Acute exercise and an elevated intraabdominal obesity: implications for cerebrovascular function

Danielle Hodson, Christopher Marley, Julien Brugniaux, R Petit, H Blundell, W Evans, Damian Bailey

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

Abstract

Introduction: An increase in body fat percentage and more so an elevated visceral adiposity has been demonstrated to decrease cerebrovascular function and increase the risk of stroke. Acute exercise is a challenge to the brain and may help highlight subtle consequences in cerebrovascular function (1). The aim of the study was to examine if elevated intraabdominal obesity impairs cerebrovascular function and to what this is further compounded by acute exercise. 
Method: Ten non-medicated aged matched obese 28 (mean) ± 8 (SD) years and 13 non-obese participants (22±5 years) classified by body mass index (BMI; 36.9±9.0 vs. 24.2±2.9kg/m2 respectively) were recruited. BMI was collected via bioelectrical impedance analysis (BC-418, Tanita), Visceral adipose tissue (VAT) was assessed via computer tomography (GE Hawkeye Scanner), body fat percentage (BF) & trunk fat percentage (TF) were collected via duel energy x-ray absorptiometry (Lunar Scanner, UK) and waist circumference (WC) was measured at the midpoint between the last palpable rib and the top of the iliac crest. Middle cerebral artery velocity (MCAv, transcranial Doppler Ultrasound) and mean arterial pressure (MAP, finger photoplethysmography) were measured pre and post exercise (cycling challenge (Lode, Sweden) to volitional exhaustion). Cerebrovascular resistance (CVR) and conductance (CVC) were calculated as MAP/MCAv, and MCAv/MAP respectively. Data were analysed using a 2-way repeated measures ANOVA and independent samples t-tests to establish between group differences. Correlations between VAT, BF, TF and WC and cerebrovascular function were performed using Pearson Moment Correlations, with significance established at P<0.05, following confirmation of distribution normality. 
Results: Obese had a higher VAT (81±28 vs. 45±23cm2), TF (34±5 vs. 26±7%) and WC (115.4±22.8 vs. 80.9±8.7cm) compared to the non-obese controls (P<0.05). Correlations were observed between CVR and VAT (r=0.53, P<0.05), TF (r= 0.47, P<0.05) and WC (r=0.41, P<0.05) and CVC and TF (r=-0.44, P<0.05) and WC (r=-0.46, P<0.05). There was no effect of acute exercise on cerebrovascular function and cerebrovascular function was not further impaired by obesity. 
Conclusion: The findings demonstrate that an increased intraabdominal obesity was associated with impaired cerebrovascular function which was not further compounded through acute exercise. The mechanisms and the long term consequences associated with body fat distribution on cerebral haemodynamic function still warrants further investigation.
Original languageEnglish
Title of host publicationProceedings of The Physiological Society
Volume34, PC074
Publication statusPublished - 2015
EventPhysiological Society 2015 Annual Meeting - Motorpoint Arena, Cardiff, United Kingdom
Duration: 6 Jul 20158 Jul 2015

Conference

ConferencePhysiological Society 2015 Annual Meeting
Abbreviated titlePhysiology 2015
Country/TerritoryUnited Kingdom
CityCardiff
Period6/07/158/07/15

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