Crisp, Rachel (2015) Effects of acute exercise and high fat diet on the inflammatory response associated with endothelial cells and lipid metabolism. (MSc(R) thesis), Kingston University, .

Abstract

Introduction: Inflammation, by definition, is a 'response of living tissue to local injury' which results in the accumulation of blood cells and fluid [Ryan and Majno, 1977]. Diet has been linked to inflammation, especially in the postprandial hours of a high-fat meal. Research has shown an increase in inflammatory markers after the consumption of a meal with a high fat content [Tsai et al, 2004]. Conversely, regular exercise has been reported to be beneficial to our well-being [Laufs et al, 2004], however reports have suggested that the shear stress experienced by the vasculature during intense exercise may induce changes in biochemical markers indicative of an inflammatory state [Laufs et al, 2005, Rehman et al, 2004]. The principal inflammatory markers used in this research so far have been Circulating Endothelial Cells (CECs) and Endotheliam Progenitor Cells (EPCs). CECs have been shown to increase in number in inflammatory states, including atherosclerosis [Boos et al, 2006, Goon et al, 2006]. EPCs are measured by their ability to form colonies (Colony Forming Units, CFUs) and have been shown to decrease in number in inflammatory states [Kunz et al, 2006]. The decrease in EPCs has been indicated as a marker of endothelial health. Taking into account current research findings and methods, it is hypothesised that the simulating an inflamed state using the consumption of a specified fatty snack, or participation intense exercise by healthy males, would cause a change in the function of the endothelium, which would be expressed as a change in measurable markers of inflammation. Methodology: Healthy male volunteers (n=31) aged between 23 and 53 years were recruited to take part in one of two studies. The participanets were required to fast for 12 hours prior to the experiment. On the day of the experiment athropometric measurements, including blood pressure, were taken. A fasted blood sample (30 mL) was taken before the participants were either provided with the fatty snack or invited to carry out an intensive exercise. The total nutritional content of the meal was 1000kcal, 54.4 g fat (58% saturated fat). The exercise task consisted of either a treadmill- or cycle-based task for more than 15 minutes. A second blood sample (30 mL) was taken one hour after consuming the snack or immediately after exercise. EPCs were cultured according to a validated method [Kunz et al, 2006] and CECs were ennumerated according to a literature method [Good et al, 2006]. Plasma was extracted from each sample and stored at -80[degrees]C for further analysis of CRP, NEFA, Triglycerides and Cholesterol. Results: The effects of the test meal and exercise protocol varied according to the inflammatory marker measured. Paired t-test statistics were applied and showed significant increases in CEC population after the test meal and exercise (p = < 0.0001 and p = < 0.0001 respectively). EPC populations showed a significant decline in activity after the test meal (p = 0.0291). The significant correlation of age with systolic and diastolic blood pressure (p = 0.16 and p = 0.29, respecticely) was also recorded. Conclusion: According to the results, age and BMI positively correlate with blood pressure, which is demonstrated in literature [Miall et al, 1967; Landahl et al, 1986]. The results obtained here have shown a significant correlation between the consumption of the chosen test meal and exercise with the number of CECs and EPCs, which appear to be independent of correlations with the other variables measured. This is an extremely significant result, which begins to confirm the hypothesis, as CECs have been reported to be a marker of endothelial damage [Lee et al, 2006; Lee et al, 2005; Boos et al, 2006, Erdbrugger et al, 2006].

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