Danielle Hodson, PhD research student
Obesity has been defined as an excess of body fat leading to ill health and is associated with serious chronic disease such as type 2 diabetes and hypertension.
An increase in an individual’s weight can be due to an increased total energy intake, sedentary lifestyle or both. One explanation to why there is a rise in obesity is the modern day diet, of energy dense, fatty and sugary foods leading to excess weight gain which the body tolerates, and it has been shown that only 3 in 10 adults report meeting the guidelines of participating in 30 minutes of moderate physical activity on 5 days a week, with 1 in 8 not participating in any physical activity (Welsh Health Survey, 2012).
The detrimental effects that a sedentary lifestyle has can be attributed at least partially to changes in lipoprotein lipases (LPL) activity, an enzyme that facilitates up regulation of free fatty acids into skeletal muscle and adipose tissue. Low levels of LPL have been associated with an increased circulating triglycerides levels, decreased HDL cholesterol and an increased risk of cardiovascular disease.
Research has suggested that obesity may exert adverse affects on the vascular system by increasing arterial stiffness, predisposing the individual to hypertension and premature aging of the vasculature. The prevalence of obesity within the UK has reached epidemic proportions; in Wales (Welsh Health Survey, 2012) it has been indicated that 1 in 4 adults were classified as obese (Body Mass Index; BMI >30kg/m2), with 3 in 5 adults been classified as overweight (BMI; 25 – 29.9kg/m2) or obese. Body mass index is a widely accepted method within the clinical setting to measure and define body mass.
It has been increasingly recognised as a risk factor for stroke, cardiovascular disease and cognitive impairment alongside various other factors such as aging, hypertension and smoking. BMI is an imprecise but useful measurement of adiposity which varies with age, sex and ethnicity but correlates well with body fat mass, however, measurements fail to distinguish between body fat, muscle mass or bone.
In healthy individuals, it has been demonstrated that a brief period of stress induces transient endothelium dysfunction. It has been stated that blocking cortisol production (a marker of inflammation) during an acute mental stress (simulated public speaking task) preserves endothelial function. Therefore, inflammation may provide a common link between mental stress and obesity. However, this link remains to be clarified in the obese population.
The current research is therefore assessing two everyday life stressors; mental agility (in the form of a paper and pen based battery of psychometric tests) and an exercise challenge to exhaustion and the impact that these two stressors have upon the cardiovascular and cerebrovascular function.
Utilising a range of techniques, to measure cerebral haemodynamic function via Transcranial Doppler Ultrasound and Near Infrared Spectroscopy; cardiovascular function via Flow Mediated Dilatation and Pulse Wave Analysis/Velocity; body composition via Duel Energy X-Ray Absorptiometry (DXA), Hydrostatic weighing and Bioelectrical Impedance Analysis (BIA) we are assessing a range of body composition from ‘healthy weight’ (BMI 18.5 – 24.99 kg/m2) to obese individuals (BMI > 30 kg/m2) during the two stressors to determine the impact on the cardiovascular and cerebrovascular system.
The objective of the current research is to establish the implication of obesity for cardiovascular and cerebral haemodynamic function, with the aim to determine if an increased body mass index will affect cardiovascular and cerebral haemodynamic function. It is hypothesised that cardiovascular function and in turn cerebral haemodynamic function will be directly related to an increased body mass index, by definition with the worst case scenario been the obese individual.