title: Dynamic cerebral autoregulation during passive heat stress in humans.
abstract: This study tested the hypothesis that passive heating impairs cerebral autoregulation. Transfer function analyses of resting arterial blood pressure and middle cerebral artery blood velocity (MCA V(mean)), as well as MCA V(mean) and blood pressure responses to rapid deflation of previously inflated thigh cuffs, were examined in nine healthy subjects under normothermic and passive heat stress (increase core temperature 1.1 +/- 0.2 degrees C, P < 0.001) conditions. Passive heating reduced MCA V(mean) [change (Delta) of 8 +/- 8 cm/s, P = 0.01], while blood pressure was maintained (Delta -1 +/- 4 mmHg, P = 0.36). Coherence was decreased in the very-low-frequency range during heat stress (0.57 +/- 0.13 to 0.26 +/- 0.10, P = 0.001), but was >0.5 and similar between normothermia and heat stress in the low- (0.07-0.20 Hz, P = 0.40) and high-frequency (0.20-0.35 Hz, P = 0.12) ranges. Transfer gain was reduced during heat stress in the very-low-frequency (0.88 +/- 0.38 to 0.59 +/- 0.19 cm.s(-1).mmHg(-1), P = 0.02) range, but was unaffected in the low- and high-frequency ranges. The magnitude of the decrease in blood pressure (normothermia: 20 +/- 4 mmHg, heat stress: 19 +/- 6 mmHg, P = 0.88) and MCA V(mean) (13 +/- 4 to 12 +/- 6 cm/s, P = 0.59) in response to cuff deflation was not affected by the thermal condition. Similarly, the rate of regulation of cerebrovascular conductance (CBVC) after cuff release (0.44 +/- 0.22 to 0.38 +/- 0.13 DeltaCBVC units/s, P = 0.16) and the time for MCA V(mean) to recover to precuff deflation baseline (10.0 +/- 7.9 to 8.7 +/- 4.9 s, P = 0.77) were not affected by heat stress. Counter to the proposed hypothesis, similar rate of regulation responses suggests that heat stress does not impair the ability to control cerebral perfusion after a rapid reduction in perfusion pressure, while reduced transfer function gain and coherence in the very-low-frequency range during heat stress suggest that dynamic cerebral autoregulation is improved during spontaneous oscillations in blood pressure within this frequency range.
authors.affiliation: Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, TX 75231, USA.
authors.forename: David A
authors.initials: DA
authors.lastname: Low
authors.forename: Jonathan E
authors.initials: JE
authors.lastname: Wingo
authors.forename: David M
authors.initials: DM
authors.lastname: Keller
authors.forename: Scott L
authors.initials: SL
authors.lastname: Davis
authors.forename: Jian
authors.initials: J
authors.lastname: Cui
authors.forename: Rong
authors.initials: R
authors.lastname: Zhang
authors.forename: Craig G
authors.initials: CG
authors.lastname: Crandall
mesh_terms: D000328:Adult; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001833:Body Temperature Regulation / Q000502:physiology; D001921:Brain / Q000098:blood supply / Q000502:physiology*; D002320:Cardiovascular Physiological Phenomena; D005260:Female; D018882:Heat Stress Disorders / Q000503:physiopathology*; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D008297:Male