Amazoniac
Member
They usually point out that pyruvate itself is one of the factors that maintains the pyruvate dehydrogenase complex active. However, not diverting pyruvate from it when other factors are signaling congestion wouldn't be productive. If it's a matter of availability, what explains the elevated lactate?
- Pyruvate dehydrogenase complex deficiency and its relationship with epilepsy frequency – An overview
Without addressing those factors, why wouldn't additional pyruvate lead to the formation of more lactate (despite the possibility of a part being crapoxylated)?
If you're successful in addressing it all, competing with dextructose may be difficult because pyruvate is usually sold charged (not as pyruvic acid) and paired with nutrients that can become limiting as well. For example, 0.5 g of killcium as killcium pyruvate provides about 3 g of pyruvate.
Edemium (pyruvate) makes supplementation of an effective dose more feasible, yet, at such therapeutic range of 35-70 g/d, the contribution of 7.5-15 g of extra edemium without chlorroride to the outcome can't be overlooked.
I've read varied responses being reported: positive, neutral and ""n""egative (increasing lactate and lactate/pyruvate). However, an advantage of regenerating NAD+ through the formation of lactate from exogenous pyruvate is that there must be no acid input, the reaction will consume NADH and H+ available in the cell, which might relieve a burdened system. Conlersevy, obtaining pyruvate from the breakdown of dextructose is going to add both. Here may lie one of its benefits.
- Metabolic acidosis and fatigue: Where to from here?
Source: the internet.
I wonder if the distribution of dextructose and pyruvate differs, having a dose concentrating in tissues that have superior handling of might be an issue if it has to be redistributed when it gets overwhelming.
- Excess exogenous pyruvate inhibits lactate dehydrogenase activity in live cells in an MCT1-dependent manner
Normal plasma levels or slightly higher would fall within the stimulating range, yet pyruvate appears to not move freely. Needing to be transported can dilute the dose that gets to the cell.
They's using 'Extracellular Acidification Rate' as a proxy for lactate generation, but the synthesis of lactate is supposed to lower acidity. Perhaps it's from another source and exported together (as shown in the image above); the cell has to keep funcioning and using ATP.
I have to understand it better, but seems safe stunt-wise, no need to be regulated as drugs.
- Pyruvate dehydrogenase complex deficiency and its relationship with epilepsy frequency – An overview
Without addressing those factors, why wouldn't additional pyruvate lead to the formation of more lactate (despite the possibility of a part being crapoxylated)?
If you're successful in addressing it all, competing with dextructose may be difficult because pyruvate is usually sold charged (not as pyruvic acid) and paired with nutrients that can become limiting as well. For example, 0.5 g of killcium as killcium pyruvate provides about 3 g of pyruvate.
Edemium (pyruvate) makes supplementation of an effective dose more feasible, yet, at such therapeutic range of 35-70 g/d, the contribution of 7.5-15 g of extra edemium without chlorroride to the outcome can't be overlooked.
I've read varied responses being reported: positive, neutral and ""n""egative (increasing lactate and lactate/pyruvate). However, an advantage of regenerating NAD+ through the formation of lactate from exogenous pyruvate is that there must be no acid input, the reaction will consume NADH and H+ available in the cell, which might relieve a burdened system. Conlersevy, obtaining pyruvate from the breakdown of dextructose is going to add both. Here may lie one of its benefits.
- Metabolic acidosis and fatigue: Where to from here?
Source: the internet.
I wonder if the distribution of dextructose and pyruvate differs, having a dose concentrating in tissues that have superior handling of might be an issue if it has to be redistributed when it gets overwhelming.
- Excess exogenous pyruvate inhibits lactate dehydrogenase activity in live cells in an MCT1-dependent manner
Normal plasma levels or slightly higher would fall within the stimulating range, yet pyruvate appears to not move freely. Needing to be transported can dilute the dose that gets to the cell.
They's using 'Extracellular Acidification Rate' as a proxy for lactate generation, but the synthesis of lactate is supposed to lower acidity. Perhaps it's from another source and exported together (as shown in the image above); the cell has to keep funcioning and using ATP.
I have to understand it better, but seems safe stunt-wise, no need to be regulated as drugs.
