I've been looking into this a bit because I've seen conflicting things, and discussed it with Jaime a bit

From studies now, it actually seems that testosterone decreases lipolysis through down regulating the # of beta adrenergic receptors.
However, it does inhibit the formation of more fat through LPL inhibition and inhibits precursor aadipocytes from differentiating fully into the lineage
It also apparently inhibits NPY and increases CART and should thus have a positive effect on (decreasing) appetite

This post was edited by Balla on Mar 28 2014 08:32pm

Last sentence was pretty wat

All of my friends who've been on cycle are like always hungry. It depends on the compound, of course; apparently stanozolol is one of the worst in that sense, but I'd assume all AAS trigger hunger, if only for the increased BMR

lmfao

I wouldnt think the increase in bmr would have such a marked increase in hunger, it must be something else.

Yeah, I said if only because of the increased BMR. I don't know exactly why, but some of them are even used to treat people with anorexia to increase appetite. As for the way it works... I wish I was knowledgeable enough to understand it even.

apetite is primarily regulated via leptin, which is predominantly regulated by %bf, so it highly depends on whether the control subs are fat/obese or regular, or even malnourished.
test on its own would definitely increase apetite, but again, only under the regulation of leptin gut cycles, which can skew any reading on any uncontrolled environment such as segmenting individuals by age/height/ffm/%bf most of all/no food allergies/etc, over a strict timeline with strict diet regimens.

a lot of studies like to pertain to perfect analysis environments, and after looking at their methods section you can see just how easily any uncontrolled variable can throw the conclusions out the window.

Aren't there any other factors besides leptin/ghrelin in hunger regulation?

Also, I'll shamelessly advertise my new article.

http://exdurisgloria.blogspot.co.uk/2014/03/overview-on-time-under-tension.html

Feedback from people more used to serious shit will be gladly welcome, and hopefully applied in future entries.

I'll try to find the study again, but apparently test DIRECTLY interferes w/ and inhibits leptin secretion, independent of changes in fat mass.. but seeing as how test decreases the level of HSL through interactions w/ beta adrenergics on adipocytes, it'd have to be a direct molecular interaction anyhow.
Also, test does, as I said, increase CART and decrease NPY, which will shift hunger towards satiety. Leptin signals through those facets anyhow, through upregulating and activating expression of MSH & CART and downregulating and inhibiting NPY & AgRP.. and it elicits these changes independent of leptin, since test inhibits it.



Well.. in the long term leptin is the main regulator of satiety. It does NOT elicit the feeling of satiety directly from a meal though.. that's through the vagal afferents that innervate the GI tract becoming activated through CCK secretion from the gut via distension sensing, and thus the vagus nerve then transmits the satiety signal to the hypothalamus.
GLP-1 also has a similar role as CCK in transmitting satiety signals, but it also interacts w/ D2 dopamine receptors in the amygdala, which are coupled to G inhibitory GPCRs, to decrease signaling, and lead to decreased reward from the food and help modulate food negatively, so it will also serve as a bit of a "long term" signaler due to that secondary mechanism.

Nice
I've also read that longer TUTs/higher volume has a propensity to activate/proliferate satellite cells as well.. although that's probably as a result of increased metabolic stress overall

We really just need Liron to make a nice post detailing the role of lactic acid and tut in hypertrophy. He by far knows the most in that regard

I remember Eric Helms stating that of all the studies he's seen regarding extended TUT, there wasn't much difference in sarcoplasmic growth between an average TUT compared to doing ungodly slow reps.