Mitochondria Fatigue - Mental and Physiological Exhaustion You Might Not Aware

Mitochondrion, found in most human cells, produces most of the energy used by the body. Mitochondria is described as the “cellular power house” because it generates most of the cell’s supply of adenosine triphosphate (ATP) used as a source of chemical energy. The number of mitochondria in a cell varies widely by organism and tissue type. Some cells have only a single mitochondrion, whereas others can contain thousands. ATP, Mitochondrial energy production, is an absolute necessity for physical strength, energy, stamina and life itself. Fatigue, weakness and cognitive difficulties can be resulted by the dropping of mitochodrial energy output, no matter how subtle. The impairment of mitochondria function is an important factor in a wide range of human conditions and diseases, such as sexual exhaustion, mental exhaustion, chronic fatigue syndrome, dementia, Alzheimer’s disease, diabetes, stroke, heart disease and cancer.
 
Fatigue can be an important response to physical exertion, emotional stress, boredom or lack of sleep. About 5-20% of people suffer this persistent and troublesome symptom. It is twice as common in women as in men but not strongly associated with age and occupation. There is some evidence that people with chronic fatigue or exhaustion are suffered from Mitochondrial fatigue, a dysfunction of Mitochondria, a typical symptom of the exhaustion would be like a catching cold or flu that never recovered fully.
 
If the body is suffered from stress, hormonal imbalance, depletion of essential growth factors due to sexual exhaustion, or toxin intake the mitochondria of cells were injured and not working up to speed and energy production falls.




A study published in the Journal of Alzheimer’s Disease investigated when changes in multiple mitochondrial proteins occurred most frequently relating to the progression of Alzheimer’s disease. The scientists used 2-dimensional liquid chromatography along with tandem mass spectrometry and the isotope coded affinity tag method to identify and quantify proteins in mitochondrial enriched fractions isolated from postmortem subjects with mild cognitive impairment (4 subjects), early AD (4 subjects), late-stage AD (8 subjects) and age-matched normal control (7 subjects) subjects. The results were identification and quantification of 112 unique proteins common to all three stages in the progression of the disease. The researchers found that the most pronounced protein changes occurred in early Alzheimer’s disease mitochondria. ^[1]