Post-prandial hyperlipidaemia impairs dynamic cerebral autoregulation

Background: It is well established that post-prandial hyperlipidaemia (PPH) impairs systemic vascular endothelium function. However, we have recently demonstrated that this is not simply confined to the systemic circulation and equally extends to the cerebral vasculature in the form of impaired cerebrovascular reactivity to carbon dioxide. To what extent PPH may influence other markers of cerebrovascular health such as dynamic cerebral autoregulation (dCA) are yet to be investigated. Methods: Forty-four males were recruited for the study of which 20 were young (age: 24 ± 5 yrs; body mass: 76 ± 13 kg) and 24 were aged (age: 67 ± 5 yrs; body mass: 82 ± 11 kg). dCA was assessed using transfer function analysis in response to forced oscillations in mean arterial pressure (MAP; finger photoplethysmography) via squat-stand manoeuvres at a frequency of 0.05Hz for 3 minutes as described previously. During these manoeuvres, continuous measurements of middle cerebral artery velocity (MCAv; transcranial Doppler) were made. Cerebrovascular resistance and conductance indices were calculated as MAP/MCAv and MCAv/MAP, respectively. Venous blood samples were also obtained from an indwelling cannula to assess triglycerides (photometry). All measurements were made prior to and 4 hours following consumption of a standardised high-fat meal (1362 kcal; 130g fat). Data were analysed using a 2-way repeated measures analysis of variance. Significance was established at P < 0.05 and data are expressed as mean ± SD. Results: By design, the high-fat meal increased circulating triglycerides by 1.38 ± 1.03 mmol/L in the young and 1.49 ± 0.90 mmol/L in the aged (P < 0.05). PPH had no effect on resting MCAv, MAP, CVRi or CVCi (Table 1; P > 0.05), but was associated with impaired dCA in the form of reduced phase (Table 1; P < 0.05). Conclusion: These findings show for the first time that PPH has the capacity to impair dCA across the lifespan. These findings have important clinical implications given that impaired dCA is associated with increased risk of stroke and neurodegenerative disease.