Joints/Tendons/Bone

First post here, so hi! Ill give some background - competed in powerlifting, never took anything performance enhancing in the slightest and am v much against them in any comps where the ethos is drug free. Other feds, not bothered in the slightest. Anyway, ive been out for a year with torn ligaments in my clavicle and have tried all conventional methods - cortisone, physio, prolo and PRP and non worked. As you all can appreciate, totally depressed and may not lift again at this rate, at least not for a v long time. So, having done some reading, im considering giving hgh a try, perhaps on prescription if possible from a doc as I think its fair to say ive tried ever other reasonable method (surgery isnt an option)
Ive read through many posts on here but couldnt quite find the anser so apologies for asking what may be an age old question - would hgh without any other stacks assist do you think? most seem to take other stacks with it. Im thinking of combining it with regular PRP to see if that helps. Any recommendations of injecting into the ligament or just the thigh? Thanks
 
I have been experiencing tendon problems lately and I suspect it is due to aas. I have never had a problem until now. I have always run eq on cycle and this current cut I'm on I ditched the eq. I'm not sure if it's related or not but if I sprint hard I pull my hamstring every single time. not bad but enough to put me out for a week or so. I'm going to add eq to my cut Friday. I hope this solves my problems
 
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


While there is no doubt essentially all AAS increase the synthesis of collagen or it's precursors there is NO evidence this collagen is destined for the supportive structures of joints including; tendons, ligaments and articular cartilage in particular.

The fact is while AAS have unequivocally been shown to selectively increase SKM protein synthesis, their ability to enhance collagen synthesis is anything but selective, and quite likely involves the deposition, in one form or another, in organs or organ systems that require collagen as their matrix.

What organs need collagen as a foundation for tensile strength, cellular cohesion, and overall structural stability, about every one in the human body.

The point, contrary to popular belief AAS DO NOT selectively enhance or strengthen articular collagenous structures via a "increased collagen production".

For this reason BB and lifters should slowly increase the weight and rate of acceleration while lifting. This is even more important for noobs or those whom have been out of the gym a while BC like SKM tendons atrophy also.

These factors alone have been shown to reduce the rate of tendon disruption.

Best
Jim
 
First post here, so hi! Ill give some background - competed in powerlifting, never took anything performance enhancing in the slightest and am v much against them in any comps where the ethos is drug free. Other feds, not bothered in the slightest. Anyway, ive been out for a year with torn ligaments in my clavicle and have tried all conventional methods - cortisone, physio, prolo and PRP and non worked. As you all can appreciate, totally depressed and may not lift again at this rate, at least not for a v long time. So, having done some reading, im considering giving hgh a try, perhaps on prescription if possible from a doc as I think its fair to say ive tried ever other reasonable method (surgery isnt an option)
Ive read through many posts on here but couldnt quite find the anser so apologies for asking what may be an age old question - would hgh without any other stacks assist do you think? most seem to take other stacks with it. Im thinking of combining it with regular PRP to see if that helps. Any recommendations of injecting into the ligament or just the thigh? Thanks

I can see this post is somewhat dated but it sure would help if you could post the FORMAL DIAGNOSIS bc this sounds like an A-C separation which for stage I-III disruptions are generally treated non-operatively and stage IV operatively.

The problem in attempting to use ANY drug to improve tendon growth is these lesions (Stage III -IV) are in constant motion of sorts, and consequently the best option is surgery if either PAIN (removal of the distal clavicle bc of underlying A-C degenerative arthritis) or INSTABILITY (attachment of a synthetic corico-clavicular ligament in stage IV lesions)

Regs
Jim
 
I was catching up on this post and had some recent thoughts to review/ and docs... I recently cracked into a bottle of DEER ANTLER VELVET or whatever the shit its called (I've never been DESPERATE ENOUGH TO try the bullshit.... I think I got the stuff because I THOUGHT it was marketed as HARD-ON / Cialis type Dik Meds. But I got massive headaches twice in a row after taking for a couple of days in a row..(not sure what that's worth..) And what I found was a bit surprising. The research APPEARS to state that the deer which the antler velvet comes from are apparently FARMED as a source to SCRAPE and HARVEST this "antler velvet' from ( So it's bigger than cruelty to animals for horns...) LOL.. ... What further surprised me is that the stated active ingredient in the Antler Velvet is supposed to be IGF-1...!?!?!?! And while they state in many studies that Deer Antler Velvet is worthless ORALLY, It makes you wonder how difficult it would be to put into solution and inject/ And is that what the smarter folks have been doing all along...???!!!!??? And also notably, the information started out as to claim some kind of ESTROGENIC property associated with Deer antler velvet, which while the advertised, I could not tell if ANTagoinistic, or Agonist/ or neither, could not be sure...
 
Tore my bicep last year and had surgery to fix it. Now I tore my tricep having surgery next week.. I only run test c was wondering if I had added Eq this wouldn't have happened
 
Tore my bicep last year and had surgery to fix it. Now I tore my tricep having surgery next week.. I only run test c was wondering if I had added Eq this wouldn't have happened

-------
The injury has nothing to do with what AAS you chose to use or not use because again AAS do NOT SELECTIVELY enhance the production of articular collagen.

Any suggestion to the contrary is "bro science" and is not supported in the literature.

Regs
Jim
 
-------
The injury has nothing to do with what AAS you chose to use or not use because again AAS do NOT SELECTIVELY enhance the production of articular collagen.

Any suggestion to the contrary is "bro science" and is not supported in the literature.

Regs
Jim
So it only weakens articular collagen?
 
So it only weakens articular collagen?

I never said or implied that because their effects are much more complex.

It's prophetic how many BB and lifters want physiological processes to occur in a vacuum, separate from other metabolic factors that influence the end product, in this case collagen.

Nonetheless their are no reliable human studies that suggest AAS weaken articulat cartilage but rather a few lifters who push the capabilities of those connections to their breaking point, (as a consequence of the heavy lifting they are now capable of because of AAS) with the end result being disruption.

The bottom line is AAS can accelerate muscular growth with such efficiency and proficiency that tendon overload may occur.

Regs
Jim
 
@Dr JIM hey sorry to bug ya .. but was wondering if you have ever seen a popping hamstring tendon at the back of the knee. there is a sublaxution, that occurs when squatting past 90 , especially with a narrow stance. It doesnt casue pain, just annoying popping sensation. coupled with very tight hamstrings. Ive been stretching , avoiding this popping during squating and foam rolling, but there seems to be very little info out there on it.

thanks in advance tile

also i have golfers elbow, and i agree i happened for several reasons creating the perfect storm.

aas increased strength. i therefore increased weight too fast. I was out of the gym for a few years, and my muscles returned quick, but tendons take longer. To little rest inbetween upper body movements. lock out in the gym with my elbows. To many chinups. All created the perfect environment to injure myself. Now i am still fighting this. took 7 day leave .. after working around it for month and a half. it didnt heal . i lift around it. change grip if it hurts. more rep lighter weight. lots of negatives. stretch day and night. foam roll my forearms. lotion them up , and rub the tendons knots the fuck out . do certain weighted pt movemtents to stretch all those components.
 
Tendon and Skeletal Muscle Matrix Gene Expression and Functional Responses to Immobilisation and Rehabilitation in Young Males: Effect of Growth Hormone Administration


Key points
· Loss of muscle and tendon function during periods of immobilisation and rehabilitation represents a challenge in clinical medicine. •
· It is not known to what extent growth hormone (GH) supplementation is able to counteract the absence of mechanical loading during immobilisation in musculo-tendinous connective tissue. •
· This study examines the effect of GH in musculo-tendinous connective tissue in humans during immobilisation and subsequent rehabilitation. •
· The main study findings were the observation that GH supplementation stimulates collagen expression in musculo-tendinous tissue and abolishes the normal decline in tendon stiffness and lysyl oxidase during immobilisation. Furthermore, GH supplementation results in an increased tendon size and stiffness during rehabilitation. •
· GH supplementation has a matrix-stabilising effect during periods of inactivity and rehabilitation in humans. •

Boesen AP, Dideriksen K, Couppe C, et al. Tendon and skeletal muscle matrix gene expression and functional responses to immobilisation and rehabilitation in young males: effect of growth hormone administration. J Physiol 2014;591(Pt 23):6039-52. http://jp.physoc.org/content/591/23/6039.abstract

We examined the effect of growth hormone (GH) on connective tissue of tendon and skeletal muscle during immobilisation and re-training in humans.

Young men (20-30 years; n = 20) were randomly assigned to daily recombinant human GH (rhGH) (33-50 mug kg(-1) day(-1)) or placebo (Plc), and had one leg immobilised for 2 weeks, followed by 6 weeks of strength training. The cross-sectional area (CSA), maximal muscle strength (maximal voluntary contraction, MVC) and biomechanical properties of the quadriceps muscle and patellar tendon were determined.

Muscle and tendon biopsies were analysed for mRNA of collagen (COL1A1/3A1), insulin-like growth factors (IGF-1Ea/Ec), lysyl oxidase (LOX), matrix metalloproteases (MMP-2 and MMP-9), decorin and tenascin-C. Fibril morphology was analysed by transmission electron microscopy (TEM) to detect changes in the fibril diameter distribution.

In muscle, CSA and MVC declined with immobilisation and recovered with rehabilitation similarly in both groups. Likewise, both groups showed increased IGF-1Ea/Ec and COL1A1/3A1 expression in muscle during re-training after immobilisation compared with baseline, and the increase was more pronounced when subjects received GH.

The tendon CSA did not change during immobilisation, but increased in both groups during 6 weeks of rehabilitation ( approximately 14%). A decline in tendon stiffness after immobilisation was observed only in the Plc group, and an increase during 6 weeks of rehabilitation was observed only in the GH group. IGF-1Ea and COL1A1/3A1 mRNA increased with immobilisation in the GH group only, and LOX mRNA was higher in the GH group than in the Plc group after immobilisation.

Both groups showed an increase in MMP-2 with immobilisation, whereas no changes in MMP-9, decorin and tenascin-C were observed. The tendon fibril diameter distribution remained unchanged in both groups.

In conclusion, GH stimulates collagen expression in both skeletal muscle and tendon, abolishes the normal inactivity-related decline in tendon stiffness and LOX, and results in increased tendon CSA and stiffness during rehabilitation. GH has a matrix-stabilising effect during periods of inactivity and rehabilitation in humans.
 
I have lateral Semitendinosus, snapping bicep formis tendon on my left back knee. My elbow tendonidis seems to be going away, but know this knee thing is really pissing me the fuck off
 
Boesen AP, Dideriksen K, Couppe C, et al. Effect of growth hormone on aging connective tissue in muscle and tendon: gene expression, morphology, and function following immobilization and rehabilitation. J Appl Physiol (1985) 2014;116(2):192-203. http://jap.physiology.org/content/116/2/192

It is unknown whether loss in musculotendinous tissue during inactivity can be counteracted by growth hormone (GH), and whether GH accelerate rehabilitation in aging individuals.

Elderly men (65-75 yr; n = 12) had one leg immobilized 2 wk followed by 6 wk of retraining and were randomly assigned to daily injections of recombinant GH (rhGH; n = 6) or placebo (Plc; n = 6). Cross-sectional area (CSA), muscle strength (MVC), and biomechanical properties of m. quadriceps and patellar tendon were determined. Muscle and tendon biopsies were analyzed for gene expressions (mRNA) of collagen (COL1A1/3A1) and insulin-like growth factors (IGF-1Ea/Ec). Fibril morphology was analyzed by transmission electron microscope (TEM).

In tendon, CSA and biomechanical properties did not change following immobilization, but an increase in CSA was found after 6 wk of rehabilitation in both groups. The changes were more pronounced when GH was injected. Furthermore, tendon stiffness increased in the GH group. Muscle CSA declined after immobilization in the Plc but not in the GH group. Muscle CSA increased during retraining, with a significantly larger increase in the GH group compared with the Plc group.

Both a time and a group effect were seen for IGF-1Ea/Ec and COL1A1/3A1 mRNA expression in muscle, with a difference between GH and Plc. IGF-1Ea/Ec and COL-1A1/3A1 mRNA expression increased in muscle following immobilization and retraining in subjects receiving GH, whereas an increase in IGF-1Ec mRNA expression was seen in the Plc group only after retraining.

In conclusion, in elderly humans, GH seems to have a matrix stabilizing effect during inactivity and rehabilitation by stimulating collagen expression in the musculotendinous tissue and increasing tendon CSA and stiffness.
 
Hansen M, Boesen A, Holm L, Flyvbjerg A, Langberg H, Kjaer M. Local administration of insulin-like growth factor-I (IGF-I) stimulates tendon collagen synthesis in humans. Scand J Med Sci Sports 2013;23(5):614-9. http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0838.2011.01431.x/abstract

Collagen is the predominant structural protein in tendons and ligaments, and can be controlled by hormonal changes. In animals, injections of insulin-like growth factor I (IGF-I) has been shown to increase collagen synthesis in tendons and ligaments and to improve structural tissue healing, but the effect of local IGF-I administration on tendon collagen synthesis in human has not been studied.

The purpose of this study was to study whether local injections of IGF-I would have a stimulating effect on tendon collagen synthesis. Twelve healthy nonsmoking men [age 62 +/- 1 years (mean +/- SEM), BMI 27 +/- 1] participated. Two injections of either human recombinant IGF-I (0.1 mL Increlex(c)) or saline (control) into each patellar tendon were performed 24-h apart, respectively.

Tendon collagen fractional synthesis rate (FSR) was measured by stable isotope technique in the hours after the second injection. Simultaneously, interstitial peritendinous (IGF-I) and [procollagen type I N-terminal propeptide (PINP)], as a marker for type I collagen synthesis, were determined by microdialysis technique.

Tendon collagen FSR and PINP were significantly higher in the IGF-I leg compared with the control leg (P < 0.05).

In conclusion, local IGF-I administration can directly enhance tendon collagen synthesis both within and around the human tendon tissue.
 
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

I am 35 with 3 knee surgeries under my belt. I powerlifted and played football most of my life. For me Deca is incredible, but understand that every one body is different, what works for me may not work for you. The only way to find out what works (for you), is to try the drugs out. I have tried EQ and Winny and neither compare to what Deca gives me, its the closest thing to a fountain of youth feeling (joint-wise) I have experienced.


Hope this helps,

Big Mike
 
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
What if you use BOTH Winstrol AND EQ?
 
[Rats] Anabolic Steroids Activate Calcineurin-Nfat Signaling and Thereby Increase Myotube Size and Reduce Denervation Atrophy

Highlights
· Calcineurin activity declined and NFATc4 was excluded from the nucleus in denervated muscle.
· Nandrolone increased calcineurin–NFAT signaling in myoblasts and denervated muscles.
· Nandrolone induced myoblast hypertrophy and protected against denervation atrophy.
· These data identify calcineurin–NFAT signaling as a novel target for androgen action.

Qin W, Pan J, Wu Y, Bauman WA, Cardozo C. Anabolic steroids activate calcineurin-NFAT signaling and thereby increase myotube size and reduce denervation atrophy. Mol Cell Endocrinol 2014;399C:336-45. https://www.sciencedirect.com/science/article/pii/S0303720714003050

Anabolic androgens have been shown to reduce muscle loss due to immobilization, paralysis and many other medical conditions, but the molecular basis for these actions is poorly understood.

We have recently demonstrated that nandrolone, a synthetic androgen, slows muscle atrophy after nerve transection associated with down-regulation of regulator of calcineurin 2 (RCAN2), a calcineurin inhibitor, suggesting a possible role of calcineurin-NFAT signaling.

To test this possibility, rat gastrocnemius muscle was analyzed at 56 days after denervation.

In denervated muscle, calcineurin activity declined and NFATc4 was excluded from the nucleus and these effects were reversed by nandrolone. Similarly, nandrolone increased calcineurin activity and nuclear NFATc4 levels in cultured L6 myotubes.

Nandrolone also induced cell hypertrophy that was blocked by cyclosporin A or overexpression of RCAN2. Finally protection against denervation atrophy by nandrolone in rats was blocked by cyclosporin A.

These results demonstrate for the first time that nandrolone activates calcineurin-NFAT signaling, and that such signaling is important in nandrolone-induced cell hypertrophy and protection against paralysis-induced muscle atrophy.
 
Wu BW, Berger M, Sum JC, Hatch GF, 3rd, Schroeder ET. Randomized control trial to evaluate the effects of acute testosterone administration in men on muscle mass, strength, and physical function following ACL reconstructive surgery: rationale, design, methods. BMC Surg 2014;14(1):102. http://www.biomedcentral.com/1471-2482/14/102/abstract

BACKGROUND: The anterior cruciate ligament (ACL) is one of four major ligaments in the knee that provide stability during physical activity. A tear in the ACL is characterized by joint instability that leads to decreased activity, knee dysfunction, reduced quality of life and a loss of muscle mass and strength. While rehabilitation is the standard-of-care for return to daily function, additional surgical reconstruction can provide individuals with an opportunity to return to sports and strenuous physical activity.

Over 200,000 ACL reconstructions are performed in the United States each year, and rehabilitation following surgery is slow and expensive. One possible method to improve the recovery process is the use of intramuscular testosterone, which has been shown to increase muscle mass and strength independent of exercise.

With short-term use of supraphysiologic doses of testosterone, we hope to reduce loss of muscle mass and strength and minimize loss of physical function following ACL reconstruction compared to standard-of-care alone.

METHODS/DESIGN: This study is a double-blinded randomized control trial. Men 18-50 years of age, scheduled for ACL reconstruction are randomized into two groups.

Participants randomized to the testosterone group receive intramuscular testosterone administration once per week for 8 weeks starting 2 weeks prior to surgery. Participants randomized to the control group receive a saline placebo intramuscularly instead of testosterone.

Lean mass, muscle strength and physical function are measured at 5 time points: 2 weeks pre-surgery, 1 day pre-surgery, and 6, 12, 24 weeks post-surgery. Both groups follow standard-of-care rehabilitation protocol.

DISCUSSION: We believe that testosterone therapy will help reduce the loss of muscle mass and strength experienced after ACL injury and reconstruction. Hopefully this will provide a way to shorten the rehabilitation necessary following ACL reconstruction. If successful, testosterone therapy may also be used for other injuries involving trauma and muscle atrophy.
 
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