UBC Theses and Dissertations

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UBC Theses and Dissertations

Effects of arterial blood gas concentrations on regional cerebral blood flow and metabolism during exercise Smith, Kurt Jason


The magnitude of the cerebral blood flow (CBF) response to exercise is primarily related to the sensitive balance between arterial blood gases (partial pressure of arterial oxygen [PaO₂] and carbon dioxide [PaCO₂]) and cerebral metabolism. However, it has remained unclear whether experimentally or environmentally manipulating the oxygen tensions alters the regulatory influence of arterial blood gases on the intracranial velocities (CBV) and regional CBF responses to incremental exercise. The goal of the experimental chapters of this thesis (Chapter 4, 5 and 6) was to quantify the independent and combined influence of PaO₂ and PaCO₂ on global and regional CBV and CBF during exercise. Chapter 4 identified a heightened (nearly twice the expected response) posterior CBV response during hyperoxic (PO₂ ∼713 mmHg) compared to normoxic (PO₂ ∼160 mmHg) exercise. In contrast, both the anterior and posterior CBV responses were unaltered during mild hypoxic (PO₂ ∼121 mmHg) exercise compared to normoxic exercise. Chapter 5 demonstrated that during exercise in severe hypoxia (PO₂ ∼413 mmHg), following partial acclimatization to high altitude (5050 m), global CBF was elevated by ∼20% compared to sea-level exercise. The elevated global CBF during exercise at high altitude served to compensate for the hypoxemia, and in turn maintained cerebral oxygen delivery equivalent to sea-level values. Chapter 6 revisited and extended the observations during hyperoxic exercise from Chapter 4, whereby measures of extra-cranial CBF were compared with the intracranial velocities during normoxic and hyperoxic (PO₂ ∼300 mmHg) exercise, and also in a separate condition in which any exercise-induced rise in PaCO₂ was prevented (i.e., isocapnia was maintained). The differences observed between regional CBV and CBF during normoxic and hyperoxic incremental exercise trials were abolished when PaCO₂ was held constant. This final chapter also demonstrated that the increased ventilation, per se, is unlikely to influence the cerebrovascular response to exercise. In conclusion, changes in arterial blood gases (hypoxia and hyperoxia) can exacerbate the cerebrovascular response to exercise; however, during incremental exercise in hyperoxia, the regional differences, as well as the differential intracranial and extra-cranial flow responses, are mediated primarily by PaCO₂.

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