CJ_Xfit89
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As some may already know, we have been picked up again by Nutra which is AWESOME NEWS.
I just wanted to start off by thanking everyone for showing their support.
NOW, down to the good stuff.
As many are aware Adipose Annihilation is very versatile in how it can be used, and stacked. There is hundreds, if not thousands of stacking options to cater all goals from fat loss to recomping to lean mass gains.
Here is just a few potential stacks that AA can be utilised effectively.
1. AAv2 + Alpha t2 (the low stim shredded stack)
Alpha Yohimbine
is a forceful α2 adrenergic antagonist; compared to standard Yohimbine, Alpha Yohimbine’s impact on α2B and α2C adrenoreceptors is three and four times more potent, respectively. As such, it capably enhances vasodilation/blood flow in adipose cells. Because Alpha Yohimbine modulates α2C prevalent in the brain, epinephrine – along with concurrent nutrient utilization, thermogenesis, and energy metabolism – is maximally activated, whilst breakdown of serotonin, noradrenaline, and dopamine are controlled.
Ginko Biloba Extract
is a compound that contains naturally-occurring flavonoids such as Kaempferol and Quercetin. Kaempferol is known to promote overall body/mind wellness through antioxidant, anti-inflammatory, cardioprotective, and neuroprotective activities. Significant improvements in insulin-stimulated glucose uptake can be provided via Kaempferol supplementation, due to an ability to "act at multiple targets to ameliorate hyperglycemia, including by acting as partial agonists of PPARγ"; this partial PPARγ modulation "activates some (insulin sensitization), but not all (adipogenesis), PPARγ-signaling pathways" . Furthermore, in a separate FDA-sponsored study, both Kaempferol and Quercetin were proven to "down-regulate the adipogenesis-related transcriptional factors PPARγ, C/EBP-α and SREBP-1 and to inhibit adipocyte differentiation during the early stage". Couple this mechanism of action with Kaempferol’s known capacity to regulate D2-mediated thyroid activity (T3 production).
Higenamine:
Higenamine (HG) is a potent cardioactive benzylisoquinoline alkaloid isolated from Aconiti tuber which has long been used as a cardiotonic in traditional Chinese medicine. HG exerts various effects on the cardio-circulatory system inotropic and chronotropic in isolated rat atria. It also relaxes isolated rat aorta. It inhibits epinephrine, ADP or collagen-induced platelet aggregation in platelet rich plasma. HG inhibits LPS-induced nitrate accumulation and the expression of iNOS mRNA in RAW 264.7 cells. HG lowers blood pressure in rats and increases the recovery rates in acute thrombosis model of mice, and lower the weight of thrombus formed in the arterio-venous shunt model of rats. Higenamine also has ameliorative effects in the LPS-induced DIC model.
Aconitine and higenamine are the components of aconite root. We investigated the cardiac effects of these compounds on murine right and left atria and the interaction of higenamine with aconitine on the rate of spontaneously beating right atria. Higenamine increased the rate (EC50 = 38 nM) and the force of contraction (EC50 = 97 nM), the maximal responses being comparable with those of isoproterenol. The positive chronotropic effect of higenamine was antagonized by propranolol (30-300 nM) and practolol (10 nM-3 microM), but not by butoxamine (1 microM), indicating that it was a beta 1-adrenoceptor-mediated action. The positive chronotropic effect of higenamine was not changed by pretreatment with reserpine (4 mg/kg, i.p., 4 hr). Aconitine (0.16-0.25 microM) induced tachyarrhythmia in right atria was attenuated by quinidine (1 microM), atropine (8.6 microM) and AF-DX 116 (8.6 microM), suggesting that aconitine activates sodium channels and muscarinic receptors. Higenamine (2.5 nM) and dobutamine (1 nM) did not cause chronotropic effects by themselves, but enhanced the aconitine-induced tachyarrhythmia. These results indicate that higenamine is a beta 1-adrenoceptor full agonist in murine atria and that the aconitine-induced tachyarrhythmia is augmented by the beta 1-adrenergic action of higenamine
In essence, a 1,2 combo punch stimulating beta receptors and blocking a2 receptors meaning ultimate shreddedness
I just wanted to start off by thanking everyone for showing their support.
NOW, down to the good stuff.
As many are aware Adipose Annihilation is very versatile in how it can be used, and stacked. There is hundreds, if not thousands of stacking options to cater all goals from fat loss to recomping to lean mass gains.
Here is just a few potential stacks that AA can be utilised effectively.
1. AAv2 + Alpha t2 (the low stim shredded stack)
Alpha Yohimbine
is a forceful α2 adrenergic antagonist; compared to standard Yohimbine, Alpha Yohimbine’s impact on α2B and α2C adrenoreceptors is three and four times more potent, respectively. As such, it capably enhances vasodilation/blood flow in adipose cells. Because Alpha Yohimbine modulates α2C prevalent in the brain, epinephrine – along with concurrent nutrient utilization, thermogenesis, and energy metabolism – is maximally activated, whilst breakdown of serotonin, noradrenaline, and dopamine are controlled.
Ginko Biloba Extract
is a compound that contains naturally-occurring flavonoids such as Kaempferol and Quercetin. Kaempferol is known to promote overall body/mind wellness through antioxidant, anti-inflammatory, cardioprotective, and neuroprotective activities. Significant improvements in insulin-stimulated glucose uptake can be provided via Kaempferol supplementation, due to an ability to "act at multiple targets to ameliorate hyperglycemia, including by acting as partial agonists of PPARγ"; this partial PPARγ modulation "activates some (insulin sensitization), but not all (adipogenesis), PPARγ-signaling pathways" . Furthermore, in a separate FDA-sponsored study, both Kaempferol and Quercetin were proven to "down-regulate the adipogenesis-related transcriptional factors PPARγ, C/EBP-α and SREBP-1 and to inhibit adipocyte differentiation during the early stage". Couple this mechanism of action with Kaempferol’s known capacity to regulate D2-mediated thyroid activity (T3 production).
Higenamine:
Higenamine (HG) is a potent cardioactive benzylisoquinoline alkaloid isolated from Aconiti tuber which has long been used as a cardiotonic in traditional Chinese medicine. HG exerts various effects on the cardio-circulatory system inotropic and chronotropic in isolated rat atria. It also relaxes isolated rat aorta. It inhibits epinephrine, ADP or collagen-induced platelet aggregation in platelet rich plasma. HG inhibits LPS-induced nitrate accumulation and the expression of iNOS mRNA in RAW 264.7 cells. HG lowers blood pressure in rats and increases the recovery rates in acute thrombosis model of mice, and lower the weight of thrombus formed in the arterio-venous shunt model of rats. Higenamine also has ameliorative effects in the LPS-induced DIC model.
Aconitine and higenamine are the components of aconite root. We investigated the cardiac effects of these compounds on murine right and left atria and the interaction of higenamine with aconitine on the rate of spontaneously beating right atria. Higenamine increased the rate (EC50 = 38 nM) and the force of contraction (EC50 = 97 nM), the maximal responses being comparable with those of isoproterenol. The positive chronotropic effect of higenamine was antagonized by propranolol (30-300 nM) and practolol (10 nM-3 microM), but not by butoxamine (1 microM), indicating that it was a beta 1-adrenoceptor-mediated action. The positive chronotropic effect of higenamine was not changed by pretreatment with reserpine (4 mg/kg, i.p., 4 hr). Aconitine (0.16-0.25 microM) induced tachyarrhythmia in right atria was attenuated by quinidine (1 microM), atropine (8.6 microM) and AF-DX 116 (8.6 microM), suggesting that aconitine activates sodium channels and muscarinic receptors. Higenamine (2.5 nM) and dobutamine (1 nM) did not cause chronotropic effects by themselves, but enhanced the aconitine-induced tachyarrhythmia. These results indicate that higenamine is a beta 1-adrenoceptor full agonist in murine atria and that the aconitine-induced tachyarrhythmia is augmented by the beta 1-adrenergic action of higenamine
In essence, a 1,2 combo punch stimulating beta receptors and blocking a2 receptors meaning ultimate shreddedness