The double-edged sword of Beta Adrenoceptor agonists

arwold

New member
I'm coming at this from a man-in-the-street perspective, and hopefully someone here can help me out.
There is numerous literature which finds that beta adrenoceptor agonists actually help to promote skeletal muscle hypertrophy, and also prevent atrophy as a result of stress hormones.
But activation of the same receptors seem to cause an adverse effect on bone, as well as risk of cardiac issues.

Does dosage make a difference to any of the above? Could the adverse effects be counteracted say with certain beta blockers or Angiotensin antagonists?
 
Beta adrenergic agonists like albuterol or clenbuterol trigger the release of epinephrine (adrenaline). The anabolic effects are minimal, and it's cortisol that will ultimately determine what happens next. As your adrenals cannot release high quantities of epinephrine indefinitely, cortisol is inevitable - which is the catabolic agent you're likely reading about.

Dosage does determine results as well as negative side effects, but there are baselines that we all have individually set for each of us at a minimal effective dose. This is why titration is so imperative when embarking on such an experiment.

Also to note, the effects of beta agonists is short lived as the body does adjust, and they will simply become ineffective without a cool down period (two weeks on, two weeks off is typical), or the use of ketotifen.

As adrenaline causes vasoconstriction, blood pressure increases, and heart rate increases. This is where the risk of cardiac complications comes from. Using a beta blocker would work, but it would do so by rendering the beta agonist inefficacious - wasting the money spent on it. I haven't looked into the usage of angiotensive agents, but I suspect they won't have the effect you're thinking of.

In all honesty, if you're looking to lose body fat, work on your diet. I've yet to meet anyone that had a perfectly controlled diet require the use of diet aids to lose body fat beyond the ten percent mark.

My .02c :)
 
Beta adrenergic agonists like albuterol or clenbuterol trigger the release of epinephrine (adrenaline). The anabolic effects are minimal, and it's cortisol that will ultimately determine what happens next. As your adrenals cannot release high quantities of epinephrine indefinitely, cortisol is inevitable - which is the catabolic agent you're likely reading about.

Dosage does determine results as well as negative side effects, but there are baselines that we all have individually set for each of us at a minimal effective dose. This is why titration is so imperative when embarking on such an experiment.

Also to note, the effects of beta agonists is short lived as the body does adjust, and they will simply become ineffective without a cool down period (two weeks on, two weeks off is typical), or the use of ketotifen.

As adrenaline causes vasoconstriction, blood pressure increases, and heart rate increases. This is where the risk of cardiac complications comes from. Using a beta blocker would work, but it would do so by rendering the beta agonist inefficacious - wasting the money spent on it. I haven't looked into the usage of angiotensive agents, but I suspect they won't have the effect you're thinking of.

In all honesty, if you're looking to lose body fat, work on your diet. I've yet to meet anyone that had a perfectly controlled diet require the use of diet aids to lose body fat beyond the ten percent mark.

My .02c :)

Thx for the reply. The connection between norepinephrine and skeletal muscle is an interesting one. I found this study that even a Norepinephrine Reuptake Inhibitor, Atomoxetine, can prevent glucocorticoid-induced muscle atrophy in mice:
ncbi.nlm.nih.gov/pubmed/25292181
 
You're overthinking things. Beta receptor agonists/adrenergic receptor antagonist (ephedrine/yohimbine) are not going to have any negative significant effect on skeletal muscle.


Ephedrine/clen have a mild anti-catabolic effect, just stick to therapeutic doses and don't abuse it and have a heart attack.



Anecdotally, Yohimbine seems to promote strength for me, most likely via the adrenaline increase. This helps preserve muscle on a cut by keeping intensity high, which is a bonus since yohimbine is an awesome addition to a caloric deficit.
 
Thx for the reply. The connection between norepinephrine and skeletal muscle is an interesting one. I found this study that even a Norepinephrine Reuptake Inhibitor, Atomoxetine, can prevent glucocorticoid-induced muscle atrophy in mice:
ncbi.nlm.nih.gov/pubmed/25292181

Two problems: The first is that mice (and most animals) studies don't always translate over to human beings. Second is that glucocorticoids operate by a different pathway to induce atrophy. Kind of like how many thought that NSAIDs were bad for hypertrophy because their steroidal cousins wreck havoc at the cellular level. Notice that they're also taking about norepinephrine, which is released in far smaller quantities than epinephrine via adrenergic stimulus.

The adrenals themselves are quite fascinating as they have the ability to make us extremely strong/alert/focused, but can also make us lethargic/weak/flaccid. The entire sympathetic and parasympathetic nervous system is a truly remarkable method used to ensure survival.

It does seem that you're trying to overthink things here.
 
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