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In nerves uncovered to a hundred Hz when bathed in 10 mM glucose, the CAP failed suggesting that even in the presence of normoglycemic glucose further vitality substrate is required when the tissue energy demand will increase. Such knowledge are essential as they present that glycogen has an necessary position under physiological circumstances. The fact that glycogen supported CAP conduction in the absence of exogenously utilized glucose most likely has no worth in ascribing a role to glycogen, since aglycaemia is an artificial experimental process, and hypoglycemia is an iatrogenic consequence of insulin therapy that did not exist prior to 1922 (Frier et al., 2014), thus can't be glycogen’s major function. However supplying lactate to axons when tissue vitality demand will increase implies a novel function for mind glycogen and suggests it acts as an power buffer rather than an vitality reserve, whose position is to not single-handedly assist conduction, but to act in concert with ambient levels of normoglycemic glucose.