[The mechanism of breathing under the conditions of prolonged voluntary hyperventilation].

Effects of voluntary hyperventilation (2 h, 70-80% of maximal lung ventilation) on external breathing, gas exchange and blood circulation were studied in 12 healthy male volunteers. Hyperventilation was shown to change structure of the respiratory cycle as variation and expiration time were decreased. Indices of the external breathing did not reduce but, on the contrary, there was a significant increase in the alveolar ventilation and a reduction in the dead space ventilation. Considerable losses of carbon dioxide with the expired air were noted only during initial 10-15 min of intensive breathing. The angular coefficient for the most steep section of the CO2 loss curve ranged from 150 to 200 ml/min as a result of which the total CO2 deficit in this period (i.e. the CO2 release exceeds the O2 consumption) was about 2 l. Hereafter, the CO2 deficit did not virtually increase despite intensive functioning of the external breathing system. This became apparent from the regain of the respiratory coefficient, a significant and gradually growing CO2 ventilation coefficient. Values of PETO2 and PETCO2 remained stable throughout the experiment with quite substantial hypocapnia: up to 15-20 mm Hg. Thus, the cardiorespiratory system has a powerful defence mechanism to prevent exacerbation of hypocapnia despite intensive ventilation of the alveolar space. This mechanism comes into action at the very first minutes of hyperventilation, reaches maximal efficiency within 10-15 min and maintains this level during the whole period of investigation (about 2 h).