Other than the fact that cyclic variations and cessation of breathing may take place at the onset of sleep, there is also a possibility of these events taking place during hypoxia and when transient hyperventilation results to subnormal levels of partial carbon dioxide. This mainly takes place in the non-rapid eye movement sleep than it does while awake. The subnormal levels of partial carbon dioxide in conscious humans that are mainly caused by a transient episode of raised rates of breathing produce only ventilator oscillations or occasional apnea (external breathing suspension). The ability of someone, who is awake to breathe in a spontaneous manner at the levels of partial carbon dioxide that is considerably low, seems to depend on chemical drives coming from the peripheral or central chemoreceptors, as well as the interplay of the neural or wakefulness drives and chemicals (Longobardo, Evangelisti, & Cherniack, 2002).
There are two major categories of excitatory neural mechanisms that are thought to play crucial roles in maintaining ventilation in humans who are conscious at low chemical level stimulations and at the same time preventing the chances of apnea occurring. The first mechanism arises from the disturbances that take place in environments such as the nose and light and mental activities that are responsible for breathing excitement. This breathing excitement occurs by a direct action of the central nervous system without interfering with any specific chemoreceptor (Longobardo, Evangelisti, & Cherniack, 2002).
The second mechanism is referred to as post-stimulus potentiation (PSP) and leads to an excitatory response, which continues for one minute or more after the termination of the respiratory stimulation and assists in the prevention of apnea from occurring when there is hypocapnia that has resulted from hyperventilation. The offset of the stimulatory effects in humans is usually done by severe hypocapnia that is sufficient and only disappear if hypoxia is maintained for a period of 5 minutes or more (Fregosi, 1991).
Individuals who are healthy awake rarely experience the periodic breathing or even apnea. However, apnea may take place in conscious healthy individuals. This only occurs in hypoxia and after voluntary hyperventilation and its occurrence is rarely repetitive and may appear during some times and fail in others. This behavior is different as the one seen during apnea or periodic breathing during non-rapid eye movement sleep. Studies have been conducted to evaluate the mechanisms that may explain the scarcity of apnea and the periodic breathing while awake. It has been found that the simplest models that may allow for the essential breathing features to be reproduced while awake as well as when sleeping have a chemical controller that is not linear. This controller is usually awake over a wide range of partial pressures of carbon dioxide and oxygen. The stability of this model is usually dependent on the shape of the curve of the chemical controller. The post-stimulus potentiation also plays a part in the stabilization of responses of the model while hypoxic depression results in destabilization effect on this model. However, the impact of post-stimulus potentiation on breathing stability in individuals who are awake is sometimes seen to be low (Longobardo, Evangelisti, & Cherniack, 2002).
Reference List
Fregosi, R. F. (1991). Short-term potentiation of breathing in humans. Journal of Applied Physiology, 71(3), 892-899.
Longobardo, G., Evangelisti, C. J., & Cherniack, N. S. (2002). Effects of neural drives on breathing in the awake state in humans. Respiration physiology, 129(3), 317-333.
