Caffiene?? Beta 2 Receptors???

[Prizz]

I've been using ECA for about 8wks straight now, and it's time to come off for a bit..... Gonna use Trex after I come off..... I want my Beta 2 receptors to clear out.... I'm wondering if Caffiene has any affinity to the Beta 2 receptor? Cause if it does, I wanna stay away from it for a few weeks..... Appreciate any info.....

rizz

 

[macrophage69alpha]

I've been using ECA for about 8wks straight now, and it's time to come off for a bit..... Gonna use Trex after I come off..... I want my Beta 2 receptors to clear out.... I'm wondering if Caffiene has any affinity to the Beta 2 receptor? Cause if it does, I wanna stay away from it for a few weeks..... Appreciate any info.....

rizz

no. thermorexin will allow for restored "intolerance" to ephedrine

 

[MTS]

check out the new muscluar devlopment...it says all about beta 2 receptors...and somewhere it says about caffine and the eca stack

 

[Makavelli]

Caffeine works by causing noradrenaline to be released, which interacts with the beta 2 receptor. So yes it does. Ephedrine works the same way, but is more powerful. Clen fits directly into the beta 2's, which is why it's more powerful, but will cause a reduction in receptors.

 

[macrophage69alpha]

Caffeine works by causing noradrenaline to be released, which interacts with the beta 2 receptor. So yes it does. Ephedrine works the same way, but is more powerful. Clen fits directly into the beta 2's, which is why it's more powerful, but will cause a reduction in receptors.

caffeine does not cause down regulation of Beta adrenoceptors, it is actually associated with greater adrenergic tone. Its does not directly interact with beta adrenoceptors. Its an adenosine receptor antagonist. It does increase NA levels, though how exactly is still at issue (what is observed is NA excretion in the urine). what is clear is that there is no central noradrenaline release (see below) only peripheral (though this is often claimed).

J Pharmacol Exp Ther. 1997 May;281(2):648-54. Related Articles, Links


Hippocampal noradrenaline release in awake, freely moving rats is regulated by alpha-2 adrenoceptors but not by adenosine receptors.

Carter AJ.

Department of Biological Research, Boehringer Ingelheim KG, Ingelheim am Rhein, Federal Republic of Germany.

In this study, the ability of the nonselective adenosine receptor antagonist caffeine to influence the concentration of noradrenaline in the central nervous system was investigated, and its effects compared with those of alpha-2 adrenoceptor modulation. The technique of microdialysis in association with microbore high-performance liquid chromatography and electrochemical detection was used to measure the extracellular concentrations of noradrenaline in the hippocampus of awake, freely moving rats. Neither the oral administration of caffeine nor its local perfusion influenced the base-line hippocampal levels of noradrenaline. Furthermore, the levels of noradrenaline were not influenced by local perfusion of the selective adenosine A1 agonist N6-cyclopentyladenosine or by the selective adenosine A2 agonist CGS 21680. In contrast, the extracellular levels of noradrenaline could be increased by the perfusion of the selective alpha-2 adrenoceptor antagonist idazoxan and decreased by local perfusion of Ca(+2)-free phosphate buffered saline, a Na(+)-channel blocker, tetrodotoxin, or the selective alpha 2-adrenoceptor agonist clonidine. The extracellular levels of noradrenaline were stimulated by the local perfusion of different concentrations of K+ (10-100 mmol/l). The K(+)-dependent increase in the extracellular levels of noradrenaline was potentiated by local perfusion of idazoxan and inhibited by local perfusion of clonidine. In contrast, neither the oral administration of caffeine nor its local perfusion influenced the K(+)-stimulated increases in hippocampal noradrenaline. Furthermore, local perfusion of N6-cyclopentyladenosine or CGS 21680 did not influence the K(+)-stimulated levels of noradrenaline either. These results indicate that base-line and K(+)-stimulated extracellular levels of noradrenaline in the hippocampus of awake, freely moving rats are regulated by alpha-2 adrenoceptors and not by adenosine receptors.

 

[Prizz]

Clen fits directly into the beta 2's, which is why it's more powerful, but will cause a reduction in receptors.

So I guess this is the reason why Clen is only effective for a few weeks, and Ephedrine gives results for weeks on end? Prob I'm having is I'm still losing some fat, but I'm not getting the energy boost, or appetite suppression I used to get with Ephedrine.... I figured it was cause my Beta 2 receptors were down regulating..... Thoughts?

rizz

 

[macrophage69alpha]

clenbuterol binds very tighty and very strongly to the beta 2 adrenoceptor causing significant down regulation within 2-3 weeks. Ephedrine does not directly bind but it increases catecholamine release (centrally and peripherally)- hence the decreased energy boost and appetite suppression with down regulation of central beta 2's

 

[Makavelli]

So I guess this is the reason why Clen is only effective for a few weeks, and Ephedrine gives results for weeks on end? Prob I'm having is I'm still losing some fat, but I'm not getting the energy boost, or appetite suppression I used to get with Ephedrine.... I figured it was cause my Beta 2 receptors were down regulating..... Thoughts?

rizz

That's right. That's why it stops working after about 2 weeks. You can prevent the decline in Beta 2's by adding in T3, which will increase the amount of beta 2's.

Macro, I don't see how that study contradicts what I said. It says it causes "peripheral" adrenaline stimulation. My point was that caffeine needs adrenaline to stimulate the beta because it doesn't do so correctly.