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There are many proposed mechanisms behind [[Overtraining Syndrome]], but none of them are generally accepted<ref name="OTPhysioReview"/><ref name="OTDepression"/>.
* '''[[Glycogen]] hypothesis'''. One hypothesis is that [[Overtraining Syndrome]] produces chronically depleted glycogen [[Glycogen]] levels leading to the problems of [[Overtraining Syndrome]]. While there is evidence of lower blood sugar in overtrained athletes, glycogen [[Glycogen]] stores are generally replenished between exercises<ref name="OTBiochemical"/>. Studies<ref name="OTCostill"/><ref name="OTSnyder"/> have concluded that glycogen [[Glycogen]] depletion was not responsible for short term [[Overtraining Syndrome]]. There is also the suggestion<ref name="OTBiochemical"/> that glycogen [[Glycogen]] depletion has a knock on effect of increasing BCAA oxidation which in turn causes [[Overtraining Syndrome]] symptoms (see below).* '''BCAA hypothesis'''<ref name="OTBiochemical"/>. This hypothesis suggests that BCAA is used in higher amounts by the muscles because of glycogen [[Glycogen]] depletion. This BCAA consumption indirectly leads to a rise in tryptophan, and tryptophan is able to enter the brain where it is converted to serotonin. This increase in serotonin is linked to clinical depression and could cause symptoms of [[Overtraining Syndrome]]. However consumption of BCAA during or after exercise has not been shown to help.
* '''Free fatty acid hypothesis'''<ref name="OTDepression"/>. As mentioned in the BCAA hypothesis the levels of brain serotonin depend largely on the level of tryptophan in the blood, and tryptophan increases with higher free fatty acid plasma levels. Because endurance training tends to increase the level of free fatty acids in the blood, this hypothesis proposes that excessive endurance training raises the blood free fatty acid which raises the tryptophan levels which in turn raise the serotonin levels.
* '''Glutamine hypothesis'''<ref name="OTBiochemical"/><ref name="OTPhysioReview"/>. Endurance exercise deplete glutamine levels and glutamine is important for immune system functioning. However decreased levels of glutamine have not been observed in overtrained athletes<ref name=" OTBiochemical "/>, and glutamine would only explain the compromised immune system, not other symptoms of [[Overtraining Syndrome]].
* '''Hypothalamus<ref name="OTBiochemical "/>/Adrenal Fatigue Syndrome<ref name="OTAdrenal"/> hypothesis'''. This hypothesis is based around compromise of the hypothalamus, pituitary gland or adrenal gland, which are all responsible for hormone levels. This hypothesis may have some limited support from the success in treating [[Overtraining Syndrome]] with hormone replacement therapy.
* '''[[Muscle ]] damage hypothesis<ref name="OTBiochemical "/><ref name="OTTrauma"/>'''. Exercise induces damage to the muscle cells and this hypothesis suggests that this damage is the underlying root cause of [[Overtraining Syndrome]]. It is deemed unlikely that [[Overtraining Syndrome]] would be caused directly muscular damage, but rather this damage would precipitate other changes leading to [[Overtraining Syndrome]]<ref name="OTBiochemical"/>. It is been observed<ref name="OTSickAnimals"/> that wounded animals exhibit "recuperative behavior", where they become lethargic, less sociable, and exhibit reduced appetite and thirst. This behavior is believed to encourage recovery by reducing activity and exposure to predators. This "recuperative behavior" in some ways mimics [[Overtraining Syndrome]] and depression in human beings. Unfortunately this hypothesis has never been supported by objective measurement<ref name="OTBiochemical"/>.
* '''Brain receptor hypothesis'''<ref name="OTDepression"/>.''' '''Exposure to chronic stress may lead to altered neurotransmitter receptors within the brain. Changes in these neurotransmitter receptors can modify the fundamental mechanisms of the brain and are believed to play a role in both [[Overtraining Syndrome]] and major depression.
* '''Brain plasticity hypothesis'''<ref name="OTDepression"/>. The human brain retains the ability to update its 'neurological wiring', which is part of our ability to adapt and learn. This neural plasticity is one of the adaptations that occurs to long-term exercise. While mild levels of exercise in harms the creation of new neurons, severe exercise stress causes neurological degradation.
