Daily Log to 2019 Show Season

[JesterBOB]

I can’t sympathize here because I’ve never had a single thought about not training on tren. If trens in I know it’s fucking go time. Change your mental state.

You are just a machine, in fact, and your level of results proves it.

 

[Mac11wildcat]

You are just a machine, in fact, and your level of results proves it.

I’m not saying everyone can excel where I have, but everyone can improve discipline which is a trainable skill. We all have days we don’t wanna train, work, get chores done, whatever. Those days are a test. Every time you pass it the rest get easier.

 

[JesterBOB]

I’m not saying everyone can excel where I have, but everyone can improve discipline which is a trainable skill. We all have days we don’t wanna train, work, get chores done, whatever. Those days are a test. Every time you pass it the rest get easier.

I agree that for everyone his goal is the most difficult and important, but if you add discipline, and especially when there is no desire and laziness, it's easy to do. Everyone is able to achieve that, because it is essentially a developed habit. The work that is done despite laziness and mood turns into a habit and success is inevitable.

 

[Jaxino]

I’m not saying everyone can excel where I have, but everyone can improve discipline which is a trainable skill. We all have days we don’t wanna train, work, get chores done, whatever. Those days are a test. Every time you pass it the rest get easier.

How is going with Masteron?

Which stack you ended up running?

 

[Mac11wildcat]

How is going with Masteron?

Which stack you ended up running?

Haven’t started. We’re still cruising, bloodwork soon, then blast off.

 

[Type-IIx]

Mast builds muscle. It’s an anabolic steroid. The differences between AAS are smaller than we all were taught, IMO. The exceptions to this are tren and halo IMO.

Well, Mast has weakened anabolism due to the ubiquity of 3α-HSD in human skeletal muscle. A lot of the "Mast as an anabolic anchor" and "all AAS are equivalent at protein deposition" guys don't understand how to distinguish between relevance in rats vs. humans. So, Mast's primary effects are in anti-estrogenic action in a tissue-selective manner (i.e., it has efficacy in male gynecomastia, breast cancer). There's a reason Mast was never even investigated for therapeutic use in wasting conditions.

 

[Jaxino]

Well, Mast has weakened anabolism due to the ubiquity of 3α-HSD in human skeletal muscle. A lot of the "Mast as an anabolic anchor" and "all AAS are equivalent at protein deposition" guys don't understand how to distinguish between relevance in rats vs. humans. So, Mast's primary effects are in anti-estrogenic action in a tissue-selective manner (i.e., it has efficacy in male gynecomastia, breast cancer). There's a reason Mast was never even investigated for therapeutic use in wasting conditions.

Behind the lines you said that Mast isn't a good direct anabolic agent... Or am I wrong?

I love how @Type-IIx answers, your answers have so much secondary content!

 

[Bigdiddy]

Copy and paste

 

[MindlessWork]

Copy and paste

Sworder style

 

[Type-IIx]

Behind the lines you said that Mast isn't a good direct anabolic agent... Or am I wrong?

I love how @Type-IIx answers, your answers have so much secondary content!

Yes, it's a weak anabolic and mostly useful for modulating estrogens in a tissue-selective manner. This can be synergistic in achieving a dry look with the right compounds, but in itself, Mast is definitely in a class of "slow bulking" compounds.

 

[Type-IIx]

Sworder style

You've been around long enough to know who someone is that I don't, so you're like a pseudo-vet of the boards. Yet not only do you not even run cycles or use gear; contribute any sort of knowledge to the forums; but you pathetically regard anyone slightly smarter than yourself that posts anything based on science as a plagiarist, unironically.

I've heard musings that you're law enforcement, but my money is on you just liking to chat with guys with big muscles.

 

[malfeasance]

I got you. Here’s my current A and B arm day. One is failure one is volume.

Arms 1 *

1. Single Arm Tricep Extension
2. Single DB Preacher Curl
3. Close Grip Bench
4. EZ Bar Curls
5. Single OH Cable Ext SS Single Cable Curl
6. Vbar Pushdown SS High Curl Machine - 3x12–15 each

* all movements except 6 are one top set to failure and one backdown set (20-30% less weight, aim for more reps than top set), rests are a good 2mins/normal breathing

Arms 2 **

1. Vbar Pushdown
2. EZBar Curls
3. Double OTS Cable Ext
4. Incline Curls
5. Close grip bench
6. Preacher Curl Machine
7. Single Cable OH Ext SS Single Cable Curl
8. Dips SS Cross body curls

** everything is 3-4 sets 10-15 reps per set with shorter rests (60-90s)

You have mentioned your split is something like Arms L P P

I was doing PPL (push pull legs), but found I had problems with deadlift/ rack pull one day and squats and stiff leg dead the next.

I had started experimenting with a separate arm day occasionally, and I liked it. I also like where you stuck legs after your arm day and before your push day, giving a day in between before pull day.

So let me ask a question. Are you doing triceps on your push day and biceps on your pull day?

Or do you do arms only on your arm day and no isolation work for bis and tris on P and P day?

I hope that question makes sense. I am trying to figure out if I might be overdoing it.

 

[MR_Midas]

You've been around long enough to know who someone is that I don't, so you're like a pseudo-vet of the boards. Yet not only do you not even run cycles or use gear; contribute any sort of knowledge to the forums; but you pathetically regard anyone slightly smarter than yourself that posts anything based on science as a plagiarist, unironically.

I've heard musings that you're law enforcement, but my money is on you just liking to chat with guys with big muscles.

I liked the way it was written. I do not know the essence of the conflict, but the writing style is chic.

 

[Looking4gainzz]

Pretty much.



I'll leave this here:


View: https://www.youtube.com/watch?v=AUMrP6-eAV4


View: https://www.youtube.com/watch?v=PSnZZv4r8WQ

That shit is all science based on rats and they have different endocrine and overall biology than they do. Within HUMANS in real life application different compounds interact with far more than just the androgen receptor and so far more than just retain nitrogen to promote the overall accrual of mass. Tren interacts with the glucocorticoid receptors as well as probably interacts with the thyroid causing up regulation which is why tren does in fact burn fat. That blows the other bro myth away about steroids not helping people lose weight because both tren and anavar have evidence to show they do. Our bodies work somewhat differently person to person, i mean think about this forum and how some people hate EQ others love it. Some people get tren anxiety and paranoia, others don’t but will have those side effects if they take deca. Don’t get me started on anti depressants and the massive amount of differences in effects felt by each of us. With all that in mind if there is that much variance within our species how can you apply word for word the effects of these compounds on rats to yourself and all of us as well. It makes no sense at all. That’s why all of us who have used cardarine haven’t needed chemo therapy…yet lol.

 

[Type-IIx]

That shit is all science based on rats and they have different endocrine and overall biology than they do. Within HUMANS in real life application different compounds interact with far more than just the androgen receptor and so far more than just retain nitrogen to promote the overall accrual of mass. Tren interacts with the glucocorticoid receptors as well as probably interacts with the thyroid causing up regulation which is why tren does in fact burn fat. That blows the other bro myth away about steroids not helping people lose weight because both tren and anavar have evidence to show they do. Our bodies work somewhat differently person to person, i mean think about this forum and how some people hate EQ others love it. Some people get tren anxiety and paranoia, others don’t but will have those side effects if they take deca. Don’t get me started on anti depressants and the massive amount of differences in effects felt by each of us. With all that in mind if there is that much variance within our species how can you apply word for word the effects of these compounds on rats to yourself and all of us as well. It makes no sense at all. That’s why all of us who have used cardarine haven’t needed chemo therapy…yet lol.

You make some good points. To expand, this study showing equivalent protein deposition by all tested androgens in rats is inapplicable to humans due to the high prevalence of, in particular, 3α-HSD isozymes in human skeletal muscle (as just the prime example of differences in metabolism). Androgens that undergo rapid and substantial metabolism by this enzyme and its isozyme chiefly present in human skeletal muscle dramatically reduces human skeletal muscle hypertrophy in man vs. rodent -- and this is only one example, but the most enlightening to sort of focus on as a case in point.

I note that we only know about tren's modulating glucocorticoids (e.g., reducing GR number) because of animal research, so it is unwise to throw the baby out with the bathwater. I'd note also that tren's anti-adipogenic effects are not mediated by thyroid function, but rather PPARγ (reducing its number) and likely some other mechanisms in lowering HOMA-IR. Rather, we must strive to meaningfully distinguish animal vs human mechanisms - take what is relevant, and dismiss at least in part that which is irrelevant. This requires greater understanding than any of these YouTube guys possess.

A particular interest of mine is boldenone, and understanding why it may be experienced so differently between individuals. I think that the distinction between boldenone (shared by primo, mast) as androgens often claimed to act as anti-estrogens may reside in its being an androgen resistant to aromatization to E2 while possessing a secondary 17β-hydroxy group. Its being resistant to ring-A aromatization is a consequence of this structural feature (not completely abolishing aromatization but rather abating it). There is significant interindividual variation in 17β-HSD isozymes. Some individuals aromatize principally to estrone (E1). Some individuals experience an anti-estrogen effect. I find this fascinating. Its primary metabolite is also rather interesting (a 17β-conjugate, though it likely lacks substantial activity as it is subjected to glucoronidation).

 

[Mac11wildcat]

You have mentioned your split is something like Arms L P P

I was doing PPL (push pull legs), but found I had problems with deadlift/ rack pull one day and squats and stiff leg dead the next.

I had started experimenting with a separate arm day occasionally, and I liked it. I also like where you stuck legs after your arm day and before your push day, giving a day in between before pull day.

So let me ask a question. Are you doing triceps on your push day and biceps on your pull day?

Or do you do arms only on your arm day and no isolation work for bis and tris on P and P day?

I hope that question makes sense. I am trying to figure out if I might be overdoing it.

I do one progressive overload movement and one “pump” movement for bis on pull and tris on pull and the

 

[Megadick3000]

You make some good points. To expand, this study showing equivalent protein deposition by all tested androgens in rats is inapplicable to humans due to the high prevalence of, in particular, 3α-HSD isozymes in human skeletal muscle (as just the prime example of differences in metabolism). Androgens that undergo rapid and substantial metabolism by this enzyme and its isozyme chiefly present in human skeletal muscle dramatically reduces human skeletal muscle hypertrophy in man vs. rodent -- and this is only one example, but the most enlightening to sort of focus on as a case in point.

I note that we only know about tren's modulating glucocorticoids (e.g., reducing GR number) because of animal research, so it is unwise to throw the baby out with the bathwater. I'd note also that tren's anti-adipogenic effects are not mediated by thyroid function, but rather PPARγ (reducing its number) and likely some other mechanisms in lowering HOMA-IR. Rather, we must strive to meaningfully distinguish animal vs human mechanisms - take what is relevant, and dismiss at least in part that which is irrelevant. This requires greater understanding than any of these YouTube guys possess.

A particular interest of mine is boldenone, and understanding why it may be experienced so differently between individuals. I think that the distinction between boldenone (shared by primo, mast) as androgens often claimed to act as anti-estrogens may reside in its being an androgen resistant to aromatization to E2 while possessing a secondary 17β-hydroxy group. Its being resistant to ring-A aromatization is a consequence of this structural feature (not completely abolishing aromatization but rather abating it). There is significant interindividual variation in 17β-HSD isozymes. Some individuals aromatize principally to estrone (E1). Some individuals experience an anti-estrogen effect. I find this fascinating. Its primary metabolite is also rather interesting (a 17β-conjugate, though it likely lacks substantial activity as it is subjected to glucoronidation).

Lets cut to the chase. On all the studies you have read, what are the most effective steroids for actual protein anabolism in muscle tissue of humans (not just glycogenesis and sarcoplasmic water swelling)?

 

[Looking4gainzz]

You make some good points. To expand, this study showing equivalent protein deposition by all tested androgens in rats is inapplicable to humans due to the high prevalence of, in particular, 3α-HSD isozymes in human skeletal muscle (as just the prime example of differences in metabolism). Androgens that undergo rapid and substantial metabolism by this enzyme and its isozyme chiefly present in human skeletal muscle dramatically reduces human skeletal muscle hypertrophy in man vs. rodent -- and this is only one example, but the most enlightening to sort of focus on as a case in point.

I note that we only know about tren's modulating glucocorticoids (e.g., reducing GR number) because of animal research, so it is unwise to throw the baby out with the bathwater. I'd note also that tren's anti-adipogenic effects are not mediated by thyroid function, but rather PPARγ (reducing its number) and likely some other mechanisms in lowering HOMA-IR. Rather, we must strive to meaningfully distinguish animal vs human mechanisms - take what is relevant, and dismiss at least in part that which is irrelevant. This requires greater understanding than any of these YouTube guys possess.

A particular interest of mine is boldenone, and understanding why it may be experienced so differently between individuals. I think that the distinction between boldenone (shared by primo, mast) as androgens often claimed to act as anti-estrogens may reside in its being an androgen resistant to aromatization to E2 while possessing a secondary 17β-hydroxy group. Its being resistant to ring-A aromatization is a consequence of this structural feature (not completely abolishing aromatization but rather abating it). There is significant interindividual variation in 17β-HSD isozymes. Some individuals aromatize principally to estrone (E1). Some individuals experience an anti-estrogen effect. I find this fascinating. Its primary metabolite is also rather interesting (a 17β-conjugate, though it likely lacks substantial activity as it is subjected to glucoronidation).

Dude thank you for the additional info I didn’t know About all of the PPAR activation! I’m also highly fascinated by the difference in expression of all these androgens on different individuals. Speaking of which do you happen to understand the actual reason behind why we aromatize at different levels? I already k ow that having an excess of fat being morbidly obese or even obese greatly increases the turnover to estrogen, but are all other differences variable like that? For instance, could we track down a lot of these and adjust our lives accordingly to reduce estrogenic turnover overall? It seems like If we could figure that out just like with guys being under 14 percent tend to aromatizr far less then maybe we can reduce the need for AI considerably. Sorry did the speech this shit is just awesome

 

[Looking4gainzz]

Lets cut to the chase. On all the studies you have read, what are the most effective steroids for actual protein anabolism in muscle tissue of humans (not just glycogenesis and sarcoplasmic water swelling)?

Superdrol, tren, anadrol, dbol, deca, Boladrol, Pheraplex, Methylstenbolone and Mithras. Boladrol may actually be the strongest mg for mg even more so than superdrol. 12 mg of Boladrol is the strongest cycle of an oral I ever ran, but it aromatizes as much or more than dbol and is heavily toxic so I had to drop out after 2 weeks but I put on 17 pounds than lost about 15 in water when I came off lol. Incredibly strong but not for beginners at all. I mean it don’t fuck around with this unless your prepared or you’ll end up with the best set of tits in your town! Sdrol is the consensus best though abs it’s a dht so no estrogen issues to worry about.

 

[Type-IIx]

Dude thank you for the additional info I didn’t know About all of the PPAR activation! I’m also highly fascinated by the difference in expression of all these androgens on different individuals. Speaking of which do you happen to understand the actual reason behind why we aromatize at different levels? I already k ow that having an excess of fat being morbidly obese or even obese greatly increases the turnover to estrogen, but are all other differences variable like that? For instance, could we track down a lot of these and adjust our lives accordingly to reduce estrogenic turnover overall? It seems like If we could figure that out just like with guys being under 14 percent tend to aromatizr far less then maybe we can reduce the need for AI considerably. Sorry did the speech this shit is just awesome

The CYP19 (Aromatase) gene. Basically CYP19A1 is principally expressed in adipose tissue, testes, brain. Different expression and activity between individuals.