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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 levels leading to the problems of [[Overtraining Syndrome]]. While there is evidence of lower blood sugar in overtrained athletes, glycogen stores are generally replenished between exercises<ref name="OTBiochemical"/>. Studies<ref name="OTCostill"/><ref name="OTSnyder"/> have concluded that glycogen depletion was not responsible for short term [[Overtraining Syndrome]]. There is also the suggestion<ref name="OTBiochemical"/> that 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 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.