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Aerobic vs Anaerobic respiration in ME/CFS--from Serg1942

Sushi

Moderation Resource Albuquerque
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19,935
Location
Albuquerque
Posted with permission from the author who is in medical school (English is his second language):

Aerobic vs Anaerobic Respiration in ME/CFS.

(I just explained this to a fellow and thought I'd share in case it may be useful to others)

There're two ways a cell can obtain energy from food, one with O2 (aerobic) and the other without O2 (anaerobic).

The aerobic one is much more efficient, so it is used preferably over the anaerobic, except when there's no choice, such as in anaerobic exercise (hence the name) where the need of energy is so great in so little time, than the only way to get the required energy is through the anaerobic respiration (note that this one is less efficient but quicker).

Note also that both routes finally recycle ADP into ATP, that is the "energetic currency" of the body. So when I talk about efficiency I mean to produce more ATP per gram of glucose used.

Ok, so what happens in ME? To oxidize glucose aerobically in order to obtain ATP, we need a pathway called Kreb's cycle (KC), that is coupled with another pathway, the electron transport chain that finally ends up into the oxidative phosphorilation, where ATP is obtained by reducing the O2 into H2O (blood, urine) plus CO2 (breath)--this occurs in the mitochondria.

In ME/CFS there's oxidative stress (OS) because we don't have a proper antioxidant mechanism (I think mainly because of a chronic low levels of glutathione). This OS is known to impair some enzymes of the KC.

Also, the electron transport chain is impaired for some reasons, and more than the normal amount of free radicals are produced, while at the same time we generate less ATP (so less energy!).

The net result of all this is that if the "entrance" into the aerobic respiration pathways (KC) is inhibited, the route is diverted towards the second possible road, the anaerobic respiration (they both share the same pathway of glucose oxidation, previous to the KC, called glycolysis) --I'm sure there're signaling mechanisms that also "tell" the cell to switch to an anaerobic state, in order to protect it, when free radicals are high. This must be regulated at a genomic level.

So, the thing is that we cannot avoid using aerobic respiration (otherwise we would be dead), but we use it less frequently and less properly than we should (still, giving off much more free radicals than in a healthy person).

On the other hand we use the anaerobic respiration more than usual, forming excess of lactic acid (related to pain, muscle stiffness, etc.)

So this is how these two ways of respiration relate to each other...

Hope I have made myself understood!

Best,
Sergio
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
One thing I might add is that several pathways likely to be active in CFS and ME might produce peroxynitrite, massively increasing oxidative stress, and perhaps an initial trigger for dropping glutathione to critical levels which are hard to replace if you have a genetic defect limiting glutathione synthesis.

What a lot of hypotheses miss though is explaining the high prevalence of EDS. To me this points to gut involvement, with increased bacterial and other toxins entering the body, overwhelming and further depleting liver glutathione and other detox mechanisms.

Further, glutathione is critical to mitochondrial function. Its needed to fold aconitase, a critical mitochondrial enzyme, and probably other enzymes too. Any enzyme that requires folding to a final shape (conformation) and is then imported to the mitochondria might be defective. I know that aconitase is a nuclear protein that is imported into mitochondria, but I bet there are others. Deficiency in functioning enzymes (but not necessarily quantity of total enzyme) will not affect the mitochondria much at rest, but will limit the maximum energy available.
 

Allyson

Senior Member
Messages
1,684
Location
Australia, Melbourne
...


What a lot of hypotheses miss though is explaining the high prevalence of EDS. To me this points to gut involvement, with increased bacterial and other toxins entering the body, overwhelming and further depleting liver glutathione and other detox mechanisms.
.......


Thanks for the post Alex; could you say what you mean by EDS please?

a
 

Allyson

Senior Member
Messages
1,684
Location
Australia, Melbourne
Allyson Ehlers-Danlos Syndrome, in all its variations including those not discovered yet: EDS.



Great thanks Alex, yes I think i has been overlooked to to a great extent; I understand they are re- classifyinghte types again too as more people get diagnosed; i think they used to think you had to be hypermobile to have it and that is now aparently ot the case so many people who havee stiff muscles for whatever reason have been excluded, erroneously.


thanks again,
cheers
Ally