countering tests inhibition of collagen synthesis

[ascendant]

i know one of the biggest concerns of long-term non-stop use of gear is the issues associated with joint problems due to testosterones inhibition of collagen synthesis. so, what i'm wondering is if there's any way to counteract this issue without having to discontinue cycles?

i was figuring maybe going without test for a bit and going on ones like deca and eq that increase collagen synthesis for a short period would help those joints and connective tissues catch up to the muscle growth, but i also know you should always have test as your foundation of a cycle or else you run into the issue of impotency.

i would seriously doubt taking things like chondroitin and glucosamine could compensate for the decrease in collagen synthesis, but figured it might be better than nothing?

anyway, if anyone knows of a way to counteract the collagen issue, i'd appreciate it. i've always done the "time on = time off" deal when i did gear in the past, but now that i'm just getting back into it again and am looking to start competing next year, i really don't have time to take breaks in between. at most, i'll maybe do like 2-3months off out of the year. a buddy of mine at work goes year round, but has had problems with his joints (knees and elbows) several times in the past, and i'd rather not run into issues like that down the road and know that without giving those joints time to build up, that i'd eventually run into the same problems down the road. well, thanks in advance for any help you guys can offer.

[Property of Steroid.com]

Testosterone doesn't inhibit collagen synthesis.

[ascendant]

Testosterone doesn't inhibit collagen synthesis.

k, been a while since i had the chance to respond, but i have to completely disagree on this one.

deca, eq, anavar, and primo will all increase muscle while at the same time dramatically increasing collagen synthesis and bone mass density. on the other hand, test, though it increases bone mass and density, also causes weaker tendons due to the inhibition of collagen synthesis. if test is used at a dose of more than 200mg/wk, collagen syn will unquestionably be inhibited. i have the info at my house on paper, but regretfully i don't have the source of the info. however, if i printed it out and stored it in my documentation at home, the source must have been very reputable because i'm very discriminatory about what i'll print and keep.

if anyone could show evidence contradictory to my statements, please send a link my way so we can see it. otherwise, i'm still caught in the dilemma of the collagen syn issue. oh, and using things that increase collagen syn along with test isn't an option as the inhibition caused from the test will far outweight the increase from the others like deca, eq, and the like.

[caddilac]

why not just run a maintenance dose of test with deca/eq at like 125mg test e EW. that way you won't be shut down while getting the benefits of deca and eq

[guest589745]

I'll post this for hooker:

I already have disproven it several times:

http://forums.steroid.com/showthread...light=%22anima
l+mass%22

http://forums.steroid.com/showthread...light=%22anima
l+mass%22

http://forums.steroid.com/showthread...light=%22anima
l+mass%22

The only way it's possible that any of those steroids will help
stimulate collagen synthesis is by (possibly) stimulating IGF
production and/or secretion, as I have postulated with Trenbolone:

http://www.*************/readTopic.do?id=1035148

[ascendant]

I'll post this for hooker:

I already have disproven it several times:

http://forums.steroid.com/showthread...light=%22anima
l+mass%22

http://forums.steroid.com/showthread...light=%22anima
l+mass%22

http://forums.steroid.com/showthread...light=%22anima
l+mass%22

The only way it's possible that any of those steroids will help
stimulate collagen synthesis is by (possibly) stimulating IGF
production and/or secretion, as I have postulated with Trenbolone:

http://www.*************/readTopic.do?id=1035148

thanks for all the info. seems as if no matter what gear you do, you'll still be inhibiting collagen syn, eh? so is the only solution to take time off? if so, how do the pros manage year-round?

[guest589745]

thanks for all the info. seems as if no matter what gear you do, you'll still be inhibiting collagen syn, eh? so is the only solution to take time off? if so, how do the pros manage year-round?

GH .

[AnabolicBoy1981]

I'll post this for hooker:

I already have disproven it several times:

http://forums.steroid.com/showthread...light=%22anima
l+mass%22

http://forums.steroid.com/showthread...light=%22anima
l+mass%22

http://forums.steroid.com/showthread...light=%22anima
l+mass%22

The only way it's possible that any of those steroids will help
stimulate collagen synthesis is by (possibly) stimulating IGF
production and/or secretion, as I have postulated with Trenbolone:

http://www.*************/readTopic.do?id=1035148

so basically in those threads the most important part was that even if deca and eq did increase the collogen III synthesis, this would still be bad for tendons because type 3 has been shown at the site of ruptures.
However, i read this,
http://www.ecmjournal.org/journal/su...lagen%20III%22
and a couple other things about collagen 3, and it seems perhaps type 3 is predominantly in cartilage. So perhaps if you had a tear in cartilage, or the labrum, deca and eq may be an option. But tendons and ligaments you might be better of with GH,igf1 etc

[ascendant]

GH .

so, that's the key, eh? good to know, thanks bro. in that case, it will probably be a while before i can consider going year-round since i'm on my first cycle now in about 2 years. don't wanna jump the gun on the GH. never did it yet, but looking forward to trying it down the road.

[cj1capp]

Testosterone doesn't inhibit collagen synthesis.

i belive this statement to be incorrect, i will be searching for info to back up what i belive. are there any more knowledgeable people out there that can confirm or deny this statement.

[cj1capp]

Testosterone doesn't inhibit collagen synthesis.

looks like i have been wrong allof these years but still looking. found this to support what AR is saying.


ACL Injury and Hormones
Ross Hauser, M.D.

Though males and females have the same musculoskeletal structures, there are some unique differences that actually make female athletes more prone to injury. In regard to skeletal differences, males usually have wide shoulders and narrow hips, whereas a female generally has a wide pelvis in relation to the width of her shoulders. This wider pelvis is necessary for childbirth. This wider pelvis is stabilized by the sacroiliac ligaments in the back and the pubic symphysis and pubic ligaments in the front. It is these ligament structures that are stressed and account for the significant back pain that occurs in 50 percent of women who are pregnant.

This wider pelvis in females leads to an increased inward slant of the thigh and, therefore, an increased Q-angle of the knee. The Q-angle, a measurement of the angle created by the line from the anterior superior iliac spine and the patella, and the line from the patella to the tibial tubercle, is normally less than 12 degrees. An increased Q-angle produces excessive lateral forces on the quadricep's mechanism and abnormal tracking of the patella. This is one of the reasons why chondromalacia patella or patellofemoral syndrome is more common in women. (Hutchinson, M. Knee injuries in female athletes. Sports Medicine. 1995; 19:288-302.)

As stated above, a female's thighs tend to slant inward towards the knees more than a male's. This puts additional strain on a woman's hips and their ligamentous support. This is one of the reasons that the majority of the 120,000 hip replacements done each year are in women. Females also have a wider carrying angle of the elbows. This is similar to the Q-angle of the knee. This wider angle places additional stress on the medial elbow stabilizers, namely the ulnar collateral ligaments, which are usually the culprits when a female athlete has medial elbow pain.

Body composition is also different between males and females. The average body fat content of the female is approximately 26 per-cent, compared with that of the male at 14 percent. The female has a lower lean body mass indicating less muscle mass. The greater muscle mass in males is due to the predominant effect of the androgen hormones, whereas estrogen, predominant in females, results in increased body fat. As it turns out, this difference in hormones is key to understanding why female athletes are more easily injured and repair more slowly than their male counterparts. Testosterone stimulates fibroblastic proliferation, whereas estrogens, especially estradiol, inhibits it.(Liu, S. Estrogen affects the cellular metabolism of the anterior cruciate ligament. A potential explanation for female athletic injury. American Journal of Sports Medicine. 1997; 25:704-709.)

It is for this primary reason that female athletes can benefit from Prolotherapy for their sports injuries. Estrogen makes a woman a woman, but they have a definite negative effect when it comes to healing sports injuries.

Females also have a smaller proportion of muscle in relation to body size because of the hormonal differences. Having less muscle tissue means there is less muscle to stabilize the joints if the ligaments are injured. This causes more stress to be placed on injured ligaments in women than in men, because women do not have as much muscle back-up. This is another reason for female athletes to become familiar with the local Prolotherapist.

Females, compared to males, have a lower metabolic rate, the rate of conversion of food to energy under conditions of total rest. This appears to be related to the greater lean body mass of the male and the greater proportion of adipose tissue in the female. This could be one explanation why females heal sports injuries slower than men and why more of them develop chronic pain, and need operations such as hip replacements.

The Hormone Factors
Walk into any chronic pain clinic and who do you see? You see women. Caring Medical and Rehabilitation Services in Oak Park is no different. About three out of every four patients coming for Prolotherapy are woman. Why are the women getting most of the arthritis and needing the majority of the artificial joint replacements? It is easy to explain when you take into account the hormone factor.

The dominant hormone in males is testosterone. Testosterone is very anabolic, which means that it stimulates the growth or repair of tissues. Men have about 10 times the amount of testosterone as women. This is why they have a sex drive that is about 10 times as strong as women do. It is also the reason why, on average, men are 33 percent stronger than women. Males are stronger because of their increased muscle mass due to testosterone. When males perform strength training, they develop increased strength and increased muscle size due to hypertrophy of the muscles. This hypertrophy is due to the effect of testosterone. Females performing strength training gain increased strength with relatively less muscle hypertrophy. This is because females have significantly less testosterone. If a woman shows up at the Olympics looking like a man, the other athletes will accuse her of using anabolic hormones like testosterone. The complaint is justified. When a woman does weight strength training, she will get stronger, but she cannot turn herself into a body shaped like a man because the hormones are just not there.

Recent epidemiological studies have recognized a significantly higher anterior cruciate ligament (ACL) injury rate in female athletes as compared with male athletes in sports such as basketball, hand-ball, gymnastics, and soccer. (Gray, J. A survey of injuries to the anterior cruciate ligament of the knee in female basketball players. International Journal of Sports Medicine. 1985; 6:314-316.; Nilsson, S. Soccer injuries in adolescents. American Journal of Sports Medicine. 1978; 6:358-361.; Slauterbeck, J. The incidence of anterior cruciate ligament tears in men and women collegiate soccer players Orthop. Trans. 1996; 20:259.; Whiteside, P. Men's and women's injuries in comparable sports. Physician and Sports Medicine. 1980; 8:130-136.) Although various causes of this phenomenon have been postulated, including differences in ligament or muscle strength, conditioning, endurance, anatomy, and training techniques, the most plausible appears to be the hormone factor.

Unique to the female athlete is her exposure to a constantly changing hormonal milieu throughout her reproductive years. For most of her life, the female athlete is exposed to rhythmic variation in either endogenous hormones during a regular menstrual cycle or exogenous hormones via oral contraceptives.

It has been only recently that it was discovered that there are estrogen receptors on the fibro-blasts of the human ACL, suggesting that female sex hormones may have an effect on the structure and composition of this ligament. Dr. Stephen Liu and associates, at the UCLA School of Medicine, made this discovery and went the next step to find out exactly how estrogen affects ligament growth. They investigated the effects of 17B-estradiol on the cellular proliferation and collagen synthesis of fibroblasts derived from the rabbit anterior cruciate ligament. Measuring 3H-thymidine and 14C-hydroxyproline incorporation assessed fibroblast proliferation and collagen synthesis, respectively. They found that collagen synthesis was significantly reduced with increasing local estradiol concentration. Declining collagen synthesis was first noted at a 17B-estradiol concentration of 0.025 ng/ml. Within physiologic levels of estrogen (0.025 to 0.25 ng/ml), collagen synthesis was reduced by more than 40 percent of control, and at pharmacological levels of 2.5 and 25 ng/ml, as typically occurs in female atheletes taking birth control pills or estrogen replacement therapy, by more than 50 percent of control. A significant reduction of fibroblast proliferation was also observed with increasing estradiol concentrations.

These results are startling. Estrogen, the female hormone, dramatically inhibits fibroblasts. These fibroblasts are what make the collagen that makes up the ligaments and tendons, which are injured during sports. Estrogen was shown in the above study to inhibit the fibroblastic growth and thus collagen formation in a dose-dependent manner.

The more estrogen a woman has, the more inhibition will occur. This has direct effects for all women taking birth control pills. Birth control pills have pharmacological levels of estrogen, which are far in excess of a woman's normal production. The simplest way for a female athlete, who is on artificial estrogen, to overcome sports injuries, is to stop taking them. Inevitably, women are placed on birth control pills because of menstrual irregularities, which are easily treated with natural medicine techniques including diet manipulation and nutritional supplements. At Caring Medical and Rehabilitation Services in Oak Park, we perform Metabolic Typing and hormonal testing on our patients. The female athletes inevitably come up essential fatty acids deficient. This means they need to injest more good fats in their diets in the form of *****-3 fatty acids as is found in fish oils. They are encouraged to drink cod liver oil and eat more fish. Better kinds of fats are also found in nuts and seeds, flaxseed oil, and olive oil. Just this mild change in diet is typically all that is needed to get rid of menstrual cramps and other menstrual irregularities. Sometimes, however, more sophisticated dietary manipulation, herbal supplementation, or other natural medicine techniques

[cj1capp]

can some one fill in the blank so i view the site
http://www.*************/readTopic.do?id=1035148