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Clenbuterol is a potent fat-burning compound with significant muscle preserving and building effects.
It was once used in feed animals to increase growth rates of lean mass. It is currently banned for over-the-counter sales and is typically seen as one of the compounds known as 'steroids' (the vague social term for it, as it is not a steroid structure) Despite the ban, it is still used amongst bodybuilding enthusiasts due to its potency.
Clen, 4-amino-alpha(t-butyl-amino)methyl-3,5-dichlorobenzyl alcohol
Clenbuterol is highly stimulatory, and has a long half life (so will stimulate for quite some time)
Clenbuterol is a potent beta2-adrenergic agonist, exerting adrenaline-like effects on the body. Doses too high or combining with other supplements can result in cardiac arrythmia or sudden death.
Clenbuterol is also a restricted or illegal compound in certain areas of the world, and is banned for usage by athletes under most sports agencies.Examine.com Medical Disclaimer
Clenbuterol should be started at a dose of 20mcg. Higher doses can be used after tolerance is assessed but caution is warranted at higher doses due to the potency of the drug. Under no circumstance should one consume more than 120mcg a day.
Most clenbuterol should be taken in the AM hours, to allow some metabolism before sleep at night (although it will still be distrubed)
If you play any high-level sports; check to see if clenbuterol is on the banned substances list. It most likely is, and could make you face legal consequences.
This compound is essentially Ephedrine's big brother, and although most research is on animals the mechanisms as well as societal usage of this compound make it more reasonable to suspect that it works just as well in humans as it does animals than to somehow suspect a species-dependent difference.
The Human Effect Matrix looks at human studies (excluding animal/petri-dish studies) to tell you what effect Clenbuterol has in your body, and how strong these effects are.
|Grade||Level of Evidence|
|A||Robust research conducted with repeated double blind clinical trials|
|B||Multiple studies where at least two are double-blind and placebo controlled|
|C||Single double blind study or multiple cohort studies|
|D||Uncontrolled or observational studies only|
Level of Evidence
||Magnitude of Effect Size
Appears to increase muscle protein synthesis
An increase in power output is noted with clenbuterol usage
|C||Skeletal Muscle Atrophy||
The rate of muscle protein breakdown is decreased with clenbuterol usage
Clenbuterol is a synthesized drug initially created to increase lean mass amounts in farm animals for human consumption purposes. It has since been contra-indicted for usage in farm animals since its metabolites can infect food and lead to food poisoning. It has since been banned for usage in most developed countries.
Clenbuterol, after ingestion, is primarily excreted via the urine as glucuronidated metabolites. The main pathway of degradation is via N-oxidation to clenbuterol's hydroxylamine and NO2-Clenbuterol metabolites; although other mechanisms of metabolization exist. Clenbuterol has a half-life of around 26 hours and still has detectable levels in the blood 48 hours after administration.
Clenbuterol is a beta-2-adrenergic agonist, although it does act on the B1 and B3 adrenoreceptors as well. Its K^D value was reported to be −7.90 ± 0.05. Its selectivity ratio (the amount of binds to one beta-adrenergic receptor, 1 being equal) was found to be 19.5 favoring B2 over B1, and 354.8 favoring B2 over B3.
Clenbuterol administration is able to increase production of kynurenic acid in rat cortical slices and glial cultures, potentially exerting a neuroprotective effect via beta-adrenergic agonism. Clenbuterol can also exert neuroprotective effects via increased mRNA synthesis of Nerve Growth Factor (NGF) and other growth factors. Via these mechanisms, it can protect against ischemic reperfusion and glutamate-induced excitotoxicity.
It has been noted that muscle protein synthesis induced by clenbuterol is mTOR-dependent, with mTOR inhibitors being able to block the effects of clenbuterol.
It has been noted that, downstream of the β2-adrenergic receptor and via CREB phosphorylation, an induction of the histone demethylase occurs and that this promoter activity positively influences androgenic signalling.
Clenbuterol may directly induce muscle protein synthesis via mTOR dependent mechanisms as well as augment androgen signalling through the genome
Clenbuterol's effects on skeletal muscle are that it is able to induce growth, alleviate breakdown, and accelerate recovery of strength post-injury. The muscle preservation effects are also retained when a caloric deficit of 50% is used for a prolonged period of time, but is not seen in periods of absolute fasting.
One study on swine noted an increase in the size of muscle fiber cells as well with clenbuterol administration.
There appear to be adaptive effects on the transcription of the beta-adrenergic receptors in fast-twitch muscle with prolonged clenbuterol treatment that does not appear in slow-twitch muscle fibers.
One study on persons with Chronic Heart Failure noted an increase in muscle mass and concomitant decrease in fat mass at 80mcg clenbuterol daily, strength also increased to a greater extent in clenbuterol compared to placebo (27% v. 14%). This study has been commented on, in that the increase in lean mass without an increase in cardiac function indicates either a worsening or stasis of cardiac performance. It was also noted that 60% of the patients on clenbuterol had muscle cramps and tremors. Although the safety of clenbuterol was touted in the study, dosages of metoprolol were used in a responsive manner to control abberations in heart rate.
Clenbuterol can induce fat burning via beta-2-adrenergic agonism; it is a highly selective B2 agonist. Via this mechanism, it induces fat burning by increases intra-cellular levels of cyclic AMP which has downstream effects on inducing protein kinase A (PKA) activity which then acts on hormone sensitive lipase (HSL) and perilipin to mediate lipolysis; insulin is a negative mediator of this pathway. PKA may also induce CREB phosphorylation, which is then able to induce JHDM2a (a histone demethylase) promoter activity and may have downstream influences on PPARα and UCP1, two proteins involved in fatty acid oxidation and uncoupling (respectively).
Clenbuterol seems to highly affect the genetic signalling of adipocytes, with one porcine study noted 82 different mRNA expression rates following adipocyte incubation with clenbuterol
Clenbuterol is a potent β2-adrenergic receptor agonist and activates the downstream consequences of β2-receptors, which is mostly fat burning with some muscle protein synthesis. This is the receptor class that adrenaline acts upon
Although it has not yet been implicated in lowering the white blood cell count, it has been shown to have significant redistributive effects on white blood cell counts.
Potassium and taurine may be depleted with usage of clenbuterol and thus their supplementation could alleviate side effects associated with cramping and hydration
(Common misspellings for Clenbuterol include clenbutrol, clenbutril, clenbutral, clenbuteral, clenbuteril)
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