone was produced by an increased deposition of collagen in the collagen structures.

Eq, primo, anavar, and deca are all good -- they increase several biomakers of collagen syn -- ie, type III, II, I, procollagen markers. GH just seems to do so most dramatically.

Use of any of these drugs @ supra-physiological levels with a maintenance dose of test will increase collagen syn while at the same time increase skeletal muscle mass. Skeletal muscle mass gains will not be as dramatic as with large testosterone doses but you have to weigh the risk/reward basis for yourself. Also, these drugs do not satisfy the libido like testosterone, but that is not the point of this thread. It is only to demonstrate that you can increase skeletal muscle and collagen syn at the same time with certain AAS --
i clicked on a link from here i dont want to advertise but heres the link What is Equipoise? | eHow.com

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?

 

[Thatshitcray]

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.

 

[new to the game]

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

 

[BigNick002]

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?

 

[Dr JIM]

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!

 

[Michael Scally MD]

[OA] [Sheep] Genomic and Lipidomic Actions of Nandrolone On Detached Rotator Cuff Muscle

Highlights

• 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

 

[Michael Scally MD]

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.

 

[Cowardly Lion]

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.

 

[Michael Scally MD]

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