It is now becoming widely accepted that mitochondria and ATP (Adeno-Triphosphate) dysfunction in the cells are the key to fatigue syndromes.

Each cell contains mitochondria whose job it is to supply energy via ATP.

This is the universal currency of energy in all living things on the planet. ATP transports energy within the cell for metabolism, but in ME/CFS and FMS this cell communication breaks down and is part of what we call Redox Signaling.

When the mitochondria in the cell are at optimum function, and the person rests following exertion, lactic acid is converted back to glucose and the lactic acid burn that causes stiffness disappears.

This biochemical process happens every single second in the body, every day of your life.

If there is reduced, or no ATP available, mitochondria will fail, lactic acid will persist for minutes or even hours causing pain and burning sensations in FMS or stiffness and muscle aches in ME/CFS.

In fatigue syndromes energy metabolism is nearly always reduced because ATP is blocked by toxins and microbes.

ATP is also a neurotransmitter directly involved in brain function, sensory perception and nervous system control of muscles and organs and fits the criteria for ME/CFS and many patients with FMS.

Mitochondria activity is also partly controlled by free radicals.

Free Radicals and Inflammation

Cells produce excessive free radical production called superoxide in response to microbes such as virus, parasite, fungus, bacteria and environmental toxins that cannot be dealt with by the Antioxidants housed inside the cell such as Co-Enzyme Q10, NAD (niconamide), Magnesium and Acetyl L-Carnitine.

If the infection or toxin is persistent and chronic, this will lead to blocking and eventually a "switching off" of mitochondria. The bodies’ natural reaction is to create inflammation in an attempt to deal with this process by producing free radicals.

This reduces your ability to detoxify and the lack of Glutathione (the cells main antioxidant protector) depletes your energy.

Mice lacking mitochondrial SOD (Super-Oxide Dismutase) die around 21 days after birth due to Neurodegeneration, Cardiomyopathy and Lactic Acidosis.

Superoxide dismutase neutralises this process and is a useful supplement in patients with FMS as it reduces free radicals.

The largest source of free radicals come from mitochondrial themselves because we have large amounts of glucose being burnt in the presence of oxygen to produce energy.

ROS Link: