Preterm birth is a risk factor for the development of cardiorespiratory complications. Infants that are born prematurely face myriad challenges due to physiological immaturity. Respiratory control impairments in early life including apnoea of prematurity with resultant disruption to systemic oxygen status can provoke long-term disability, including increased propensity to develop morbidities in later life such as sleep-disordered breathing. In rodents, exposure to intermittent hypoxia mimicking recurrent episodes of oxygen desaturation that are characteristic of apnoeas, provokes plasticity at multiple sites of the respiratory control network culminating in breathing instabilities, altered chemoreflex control of breathing and impaired respiratory motor nerve and muscle function. Persistent effects of stressors presenting during critical periods of early development may be sustained by epigenetic mechanisms. Such changes may be especially relevant to perinatal exposure to intermittent hypoxia since it is established that hypermethylation of genes encoding antioxidant enzymes underlies carotid body chemoreceptor sensitization and respiratory instability following exposure to intermittent hypoxia during postnatal development.