Clenbuterol focus: Research on Clen & Beta2- Adrenergic Compounds, Protocols

[svenrpb]

What would be the recommend starting dose @Type-IIx? How fast do you increase the dose and what will be the best dose risk/health wise?

 

[juggy38]

What would be the recommend starting dose @Type-IIx? How fast do you increase the dose and what will be the best dose risk/health wise?

Not type 2, but 20-40mcg would probably be the highest I’d want to start. I’ve seen guys ramp up to 120mcg….but I bet their heart is beating out of their chest all damn day. I wouldn’t want to go that high.

And thanks for the responses. Indefinitely get no mental drive from clen. Sweat A LOT during lifting though

 

[cmryan]

What would be the recommend starting dose @Type-IIx? How fast do you increase the dose and what will be the best dose risk/health wise?

Just my opinion but 20µg is a good starting dose since clen can cause a variety of issues even at low doses. Personally, I don't get much of an increase in rhr at low doses but I do get significant cramping issues even at 40µg/day. So it gets problematic for me at low doses. Some guys even experience significant rhr increases and tremors at low doses as well.

 

[SDRaver]

Can you dumb things down if i hire you ?

This was me receiving the information

 

[idan707]

Great read!
But if ketotifen like you say Inhibits cAMP activity what can i take to make the beta receptors upregulation?
(To run it 4-8 weeks)

 

[Type-IIx]

Great read!
But if ketotifen like you say Inhibits cAMP activity what can i take to make the beta receptors upregulation?
(To run it 4-8 weeks)

It does not seem that there are any known viable agents for our purposes (hypertrophy, lipolysis, etc.) to attenuate β₂AR desensitization. The only agents supported by evidence after my searching into the matter are glucocorticoids (e.g., prednisone) & ketotifen. Since glucocorticoids are potently muscle catabolic and ketotifen inhibits cAMP activity, neither agent/class are acceptable for our purposes.

 

[idan707]

It does not seem that there are any known viable agents for our purposes (hypertrophy, lipolysis, etc.) to attenuate β₂AR desensitization. The only agents supported by evidence after my searching into the matter are glucocorticoids (e.g., prednisone) & ketotifen. Since glucocorticoids are potently muscle catabolic and ketotifen inhibits cAMP activity, neither agent/class are acceptable for our purposes.

So you suggest not to take clen straight for more then 2 weeks?
If i will take clen for 8 weeks what can be the damage?

 

[svenrpb]

@Type-IIx would you always split the clen dose, if so why?

 

[TheRoid]

@Type-IIx would you always split the clen dose, if so why?

Since the thread just got resurrected...
Any worthwhile benefit from using clen on a caloric surplus, in terms of repartitioning effect? If so, said surplus is better coming from fats or CHO?

 

[Type-IIx]

Since the thread just got resurrected...
Any worthwhile benefit from using clen on a caloric surplus, in terms of repartitioning effect? If so, said surplus is better coming from fats or CHO?

Yes its use as an anabolic agent (indeed what it classified as) makes sense, however, I believe that the prevailing effects (increased RMR, ↑lipolysis, ↓lipogenesis) should be harnessed. That is, it is best used in bodybuilding for recomp (at maintenance calories or perhaps slightly below, accounting for the increased RMR) to recomp (↑skeletal muscle & ↓adipose tissue). I'd focus on increasing PRO (i.e., 3.3 g/kg / 1.5 g/lb) & decreasing fats (primarily monounsaturated) to as low as possible, with the remainder coming from CHO.

 

[Type-IIx]

ADDENDUM

Class effects of β2 agonists

- Biochemical and haemodynamic changes; basic

- ↑HR
- ↑BP (systolic) [in combination with ↑HR, indicates sympathomimetic effects]
- ↓K (serum)
- ↑glucose (serum)
- ↑insulin (serum)

[25]

- Haemodynamic changes; detailed

* increases in heart rate and systolic blood pressure, decreases in diastolic blood pressure and shortening of the systolic time intervals (STIs), heart rate corrected duration of electromechanical systole (QS2c) and pre-ejection period (PEP; as a measure of inotropism)...

- ↑HR
- ↑BP (systolic) [in combination with ↑HR, indicates sympathomimetic effects]
- ↓BP (diastolic)
- ↓systolic time intervals (STIs) [shortening of STIs]
- ↓electromechanical systole duration (QS₂c) [HR-corrected value]
- ↓pre-ejection period (PEP) [inotropism]

[26]

Ketotifen ?

Ketotifen is a relatively selective, non-competitive histamine antagonist (H1-receptor) and mast cell stabilizer. Ketotifen inhibits the release of mediators from mast cells involved in hypersensitivity reactions. Decreased chemotaxis and activation of eosinophils have also been demonstrated. Ketotifen also inhibits cAMP phosphodiesterase [thereby increasing cAMP activity]. Properties of ketotifen which may contribute to its antiallergic activity and its ability to affect the underlying pathology of asthma include inhibition of the development of airway hyper-reactivity associated with activation of platelets by PAF (Platelet Activating Factor), inhibition of PAF-induced accumulation of eosinophils and platelets in the airways, suppression of the priming of eosinophils by human recombinant cytokines and antagonism of bronchoconstriction due to leukotrienes. Ketotifen inhibits of the release of allergic mediators such as histamine, leukotrienes C4 and D4(SRS-A) and PAF.

Ketotifen is a non-bronchodilator antiasthmatic drug which inhibits the effects of certain endogenous substances known to be inflammatory mediators, and thereby exerts antiallergic activity. Ketotifen possesses a powerful and sustained non-competitive histamine (H1) blocking property. Ketotifen's antihistamine (H1) effect seems to be distinct from it antiallergic properties. Properties of ketotifen which may contribute to its antiallergic activity and its ability to affect the underlying pathology of asthma include: In Vivo results: Inhibition of the development of airway hyperreactivity associated with activation of platelets by PAF (Platelet Activating Factor) or caused by neural activation following the use of sympathomimetic drugs or the exposure to allergen; inhibition of PAF-induced accumulation of eosinophils and platelets in the airways; suppression of the priming of eosinophils by human recombinant cytokines and thereby suppression of the influx of eosinophils into inflammatory loci; antagonism of bronchoconstriction due to leukotrienes. In Vitro results: inhibition of the release of allergic mediators such as histamine, leukotrienes C4 and D4 (SRS-A) and PAF. /Ketotifen fumarate (systemic)/

Source: PubChem

...[W]hen each patient's response to [β₂AR activation] was examined relative to his or her non-stimulated levels, the results that ketotifen therapy increased the responsiveness... to β₂-adrenergic stimulation...

t appears likely that... kektotifen-treated patients are therefore more sensitive to... β-agonist drugs than patients not receiving ketotifen [in peripheral blood lymphocytes]

[27]

The data from [27] indicates that high ketotifen concentrations can increase cAMP levels, and is consistent with data that suggests that lower concentrations of ketotifen achieved in vivo could produce similar effects after weeks of accumulation of the drug within target cells, and is associated with greater β₂AR responsiveness. Further, the tachyphylaxis of β₂AR agonists can apparently be abated by the addition of ketotifen (as indicated by β₂AR receptor number).

The data from [26] is consistent with ketotifen attenuating the desensitization of β₂AR [in cardiac cells] as reflected by the Class effects of β2 agonists: Haemodynamic changes; detailed § of β₂AR agonists.

Conclusion:

+ Ketotifen enhances cAMP activity [in cardiac cells & lymphocytes] by attenuation of β₂AR downregulation (attenuating the decrease to receptor number)... promotes maintenance of Class effects of β2 agonists: Haemodynamic changes; detailed §

- Unclear whether the Myostatin regulation (refer to Mechanisms of skeletal muscle hypertrophy §) of β₂AR-induced hypertrophy is altered

* It is unclear to this author whether the adjuvant use of ketotifen serves to enhance the long-term partitioning ("recomp") effects of clenbuterol. It [ketotifen combination], however, does likely promote more chronic ↑fat loss [by ↑lipolysis, ↓lipogenesis,↓FA synthesis, etc.]). Preservation or loss of the anabolic effects depends on the nature of myostatin cross-talk with β₂AR [i.e., whether downstream from cAMP]).

References:
[25] Nuttall SL, Routledge HC, Kendall MJ. A comparison of the beta1-selectivity of three beta1-selective beta-blockers. J Clin Pharm Ther. 2003 Jun;28(3):179-86. doi: 10.1046/j.1365-2710.2003.00477.x. PMID: 12795776.

[26] Poller, U., Fuchs, B., Gorf, A., Jakubetz, J., Radke, J., Pönicke, K., Brodde, O.E., Terbutaline-induced desensitization of human cardiac β2-adrenoceptor-mediated positive inotropic effects: attenuation by ketotifen, Cardiovascular Research, Volume 40, Issue 1, Oct 1998:211–222, doi:10.1016/S0008-6363(98)00101-1

[27] Polson, J. B., Lockey, R. F., Bukantz, S. C., Lowitt, S., Krzanowski, J. J., & Szentivanyi, A. (1988). Effects of ketotifen on the responsiveness of peripheral blood lymphocyte β-adrenergic receptors. International Journal of Immunopharmacology, 10(6), 657–663. doi:10.1016/0192-0561(88)90019-7

 

[Othello]

@Type-IIx

does low dose (20mcg) have any place in a gaining phase?

 

[Type-IIx]

@Type-IIx

does low dose (20mcg) have any place in a gaining phase?

At the end of a gaining phase it does, yes.