reaching THR is a major method of fat burning, beta-blockers disable this occurrence, so taking these stims just fucks up your CNS in the meantime, with lackluster results, taxes your adrenals etc, clen is a horrible drug, ephedra is much more forgiving. I tore a muscle on clen just doing a pullup this summer. lameI assume this is just because these two will sort of “offset” each other; thereby rendering the beta blocker and it’s intended purpose, relatively useless.
Edumacate me. Any other reasons I missing here?
Another thing to consider is that you are taking a beta blocker to lower blood pressure and slow heart rate, and the other drugs reverse that. So if you have a heart that is compromised, taking the stimulants is going to put you into danger.reaching THR is a major method of fat burning, beta-blockers disable this occurrence, so taking these stims just fucks up your CNS in the meantime, with lackluster results, taxes your adrenals etc, clen is a horrible drug, ephedra is much more forgiving. I tore a muscle on clen just doing a pullup this summer. lame
sounds like a legal speedballAnother thing to consider is that you are taking a beta blocker to lower blood pressure and slow heart rate, and the other drugs reverse that. So if you have a heart that is compromised, taking the stimulants is going to put you into danger.
I will borrow from wiki as they explain this pretty well, basically propranolol is terribly NON-SELECTIVE which is why it has so many other benefits beyond BP control but also makes it more contraindicated in certain situations.sounds like a legal speedball
This much I can tell you guys, I get zero pump if I take 20mg propranolol within 4 hours of pre workout, strongly dislike. but it is a very good drug for PTSD. coincidentally it also helps with BP. It helps me because sometimes I will walk into lets say walmart, and start sweating (happens usually when I walk into a store) anxiety. The onset is normally my diaphram is constricted and flexed, then I realize I am holding my breath, and once i become cognizent about that part The sweating bath. Still anxiety is a domino effect of the ptsd. I try to only take the propranolol before bed now as it helps with body jerking and convulsions
+ you can dose the stimulants higher because you aren't limited by your HR which is capped at a certain level.
see my post above, selective blocking of beta-1 is NOT going to negate the beneficial aspect of stims, all beta blockers are not created equal when it comes to selectivityIf stims exert the majority of their effects by way of increased CNS activity, and beta blockers’ MOA ramp this down, aren’t these 2 directly antagonist?
What benefits can still be achieved w such use?
Lastly, won’t “taking more stims” simply negate any benefit the BB confers?
yes, I had to describe to my doctor that I overproduce norepinephrine and noradrenaline to get the script, she is fucking clueless, my highschool freshman football coach told me i was the most wound kid he has ever met. Even when I was 7 I remember being this way. Being aggressive and explosiveI will borrow from wiki as they explain this pretty well, basically propranolol is terribly NON-SELECTIVE which is why it has so many other benefits beyond BP control but also makes it more contraindicated in certain situations.
Propranolol is classified as a competitive non-cardioselective sympatholytic beta blocker that crosses the blood–brain barrier. It is lipid soluble and also has sodium channel blocking effects. Propranolol is a non-selective β-adrenergic receptor antagonist, or beta blocker;[54] that is, it blocks the action of epinephrine (adrenaline) and norepinephrine (noradrenaline) at both β1- and β2-adrenergic receptors. It has little intrinsic sympathomimetic activity, but has strong membrane stabilizing activity (only at high blood concentrations, e.g. overdose).[55] Propranolol is able to cross the blood–brain barrier and exert effects in the central nervous system in addition to its peripheral activity.[13]
In addition to blockade of adrenergic receptors, propranolol has very weak inhibitory effects on the norepinephrine transporter and/or weakly stimulates norepinephrine release (i.e., the concentration of norepinephrine is increased in the synapse).[56][52] Since propranolol blocks β-adrenoceptors, the increase in synaptic norepinephrine only results in α-adrenoceptor activation, with the α1-adrenoceptor being particularly important for effects observed in animal models.[56][52] Therefore, it can be looked upon as a weak indirect α1-adrenoceptor agonist in addition to potent β-adrenoceptor antagonist.[56][52] In addition to its effects on the adrenergic system, there is evidence that indicates that propranolol may act as a weak antagonist of certain serotonin receptors, namely the 5-HT1A, 5-HT1B, and 5-HT2B receptors.[57][58][43] The latter may be involved in the effectiveness of propranolol in the treatment of migraine at high doses.[43]
see my post above, selective blocking of beta-1 is NOT going to negate the beneficial aspect of stims, all beta blockers are not created equal when it comes to selectivity
I personally really like Nebivolol(when needed of course)Thanks TR, still trying to interpret it lol. Just began Nebivolol