The doses vary given to chronic heart failure patients. Raging from 20mcg, right upto 720mcg/ED (tirated over 3 months).
Yes, you read that right.
720mcg/ED to a patient with chronic heart failure.
The dose has nothing to do with it.
This paper, titled "
Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure.
I'll quote, "Clenbuterol, a beta(2)-agonist with potent anabolic properties, has been shown to improve skeletal muscle function in healthy subjects, and in high doses, promotes cardiac recovery in patients with left ventricular assist devices. In a small, randomized controlled study, we investigated the effect of clenbuterol on skeletal muscle function, cardiac function, and exercise capacity in patients with chronic heart failure."
In another human study, they slowly titrated the dose by 20mcg/wk for three months reaching a maximum dose of "720mcg/ED". It was tirated to avoid dsensitisation.
"High-dose clenbuterol (a selective beta2-adrenergic agonist) has
been proposed to promote myocardial recovery during left ventricular assist device (LVAD) support, but its effects on cardiac and skeletal muscle are largely unknown."
"CONCLUSIONS:
Cardiac function did not improve in this cohort of LVAD patients treated with high-dose clenbuterol. However, clenbuterol therapy increased skeletal muscle mass and strength and prevented the expected decrease in myocyte size during LVAD support."
As if I'm going to get you to post something to contradict my views.
I'm asking you so I can point the holes in it.
I'm pretty sure you're going to post
this study on rodents.
Thats extrapoliates to a dose of 100mcg in humans. However, who starts on a dose of 100mcg? No one does. The dose dose not matter, but the dose relevant to sensitivity. Therefore 100mcg in a starting dose, sounds dangerous. The dose is tirated to avoid this over days/weeks.
Anyway, the study above states that "the available information suggests that b2-AR stimulation is antiapoptotic and that it may even be beneficial to the failing heart." It's often missed, but the abstract says "...clenbuterol-induced myocardial apoptosis was mediated through neuromodulation of the sympathetic system and the cardiomyocyte beta 1-adrenoreceptor..." So it wasn't beta-2 agonism in the heart that caused apoptosis; that's actually protective. Rather, it was excessive beta-1 agonism from the local release of noradrenaline. And this is exactly what we see when excessive doses of clen are taken by humans. Side effects that are actually specific to the beta-1 receptor become apparent, including increased heart rate and blood pressure. Low doses of beta-2 agonists, however, don't do this.
Thanks.
Exactly. Its cardioprotctive, not the other way around.
Typical parotting.