Functionalnaya Mezhpolusharnaya Asymmetriya e Plastichnost Mozga. (Materials of the All-Russian conference with international participation), 2012, pp 338-340, Moscow, Russia.
Changes in EEG-activity after standard and nasal hyperventilation.
Nabieva T.N., Damyanovich E.V., Baziyan B.Kh.
Brain Research Department, Scientific Center
of Neurology, Russian Academy of Medical Sciences
A number of investigations prove that air passing through the nasal or mouth cavities induce different changes in brain bioelectrical activity. Intensive air passing through the nasal cavity (insufflation) of lower vertebrates activates olfactory generator of electrographic respiratory response and elicit paroxysmal high-voltage activity in the theta-frequency range in bulbus olfactorius, hippocampus, pyryform cortex, amygdale, thalamus and general cortex (Arduini&Moruzzi, 1953; Domino&Ueki, 1960; Gault&Coustan, 1965; Servít&Strejcková 1979; Servít, 1980). For the purpose of finding the effect of intensive nasal breathing on the theta-activity in human central nervous system we implemented EEG-investigation. We recorded electroencephalogram in 8 healthy adult volunteers under 3 experimental conditions: 1) baseline - 3 minutes of quiet respiration; 2) 3 minutes of intensive nasal hyperventilation with mouth closed; 3) 3 minutes of intensive mouth hyperventilation. Theta-band spectral power was analyzed from fourteen bipolar leads.
Following the instructions, our subjects breathed with equal intensity and frequency during nasal and oral hyperventilation. It appeared that maximal attainable frequency of nasal hyperventilation was limited by 15 breathing movements per minute. The more frequent, than 15/min deep nasal respiration was impracticable, because translaryngeal inspiratory and expiratory resistance during nasal breathing is higher than during the mouth breathing. Thus our subjects breathed with equal frequency (15/min) during nasal and oral hyperventilation.
We analyzed the theta-band spectral power from 14 bipolar leadings but didn’t reveal any significant alteration of baseline activity in response to nasal or oral hyperventilation. It should be noted that nasal respiration differs from mouth respiration by considerable resistance in pharyngeal and laryngeal cavity both during quiet breathing and nasal hyperventilation. In inspiration phase of respiration cycle muscles surmount dynamic resistance of shifted tissues and aerodynamical resistance of respiratory pathway.
The frequency rate during standardized classic hyperventilation with open mouth is about 30 breathing movements per minute; besides oral inspiration is deeper as compare with nasal inhalation. During the equal time lungs get much more air and oxygen through the open mouth than through the nose.
We suppose that the frequency rate used by subjects in our investigation - 15 breathing movements per minute - is not sufficient for evoking the changes in blood gas composition and therefore, alterations in human electroencephalogram. Such hyperventilation couldn’t lead to that degree of hypocapnia that elicits changes in brain bioelectric activity that could be generally observed after the standardized hyperventilation (about 30 breathing movements per minute). Intensive nasal breathing can’t lead to that concentration of oxygen and carbon dioxide in blood that is usually observing after the standardized mouth hyperventilation. It is quite possible that presence and degree of alterations in brain bioelectric activity in response to hyperventilation is conditioned by intensity of breathing but not the modality (nose vs. mouth).
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