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In nerves exposed to 100 Hz when bathed in 10 mM glucose, the CAP failed suggesting that even in the presence of normoglycemic glucose additional vitality substrate is required when the tissue vitality demand increases. Such data are vital as they present that glycogen has an necessary function under physiological circumstances. The fact that glycogen supported CAP conduction in the absence of exogenously applied glucose in all probability has no worth in ascribing a task to glycogen, since aglycaemia is an artificial experimental process, and hypoglycemia is an iatrogenic consequence of insulin therapy that didn't exist prior to 1922 (Frier et al., 2014), thus cannot be glycogen’s important position. However supplying lactate to axons when tissue vitality demand increases implies a novel role for brain glycogen and suggests it acts as an power buffer moderately than an power reserve, whose function is to not single-handedly support conduction, however to act in concert with ambient ranges of normoglycemic glucose.

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