I ran a recomp cycle of Test with EQ and Var which worked wonders for ailing knees. I am a firm believer in the ability of Boldenone and Anavar to increase cartilage production, as my anecdotal experience serves to support such.Yep. Carrying a little extra water always makes my joints feel more secure as well. I like eq also for it’s supposed ability to increase collagen production
Boldenone works even better for me than deca for joints. I like running eq in the 1000-1200 Mg rangeI ran a recomp cycle of Test with EQ and Var which worked wonders for ailing knees. I am a firm believer in the ability of Boldenone and Anavar to increase cartilage production, as my anecdotal experience serves to support such.
If that is the case then deca (At least in micro doses of 50-75mg or even 100mg per week) should be an absolute staple in all TRT/cycle regimes. I know that amount may seem so insignificant but it's really not. We need all of the collagen synthesis and joint lubrication we can get in this game.Prolly related 2 d collagen synthesis increase. Which is why it also makes it safer against ur bones etc breaking.
Can you speak more to the heart affects? I have a personal vested interest in this now13 joint reconstructions later. Deca is not what people think it is. It’s a wolf in Sheep’s clothing gentleman. And it’s also very hard on the heart as well.
Can you speak more to the heart affects? I have a personal vested interest in this now
If you're referring to the studies on blood vessels, I believe those were done on rats. A few of the science minds here like @Stewie have gone through them and they don't translate 100% to humans. Not saying there isn't any risk with it, but it's not a 1:1 comparison.Start digging you’ll find info on it.
The reason why im pressing you for some details is bcuz of a previous thread I started. Had a nuclear stress test done after having chest pains and it showed my ejection fraction reduced to 38% and my heart was globally hypokinetic. I was a big deca guy for many years.There are studies out there done on it. But my main concern was when my endocrinologist at university of Washington who is a doctor for many pro athletes advised me that they are aware that nandrolone has negative effects on the heart specifically. This doctor is well versed in anabolics that’s why I went to her.
I just read over that brazilian article you cite. It's interesting that they are able to show differences in ACE I signaling but they show no data on collagen ynthesis, tendon strength measurements or other experiments to really monitor downstream effects of nandrolone dependant ACE I signaling. Nandrolone is still a bit of a mystery when it comes to reduced joint pain. Sicne it is used in a number of inflammatroy diseases it seems to me that other mechanisms may be in place. I think probably the drug also has impact on joint tissue renewal and/or repair but it's probably more complex than increased synthesis of one or a subset of collagen types. It is probably so that dysregulated collagen synthesis, or for instance, improper temporal or coordinated collagens I, II and III synth would not be an advantage to arthritic or injury repair. I can state that I used ND long in the past when I had a knee injury that would not heal and it worked very well.I've collated quite a bit on the topic and may write more about, for example, what makes stanozolol so bad for healthy joints despite increased collagen synthesis markers. But just to address this question, I'll use one relevant study that implicates the RAS, because I think it's probably the most relevant system in what's occurring with apparent joint benefits while on a deca cycle.
The two major mechanisms that may explain deca's effects on joints are:
A) increased collagen deposition in the tendon, and
B) synovial joint fluid retention
Both mechanisms (increased collagen deposition in i.e. flexor tendon) and synovial joint fluid retention may be positively acted upon by the renin-angiotensin system (RAS). The RAS regulates water and electrolyte balance, connective tissue cell growth, and the metabolism of loose and dense connective tissue and sites of tissue repair [1]. Pathologically, RAS activation increases vascoconstriction, cardiac hypertrophy, and fibrosis (resulting in myocardial infarction, fibrosis of the liver) [1]. Therefore, it is important to consider the duality of the potential joint-tendon (i.e., knee extensor tendon) augmentation while on nandrolone: you may have a transient benefit in tendon remodeling (i.e., extensor tendon) and fluid balance, but via this same mechanism, may be accruing fibrotic or cardiac/left ventricular maladaptations.
So, to the potential transient benefits: Angiotensin-I converting enzyme (ACE) is a marker positively correlated with collagen type I mRNA activity, and may reflect ECM remodeling wherein collagen synthesis outstrips degradation.
Whereas AAS generally decrease matrix metalloproteases (MMP), collagen gene expression, nandrolone increases ACE activity and increases matrix type I collagen deposition. The results of [1] showed Nand + jump training >> Nand > jump training > sedentary in ACE activity in tendon (i.e., knee extensor). Consider, however, that this same pathway is implicated in cardiac tissue remodeling and pathological action.
[1] Marqueti, R. de C., Hashimoto, N. Y., Durigan, J. L. Q., Batista e Silva, L. L., Almeida, J. A. de, Silva, M. da G. da, … Araújo, H. S. S. de. (2015). Nandrolone increases angiotensin-I converting enzyme activity in rats tendons. Revista Brasileira de Medicina Do Esporte, 21(3), 173–177. doi:10.1590/1517-869220152103143667
What makes stanozolol cause joint pain is fairly simple, new collagen is type III and healthy tendons are type I. Type III are stiff and lack elasticity, which makes it extremely prone to tendinopathy, especially from resistance training. What makes it even worse is that many if not most weightlifters have some level of tendinosis plus tendonitis already present in many tendons which are rapidly exacerbated by the increase in type III collagen.I've collated quite a bit on the topic and may write more about, for example, what makes stanozolol so bad for healthy joints despite increased collagen synthesis markers. But just to address this question, I'll use one relevant study that implicates the RAS, because I think it's probably the most relevant system in what's occurring with apparent joint benefits while on a deca cycle.
The two major mechanisms that may explain deca's effects on joints are:
A) increased collagen deposition in the tendon, and
B) synovial joint fluid retention
Both mechanisms (increased collagen deposition in i.e. flexor tendon) and synovial joint fluid retention may be positively acted upon by the renin-angiotensin system (RAS). The RAS regulates water and electrolyte balance, connective tissue cell growth, and the metabolism of loose and dense connective tissue and sites of tissue repair [1]. Pathologically, RAS activation increases vascoconstriction, cardiac hypertrophy, and fibrosis (resulting in myocardial infarction, fibrosis of the liver) [1]. Therefore, it is important to consider the duality of the potential joint-tendon (i.e., knee extensor tendon) augmentation while on nandrolone: you may have a transient benefit in tendon remodeling (i.e., extensor tendon) and fluid balance, but via this same mechanism, may be accruing fibrotic or cardiac/left ventricular maladaptations.
So, to the potential transient benefits: Angiotensin-I converting enzyme (ACE) is a marker positively correlated with collagen type I mRNA activity, and may reflect ECM remodeling wherein collagen synthesis outstrips degradation.
Whereas AAS generally decrease matrix metalloproteases (MMP), collagen gene expression, nandrolone increases ACE activity and increases matrix type I collagen deposition. The results of [1] showed Nand + jump training >> Nand > jump training > sedentary in ACE activity in tendon (i.e., knee extensor). Consider, however, that this same pathway is implicated in cardiac tissue remodeling and pathological action.
[1] Marqueti, R. de C., Hashimoto, N. Y., Durigan, J. L. Q., Batista e Silva, L. L., Almeida, J. A. de, Silva, M. da G. da, … Araújo, H. S. S. de. (2015). Nandrolone increases angiotensin-I converting enzyme activity in rats tendons. Revista Brasileira de Medicina Do Esporte, 21(3), 173–177. doi:10.1590/1517-869220152103143667
Given the tone of the paper, you likely picked up on their tendency to REALLY want a different finding, and to be able to say "DECA BAD!" right? Given the Declaration of Helsinki we'll never get a perfect study to look at what we want, and all studies have limitations. Given practical limitations, the Brazilian article stands out because it used a relevant exercise model and looks at the RAS as a system, which can account for the likely mechanisms behind transient joint benefits in deca. We'll never get a study that perfectly suits our interests on this, unfortunately. There's no legitimate interest in following the thread left by this study to show joint benefits, when by the same mechanism, cardiac maladaptations are more justified.I just read over that brazilian article you cite. It's interesting that they are able to show differences in ACE I signaling but they show no data on collagen ynthesis, tendon strength measurements or other experiments to really monitor downstream effects of nandrolone dependant ACE I signaling. Nandrolone is still a bit of a mystery when it comes to reduced joint pain. Sicne it is used in a number of inflammatroy diseases it seems to me that other mechanisms may be in place. I think probably the drug also has impact on joint tissue renewal and/or repair but it's probably more complex than increased synthesis of one or a subset of collagen types. It is probably so that dysregulated collagen synthesis, or for instance, improper temporal or coordinated collagens I, II and III synth would not be an advantage to arthritic or injury repair. I can state that I used ND long in the past when I had a knee injury that would not heal and it worked very well.
Is it that simple? My understanding is stanozolol doesn't even increase collagen deposition except for in skin fibroblasts. Evidence that it suppresses DNA synthesis in synovial fibroblasts. GH increases collagen I mRNA by 2.3-fold and collagen III by 2.5-fold, so it's good for tendons, right?What makes stanozolol cause joint pain is fairly simple, new collagen is type III and healthy tendons are type I. Type III are stiff and lack elasticity, which makes it extremely prone to tendinopathy, especially from resistance training. What makes it even worse is that many if not most weightlifters have some level of tendinosis plus tendonitis already present in many tendons which are rapidly exacerbated by the increase in type III collagen.
Just as a note for everyone, I've explained this many times in the past, how tendinosis and tendonitis work: Tendonitis is caused when the tendon is broken down from repetitive activity, it becomes frayed which leads to further tendon injury as it irritates itself in the tendon sheath. This tendon then repairs itself with type III fibers, these fibers need time and use to mature to type I, and before this happens they are less elastic and more prone to getting tendonitis, this is tendinosis. More tendonitis leads to more tendinosis and more tendinosis leads to more tendonitis. To make it even WORSE: resistance training is needed to mature type III fibers and this can lead to further tendonitis.
Writing tendonitis and tendinosis over and over is super annoying.
It's also possible there is some kind of anti-cortisol effect playing a role here, I'm just guessing but it certainly makes sense, especially because most will already have tendinopathy on some level as I mentioned above which would need cortisol to heal. However, all AAS are anti-cortisol to some degree and winny does have an oddly higher effect on collagen synthesis so you be the judge.
It's possible there are other factors but given winny's unique effect on collagen and its definite effect on "joints," this seems by far the biggest contributor. GH does all sorts of positive things for joints, but I'm not sure it has a positive effect on tendinopathy in particular.Is it that simple? My understanding is stanozolol doesn't even increase collagen deposition except for in skin fibroblasts. Evidence that it suppresses DNA synthesis in synovial fibroblasts. GH increases collagen I mRNA by 2.3-fold and collagen III by 2.5-fold, so it's good for tendons, right?
Collagen fibers in tendon repair start out as type III so if GH is increasing type I then it has to be increasing the rate of type III becoming type I.Is it that simple? My understanding is stanozolol doesn't even increase collagen deposition except for in skin fibroblasts. Evidence that it suppresses DNA synthesis in synovial fibroblasts. GH increases collagen I mRNA by 2.3-fold and collagen III by 2.5-fold, so it's good for tendons, right?
Collagen fibers in tendon repair start out as type III so if GH is increasing type I then it has to be increasing the rate of type III becoming type I.
Agreed, GH does seem good for joints and at least healthy tendons. There's some evidence it can be used (i.e., directly into the tendon) to accelerate procollagenous activity... now whether that's good, e.g., if it's leading to fibrotic tissue in some cases, not sure. I need to look into the mechanisms of tendon remodeling more.It's possible there are other factors but given winny's unique effect on collagen and its definite effect on "joints," this seems by far the biggest contributor. GH does all sorts of positive things for joints, but I'm not sure it has a positive effect on tendinopathy in particular.
I just started up GH and I have lots of joint issues, they all feel great from the GH except for my biceps tendons that I know have issues.