Cerebral vasoreactivity: impact of heat stress and lower body negative pressure

Abstract

Objective Cerebrovascular reactivity represents the capacity of the cerebral circulation to raise blood flow in the face of increased demand, and may be reduced in some clinical and physiological conditions. We tested the hypothesis that the hypercapnia-induced increase in cerebral perfusion is attenuated during heat stress (HS) compared to normothermia (NT), and this response is further reduced during the combined challenges of HS and lower body negative pressure (LBNP). Methods Ten healthy individuals (9 men) undertook rebreathing-induced hypercapnia during NT, HS, and HS+20 mmHg LBNP (HSLBNP) while cerebral perfusion was indexed from middle cerebral artery blood velocity (MCA Vmean). Cerebrovascular responses were calculated from the slope of the change in MCA Vmean and cerebral vascular conductance (CVCi) relative to the increase in end tidal carbon dioxide (PETCO2) during rebreathing. Results MCA Vmean was similar in HS (55±19 cm·s−1) and HSLBNP (52±16 cm·s−1), and both values were reduced relative to NT (66±20 cm·s−1), yet the rise in MCA Vmean per Torr increase in PETCO2 during rebreathing was similar in each condition (NT: 2.5±0.6 cm/s·Torr−1; HS: 2.4±0.8 cm/s·Torr−1; HSLBNP: 2.1±1.1 cm/s·Torr−1). Likewise, the rate of increase in CVCi was not different between conditions (NT: 2.1±0.65 cm/s/mmHg·100·Torr−1; HS: 2.4±0.8 cm/s/mmHg·100·Torr−1; HSLBNP: 2.0±1.0 cm/s/mmHg·100·Torr−1). Interpretations These data indicate that cerebrovascular reactivity is not compromised during whole body heat stress alone or when combined with mild orthostatic stress relative to normothermic conditions.

Global REACH 2018: The influence of acute and chronic hypoxia on cerebral haemodynamics and related functional outcomes during cold and heat stress

“…7). Although counter to previous findings that show heating does not affect (Low et al 2008;Lee et al 2015) or slightly decreases (Lee et al 2014) CVRCO 2 , this is the first investigation (to our knowledge) to directly compare normothermic and heated CVRCO 2 using volumetric measures of CBF from all arteries. Moreover, we investigated CVRCO 2 solely within the same hypocapnic range between 20 and 40 mm Hg to ensure linearity between CBF and P a,CO 2 and direct comparisons for all stressors.…”

“…; Lee et al . ) or slightly decreases (Lee et al . ) CVRCO 2 , this is the first investigation (to our knowledge) to directly compare normothermic and heated CVRCO 2 using volumetric measures of CBF from all arteries.…”

Cerebral Vascular Control and Metabolism in Heat Stress

“…Increasing pH appears to increase Ca 2+ intracellular influx, while decreasing pH inhibits it (245,247). Although pH and temperature are inversely related, the majority of data indicate that heat stress does not alter cerebrovascular reactivity (i.e., changes in CBF for a given change in PaCO 2 ) (141,250,265). On the other hand, a recent study suggests that reactivity in the ICA, but not in the VA or in MCAv, may be reduced during passive heat stress (338).…”

Integrative cardiovascular control in women: Regulation of blood pressure, body temperature, and cerebrovascular responsiveness

“…48 Cerebrovascular reactivity is often defined as the ability of the cerebral vasculature to respond to vasoactive stimuli. When using changes in arterial CO 2 as the stimulus to measure cerebrovascular reactivity, many studies show no change in cerebrovascular reactivity, 49,50 whereas others report increases 43 or even decreases in cerebrovascular reactivity. 51 Thus, the existing data suggests that thermal stress challenges cerebral blood flow regulatory mechanisms, but more research is needed to understand the interaction of thermoregulation and cerebrovascular regulation.…”