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Ventrolin??
- Thread starter JKurz1
- Start date
wnt2bBeast
New member
Ive used ventolase by Juste..spanish drug company that makes clen!!!not sure if thats what you mean?
b1ewsw32
New member
Ventolin(salbutamol) is a selective B2 agonist bronchiodilator.JKurz1 said:
It produces bronchiodilation through stimulation of B2 adrenergic receptors in bronchial smooth muscle, thereby causing relaxation of muscle fibres. This action is manifested by an increase in pulmonary function as demonstrated by spirometric measurements.
Even oral(tablet or liquid) versions of salbutamol, which have a much better bioavailability then the aerosol inhaler, the thermogenic effect's are present, but minimal. I believe B2 stimulants are inferior to activation of the B1 or B3 receptors. Better results can be achieved by incorporating agonism of the alpha1 receptor with B1 and B3, or antoginism of the alpha2 receptor(yohimbine) combined with B1 and B3 . I also believe B2 activation to be slightly catabolic, as mentioned in an earlier thread.
Effect of beta1- and beta2-adrenergic stimulation on energy expenditure, substrate oxidation, and UCP3 expression in humans
Hoeks J, van Baak MA, Hesselink MK, Hul GB, Vidal H, Saris WH, Schrauwen P.
NUTRIM, Department of Human Biology, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands. [email protected]
In humans, beta-adrenergic stimulation increases energy and fat metabolism. In the case of beta1-adrenergic stimulation, it is fueled by an increased lipolysis. We examined the effect of beta2-adrenergic stimulation, with and without a blocker of lipolysis, on thermogenesis and substrate oxidation. Furthermore, the effect of beta1-and beta2-adrenergic stimulation on uncoupling protein 3 (UCP3) mRNA expression was studied. Nine lean males received a 3-h infusion of dobutamine (DOB, beta1) or salbutamol (SAL, beta2). Also, we combined SAL with acipimox to block lipolysis (SAL+ACI). Energy and substrate metabolism were measured continuously, blood was sampled every 30 min, and muscle biopsies were taken before and after infusion. Energy expenditure significantly increased approximately 13% in all conditions. Fat oxidation increased 47 +/- 7% in the DOB group and 19 +/- 7% in the SAL group but remained unchanged in the SAL+ACI condition. Glucose oxidation decreased 40 +/- 9% upon DOB, remained unchanged during SAL, and increased 27 +/- 11% upon SAL+ACI. Plasma free fatty acid (FFA) levels were increased by SAL (57 +/- 11%) and DOB (47 +/- 16%), whereas SAL+ACI caused about fourfold lower FFA levels compared with basal levels. No change in UCP3 was found after DOB or SAL, whereas SAL+ACI downregulated skeletal muscle UCP3 mRNA levels 38 +/- 13%. In conclusion, beta2-adrenergic stimulation directly increased energy expenditure independently of plasma FFA levels. Furthermore, this is the first study to demonstrate a downregulation of skeletal muscle UCP3 mRNA expression after the lowering of plasma FFA concentrations in humans, despite an increase in energy expenditure upon beta2-adrenergic stimulation.
alpha1-Adrenergic stimulation potentiates the thermogenic action of beta3-adrenoreceptor-generated cAMP in brown fat cells.
Zhao J, Cannon B, Nedergaard J.
Wenner-Gren Institute, the Arrhenius Laboratories F3, Stockholm University, S-106 91 Stockholm, Sweden.
The relationship between cAMP levels and thermogenesis was investigated in brown fat cells from Syrian hamsters. Irrespective of whether the selective beta3-, beta2-, and beta1-agonists BRL 37344, salbutamol, and dobutamine or the physiological agonist norepinephrine was used to stimulate the cells, increases in cAMP levels were mediated via the beta3-receptor, as were the thermogenic effects. However, the relationship "thermogenesis per cAMP" was much lower for agents other than norepinephrine. Similarly, forskolin, although more potent than norepinephrine in elevating cAMP, was less potent in inducing thermogenesis. The selective alpha1-agonist cirazoline was in itself without effect on cAMP levels or thermogenesis, but when added to forskolin-stimulated cells, potentiated thermogenesis, up to the norepinephrine level, without affecting cAMP. This potentiation could not be inhibited by chelerythrine, but could be mimicked by Ca2+ ionophores. It was apparently not mediated via calmodulin-dependent protein kinase and was not an effect on mitochondrial respiratory control. The ability of all cAMP-elevating agents to induce thermogenesis in brown fat cells has earlier been interpreted to mean that it is only through the beta-receptors and the resulting increase in cAMP levels that thermogenesis is induced. However, it is here concluded that the thermogenic response to norepinephrine involves two interacting parts, one mediated via beta-receptors and cAMP and the other via alpha1-receptors and increases in cytosolic Ca2+ levels.
B32
Last edited:
bicepts101
New member
E-Swift25 said:
why? what do think clen and ephedra are for?
junk
New member
Thanks b1ewsw32, excellent answer. So I believe clen being also a selective B2 agonist bronchiodilator may be quite catabolic, particularely in large doses am I right? Also I guess your opinion on it being good for fat loss is not all that great?
I've taken T-Rex for 3 weeks and thought about cycling with 1-2 weeks of clens before going back to T-rex.. what's your thought?
I've taken T-Rex for 3 weeks and thought about cycling with 1-2 weeks of clens before going back to T-rex.. what's your thought?
