quote:

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Originally posted by macrophage69alpha:
Ephedrine, through its actions upon the beta adrenoceptors increases the release of fatty acids (it burns fat).

However it is at the same time Ephedrine is inhibiting the release of fatty acids from adipose tissue with high #'s A2 adrenoceptors. It does this by agonizing the A2 adrenoceptor.

What does this mean?

EPHEDRINE makes estrogenic (estrogen plays a key role in #/activation/sensitivity of A2 receptors) fatty deposits more "stubborn" and may actually increase fat storage in those deposits.

peace

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QUOTE]Originally posted by macrophage69alpha:
yohimbine

Yes that is part of the solution.

However, Yohimbine cannot be taken all the time. Though it can be taken for extended time periods

Additional measures:

Estrogen must also be minimized, Not through the use of Anti-E (misnomer) which I have come to believe also agonize the A2 adrenoceptor, but through the use of aromatase inhibitors. THIS IS ESPECIALLY IMPORTANT ON CYCLE (test/dbol).

Switching beta- agonists every 2-4 weeks, with different beta and Alpha activities will also enhance fatburning and maintain some of the CNS effects which inevitably improve training intensity.

More thoughts to come....

peace

[/QUOTE]

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Originally posted by cockdezl:
This may be true, since ephedrine is not a selective beta agonist at all. It increases the release of norepinephrine from the nerve terminals, which as MACRO is alluding to, will also agonise the alpha receptors. But, it may be premature to assume that the a-2 populations will overpower the effect of chronic adrenergic use. I have not heard many complain of problems with lower body fat and ECA use.

Yohimbine would be the first thought in fighting this side effect, the other would be the use of selective beta agonists, such as clenbuterol, terbutaline, albuterol (salmeterol). These would not agonize the alpha receptors, but, clen, as we know, does not work after a short while.

Synephrine would not work, as it is an alpha-agonist, and may also cause norepinephrine release.

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quote:

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Originally posted by macrophage69alpha:
COCKDEZL,

I am not implying that ephedrine does not work, quite to the contrary. However, for those with large # of A2 adrenoceptor laden fatty tissue- ephedrine will inhibit the breakdown of those fatty tissue areas. Specifically -WOMEN, men with FEMALE bodyfat patterns, and chronic users of ANTI-E's which I have come to believe may have A2 agonist binding capabilities (as we all know they are mixed estrogen agonist/antagonists)

PLUS in the presence of high levels of Estrogen it is likely to increase the the size of those fatty deposits.( this last part is pure surmise- so take with a grain of salt)

However there is a definite Estrogen connection, How the agonizing of the A2 by both Estrogen and Ephedrine will effect fatty storage is unclear.

glad that you joined the discussion

peace

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Originally posted by Fonz:
[b]Damn, just woke up to find this thread by Macro.
I have to agree.
I'll give you an example:
Ephedrine will at the same time increase fat
breakdown and increase fat-storage. The
reason it works is that: Fat broken down is greater
than fat stored.
The highest amount of fat is lost in the cells
containing a high amount of B1 receptors.
Since ephedrine stimulates the A1,2's too
STORE MORE FAT, cells high in A2 are
going to get filled with more fat.
BUT YOU WILL STILL LOSE FAT AS THE
EPHEDRINE IS STIMULATING THE LOSS
OF HIGH-B1 CELLS, WHICH IS GREATER
THAN THE GAIN OF THE A2 CELLS.
Over time, those A2's will become fuller of
fat at the expense of the high B1's. Therefore
creating "fat deposits", so-to-speak.

Godspeed

But, one thing that might make Macro wrong,
will expand on this later.

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Macro forgot to mention the beta-3 receptors.
It has been proven that ephedrine works via
the stimulation of the B1,B2,B3 receptors
in the following manner. 20% B1, 43%B2,37%
B3. B1,B2 create the problem of excess A2 fat
storage, BUT THE BETA-3 RECEPTOR SOLVES
IT. It works by a mechanism known as
thermogenesis, by BURNING WAT(WHITE ADIPOSE
TISSUE) WHICH IS INDEPENDENT OF ANY
ALPHA OR BETA CLASSIFICATION.
Thats why ephedrine users don't have fatty deposits.
The beta-3's take care of the A-2 receptor induced
fat accumulation TO A DEGREE. In order to get
ripped yohimbe HCL is still a must to lose that
A2-stored fat.
I wonder what Macro is going to say.......

Godspeed[/B][/QUOTE]

quote:

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Originally posted by macrophage69alpha:
This problem- fatty acid release inhibition- affects a greater percentage of the population than many are aware of- since it effect almost all women that about 55% and then add men with female fat storage patterns (naturally high estrogen- endogenous or environmental) and then add men who have use aromatics without arimidex then add men who are older and have greater levels of aromatase.....might be a slightly larger population than some beleive. ALL of these groups will have pockets with HIGH A2 concentrations- in some these pockets will be larger than other but the fact still remains that ephedrine will inhibit fat loss in these areas.

Arimidex will help, but I am unsure whether clomid will or will not because of its mixed activity binds to the A2 (and whether it activates or inactivates the A2)- I beleive, from anecdotal evidence that clomid, either binds to and activates the A2 or that it does not bind at all and Estradiol is free to do so.

Ideall Arimidex should be used during cycle and after- considering the amount of environmental estrogens we are exposed to perhaps used a low doses continously- I EXPECT that it, or another aromatase inhibitor, will become a standard prescription for men over 30- whose levels of aromatase have begun to increase. ALL this estrogen is very Unhealthy for men, especially in the face of exposure to so much environemntal estrogen- these high levels of Estrogen have led to a 50% drop in male fertility rates worldwide and an increase in prostate cancer.

peace

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quote:

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Originally posted by Fonz:
Analyzing Beta-3's further, I thought this of
interest to you Macro:

Ephedrine increases calories burned by 15%
via increased thermogenesis.

43% of the thermogenesis comes from the
Beta-3's.(See my study quoted above)

If a normal 200lb bodybuilder, who has a
normal maintenance level of 3000Kcal a
day, he would burn 3450Kcal/day(115%).

Now, out of those extra 450Kcal, 194Kcal will
come through the burning of calories via
the beta-3 receptor that works through
BAT thermogenesis.
Now, here is the kicker:
A NORMAL ADULT MALE HAS ABOUT 70G
OF BAT TISSUE.
Therefore, BAT tisue burns about 2.8KCAL PER
GRAMME!!!! Thats 1271Kcal per pound of BAT!!!

It has also been surmised THAT CONTINUOUS USE
OF EPHEDRINE WILL INCREASE THE NUMBER
OF BAT TISSUES!!!!

Godspeed

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peace