RHR and HRV on Reta/GLPs

shcidheuddvv

New Member
Hey guys! I'm wondering what strategies, if any, y'all have implemented to mitigate the RHR raising and HRV lowering effects of Reta. 2mg a week has been enough to drop my HRV from 120s to 50s and raise my RHR from 50s to 70s.
 
The glucagon component in Retatrutide is what sets it apart from Segmaglutide and Tirzepitide. The glucagon competent is responsible for the increased heart rate, which produces a thermogenic effect and increasing daily caloric expenditure. This is what makes it more effective than both Tirz and Segma.

If you don't like it, you could try lowering the dose or switching to another GLP-1.
 
Probably would be better to run tirz. However, some of the kidney protection benefits that I've read on reta is what keeps me on it.
Yeah, the glucagon agonism was what originally got me interested, as the last cut I did my RHR dropped just below 40 at the very end and my daily expenditure was nuked. I didn't realize how strong it would be though, so I may have to reserve Reta for cuts, and then stock up on some Triz for general metabolic/cardiovascular health going forward. Hopefully Triz is less harsh on my RHR.
 
I have been running Reta since the end of September. Titrated up to 4mg per week.

My RHR climbed from the 60s to the 70s at first but has since dropped back down into the low 60s.

It never got to a point that concerned me personally and I like the Glucagon component.

Down almost 20lbs
 
I‘ve tried both Tirz and Reta. Both nuke my rhr and hrv similarly (rhr: mid 40 to high 60; hrv: 130 to 30). Staying longer on one dose and pinning in butt fat helped me a little (25 ish % better). Reducing dose even more.
Trying Ivabradine next and if not satisfied switch to Sema. I think it‘s the gip part of both Tirz and Reta that lead to the changes.
 
But wouldn’t that stop the thermogenic effect?
The thermogenic effect of reta, if it’s real in humans and not just mice, has nothing to do with heart rate. It’ll be something more along the lines of futile lipid cycling, ATP-consuming conversion of diglycerides into triglycerides and then conversion of triglycerides into diglycerides, back and forth creating no actual change or net product but wasting a bunch of ATP in the process.

No reason to think that ivabradine would affect that at all.
 
The idea that the increase in heart rate is linked to increased energy expenditure exists because people get causality reversed. We know that if we go for a hard run it creates metabolic demand and our body increases heart rate to help supply oxygen and energy to meet that metabolic demand. We can even use heart rate as a proxy measure of metabolic demand during a workout to estimate how many calories we’re burning.

But it doesn’t follow that just because we increase heart rate that we must be going for a hard run. Heart rate can increase independently of increased metabolic demand, for example if you take a drug that directly acts on the sinoatrial node to increase heart rate. Sure your heart is beating faster but there was no systemic increase in metabolic demand. You’re not actually going for a hard run. And considering that cardiac workload doesn’t really change (heart rate increases but blood pressure and vascular resistance decrease), you could probably count the calories burned each day from the increased heart rate on your knuckles.
 
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