Lactate dehydrogenase supports lactate oxidation in mitochondria isolated from different mouse tissues, 2019, Young et al

Open access, https://www.sciencedirect.com/science/article/pii/S2213231719311176

 

Lactate serves as a substrate for H2O2 production.

H2O2 can destroy pathogens.

 

@Andy I remember reading somewhere that 2 pyruvate are required to enter the mito and operate the PDC. One gets turned into Acetyl-CoA and in turn produces NADH, the other pyruvate uses the generated NADH with LDH to turn into lactate, regenerating the NAD+ so that the 2 new Pyruvates can enter the TCA and repeat the process. Therefore the healthy ratio between pyruvate and lactate (in the mitochondria I presume) is 1:1.

I think it would be possible that in a subset of ill people, that for whatever reason lots more lactate is being produced in comparison to pyruvate being oxidized resulting from burning muscles upon slight exertion that isn't anything to do with deconditioning (I experience this).

Does the study address this? Perhaps if you add some lactate then pyruvate can compensate and maintain a healthy ratio whilst stimulating more mito activity but then at some threshold the lactate becomes a negative.

 

I've not the brain or science knowledge to answer you specifically, but my general comments are:

* this isn't an ME/CFS specific study. They say

so this study has been done to counter a previous one which claimed that lactate can't be/isn't used as a fuel.

* I've posted it because it discussed things of general interest to us, i.e. mitochondria, lactate and reactive oxygen species (ROS), and my thought was that, theoretically, it could be we see an increase in lactate because it's not being consumed in the same way that it is in someone healthy, rather than we are generating more than normal.

* They say

which certainly seems interesting to me given that pyruvate dehydrogenase has been found to be inhibited by Fluge and Mella, although they, to my knowledge, didn't identify the cause.

Hope that helps some?