Anthony R. Bain, Shawnda A. Morrison and Philip N. Ainslie
Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan, BC, Canada
Faculty of Professional Studies, Kinesiology, Acadia University, Wolfville, NS, Canada
Hyperthermia is associated with marked reductions in cerebral blood flow (CBF). Increased distribution of cardiac output to the periphery, increases in alveolar ventilation and resultant hypocapnia each contribute to the fall in CBF during passive hyperthermia; however, their relative contribution remains a point of contention, and probably depends on the experimental condition (e.g., posture and degree of hyperthermia). The hyperthermia-induced hyper-ventilatory response reduces arterial CO2 pressure (PaCO2) causing cerebral vasoconstriction and subsequent reductions in flow. During supine passive hyperthermia, the majority of recent data indicate that reductions in PaCO2 may be the primary, if not sole, culprit for reduced CBF. On the other hand, during more dynamic conditions (e.g., hemorrhage or orthostatic challenges), an inability to appropriately decrease peripheral vascular conductance presents a condition whereby adequate cerebral perfusion pressure may be compromised secondary to reductions in systemic blood pressure. Although studies have reported maintenance of pre-frontal cortex oxygenation (assessed by near-infrared spectroscopy) during exercise and severe heat stress, the influence of cutaneous blood flow is known to contaminate this measure. This review discusses the governing mechanisms associated with changes in CBF and oxygenation during moderate to severe (i.e., 1.0◦C to 2.0◦C increase in body core temperature) levels of hyperthermia. Future research directions are provided.
The dependence to maintain body core temperature within critically functioning limits (i.e., 37 ± 3◦C) has led to seminal thermoregulatory research spanning the past 100 years (e.g., Haldane, 1905; Lindhard, 1910). From this, the capacity to effectively dissipate heat through convective and evaporative means and the concomitant cardiovascular adjustments to maintain thermoregulatory homeostasis has been topic of several extensive literature reviews (e.g., Rowell, 1974; Crandall and González-Alonso, 2010; Johnson and Proppe, 2011). Only in the last decade, however, have we begun to appropriately understand the cerebrovascular adjustments to hyperthermia. The integrative components of cerebrovascular control and ultimately oxygenation, with focus on commonly occurring levels of hyperthermia (i.e., up to +2◦C core temperature) form the basis of this review. Adjustments to the three variables germane to cerebral oxygenation, fundamentally the components of the Fick equation; (1) cerebral metabolism, (2) cerebral O2 extraction, and (3) oxygen delivery (cerebral blood flow—CBF), are discussed. We further highlight the implications of cerebral heat balance and oxygenation during hyperthermic exercise, and provide methodological considerations for future work.