Key pointsEpisodes of intermittent hypoxia, as produced in obstructive sleep apnoea, cause a carotid‐driven sympathetic hyperactivity and an oxidative status leading to cardiovascular and metabolic pathologies, which are less pronounced in patients >60–65 years old.In young rats (3–4 months) chronic intermittent hypoxia augments carotid body hypoxic responses, plasma catecholamine, renal catecholamine content and turnover, produces an oxidative status, and causes hypertension.In aged rats (22–24 months) chronic intermittent hypoxia does not alter carotid body responses, catecholamine‐related parameters or redox status, and does not cause hypertension.It is concluded that age affords protection to harmful effects produced by chronic intermittent hypoxia.Possible mechanisms involved in age protection and the significance of our findings in the diagnosis and therapeutic approaches to obstructive sleep apneoa in the elderly are considered.AbstractObstructive sleep apnoea (OSA) affects an estimated 3–7% of the adult population, the frequency doubling at ages >60–65 years. As it evolves, OSA becomes frequently associated with cardiovascular, metabolic and neuropsychiatric pathologies defining OSA syndrome (OSAS). Exposing experimental animals to chronic intermittent hypoxia (CIH) can be used as a model of the recurrent hypoxic and O2desaturation patterns observed in OSA patients. CIH is an important OSA event triggering associated pathologies; CIH induces carotid body (CB)‐driven exaggerated sympathetic tone and overproduction of reactive oxygen species, related to the pathogenic mechanisms of associated pathologies observed in OSAS. Aiming to discover why OSAS is clinically less conspicuous in aged patients, the present study compares CIH effects in young (3–4 months) and aged (22–24 months) rats. To define potential distinctive patterns of these pathogenic mechanisms, mean arterial blood pressure as the final CIH outcome was measured. In young rats, CIH augmented CB sensory responses to hypoxia, decreased hypoxic ventilation and augmented sympathetic activity (plasma catecholamine levels and renal artery content and synthesis rate). An increased brainstem integration of CB sensory input as a trigger of sympathetic activity is suggested. CIH also caused an oxidative status decreasing aconitase/fumarase ratio and superoxide dismutase activity. In aged animals, CIH minimally affected CB responses, ventilation and sympathetic‐related parameters leaving redox status unaltered. In young animals, CIH caused hypertension and in aged animals, whose baseline blood pressure was augmented, CIH did not augment it further. Plausible mechanisms of the differences and potential significance of these findings for the diagnosis and therapy of OSAS are discussed.