Video by drtrevorbachmeyer

Here's the secret to keeping muscle on all GLP-1s. So when you use semaglutide and terzepatide, even retitrutide, you activate GLP-1 receptors and suppress appetite signals in the hypothalamus. That's the part that every Insta expert online knows about it. Except what they don't know is tapping the GLP-1 receptor also suppresses mTOR signaling, which is what biology uses for muscle

protein synthesis. When it's turned off, biology is catabolic, period. Tapping GLP-1 receptors mimics a fasting state. Biology thinks that calories are limited and the nervous system goes into a metabolic defense mode. In a caloric deficit, especially a severe one like on GLP-1s, biology breaks down muscle tissue through a process called the ubiquitin proteasome pathway

or UPP. It's designed to recycle amino acids from muscle to keep the brain, the heart, and the immune system functioning properly. Here's the Cliff Notes version. Enzymes tag muscle proteins with ubiquitin. It's like putting a giant red sticker on a package. Proteasomes see the tags and then they chew up the muscle protein into amino acids, which head to the liver for gluconeogenesis to

make glucose to feed your starving brain. This entire process is independent of protein intake and Instabros and doctors and Insta experts will argue, just eat more protein, problem solved. Wrong. I'll even show you how and I'll solve it for you. Yes, protein intake matters for providing amino acid substrate for muscle protein synthesis You can have all the amino acids you want and the UPP will still tear apart your muscle because the signal driving the breakdown isn low amino acids The signal is biology is in energy

scarcity, fire up the catabolic reactor. So when you're on GLP-1s, especially semaglutide or terzepatide, don't get mad. The nervous system is saying the opposite. It's saying danger, crank up the UPP and recycle all the muscle for energy. Protein provides the raw materials, but the nuclear meltdown needs to be shut down and the meltdown is the ubiquitin proteasome pathway