Joints/Tendons/Bone

[BBC3]

This one should prove interesting where-AS studies and real use application will ultimately FAIL and due to lack of proper understanding caused by the steroid witch hunt damage now manifesting...

What I am saying is that while the application of synthetic testosterone may bolster "Protein synthesis" in the body (no data seen yet/ i think inconclusive and may bolster USE of protein synthesis), and may speed RECOVERY or muscle-skeletal tissue, the protocol and administration routines should be critical to any potential success - ELSE it's a set up.

For example. Testosterone supplementation in excess of 400mgs/week tends to get muscles so fucking pumped, THAT THEY ARE PUMPED...! This can cause problems however if things are not balanced. In my example I use the Dreaded "D-Bol lower back pump" as example. And - AS - this type pump DOES occur from T-cyp supplementation alone..! What I found was that the negative effects of the lower back pump on the body are not as profound if OPPOSING ABDOMINAL Muscles are well trained. This is a "Bust-Tel-Point", as many folks just don't like to work abz. So the long and short is you get your back to pumped and ABs all weak and you jerk yer spine out of alignment... The spine being a particularly clear "Tell" as once the muscles related to spinal vertebra and CNS get out of what, a "Pull" tends to result in MORE PULL. Thus the vicious cycle and spin of course mean a REPORT somewhere ELSE...

All that said. The patients potentially using testosterone in conjunction with any surgical rehab protocol will need to be sure to have a PROPER application plan in place. Else the T will EQUAL TROUBLE... In more ways than one too..

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.

 

[Michael Scally MD]

Zolin SJ, Vodovotz Y, Forsythe RM, Rosengart MR, Namas R, et al. The early evolving sex hormone environment is associated with significant outcome and inflammatory response differences after injury. J Trauma Acute Care Surg. 2015;78(3):451-8. http://journals.lww.com/jtrauma/pages/futuretoc.aspx?futuretocid=20

BACKGROUND: Clinical research characterizing the mechanisms responsible for sex-based outcome differences after injury remains conflicting. Currently lacking is an understanding of the early sex hormone milieu of the injured patient and the effects these early hormone differences have on clinical outcomes and the innate immune response following injury.

METHODS: A prospective cohort study was performed over a 20-month period. Blunt injury patients requiring intensive care unit admission were enrolled. Samples were collected within 6 hours and at 24 hours after injury and were analyzed for total testosterone (TT) and estradiol concentrations.

Outcomes of interest included multiple-organ failure (MOF; Marshall Multiple Organ Dysfunction Score [MODScore] > 5), nosocomial infection (NI), mortality, and serial cytokine/chemokine measurements. Multivariate logistic regression was used to determine the independent risks associated with early sex hormone measurements.

RESULTS: In 288 prospectively enrolled patients, 69% were male, with a median Injury Severity Score (ISS) of 16 (interquartile range 10-21). Elevated TT levels at 6 hours were associated with elevated interleukin 6 levels and cytokine/chemokine measurements (18 of 24 measured).

Rising TT levels were significantly associated with more than a fivefold and twofold higher independent risk of MOF and NI, respectively (odds ratio [OR], 5.2; p = 0.02; 95% confidence interval [CI], 1.2-22.3; and OR, 2.1; p = 0.03; 95% CI, 1.02-4.2).

At 24 hours, TT levels were no longer associated with poor outcome, while estradiol levels were significantly associated with nearly a fourfold higher independent risk of MOF (OR, 3.9; p = 0.04, 95% CI, 1.05-13).

CONCLUSION: Early elevations and increasing testosterone levels over initial 24 hours after injury are associated with an exaggerated inflammatory response and a significantly greater risk of MOF and NI. High estrogen levels at 24 hours are independently associated with an increased risk of MOF.

The current analysis suggests that an early evolving testosterone to estrogen hormonal environment is associated with a significantly higher independent risk of poor outcome following traumatic injury.

LEVEL OF EVIDENCE: Prognostic/epidemiologic study, level II.

 

[BBC3]

Man!! You KNOW I LIKE THIS ONE....!

*** So I find this interesting sentence here essentially stating that the study is BORDERLINE "ANECDOTAL". This must be the "Scientific way" of acknowledging that there MAY BE little difference in "Hearing a tale" (if a sound story teller), and actually watching something happen and recording it (Science). Else its just an introverted nerdy attempt at a sense of humor. Kicks reserved... Bla..

"LEVEL OF EVIDENCE: Prognostic/epidemiologic study, level II."

L................... O......................... L..................................................


But to interpret the study...:

1) They ASSUMED or KNEW that Sex Hormones ELEVATE Post traumatic injury..?

2) So are the trying to determine if MEN are "Stronger Survivors"...?!?

3) Or would they like to prove that Estrogen laden MEN (fat boys) AND Just-Women are weaker and don't recover as well as otherwise...?

4) IN SHORT, one might interpret that THEY DEDUCE that after an initial heavy TT response to injury, Those with High E2 turnover rate at 24 hours had worse outcomes...

5) The study principle mechanism reviewed appears to pertain to the FLESH and SOFT TISSUE - As the MEANS IN I am speculating....

- This would make sense to me as the injury to my knee in which a Strep A infection ensued almost like a VIRAL WEB POST - and I'm in no short supply of Estrogen right now. LOL

- ALSO INTERESTING as I recall my leg swelling up like a balloon about 24 hours after the strep took hold good... BUT 48-72 Hrs post injury....

- Does Estrogen DELAY inflammatory immune Type response...?

- Would my heart and spleen have been next on the menu...?

** From WIKI - (Funny they use the TERM - NECROSIS)...

• Tumor necrosis factor (TNF), formerly known as TNFα or TNF alpha, is the best-known member of this class. TNF is amonocyte-derived cytotoxin that has been implicated in tumor regression, septic shock, and cachexia.[2][3] The protein is synthesized as a prohormone with an unusually long and atypical signal sequence, which is absent from the mature secreted cytokine.[4] A short hydrophobic stretch of amino acids serves to anchor the prohormone in lipid bilayers.[5] Both the mature protein and a partially processed form of the hormone can be secreted after cleavage of the propeptide.[5]
• Lymphotoxin-alpha, formerly known as Tumor necrosis factor-beta (TNF-β), is a cytokine that is inhibited by interleukin 10.[6]

*** (definition from another source)
"Interleukin 6 (IL-6) is an interleukin that acts as both a pro-inflammatory cytokine and an anti-inflammatory myokine. In humans, it is encoded by the IL6 gene."

(Now here is a killer laymanizing site I stumbled on...)
http://www.news-medical.net/health/Interleukin-6-What-is-Interleukin-6.aspx

EXCERPT..:
What is Interleukin 6?
Interleukin-6 (IL-6) is a protein that in humans is encoded by the ''IL6'' gene.

IL-6 is an interleukin that acts as both a pro-inflammatory and anti-inflammatory cytokine. It is secreted by T cells and macrophages to stimulate immune response to trauma, especially burns or other tissue damage leading to inflammation.

In terms of host response to a foreign pathogen, IL-6 has been shown, in mice, to be required for resistance against the bacterium, ''Streptococcus pneumoniae''. IL-6 is also a "myokine," a cytokine produced from muscle, and is elevated in response to muscle contraction. It is significantly elevated with exercise, and precedes the appearance of other cytokines in the circulation.

During exercise, it is thought to act in a hormone-like manner to mobilize extracellular substrates and/or augment substrate delivery (Petersen, J Appl Physiol 2005). Additionally, osteoblasts secrete IL-6 to stimulate osteoclast formation. Smooth muscle cells in the tunica media of many blood vessels also produce IL-6 as a pro-inflammatory cytokine.

IL-6's role as an anti-inflammatory cytokine is mediated through its inhibitory effects on TNF-alpha and IL-1, and activation of IL-1ra and IL-10.

Interleukin 6 has been shown to interact with interleukin-6 receptor and glycoprotein 130.


* There's more too if you go there...

I am not going to get on my soap box about hormone levels HAVING NOTHING TO DO WITH ACTUAL METABOLISM AS DIRECT RELATION FOR SURE...

** BUT YOU MUST WONDER IF E2 being an "end-road" hormone CREATES A "BOTTLE-NECK" of sorts..?!? And thus harder to metabolize OUT. And potentially a MORE POTENT hormone and simply because it is the end of the primary "hormonal food chain"..!? So those with propensity to make E2 (fat men and just women) have an immune issue of sorts...!

The REAL QUESTION I THINK is "blood interference". And WHAT the hormone levels may do to other "blood reactants" as affecting their abilities to PERFORM NORMALLY.

Again, I DO want to make merit of the POINT that the PROCESSING or METABOLISM RATES of hormones MAY have play here - And SIMPLY by population alone. To WHAT their "Then device" is I don't pretend to have a clue. But it should be noted as AGAIN MEDICAL SCIENCE IS TAKING "SNAP SHOTS" and FAILING TO WATCH THE MOVIE IN PROGRESS! It's like the same nerds that cheated paying for "Cliff Notes" are STILL fucking relying on CLIFF NOTES. But WORSE is ones that the MANUFACTURE themselves...!

The real MAGIC TRICK to all that Human Body Dance is WHAT is determining WHAT swells up and WHAT Gets turned off. MOST IMPORTANTLY - The WHEN....! And this is VERY IMPORTANT because INFLAMMATION IS THE ROOT OF MOST "SELF-AUTOMATED INCIDENTAL TISSUE DESTRUCTION"...! This is where the Manual Application of "hot/cold" comes into play. And the Critical nature of getting the flow of O2 back to tissue. Its like the body goes into "Self-Amputation mode", and bluntly attempting to kill the few to save the many. But with no logical REGULATION. As this either seems to be where the Human body was failed by its creator, or there are other players which we are unaware...!

** NOTE that one of the sources I pulled from discusses "osteoclast formation". THUS IMPLYING Muscle & Skeletal involvement as pertaining to higher perceived overall immune response as MORE Primary production factors... Again, fat boys and girls take note.

- The study should have considered BMI of the subjects...

- I also wonder what TIME of the MONTH was it for these women in the study..?

I am discerning a common denominator as the KEY TO LONGEVITY IN LIFE appears to be CIRCULATION. Essentially, this is what "Medicine" does with the application of ASPIRIN and later created NSAIDS. Which tend to apply to injury sites LOCALLY and DO THEIR JOBS via increasing OR RESTORING Circulation....! Turn the blood to "firewater" essentially - But HEY- It's flowing again at least right???!!!! In short, NSAIDS essentially having the NET EFFECT of acting like HOT and COLD application but SIMULTANEOUSLY and with no swapping.. Another story for another thread though...

So the moral of the story appears to be - Don't trip and hurt yerself there fatboy...!

Zolin SJ, Vodovotz Y, Forsythe RM, Rosengart MR, Namas R, et al. The early evolving sex hormone environment is associated with significant outcome and inflammatory response differences after injury. J Trauma Acute Care Surg. 2015;78(3):451-8. http://journals.lww.com/jtrauma/pages/futuretoc.aspx?futuretocid=20

BACKGROUND: Clinical research characterizing the mechanisms responsible for sex-based outcome differences after injury remains conflicting. Currently lacking is an understanding of the early sex hormone milieu of the injured patient and the effects these early hormone differences have on clinical outcomes and the innate immune response following injury.

METHODS: A prospective cohort study was performed over a 20-month period. Blunt injury patients requiring intensive care unit admission were enrolled. Samples were collected within 6 hours and at 24 hours after injury and were analyzed for total testosterone (TT) and estradiol concentrations.

Outcomes of interest included multiple-organ failure (MOF; Marshall Multiple Organ Dysfunction Score [MODScore] > 5), nosocomial infection (NI), mortality, and serial cytokine/chemokine measurements. Multivariate logistic regression was used to determine the independent risks associated with early sex hormone measurements.

RESULTS: In 288 prospectively enrolled patients, 69% were male, with a median Injury Severity Score (ISS) of 16 (interquartile range 10-21). Elevated TT levels at 6 hours were associated with elevated interleukin 6 levels and cytokine/chemokine measurements (18 of 24 measured).

Rising TT levels were significantly associated with more than a fivefold and twofold higher independent risk of MOF and NI, respectively (odds ratio [OR], 5.2; p = 0.02; 95% confidence interval [CI], 1.2-22.3; and OR, 2.1; p = 0.03; 95% CI, 1.02-4.2).

At 24 hours, TT levels were no longer associated with poor outcome, while estradiol levels were significantly associated with nearly a fourfold higher independent risk of MOF (OR, 3.9; p = 0.04, 95% CI, 1.05-13).


CONCLUSION: Early elevations and increasing testosterone levels over initial 24 hours after injury are associated with an exaggerated inflammatory response and a significantly greater risk of MOF and NI. High estrogen levels at 24 hours are independently associated with an increased risk of MOF.

The current analysis suggests that an early evolving testosterone to estrogen hormonal environment is associated with a significantly higher independent risk of poor outcome following traumatic injury.

LEVEL OF EVIDENCE: Prognostic/epidemiologic study, level II.

 

[barbelle]

So 12 pages of studies, and to sum it up: it has been well studied that we just don't know yet.

Does anybody think boldenone might work after all? What about 3 weeks of winstrol and high reps to increase brittle collagen, followed by a couple of weeks of bold to make them stronger?

 

[antipcman]

Re: *EQ increases tendon strength*

I LOVE EQ. it works but you'll want to run it 12 weeks for optimal performance at any where between 400-600mg per week. You will feel it brother. I've ran it in so many of my cycles it's basically a staple for me. Some just plain don't like it though. To each his own.

I've read TB500 is great for the joints. Some articles state to site inject and others say sub-Q works just as effectively. There is always GHRPs like ghrp-6, and 2 and 3rd generation ghrp Ipamorelin. The latter-most is the most expensive but is more selective in that you do not get a prolactin spike.

Re: *EQ increases tendon strength*

Has anyone on here ever ran EQ at 900mg/wk? For 12-13 weeks? How do you guys think that would work out?

I had to go somewhere for a week so I took a 3rd pin of EQ (400mg) but I doubt doing that for one week would give me a guage of 900+. However, whenever I run EQ I run it at 800mg/wk and I love it. I donate blood every 4 weeks on it. As somebody previously stated, some people loathe the idea of EQ in a cycle, others like it. I'm an athlete so I enjoy it. I run it every summer. I like being between 190-210 pounds with low bodyfat so I run it with mast and prop. The "increased hunger" does not affect me negatively as I need to bring in clean fats and carbohydrates anyway due to my summer training sessions and weightlifting sessions.

 

[Juri Osa]

There is a new shop that sells out its stock:

http://maxmanpower.biz

 

[mands]

Wtf^^^^ Get outta here!

mands

 

[Swedishsteel]

So 12 pages of studies, and to sum it up: it has been well studied that we just don't know yet.

Does anybody think boldenone might work after all? What about 3 weeks of winstrol and high reps to increase brittle collagen, followed by a couple of weeks of bold to make them stronger?

EQ won't make your joints stronger. The collagen that EQ produce isn't crosslinking
so the collagen will be weak and brittle.

 

[Michael Scally MD]

Chung KJ, Kim KH. Forbidden fruit for athletes, but possible divine blessing for rehabilitation: testosterone. J Exerc Rehabil. 2015;11(1):2-4. http://www.e-jer.org/journal/view.php?number=2013600172

Testosterone is regarded as an attractive supplement for obtaining masculinity and sexuality; however, there have been pros and cons regarding its application as a treatment.

In addition, there is also conventional repulsion on adoption of testosterone to any kind of exercise to anyone with concern with sports.

However, we should keep in mind that in terms of rehabilitation, our main concern is not fairness but efficiency. And there are obvious advantages of testosterone in recovery and rejuvenation.

We aim to introduce the possibility of testosterone in recovery and rejuvenation and are to bring up a topic the application of testosterone in exercise rehabilitation.

Considering the light and darkness in testosterone, moderate use of testosterone under professional medication counseling might be an effective possibility to those with sickness and illness and should be considered as a possible option to assist the recovery from frailty and illness.

 

[Volley_Fire]

EQ won't make your joints stronger. The collagen that EQ produce isn't crosslinking
so the collagen will be weak and brittle.

Interesting. Do you have a source for this information?

 

[Izk]

I would love to see more research regarding the use of peptides, specifically IGF-1 or alternative versions (IGF-1 LR3, etc.), to repair tendons or joints.
Although I'm doing my own research, you guys especially Dr. Scally, probably have more resources and know which sites are more reliable.

 

[leanedout]

Nothing that ive ever used helped tendons like ghrp2 and also researched semorelin together ....healed a nagging shoulder, it was getting to the point where lowering bench weight was necessary .......4 months of research and its healed......deca helps while on, then pain came back.

 

[leanedout]

Re: *EQ increases tendon strength*

I don't think collagen synthesis from EQ can cause "hyperplasia" of the skin or growth. In my experience my skin has been great on EQ. Everytime I take it my acne seems to clear up and my skin dryness goes away. I really don't think that's a coincidence.

BTW, for the record....the best cycle I've ever run as a bulker...


Dbol 40mg ED weeks 1-4
Test E 500mg EW weeks 1-14
Deca 500mg EW weeks 1-12
EQ 600mg EW weeks 1-12

gained a sick amount of mass with very little water weight. I'm going to be running a similar cycle soon but replacing Deca with Tren....I'm excited

Never ran deca and eq togeth? Sounds good though......waiting on new bloodwork for my summer funtime!! Tren is on the menu for sure.....my kidney kevels were weird so i dont want to push it but it wont be the same without it.
Researching 500e, 500eq, 50a-bombs ed till i get the greenlight

My best research last winter was 750-1000cyp....40dbol ed....75 tren every 3rd day-retarded gains

 

[Izk]

Never ran deca and eq togeth? Sounds good though......waiting on new bloodwork for my summer funtime!! Tren is on the menu for sure.....my kidney kevels were weird so i dont want to push it but it wont be the same without it.
Researching 500e, 500eq, 50a-bombs ed till i get the greenlight

My best research last winter was 750-1000cyp....40dbol ed....75 tren every 3rd day-retarded gains

When you say research, you mean cycling/using, right? This place is uncensored.

 

[Justicexx]

look at this www dot legitsteroidpowder dot com it sells legit ones

 

[anky15]

After reading all this i still feel we haven't got the bottom of whether AAS use can help heal ligament/tendon injuries. I recently severely injured my ankle whilst i was using NPP, Tren and test and am due for some surgery to put things back together. I feel that the injury was more of a freak injury rather than me being more prone to it because of AAS use but the thought still comes to my head about what if I wasn't using anything and had the same accident. Although I do not want to pressure my ligaments and tendons to much but I would like to prevent muscle wasting. Another issue is the fact that during this time i would like to give my body a rest from 19 nor steroids due to the fact that I just Don't see the point of putting up with all the side effects while I can not train at my full potential at the gym. Now while saying this I have access to legit primo and eq. Would it be worthwhile adding these things into the mix? or just some gh? I would like to know everyones thoughts. I am also thinking that instead of test I will do HCG 250iuX3 Weekly just to avoid further Collagen issues. Another issue I can think of is the kicking time for EQ any suggestions here as well? Help would be much appreciated. All bloods are in check so no issues there and I'm allowed to start doing upper body work in the gym the week after surgery.

 

[antipcman]

I would love to see more research regarding the use of peptides, specifically IGF-1 or alternative versions (IGF-1 LR3, etc.), to repair tendons or joints.
Although I'm doing my own research, you guys especially Dr. Scally, probably have more resources and know which sites are more reliable.

Don't know if anybody said this yet but BPC-157 is a miracle. I'll find you peer reviewed research. I had an MRI on my shoulder and it turned out to be a partially torn pec and torn labrum. Injecting minimal dose of BPC-157 healed it in a month. I couldn't put up 60 lb DBells in April and was repping 100s in June. Same with the hammer strength Bench. I maxxed out the rack in June. I have babied it with 125 lb dumbbells and haven't touched them in awhile but I'll try again soon. There is a write-up on this site about it. I haven't gotten a post-bpc MRI done yet but the injury was nagging for 5 months.

 

[Izk]

Don't know if anybody said this yet but BPC-157 is a miracle. I'll find you peer reviewed research. I had an MRI on my shoulder and it turned out to be a partially torn pec and torn labrum. Injecting minimal dose of BPC-157 healed it in a month. I couldn't put up 60 lb DBells in April and was repping 100s in June. Same with the hammer strength Bench. I maxxed out the rack in June. I have babied it with 125 lb dumbbells and haven't touched them in awhile but I'll try again soon. There is a write-up on this site about it. I haven't gotten a post-bpc MRI done yet but the injury was nagging for 5 months.

I have been loking into buying some!
All the reviews I've seen are excellent but all anecdotal.
Also most people only use extremes when describing something, so it's hard to believe anyone's review, e.g "I LOVE chipotle it has the BEST food".

Keen to see the studies though!

 

[Michael Scally MD]

Gerber C, Meyer DC, Fluck M, Benn MC, von Rechenberg B, et al. Anabolic Steroids Reduce Muscle Degeneration Associated With Rotator Cuff Tendon Release in Sheep. Am J Sports Med. http://ajs.sagepub.com/content/early/2015/08/24/0363546515596411.abstract

BACKGROUND: Chronic rotator cuff tendon tearing is associated with irreversible atrophy, fatty infiltration, and interstitial fibrosis of the corresponding muscle.

HYPOTHESES: Anabolic steroids can prevent musculotendinous degeneration during retraction and/or can reverse these changes after operative repair of the retracted musculotendinous unit in sheep.

STUDY DESIGN: Controlled laboratory study.

METHODS: The infraspinatus tendon was released in 18 alpine sheep. All sheep underwent repair of the retracted musculotendinous unit after 16 weeks and were sacrificed after 22 weeks; 6 sheep served as controls, 6 sheep were treated with weekly intramuscular injection of 150 mg of nandrolone decanoate after infraspinatus (ISP) repair (group N6W), and 6 sheep were treated with 150 mg of nandrolone decanoate immediately after tendon release (group N22W). Muscle biopsy specimens were taken before tendon release and after 16 and 22 weeks. Muscle volume and fatty infiltration (on MRI), myotendinous retraction, and muscle density (on computed tomography) were measured immediately after ISP release, after 6 weeks, and before ISP repair and sacrifice.

RESULTS: Muscle volume on MRI decreased to a mean (+/-SD) of 80% +/- 8% of the original volume after 6 weeks, remained stable at 78% +/- 11% after 16 weeks, and decreased further to 69% +/- 9% after 22 weeks in the control group. These findings were no different from those in group N22W (72% +/- 9% at 6 weeks, 73% +/- 6% at 16 weeks, and 67% +/- 5% at 22 weeks). Conversely, the N6W group did not show a decrease in ISP volume after repair; this finding differed significantly from the response in the control and N22W groups. Fatty infiltration (on MRI) continuously increased in the control group (12% +/- 4% at tendon release, 17% +/- 4% after 6 weeks, 50% +/- 9% after 16 weeks, and 60% +/- 8% after 22 weeks) and the N6W group. However, application of anabolic steroids at the time of tendon release (N22W group) significantly reduced fatty infiltration after 16 (16% +/- 5%; P < .001) and 22 weeks (22% +/- 7%; P < .001).

CONCLUSION: In a sheep model of rotator cuff tendon tear, further muscle atrophy can be prevented with the application of anabolic steroids starting immediately after tendon repair. In addition, fatty muscle infiltration can largely be prevented if the steroids are applied immediately after tendon release.

CLINICAL RELEVANCE: Study findings may lead to the development of treatment strategies to prevent or reduce muscle degeneration caused by rotator cuff tendon tearing.

 

[BBC3]

WOW..!

Gerber C, Meyer DC, Fluck M, Benn MC, von Rechenberg B, et al. Anabolic Steroids Reduce Muscle Degeneration Associated With Rotator Cuff Tendon Release in Sheep. Am J Sports Med. http://ajs.sagepub.com/content/early/2015/08/24/0363546515596411.abstract

BACKGROUND: Chronic rotator cuff tendon tearing is associated with irreversible atrophy, fatty infiltration, and interstitial fibrosis of the corresponding muscle.

HYPOTHESES: Anabolic steroids can prevent musculotendinous degeneration during retraction and/or can reverse these changes after operative repair of the retracted musculotendinous unit in sheep.

STUDY DESIGN: Controlled laboratory study.

METHODS: The infraspinatus tendon was released in 18 alpine sheep. All sheep underwent repair of the retracted musculotendinous unit after 16 weeks and were sacrificed after 22 weeks; 6 sheep served as controls, 6 sheep were treated with weekly intramuscular injection of 150 mg of nandrolone decanoate after infraspinatus (ISP) repair (group N6W), and 6 sheep were treated with 150 mg of nandrolone decanoate immediately after tendon release (group N22W). Muscle biopsy specimens were taken before tendon release and after 16 and 22 weeks. Muscle volume and fatty infiltration (on MRI), myotendinous retraction, and muscle density (on computed tomography) were measured immediately after ISP release, after 6 weeks, and before ISP repair and sacrifice.

RESULTS: Muscle volume on MRI decreased to a mean (+/-SD) of 80% +/- 8% of the original volume after 6 weeks, remained stable at 78% +/- 11% after 16 weeks, and decreased further to 69% +/- 9% after 22 weeks in the control group. These findings were no different from those in group N22W (72% +/- 9% at 6 weeks, 73% +/- 6% at 16 weeks, and 67% +/- 5% at 22 weeks). Conversely, the N6W group did not show a decrease in ISP volume after repair; this finding differed significantly from the response in the control and N22W groups. Fatty infiltration (on MRI) continuously increased in the control group (12% +/- 4% at tendon release, 17% +/- 4% after 6 weeks, 50% +/- 9% after 16 weeks, and 60% +/- 8% after 22 weeks) and the N6W group. However, application of anabolic steroids at the time of tendon release (N22W group) significantly reduced fatty infiltration after 16 (16% +/- 5%; P < .001) and 22 weeks (22% +/- 7%; P < .001).

CONCLUSION: In a sheep model of rotator cuff tendon tear, further muscle atrophy can be prevented with the application of anabolic steroids starting immediately after tendon repair. In addition, fatty muscle infiltration can largely be prevented if the steroids are applied immediately after tendon release.

CLINICAL RELEVANCE: Study findings may lead to the development of treatment strategies to prevent or reduce muscle degeneration caused by rotator cuff tendon tearing.