Mitochondria are rod-shaped organelles that can be considered the power generators of the cell, converting oxygen and nutrients into a substance known as Adenosine Tri-Phosphate (ATP).
ATP is the chemical energy “currency” of the cell that powers the cell’s metabolic activities. This process is called aerobic respiration and is the reason we breathe oxygen.
Without mitochondria humans and animals would likely not exist because we need large amounts of energy in order to survive. In fact, mitochondria enable cells to produce 15 times more ATP (energy currency) than they could otherwise.
Chronic Fatigue Syndrome as we have discussed is a multi-factorial health condition, with a number of imbalances contributing to the over-all experience of CFS. However mitochondrial imbalance can explain more than any other contributory factor Post Exertional Fatigue, which is a key player within differential diagnosis.
Mitochondria’s key function is the Recycling of ATP to ADP and back to ATP.
This cycle relies upon various nutrient substrates such as D Ribose, Carnitine, B3, Co-enzyme A, Co-enzyme Q10. The role of these substrates is to move into the cell in the process of completing the important recycling metabolic process.
As the nutrients are harnessed, Adenosine Tri-Phosphate becomes Adenosine Di-Phosphate (ATP > ADP). This process actually releases energy, whilst becoming carbon dioxide and water.
Rate Limiting Factors:
Firstly a deficiency in any of the substrates mentioned above create a BLOCK within the cycle. Therefore nutrient deficiency plays into mitochondrial insufficiency.
And because Carnitine, Co-enzyme Q10 and other substrates result from a process called methylation (a biological process that will be expanded on in subsequent Blog posts), when a person under-methylates there is automatically a material deficiency regarding these substrates.
However others things also BLOCK this cycle, like heavy metals, hair dyes and excessive oxidative stress. Excessive oxidative stress destroys both the fatty membrane of the cells and the mitochondria itself.
Further to, there is a protein called trans locator protein responsible for moving ATP and ADP from the mitochondria cell to the cytosol of the cell. When mitochondria senses that ADP/ATP have been depleted, used up for cells function etc, then this triggers mitochondria to produce more ATP. So this constant re-cycling occurs.
The key thing about those individuals who struggle with a rate limiting factor is when they push through, meaning that they carry on doing exercise when or even in some cases just daily chores and tasks throughout their day, and they are not capable recycling the ADP to ATP then the body goes into emergency mode. What this means is that the body then targets ADP to be broken down instead because there is not ample ATP because boundaries have been crossed.
ADP is then broken down to AMP, which is a purine, and is lost to the system since it is then urinated out of the body. Understood by leaders in the field of CFS to be a metabolic disaster. This is where Post Exertional Fatigue comes from. Usually the person pushes through and can feel fine, and even feel fine the following day. But the day after that could be when they crash!!!
AMP cannot be recycled. ADP then has to be built from scratch before it is then recycled to ATP.
However Mitochondrial function is not enough to create CFS on it’s own. Rather understood a down-steam consequence of other factors.
A key factor in how the disease is managed as well as forged is the personality type of the person. If you are a perfectionist for instance who finds it hard to pace, then typically as soon as the person has some energy they use it up again.