One of the first definitions of intermittent (interval) hypoxia is a repeated episode of hypoxia interspersed with episodes of normoxia Burtscher et al.. The term “intermittent hypoxia” is widely used with negative connotations in reference to obstructive sleep apnoea . For this reason, Burtscher et al. proposed using the term “interval hypoxia” in connection with treatment.
Hypoxia can be achieved in two ways: through a reduction of the oxygen level in the air – Normobaric IH (NIH) or through a decrease in the overall pressure level, resulting in the supply of a lower oxygen volume to the body in a hypobaric chamber – Hypobaric IH (HIH). There are several complications associated with the HIH method and our main focus is directed at the development of the Normobaric approach.
The duration of a single hypoxic episode can be divided into two categories: short-duration IH, comprised of several 5-minute bouts of low level oxygen, separated by 5-minute bouts of room air, and long-duration IH, consisting of being exposed for one hour to a low level of O2 Koehle et al.
Oxygenation intervals have a peculiar regulatory, normalising role. They attenuate the hypoxia effect and prevent the possibility of overdosing the affecting factor. When an INH exposure is repeated many times, the oxygenation intervals attenuate the hypoxia exposure intensity to optimise the conditions required for the development of long-term adaptation.
During the re-oxygenation phase, an induction of ROS takes place within the cell, leading to the initiation of a cascade of reactions. The key result is the activation of transcription factors (NF-kB, АР-1, HIF-1-alpha, HIF-3-alpha) which induce protective proteins – anti oxidative enzymes, HSP, FeRP and repair enzymes. As a result, the cells become saturated with protective molecules.
Induction of the ROS synthesis depends on the degree of hypoxia. At the same time, the use of breathing mixtures with concentrations below 10% is rather complicated.
The replacement of normoxia periods with hyperoxic ones (from 30% to 40% O2) significantly increases the amplitude of the treatment factor, resulting in a stronger ROS signal without more intense hypoxia.