Abstract
[Truncated abstract] Recent and profound changes associated with ubiquitous exposure to television, mobile devices and the internet have rapidly accelerated an underlying trend in sedentary behaviour related to urbanisation, automation and the widespread use of motorised personal transport. These technological "advances" have fundamentally altered vocational and lifestyle behaviours in the space of one or two generations. There has never been a more sedentary population of humans than 21st century western society. It was estimated that, in 2008, physical inactivity caused 6–10% of all deaths from the major non-communicable diseases (coronary heart disease, type 2 diabetes and breast and colon cancers), or more than 5.3 of the 57 million deaths that occurred worldwide. It is clear that lifestyle changes are having profound impacts on human disease and healthcare costs and one of the most predominant health conditions is atherosclerotic cardiovascular disease.
Regular exercise has been shown to significantly reduce cardiovascular risk, an impact which is partly mediated by improvements in traditional modifiable risk factors such as hypercholesterolemia, hypertension and obesity. However, recent evidence suggests there is a ‘risk factor gap’, whereby the cardio-protective benefits of exercise cannot be fully accounted for by improvements in traditional risk factors. There is growing evidence that one element that may fill the risk factor gap relates to the direct effects of exercise on the vasculature. It is now believed that increases in blood flow and attendant shear stress associated with bouts of exercise are key mechanisms capable of inducing arterial adaptation. However, exercise is a complex stimulus associated with the release of hormones, metabolic by-products from working muscles and neural activation. The independent role of shear stress as the principal modulator of endothelial and vascular adaptation is therefore difficult to dissect in exercise studies. The broad aim of this thesis was to investigate the effects of changes in shear stress, induced by exercise-independent modalities, on both macro- and micro-vascular adaptation. The thesis is presented in two sections, containing data on conduit artery adaptation and changes in the cutaneous microvessels...
Regular exercise has been shown to significantly reduce cardiovascular risk, an impact which is partly mediated by improvements in traditional modifiable risk factors such as hypercholesterolemia, hypertension and obesity. However, recent evidence suggests there is a ‘risk factor gap’, whereby the cardio-protective benefits of exercise cannot be fully accounted for by improvements in traditional risk factors. There is growing evidence that one element that may fill the risk factor gap relates to the direct effects of exercise on the vasculature. It is now believed that increases in blood flow and attendant shear stress associated with bouts of exercise are key mechanisms capable of inducing arterial adaptation. However, exercise is a complex stimulus associated with the release of hormones, metabolic by-products from working muscles and neural activation. The independent role of shear stress as the principal modulator of endothelial and vascular adaptation is therefore difficult to dissect in exercise studies. The broad aim of this thesis was to investigate the effects of changes in shear stress, induced by exercise-independent modalities, on both macro- and micro-vascular adaptation. The thesis is presented in two sections, containing data on conduit artery adaptation and changes in the cutaneous microvessels...
Original language | English |
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Qualification | Doctor of Philosophy |
Publication status | Unpublished - 2013 |