Unanswered Do some anabolics have a greater ability to increase myonuclei than others?

[SuppBro]

When I look into the topic of anabolics increasing myonuclei it keeps going back to supraphysiological levels of testosterone increasing nitrogen retention and satellite cell recruitment, but this isn't necessarily exclusive to testosterone. Does the increase in myonuclei gains have a linear correlation to how anabolic the compound or cycle is, or do some anabolics have a greater effect on increasing myonuclei by activating certain pathways?

There's test which aromatizes leading to increases in estrogen which supports blood circulation and IGF-1 levels.

DHT doesn't aromatize. Although DHT on it's own is hardly anabolic, derivative designer steroids like Anavar or Winstrol are anabolic but dry unlike test. Would they be less effective than test relative to their anabolic strength due to being dry?

Nandrolone on the other hand interacts with the progesterone receptors taking a completely different approach, so where does this stand?

 

[Renew1]

Sorry man, I don't quite get what you are asking.

 

[SuppBro]

Sorry man, I don't quite get what you are asking.

Heard about how taking anabolics leads to a permanent increase in myonuclei? This means that even after you come off you're ability to put on and hold muscle will be forever increased, effectively breaking past your natty limits. This is why people say that once you run a cycle you can never truly be considered a natural.

The literature on anabolics is predominantly focussed on testosterone but I'm wondering how DHT, nandrolone, and designer compounds compare based on the mechanisms of action they deploy and what is known about increasing myonuclei.

 

[Alchemist11]

I love when someone goes this deep into the one subject to explore. I've read a few things about this. Yes, you do have forever increased number of myonuclei in muscles (that's why some sports federations want to ban someone for life if caught on ped's). It's hard to say man, only few studies were done and they used only Testosterone for 12 weeks and thats it.

 

[SuppBro]

I love when someone goes this deep into the one subject to explore. I've read a few things about this. Yes, you do have forever increased number of myonuclei in muscles (that's why some sports federations want to ban someone for life if caught on ped's). It's hard to say man, only few studies were done and they used only Testosterone for 12 weeks and thats it.

I used to go very deep years ago before work and studying pulled me away. I never got into posting these topics back than so I don't have any archive of the studies I saw in the past. I'm just going to post any studies I find to this thread that might contribute and my own notes of interpretation.

https://pdfs.semanticscholar.org/bd52/208788c12203bdc88d5e79cb4fb9bcbc77df.pdf

In this study they found that nandrolone increased myonucleur domain size and myonuclei per muscle fiber length. Myonucleur domain would appear to mean how much nuclei there is among the entire muscle which would include cytoplasm and sarcoplasm.

From the discussion: It would seem that nandrolone may increase androgen receptor density and it's possible that a driving force that makes satelite cells differentiate into myonuclei is to maintain a balance between myonuclei and cytoplasmic volume.
"Bovine muscle cell cultures responded to nandrolone treatment by increasing the expression of androgen receptors (Lee et al. 2007), and satellite cells are the predominant site of androgen receptor expression(Sinha-Hikim et al. 2004). It is held that satellite cells in mature muscle areconverted to myonuclei to maintain the ratio between cytoplasmic volume and number of myonuclei (Allen etal., 1999; Alway and Sui, 2008). "

 

[Jeremyk1]

First of all, I doubt you’re going to find anything comparing rates of myonuclei increase. Anabolics really aren’t a big interest in research.

Another thing I want to say is does this really even matter? At the end of the day, all we’re really looking for is increased anabolism, and I think we have a pretty good idea about how anabolic most compounds are. Looking at cellular differences doesn’t really affect the end goal of muscle growth.

All that said, I freaking love discussions like this! Anyway, the hormonal component is obviously extremely complex. I’ve also long wondered how various effects translate to other similar compounds. For example, YK11 is always advertised as being an amazing myostatin inhibitor, but all androgens inhibit myostatin to a degree. To what degree, I have no idea.

Back to the topic, I’m sure there will be differences, but I don’t know if the data is there to say how significant they will be. There will also be differences based on effects some anabolics have outside of androgenic ones. For example, I think you mentioned estrogen and it’s effects on IGF-1, but I’ve also seen it suggested that estrogen can actually increase the “pool” of satellite cells available to be incorporated into muscle cells. Also, I recall seeing a paper showing that estrogen treatment was able to attenuate the downregulation of androgen receptors from androgen treatment. So in theory, any wet compound should be a superior muscle builder. But I think you also alluded to the idea that some DHTs are actually considered to be some of the strongest anabolics. Superdrol comes to mind. That said, DHT itself is generally considered to be extremely weakly anabolic. What causes that discrepancy, I wish I knew.

I’m definitely interested to see what info you can come up with, this is super interesting.

 

[Chados]

No muscle mass is muscle no matter what. Dry or wet, the amount you gain depends on the steroid you use. The keepable gains are decided by diet, shutdown, cortisol etc. If by coincidence youd have the same shutdown, pct etc and youll recover as fast you gain more on a stronger steroid then a weaker one and if you gain 2lbs on steroid (A) and 10lbs on steroid (B) and loose 50% of the gains youd easily keep more size on steroid (B) making the other steroid useless in comparison.

 

[SuppBro]

First of all, I doubt you’re going to find anything comparing rates of myonuclei increase. Anabolics really aren’t a big interest in research.

Another thing I want to say is does this really even matter? At the end of the day, all we’re really looking for is increased anabolism, and I think we have a pretty good idea about how anabolic most compounds are. Looking at cellular differences doesn’t really affect the end goal of muscle growth.

All that said, I freaking love discussions like this! Anyway, the hormonal component is obviously extremely complex. I’ve also long wondered how various effects translate to other similar compounds. For example, YK11 is always advertised as being an amazing myostatin inhibitor, but all androgens inhibit myostatin to a degree. To what degree, I have no idea.

Back to the topic, I’m sure there will be differences, but I don’t know if the data is there to say how significant they will be. There will also be differences based on effects some anabolics have outside of androgenic ones. For example, I think you mentioned estrogen and it’s effects on IGF-1, but I’ve also seen it suggested that estrogen can actually increase the “pool” of satellite cells available to be incorporated into muscle cells. Also, I recall seeing a paper showing that estrogen treatment was able to attenuate the downregulation of androgen receptors from androgen treatment. So in theory, any wet compound should be a superior muscle builder. But I think you also alluded to the idea that some DHTs are actually considered to be some of the strongest anabolics. Superdrol comes to mind. That said, DHT itself is generally considered to be extremely weakly anabolic. What causes that discrepancy, I wish I knew.

I’m definitely interested to see what info you can come up with, this is super interesting.

The reason I want to boost up myonuclei is because I don't want to be that person who cycles on and off forever chasing gains. I just want to do a minimal amount of cycles that will increase my "natty" limit for decades after.

The case for androgen receptor up and down regulation is something I'm interested in but it's not long term as myonuclei so I'm more focussed on that. I recall a thread on Primordial Performance that was going into the effects of DHT with someone suggesting the DHT prohormones would increase androgen receptor density, also resulting in a decreased rate of testosterone aromatization post cycle leading to an increased test/e2 ratio long term. The web archives didn't back up the PP forums so that discussion is history.

You said that esrogen treatment attenuated the downregulation of androgen receptors from androgen treatment, so cycles and more particularly dryer androgens like DHT should decrease androgen receptor density? It's consistent with neurons and neurotransmitters but inconsistent with the DHT example from the Primordial Performance forums, and the once citation from the Nandrolone study. I've read people on forums saying androgen receptors increase from cycles but there were never sources or explanations.