Post-prandial hyperlipidaemia (PPH) acutely impairs systemic vascular endothelial function, potentially attributable to a free radical-mediated reduction in vascular nitric oxide (NO) bioavailability (oxidative-nitrosative stress). However, it remains to be determined whether this extends to the cerebrovasculature. To examine this, 38 (19 young (≤ 35 years) and 19 aged (≥ 60 years)) healthy males were recruited. Cerebrovascular function (middle cerebral artery velocity, MCAv) and cerebrovascular reactivity to hypercapnea (CVRCO2Hyper) and hypocapnea (CVRCO2Hypo) were determined via trans-cranial Doppler ultrasound and capnography. Venous blood samples were obtained for the assessment of triglycerides (photometry), glucose (photometry), insulin (radio-immunoassay), ascorbate free radical (A•−, electron paramagnetic resonance spectroscopy) and nitrite (NO2-, ozone-based chemiluminescence) in the fasted state prior to and 4 hours following consumption of a standardised high-fat meal (1,362 kcal; 130g of fat). Circulating triglycerides, glucose and insulin increased in both groups following the high-fat meal ( P < 0.05), with triglycerides increasing by 1.37 + 1.09 mmol/L in the young and 1.54 + 1.00 mmol/L in the aged ( P < 0.05). This resulted in an increased systemic formation of free radicals in the young ( P < 0.05) but not the aged ( P > 0.05) and corresponding reduction in NO2- in both groups ( P < 0.05). While the meal had no effect on MCAv in either age group, CVRCO2Hyper was selectively impaired in the aged ( P < 0.05). These findings indicate that PPH causes acute cerebrovascular dysfunction in the aged subsequent to systemic nitrosative stress.