Visceral adiposity and its differential impact on systemic and cerebrovascular function

Introduction: Traditionally, much interest has focused on the cardiovascular complications of obesity while its impact on the cerebrovasculature is comparatively less well established. This is surprising given its association with stroke, cognitive decline, dementia and depression which ultimately decrease an individual's functional quality of life (1). To explore this in more detail, the present study was designed to examine to what extent abdominal obesity and the excessive accumulation of visceral adipose tissue (VAT) is associated with impaired cerebrovascular function in the form of cerebral hypoperfusion and decreased vasoreactivity.

Method: We recruited 10 non-medicated obese aged 28 (mean) ± 8 (SD) years and 13 non-obese participants (22±5 years). Total body mass (TBM), body fat % (BF) and body mass index (BMI) were collected via bioelectrical impedance analysis (BC-418, Tanita) and VAT assessed using computer tomography scans (GE Hawkeye Scanner). Aortic (carotid to femoral) pulse wave velocity (PWV) was performed via applanation tonometry (SphygomoCor BPAS-1). Middle cerebral artery velocity (MCAv, transcranial Doppler Ultrasound), mean arterial pressure (MAP, finger photoplethysmography) and end-tidal carbon dioxide (PETCO2, capnography) were measured during steady-state exposure to hypercapnea (5% CO2 in balanced air) and hypocapnea (hyperventilation) as previously outlined (2). Cerebrovascular resistance (CVR) and conductance (CVC) were calculated as MAP/MCAv, and MCAv/MAP respectively. Cerebrovascular reactivity (CVRCO2) was calculated as the percent change in MCAv per mmHg change in PETCO2. Data were analysed using a 2-way repeated measures ANOVA and independent sample t-tests to establish between group differences. Correlations between VAT and haemodynamic variables were performed using Pearson Moment Correlations, with significance established at P < 0.05.

Results: By design, obese had a higher BM (119.3±34.9 vs. 69.7±2.3 kg, respectively), BF (29±6 vs.22±8%), BMI (36.9±9.0 vs. 24.2±2.9 kg.m2) and VAT (81±27 vs. 45±23) compared to the non-obese controls (P < 0.05). Aortic PWV was shown to be elevated in the obese (6.8±1.0 vs. 5.8±0.9 (m/s, P < 0.05) and associated with VAT (r = 0.41, P < 0.05). In contrast, we failed to observe any between group differences in cerebral haemodynamic function.

Conclusions: Collectively, the present findings demonstrate that while excess visceral adiposity is associated with impaired systemic vascular function, such adverse effects fail to "translate" to the cerebrovasculature which appears comparatively more "preserved". The mechanisms and indeed long-term clinical consequences associated with the differential impact of VAT on the human circulation warrant further investigation.