If you take forskolin as a test. booster, get in here.

[BringnIt]

Per this, http://www.ergo-log.com/lactatetest.html

Would this theoretically suggest that forskolin-based test. boosters would ideally be used during power/strength type training as opposed to training that causes greater rises in lactate such as drop sets/high reps/etc.?

[JornT]

Per this, http://www.ergo-log.com/lactatetest.html

Would this theoretically suggest that forskolin-based test. boosters would ideally be used during power/strength type training as opposed to training that causes greater rises in lactate such as drop sets/high reps/etc.?

Training induced hormone fluctuations are transient, so it won't matter much.

The Taiwanese study is interesting for natural athletes who want to optimise their muscle building. The more your power training stimulates testosterone production, the better your muscle bulk and power results will be.

Nope, exercise induced hypertrophy is an intrinsic process.

Also, he makes the usual error: looking at the effects on an intermediate endpoint (testosterone) and conclucing that it will positively influence muscle growth (the relevant endpoint). cAMP does a whole lot more than just influence test and you can't conclude **** based on it's effect on just one factor involved in muscle growth. For example, cAMP also increase cortisol. Just imagine cAMP would double T levels, but would increase your C levels 10x. Would you still expect a net positive effect of cAMP? Not really right? Therefore you have to look at the whole picture, not just one part of the puzzle. Even better, look at measurements that have more relevance to our interest, like cAMPs effect on protein synthesis.

[BringnIt]

Training induced hormone fluctuations are transient, so it won't matter much.



Nope, exercise induced hypertrophy is an intrinsic process.

Also, he makes the usual error: looking at the effects on an intermediate endpoint (testosterone) and conclucing that it will positively influence muscle growth (the relevant endpoint). cAMP does a whole lot more than just influence test and you can't conclude **** based on it's effect on just one factor involved in muscle growth. For example, cAMP also increase cortisol. Just imagine cAMP would double T levels, but would increase your C levels 10x. Would you still expect a net positive effect of cAMP? Not really right? Therefore you have to look at the whole picture, not just one part of the puzzle. Even better, look at measurements that have more relevance to our interest, like cAMPs effect on protein synthesis.

So you are saying that the hormonal changes associated with training are short-term and not relevant, or am I misinterpreting you?

For your second part, and honest disclaimer is I question the relevancy of herbal testosterone boosters, but isn't forskolin's studied body composition improvements entirely mediated by cAMP?

Also, aren't certain types of training like occlusion training at least theorized to partially work through increased lactate?

EDIT: this is all speaking theoretically, not definitive, and is on the basis of conjecture

[BringnIt]

http://www.ncbi.nlm.nih.gov/pubmed/20959702

Edit, scary post count

Interesting. Do you have the full-text?

For what it's worth, I'm not suggesting that the temporary increase in testosterone/especially GH after a workout is a large factor.

Here's my thought process, again in theory:

Forskolin has at least one positive body composition study behind it, and the theory is that cAMP--->increased testosterone--->increased lean muscle mass. Obviously there are pathways between that, but that seems to be the relevant endpoint.

Now the thing from ergo-log showed that high lactate induces cAMP mediated improvements in body composition, and they tested that by giving forskolin and there wasn't really an additive response.

So, to me, it makes sense that people who like to use forskolin as a testosterone booster, would best be served to use it while they are doing training styles that aren't designed to elicit high lactate responses (such as lower volume/rep schemes) to keep testosterone elevated, and then during their time to cycle the forskolin at that point would incorporate drop sets/high volume/etc. to keep testosterone elevated above normal more consistently.

Again, that's just conjecture and the logic I applied to it, but I'm just curious if I made any logical/biological fallacies that would make it an absurd theory, or if it sounds plausible.

[THEHUGE]

Interesting. Do you have the full-text?

For what it's worth, I'm not suggesting that the temporary increase in testosterone/especially GH after a workout is a large factor.

Here's my thought process, again in theory:

Forskolin has at least one positive body composition study behind it, and the theory is that cAMP--->increased testosterone--->increased lean muscle mass. Obviously there are pathways between that, but that seems to be the relevant endpoint.

Now the thing from ergo-log showed that high lactate induces cAMP mediated improvements in body composition, and they tested that by giving forskolin and there wasn't really an additive response.

So, to me, it makes sense that people who like to use forskolin as a testosterone booster, would best be served to use it while they are doing training styles that aren't designed to elicit high lactate responses (such as lower volume/rep schemes) to keep testosterone elevated, and then during their time to cycle the forskolin at that point would incorporate drop sets/high volume/etc. to keep testosterone elevated above normal more consistently.

Again, that's just conjecture and the logic I applied to it, but I'm just curious if I made any logical/biological fallacies that would make it an absurd theory, or if it sounds plausible.

Does it sound plausible? Sure.
Is it going to be relevant in the real world? Nobody knows.

[PinchTheBear]

I remember THEHUGE theorizing about another cAMP pathway (besides it's effect on lipolysis), so maybe he can jump in.

Connect the [transcription] dots.
http://www.sabiosciences.com/pathway...n=cAMP_Pathway

cAMP does a shit-ton of stuff, especially downstream.

[THEHUGE]

Connect the [transcription] dots.
http://www.sabiosciences.com/pathway...n=cAMP_Pathway

cAMP does a shit-ton of stuff, especially downstream.

To say the least. Just to stay on topic, luteinizing hormone release is facilitated by agents that alter cyclic AMP-generating system like forskolin.

[PinchTheBear]

To say the least. Just to stay on topic, luteinizing hormone release is facilitated by agents that alter cyclic AMP-generating system like forskolin.

I would consider both pre and post transcriptional PKA-mediated StAR activity significant as well. (Phosphorylation of SF-1 transcription factor and post-transcriptional phosphorylation of the StAR protein itself).

edit: ^^ I say that because it's unique to PKA. IIRC, PKG isoforms modify StAR but lack the pre-transcriptional activity.

[THEHUGE]

I would consider both pre and post transcriptional PKA-mediated StAR activity significant as well. (Phosphorylation of SF-1 transcription factor and post-transcriptional phosphorylation of the StAR protein itself).

edit: ^^ I say that because it's unique to PKA. IIRC, PKG isoforms modify StAR but lack the pre-transcriptional activity.

Forskolin also markedly inhibits DAX-1 expression at the mRNA and protein level. Fashinating stuff.

[PinchTheBear]

Forskolin also markedly inhibits DAX-1 expression at the mRNA and protein level. Fashinating stuff.

Yeah that's the primarily-studied negative transcription factor. Solid read:
http://www.springerlink.com/content/...0/fulltext.pdf

[sctp]

In simple terms,how bad is the repression of StAR,how sure you are about the carryover from a study on rats to humans and if it worths supplementing forskolin?

[THEHUGE]

In simple terms,how bad is the repression of StAR,how sure you are about the carryover from a study on rats to humans and if it worths supplementing forskolin?

Que?

[sctp]

Que?

https://springerlink3.metapress.com/...ringerlink.com

"Repression of the rat steroidogenic acute regulatory (StAR) protein gene by PGF2α is modulated by the negative transcription factor DAX-1"

[rhizome]

https://springerlink3.metapress.com/...ringerlink.com

"Repression of the rat steroidogenic acute regulatory (StAR) protein gene by PGF2α is modulated by the negative transcription factor DAX-1"

I'd be more worried about the HSP40/70/90/Hop/SRH chaperone complex not being able hydrolyze ATP to prime the receptor for HRE interaction.

[THEHUGE]

https://springerlink3.metapress.com/...ringerlink.com

"Repression of the rat steroidogenic acute regulatory (StAR) protein gene by PGF2α is modulated by the negative transcription factor DAX-1"

Sorry, I misread your post.

[PinchTheBear]

In simple terms,how bad is the repression of StAR,how sure you are about the carryover from a study on rats to humans and if it worths supplementing forskolin?

All the text shows is that DAX-1 is a negative transcription factor through binding to the StAR gene's promoter region, not directly to the transcription factor SF-1.... it has nothing to do with supplementing forskolin.

And yes, it is relevant in humans, not only because humans express DAX-1, but because the DNA sequence of the promoter regions are homologous in the mouse and human StAR genes.

I'd be more worried about the HSP40/70/90/Hop/SRH chaperone complex not being able hydrolyze ATP to prime the receptor for HRE interaction.