08-21-2003, 09:44 PM #1
T3 more "cardiovascular friendly" than Clen/ECA?
This is one of those times that I really wish i possessed the knowledge and general vernacular of physiology that many of you do, as it would be quite helpful in helping me ask this question correctly. In doing my best, though, here's what i have:
I was speaking with someone this week who mentioned that T3 has a reputation for being more cardiovascular/heart "friendly" than clen , eca and similar CNS stimulants. Or perhaps it wasn't so much that it was more friendly as it was that it simply didn't "attack" or stress the CV system in the same way those drugs might. He described the pathways through which each work and where the CV system is involved in each and it did make sense to me. Keep in mind, however, that my understanding of physiology is quite limited.
Would you guys care to comment on the merit of this guy's assertion? Thanks.
08-21-2003, 09:51 PM #2
Sounds right since both clen and ECA speed your heart up a great deal and therfore stress it out more but t3 is a synthetic thyroid hormone which i dont believe speeds the heart up at lesat not that noticably with me anyhow.
08-22-2003, 02:39 PM #3AR-Hall of Famer / Retired
- Join Date
- Aug 2001
- Wherever necessary
that is correct - t3 has little to do with increased heart beat whereas CNS stimulants increase both Blood pressure as well as induce a level of tachycardia in order to burn more energy - t3 increases the body heat without much change in RHR or BP
08-22-2003, 03:29 PM #4
yup, what he^ said.
08-22-2003, 04:36 PM #5
Your buddy is wrong.
What most people do not know is that T-3 is an adrenergic agonist (i.e. it's basically same as clen , ephedrine).
It directly increases myocardial contractility, HR and oxygen consumption. You can quite literally give yourself an ischemic heart attack with T-3.
The guy is an assclown if he doesn't know what a huge stress excessive T3 levels place on the cardiovascular system.
08-22-2003, 04:57 PM #6Originally Posted by longhornDr
08-24-2003, 03:48 PM #7
Bumping this for some clarification
08-24-2003, 05:20 PM #8
For the dumb asses like me:
Will T-3 Cause Harm to Users Who Do Lots of Cardio (2-4 miles a day)?
08-24-2003, 09:13 PM #9AR-Hall of Famer / Retired
- Join Date
- Aug 2001
- Wherever necessary
While I was wrong in saying that T3 has no effect at all but in experience, compared to clen it is far milder because its effect is NOT direct - and in fact, its mechanism of action is not really understood at this time: note the two studies:
Cardiovascular effects of clenbuterol are beta 2-adrenoceptor-mediated in steers
A. J. Hoey, M. L. Matthews, T. W. Badran, G. G. Pegg and M. N. Sillence
Tropical Beef Centre, Rockhampton, Queensland, Australia.
The mechanism through which the repartitioning agent clenbuterol increases heart rate was investigated. First, the relative importance of the beta 1- and beta 2-adrenoceptors was established in rat and bovine right atria in vitro. The positive chronotropic and inotropic effects of (+/-)isoproterenol in rat and bovine right atria, respectively, were markedly antagonized (P < .001) by the beta 1-adrenoceptor antagonist CGP 20712A but were antagonized less by the beta 2-adrenoceptor antagonist ICI 118 551 in rat (P < .01), but not in bovine atria, indicating a major role of the beta 1-adrenoceptors. Clenbuterol was only a partial agonist in rat right atria, increasing heart rate at high concentrations through stimulation of beta 1-adrenoceptors. In studies in vivo, clenbuterol decreased the plasma potassium concentration (P < .05) and increased the plasma glucose concentration (P < .05). Clenbuterol also reduced diastolic blood pressure (P < .01) and increased heart rate (P < .001). The increase in heart rate was not due to direct stimulation of cardiac beta 1-adrenoceptors by clenbuterol but was consistent with a reflex response to beta 2-adrenoceptor-mediated hypotension. This would have caused the activation of baroreceptors, which in turn would have resulted in both the release of norepinephrine to stimulate cardiac beta 1-adrenoceptors and the inhibition of cholinergic input to the heart. Thus, the effects of clenbuterol could be eliminated completely by ICI 118 551 or reduced by approximately 50% using CGP 20712A. The combination of treatment of clenbuterol and CGP 20712A could be useful. It may allow the full repartitioning effects seen with the beta 2-agonist alone, but with a markedly attenuated effect on the heart. Such a treatment regimen may also help reduce the increased energy expenditure and loss of appetite seen following the initial administration of clenbuterol.
Triiodothyronine increases contractility independent of beta-adrenergic receptors or stimulation of cyclic-3',5'-adenosine monophosphate.
Ririe DG, Butterworth JF 4th, Royster RL, MacGregor DA, Zaloga GP.
Department of Anesthesia, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157-1009, USA.
BACKGROUND: Triiodothyronine regulates cardiac contractility; however, the mechanisms by which it produces its acute contractile effects remains unknown. We compared the acute effects of thyroid hormones (triiodothyronine [T3] and thyroxine [T4]) and of isoproterenol on the contractility of isolated rat hearts. In addition, we sought to determine whether the acute inotropic effects of thyroid hormones were mediated by beta-adrenergic receptors or by increased production of cyclic-3',5'-adenosine monophosphate (cAMP). METHODS: A Langendorff heart preparation harvested from euthyroid male Sprague-Dawley rats was used. Drugs were administered through an aortic perfusion catheter. A pressure-transduced left-ventricular balloon catheter measured pressure and heart rate changes. Changes in the maximum positive rate of change in pressure (dP/dT) and maximum negative dP/dT were determined. Responses to varying doses of T3, T4, and isoproterenol were assessed in the presence and absence of beta-adrenergic receptor blockade with propranolol. cAMP production, measured by radioimmunoassay, was determined in myocardial cell suspensions after incubation with T3 or isoproterenol. RESULTS: T3 0.74 nmol rapidly and significantly increased maximum dP/dT by 335 +/- 38 mmHg/s within 30 s after bolus injection; however, contractility was unchanged after as much as 12.9 nmol T4. The maximal increase in dP/dT after 0.8 nmol isoproterenol was comparable to that produced by T3. However, the cardiotonic actions of isoproterenol were significantly slower to develop (peaking at 60 vs. 15 s) and lasted longer than those of T3. Pretreatment with propranolol 1 mumol diminished the contractile effects of isoproterenol but had no effect on those of T3. Concentrations of isoproterenol that increase contractility also significantly increased cAMP production in isolated rat myocardial cells. However, T3 failed to increase cAMP production. CONCLUSIONS: These results demonstrate that the acute inotropic effects of T3 are not shared by T4 and appear unrelated to beta-adrenergic receptor mechanisms or to generation of cAMP. Thus, T3 acutely stimulates cardiac contraction by mechanisms that differ from those of the more commonly used beta-adrenergic receptor agonists and phosphodiesterase inhibitors. Further studies are needed to identify the mechanisms underlying the acute contractile effects of T3 and to determine whether T3 will prove useful for increasing ventricular function in patients.
Users Browsing this Thread
There are currently 1 users browsing this thread. (0 members and 1 guests)