Dynamic cerebral autoregulation (dCA), the capacity of the cerebrovasculature to buffer transient fluctuations in arterial blood pressure, is critical for maintaining cerebral perfusion. Impaired dCA has been reported in individuals with type 2 diabetes, a population at elevated risk of cognitive decline. However, whether similar cerebrovascular dysfunction is evident in pre-diabetes (PD), an early stage of glycaemic dysregulation, remains unexplored. Furthermore, aerobic fitness is proposed to modulate cerebrovascular function, though its influence may be population-dependent.
Therefore, this pilot study used transfer function analysis (TFA), to assess whether (1) dCA is impaired in individuals with PD and (2) TFA-derived indices of dCA are associated with aerobic fitness.
Seven individuals with PD (5 females; 66 ± 6.6 years) and seven normoglycemic controls (CON) (4 females; 59 ± 3.55 years) volunteered to take part in this study, completing two visits. On visit one, participants performed a ramp incremental cycling test to exhaustion followed by a verification bout to determine maximal oxygen uptake (V̇O₂max). On visit two, dCA was assessed using a 5-minute repeated sit-to-stand manoeuvre completed at 0.05 Hz. Middle cerebral artery velocity (MCAV) and mean arterial pressure (MAP) were measured via Transcranial Doppler Ultrasonography and finger photoplethysmography respectively. dCA was quantified using TFA of mean MCAv and MAP, yielding values of gain, normalised gain, phase and coherence. Group differences were assessed using independent-sample t-tests, while Pearson correlations examined associations between V̇O₂max and indices of dCA.
No between group differences were observed in gain (P=0.91), normalised gain (P=0.15), phase (P=0.32) or coherence (P=0.07). V̇O₂max was not associated with gain, normalised gain, or phase in either group (all p > 0.28).
These preliminary findings suggest that dynamic cerebral autoregulation is preserved in pre-diabetes and is not associated with aerobic fitness. Although these findings suggest that early glycaemic dysregulation may not yet compromise dCA, larger studies are required to confirm these observations and to establish whether impairments develop with disease progression.