Cerebral Vascular Control and Metabolism in Heat Stress

Abstract

This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

Suppression of cognitive function in hyperthermia; From the viewpoint of executive and inhibitive cognitive processing

“…Impairments induced in cognitive performance during heat stress have been suggested to depend on the complexity and/or duration of cognitive tasks17181920 as well as the severity and duration of heat stress21. We previously demonstrated, even in ‘simple’ auditory oddball tasks, that hyperthermia reduced the cognitive processing index (i.e.…”

“…Mild hyperthermia reduces cerebral perfusion521, indicating that restricted cerebral perfusion contributes to an impaired brain neural network and reduced cognitive processing. We previously demonstrated that passive heat stress decreased ICA blood flow, but increased ECA for heat dissipation15.…”

Effects of a Training Program Involving Body Cooling on Physical and Cognitive Capacities and Quality of Life in Multiple Sclerosis Patients: A Pilot Study

“…Another hypothesis presented by D'haeseleer et al [31] states that there is widespread cerebral hypoperfusion in PwMS, which is associated with cognitive dysfunction and fatigue. These symptoms could intensify with hyperthermia [32]. Additionally, there is evidence that acute and chronic exercises increase brain perfusion [33].…”

Mechanisms of orthostatic intolerance during heat stress

“…Insufficient cerebral perfusion, and thus oxygen delivery, is the primary mechanism for loss of consciousness during central hypovolemia (Meendering et al, 2005; Van Lieshout et al, 2003). It is noteworthy that passive heat stress itself reduces cerebral perfusion (Bain et al, 2013; Brothers et al, 2009b; Fan et al, 2008; Fujii et al, 2008; Lucas et al, 2008, 2010; Nelson et al, 2011b; Ogoh et al, 2013, 2014; Ross et al, 2012; Schlader et al, 2013a; Wilson et al, 2002b, 2006); see the following citations for comprehensive reviews on this topic (Bain et al, 2015; Crandall and Wilson, 2014). After a threshold is achieved, the magnitude of the reduction in cerebral perfusion is related to the severity of the heat stress (Bain et al, 2015).…”

“…It is noteworthy that passive heat stress itself reduces cerebral perfusion (Bain et al, 2013; Brothers et al, 2009b; Fan et al, 2008; Fujii et al, 2008; Lucas et al, 2008, 2010; Nelson et al, 2011b; Ogoh et al, 2013, 2014; Ross et al, 2012; Schlader et al, 2013a; Wilson et al, 2002b, 2006); see the following citations for comprehensive reviews on this topic (Bain et al, 2015; Crandall and Wilson, 2014). After a threshold is achieved, the magnitude of the reduction in cerebral perfusion is related to the severity of the heat stress (Bain et al, 2015). For example, during mild to moderate heating, when internal temperature increases between ~0.5 and 1.2 °C, cerebral perfusion either does not change or only modestly decreases (Low et al, 2009; Lucas et al, 2008; Schlader et al, 2013a; Wilson et al, 2002b, 2006).…”