Although a sleep debt amasses during torpor, the dissimilarity of SWA curves described above show it was not the trigger for an arousal episode. Although the postponement of the first phase of arousal by sleep deprivation should have also postponed the initial enhancement of SWA seen during normal sleep processes, the initial SWA peak was independent of the induced sleep deprivation. The results from this experiment allowed Daan and Strijkstra to conclude that the effects of deep torpor on NREM sleep EEG are dissimilar from the effects of normal sleep processes on NREM sleep. Sleep homeostatis, therefore, does not play a significant role in the timing or the onset of the arousal episodes. Since sleep debt does not appear to be the trigger that initiates euthermy in hibernating animals, a different internal cue must control the onset of euthermy.
Research focuses now on the connection between euthermy and synaptogenesis.
Low hibernation temperatures are known to decrease electrical brain activity. Adenosine is one of the chemicals that may act as a trigger that initiates euthermy and, simultaneously, act as an energy conservation measure by inducing sleep during arousal. Adenosine acts as both an inhibitor of neuronal activity as well as a sleep-inducer. These two functions, although quite distinctive, correlate well with the proposed theories of euthermy. Adenosine controls neurons whose discharge activity plays a large role in the elevation of EEG readings by inhibiting postsynaptically the hyperpolarization-activated current of the neurons.