Central nervous system fatigue is a complex and multifaceted phenomenon that involves peripheral muscle fatigue and the failure to initiate and sustain voluntary drive to the muscles by the central nervous system. Recent studies have found that elevated levels of neurotransmitters such as serotonin, dopamine and acetylcholine play a part in CNS fatigue. Additionally, inadequate nutrition and abnormal immune responses are also believed to initiate central nervous system fatigue.
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Research on central nervous fatigue has shown a direct correlation between serotonin (5-HT), dopamine and acetylcholine and the onset of CNS fatigue. Acetylcholine is released in the peripheral nervous systems to activate muscle fibers; thus, decreased levels of acetylcholine leads to noticeable muscle fatigue and a decrease in muscle strength. According to NCBI.gov, an imbalance in the level of serotonin and dopamine, specifically a spike in serotonin and a drop in dopamine, is associated with the onset of central nervous system fatigue.
Research on carbohydrates and branched chain amino acids have shown their direct impact on serotonin and dopamine levels in the brain. Carbohydrates are needed for the production of ATP, the body's energy source. Low blood sugar and low levels of muscle glycogen effectively lowers the rate at which ADP is converted to APT and, consequently, the build of ADP results in muscle fatigue.
Furthermore, carbohydrates and branched amino acids fight the onset of central nervous system fatigue due to their impact on amino acids such as tryptophan, which directly affect the levels of serotonin and dopamine in the brain. According to the National Forum.org, branched amino acids and trytophan have the same receptor carriers, thus when the blood level of branched amino acids is low, tryptophan freely enters the brain and stimulates the formation of serotonin, a neurotransmitter proven to initiate central nervous fatigue if rapidly increased.
Elevated levels of circulating cytokines, particularly TNF-alpha, IL-6, and IL-1beta are known to mediate the effect of fatigue from the muscle to the brain. Further more, abnormal immune response to viral infections are also associated with central nervous system fatigue. Antiviral enzymes Rnase L and another enzyme known a protein-kinase R are elevated in patients with central nervous system fatigue. Additionally, according to the Cleveland Clinic, B lymphocytes, T lymphocytes as well as phagocytic and complement system immune cells are believed to be a factor in central nervous system fatigue.