When the arterial CO2 level falls below the apnea threshold, ventilatory effort ceases and central apnea occurs. The high ventilatory response to CO2 tends to have pCO2 levels close to the apnea threshold and to hyperventilate with small changes in arterial pCO2 whereby only a small increase in ventilation is required for CO2 to fall below the apnea threshold and this occurs. This is what appears to occur in the wake-sleep transition where an elevated CO2 response would lead to unstable ventilation and central sleep apnea. This model of hyperresponsiveness to CO2 is based on sleep apnea that arises at high altitudes and results from hyperventilation, in response to low pO2, leading to hypocapnia and subsequent apnea due to an increased CO2 threshold. On the other hand, when there is a low response to hypercapnia, there is little stimulation for ventilation during sleep (where the stimulation of wakefulness ceases), which favors the appearance of central apneas.