Enhanced Fat Metabolism

Fats and sugars are the main fuels that the mitochondria uses as the main fuel in each cell. Usually sugar is the main and easiest fuel of choice.

When nutrients are scarce, in time of starvation or extreme exertion, cells will switch to breaking down fats instead. 

This approach is a little different, what is done here is the enzyme prolyl hydroxylase 3 (PHD3) is inhibited, PHD3 acts as a brake that inhibits unnecessary fat metabolism. This brake is released when fuel is low and more energy is needed, such as during exercise. By inhibiting PHD3 production, we allow for more fat metabolism.

AMPK production is also induced to compound this effect along with some enhanced nutrient absorbtion directly to muscles which altogether works toward super charging muscle recovery and increasing the usage to fat for energy which can lead to the loss or rather 'usage' of fat stores.

Here is a summary from an article on neuro science news

"Rapid alterations in cellular metabolism allow tissues to maintain homeostasis during changes in energy availability. The central metabolic regulator acetyl-CoA carboxylase 2 (ACC2) is robustly phosphorylated during cellular energy stress by AMP-activated protein kinase (AMPK) to relieve its suppression of fat oxidation. While ACC2 can also be hydroxylated by prolyl hydroxylase 3 (PHD3), the physiological consequence thereof is poorly understood. We find that ACC2 phosphorylation and hydroxylation occur in an inverse fashion. ACC2 hydroxylation occurs in conditions of high energy and represses fatty acid oxidation. PHD3-null mice demonstrate loss of ACC2 hydroxylation in heart and skeletal muscle and display elevated fatty acid oxidation. Whole body or skeletal muscle-specific PHD3 loss enhances exercise capacity during an endurance exercise challenge. In sum, these data identify an unexpected link between AMPK and PHD3, and a role for PHD3 in acute exercise endurance capacity and skeletal muscle metabolism."

2- 3 times