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ultrasafe
11-11-2008, 12:27 PM
This is a great read for anybody cocerned about joints/ligaments while deciding what AAS to use..

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,

big_luse
11-11-2008, 06:28 PM
This only applies to high dose test ... moral of the story? Eq, Deca, or Var should alwsys be run with it.

ultrasafe
11-11-2008, 07:58 PM
high does test?? Anything over 200mg per week and you are weaken your joints.

chan_ho_nam
11-11-2008, 11:27 PM
I didnt know that about anavar, might have to pony up to give it a go.

liquidfire
12-11-2008, 12:10 AM
Good post bro.

Kilburn
12-11-2008, 04:31 AM
what about tren? it is sort of like deca. it must do something.

muscleshark
12-11-2008, 10:31 PM
what about tren? it is sort of like deca. it must do something.

Tren is nothing like deca. One is a prolactin, one is a progesterone, only thing they hold in common as they won't induce estrogen related gyno.

Rhinobolt10
12-11-2008, 10:36 PM
I've never seen info on tren for the joints... but I'd like to

azian257
12-11-2008, 10:49 PM
Tren and collagen synthesis

originally posted by hooker on qualitymuscle


Actually, it stands to reason that Tren does, in fact, stimulate collagen synthesis.

You see, tren increases IGF-1 to a great degree, which ought to stimulate the growth of tendons, as we all know.

Endocrinology. 1989 May;124(5):2110-7.

Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin-like growth factor I.

Thompson SH, Boxhorn LK, Kong WY, Allen RE.

Department of Animal Sciences, University of Arizona, Tucson 85721.

The potential role of satellite cells in mediating the effect of trenbolone [17 beta-hydroxyestra-4,9-11-trien-3-one (TBOH)] on skeletal muscle hypertrophy was examined. Young female Sprague-Dawley rats received TBOH injections daily for 2 weeks; growth, body composition, and the composition of selected muscles were assessed. Treated rats grew more rapidly and deposited less body lipid and more protein. The semimembranosus muscle from treated rats was larger and had approximately 60% more DNA per muscle than muscles from control rats. The addition of trenbolone directly to the medium of cultured satellite cells did not stimulate cell proliferation, nor did it augment the stimulatory response of these cells to fibroblast growth factor (FGF) or insulin-like growth factor I (IGF-I). In contrast, satellite cells cultured from TBOH-treated rats exhibited greater proliferative responses to FGF and IGF-I than satellite cells from control rats. In addition, serum from TBOH-treated rats stimulated greater cell proliferation in satellite cell cultures than serum from control rats. These experiments suggest that one possible mechanism responsible for the ability of TBOH to stimulate skeletal muscle hypertrophy may be through enhanced proliferation and differentiation of satellite cells as a result of the increased sensitivity of these cells to IGF-I and FGF.

PMID: 2707149 [PubMed - indexed for MEDLINE]
You will also note that Tren treated satellite cells showed an increased response to FGF (fibroblast growth factor). Again, as we know, (basic)FGF stimulates collagen synthesis:

Sports Med. 2003;33(5):381-94.The roles of growth factors in tendon and ligament healing.

Molloy T, Wang Y, Murrell G.

Orthopaedic Research Institute, St George Hospital Campus, University of New South Wales, Sydney, Australia.

Tendon healing is a complex and highly-regulated process that is initiated, sustained and eventually terminated by a large number and variety of molecules. Growth factors represent one of the most important of the molecular families involved in healing, and a considerable number of studies have been undertaken in an effort to elucidate their many functions. This review covers some of the recent investigations into the roles of five growth factors whose activities have been best characterised during tendon healing: insulin-like growth factor-I (IGF-I), transforming growth factor beta (TGFbeta), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and basic fibroblast growth factor (bFGF). All five are markedly up-regulated following tendon injury and are active at multiple stages of the healing process. IGF-I has been shown to be highly expressed during the early inflammatory phase in a number of animal tendon healing models, and appears to aid in the proliferation and migration of fibroblasts and to subsequently increase collagen production. TGFbeta is also active during inflammation, and has a variety of effects including the regulation of cellular migration and proliferation, and fibronectin binding interactions. VEGF is produced at its highest levels only after the inflammatory phase, at which time it is a powerful stimulator of angiogenesis. PDGF is produced shortly after tendon damage and helps to stimulate the production of other growth factors, including IGF-I, and has roles in tissue remodelling.In vitro and in vivo studies have shown that bFGF is both a powerful stimulator of angiogenesis and a regulator of cellular migration and proliferation. This review also covers some of the most recent studies into the use of these molecules as therapeutic agents to increase the efficacy and efficiency of tendon and ligament healing. Studies into the effects of the exogenous application of TGFbeta, IGF-I, PDGF and bFGF into the wound site singly and in combination have shown promise, significantly decreasing a number of parameters used to define the functional deficit of a healing tendon. Application of IGF-I has been shown to increase in the Achilles Functional Index and the breaking energy of injured rat tendon. TGFbeta and PDGF have been shown separately to increase the breaking energy of healing tendon. Finally, application of bFGF has been shown to promote cellular proliferation and collagen synthesis in vivo.



Therefore, Trenbolone, by stimulating (b)FGF as well as IGF-1 - certainly would stimulate collagen synthesis. I don't know of anyone who claims tren healed any injuries...but the evidence is here to suggest it.

big_luse
13-11-2008, 12:10 AM
ALL AAS will increase IGF-1 levels through various mechanisms (nitrogen retention is a biggy I think).

SteveMan
13-11-2008, 11:06 AM
So using test could increase chances of tendonitis? Because recently I have had tendonitis in my elbow joints, severe enough where I had to quit playing rugby. I only use 500mg test e/week, I have been on for the last 4 months.

ultrasafe
13-11-2008, 12:12 PM
Anatomically it could. Remember everybody is different but the science and research is there.

When your on cycle if you really want to have a concern for your connective tissue keep these 2 things in mind.




1=Skeletal muscle adaptations (i.e.hypertrophy and strength increases) take place rather rapidly in comparison to connective tissue.
Therefore, tendon injuries in athletes are thought to occur from a rapid increase in training intensity and volume where connective tissue fails to withstand the overload.

As you become stronger increase you progressions of weight slowly. Why? tendon injuries in athletes are thought to occur from a rapid increase in training intensity and volume. The excitement of feeling stronger leads people to want to one rep max every session to see how strong they really are. Say no to EGO! This isn't saying you can't lift heavy weights, this is saying don't pile on large amounts of weight for excitement sake. It's a natural reaction even if you are training as a bodybuilder/athlete to take on a powerlifting mentality when you feel strong. Keep it in check.


2=Strength levels fluctuate on a daily basis.. This means you could lift for two weeks and increase weight and in the third week for whatever reason you don't feel as strong on a given day. Don't be of the mind set that you have to fail at max effort. The percentage of one rep max and total maximum effort is a small percentage in even an elite powewrlifter/athlete.

So don't be of the mindset that you have to push through the sets and reps every single workout. Why? Strength levels fluctuate on a daily basis. Even though your on steroids outside stresses can still cause you to have a bad day on occasion. Weightlifting is an external stressor. If your having a bad day don't pound your body.

If you keep these 2 points in mind it could help releave stress to you body and connective tissue, still have productive workouts and most likely help you to enjoy the ride.

drdnj
13-11-2008, 12:29 PM
This is good advice....
I am paying for this now with having two full distal biceps tendon ruptures in 3 years (1 on left arm and 1 on right arm). When the surgeons went in they said my tendons were brittle and calcified-----

Kilburn
13-11-2008, 03:53 PM
Tren and collagen synthesis

originally posted by hooker on qualitymuscle


Actually, it stands to reason that Tren does, in fact, stimulate collagen synthesis.

You see, tren increases IGF-1 to a great degree, which ought to stimulate the growth of tendons, as we all know.

Endocrinology. 1989 May;124(5):2110-7.

Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin-like growth factor I.

Thompson SH, Boxhorn LK, Kong WY, Allen RE.

Department of Animal Sciences, University of Arizona, Tucson 85721.

The potential role of satellite cells in mediating the effect of trenbolone [17 beta-hydroxyestra-4,9-11-trien-3-one (TBOH)] on skeletal muscle hypertrophy was examined. Young female Sprague-Dawley rats received TBOH injections daily for 2 weeks; growth, body composition, and the composition of selected muscles were assessed. Treated rats grew more rapidly and deposited less body lipid and more protein. The semimembranosus muscle from treated rats was larger and had approximately 60% more DNA per muscle than muscles from control rats. The addition of trenbolone directly to the medium of cultured satellite cells did not stimulate cell proliferation, nor did it augment the stimulatory response of these cells to fibroblast growth factor (FGF) or insulin-like growth factor I (IGF-I). In contrast, satellite cells cultured from TBOH-treated rats exhibited greater proliferative responses to FGF and IGF-I than satellite cells from control rats. In addition, serum from TBOH-treated rats stimulated greater cell proliferation in satellite cell cultures than serum from control rats. These experiments suggest that one possible mechanism responsible for the ability of TBOH to stimulate skeletal muscle hypertrophy may be through enhanced proliferation and differentiation of satellite cells as a result of the increased sensitivity of these cells to IGF-I and FGF.

PMID: 2707149 [PubMed - indexed for MEDLINE]
You will also note that Tren treated satellite cells showed an increased response to FGF (fibroblast growth factor). Again, as we know, (basic)FGF stimulates collagen synthesis:

Sports Med. 2003;33(5):381-94.The roles of growth factors in tendon and ligament healing.

Molloy T, Wang Y, Murrell G.

Orthopaedic Research Institute, St George Hospital Campus, University of New South Wales, Sydney, Australia.

Tendon healing is a complex and highly-regulated process that is initiated, sustained and eventually terminated by a large number and variety of molecules. Growth factors represent one of the most important of the molecular families involved in healing, and a considerable number of studies have been undertaken in an effort to elucidate their many functions. This review covers some of the recent investigations into the roles of five growth factors whose activities have been best characterised during tendon healing: insulin-like growth factor-I (IGF-I), transforming growth factor beta (TGFbeta), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and basic fibroblast growth factor (bFGF). All five are markedly up-regulated following tendon injury and are active at multiple stages of the healing process. IGF-I has been shown to be highly expressed during the early inflammatory phase in a number of animal tendon healing models, and appears to aid in the proliferation and migration of fibroblasts and to subsequently increase collagen production. TGFbeta is also active during inflammation, and has a variety of effects including the regulation of cellular migration and proliferation, and fibronectin binding interactions. VEGF is produced at its highest levels only after the inflammatory phase, at which time it is a powerful stimulator of angiogenesis. PDGF is produced shortly after tendon damage and helps to stimulate the production of other growth factors, including IGF-I, and has roles in tissue remodelling.In vitro and in vivo studies have shown that bFGF is both a powerful stimulator of angiogenesis and a regulator of cellular migration and proliferation. This review also covers some of the most recent studies into the use of these molecules as therapeutic agents to increase the efficacy and efficiency of tendon and ligament healing. Studies into the effects of the exogenous application of TGFbeta, IGF-I, PDGF and bFGF into the wound site singly and in combination have shown promise, significantly decreasing a number of parameters used to define the functional deficit of a healing tendon. Application of IGF-I has been shown to increase in the Achilles Functional Index and the breaking energy of injured rat tendon. TGFbeta and PDGF have been shown separately to increase the breaking energy of healing tendon. Finally, application of bFGF has been shown to promote cellular proliferation and collagen synthesis in vivo.



Therefore, Trenbolone, by stimulating (b)FGF as well as IGF-1 - certainly would stimulate collagen synthesis. I don't know of anyone who claims tren healed any injuries...but the evidence is here to suggest it.

thanks for this. i was wondering about tren because my cycle right now. is

625mg test e
300mg tren e
150mg EQ

so i hope that tren is helping my tendons cause that's alot of test and not alot of EQ. i'm also taking winny right now too which could also make it worse. fingers crossedthat i have no problems.


This is good advice....
I am paying for this now with having two full distal biceps tendon ruptures in 3 years (1 on left arm and 1 on right arm). When the surgeons went in they said my tendons were brittle and calcified-----

really? how old are you?

tendon rupture is basically like a tear right? do your biceps look sort of fuked up afterwards? i think i might have partially torn my left bicep back when i was natural and skrawny as fuk. pretty sure it was concentration curls and cheating up the last reps that did it. god i was such a frail, weak pathetic excuse for a human back then. people say youre more prone to injury when juicing but so far the opposite has been true for me.