Intermittent hypoxia stimulates the development of adaptive responses, called preconditioning. This process is partially mediated by genetic remodeling, via hypoxia inducible factor (HIF), which induces long-term adaptation processes and is responsible for the increase of levels of vascular endothelial growth factor (VEGF), erythropoietin (Epo), atrial natriuretic peptide (ANP), and nitric oxide (NO). The synthesis of brain-derived neurotrophic factor (BDNF) participates in the control of neural plasticity after hypoxia. The mechanisms of neuroprotection against hypoxia may be related to vascular adjustments and to central neurogenic neuroprotection. Some of the factors known to be involved in the development of the mechanism of neuroprotection are also present in the responses to repetitive apneas that occur during sleep in patients with obstructive sleep apnea (OSA) syndrome, who are frequently exposed to severe sleep hypoxemia. It appears that OSA syndrome represents a clinical example of preconditioning and the development of adaptive responses to intermittent hypoxia.