title: The magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage.
abstract: The mechanisms responsible for heat stress-induced reductions in tolerance to a simulated hemorrhage are unclear. Although a high degree of variability exists in the level of reduction in tolerance amongst individuals, syncope will always occur when cerebral perfusion is inadequate. This study tested the hypothesis that the magnitude of reduction in cerebral perfusion during heat stress is related to the reduction in tolerance to a lower body negative pressure (LBNP) challenge. On different days (one during normothermia and the other after a 1.5°C rise in internal temperature), 20 individuals were exposed to a LBNP challenge to presyncope. Tolerance was quantified as a cumulative stress index, and the difference in cumulative stress index between thermal conditions was used to categorize individuals most (large difference) and least (small difference) affected by the heat stress. Cerebral perfusion, as indexed by middle cerebral artery blood velocity, was reduced during heat stress compared with normothermia (P < 0.001); however, the magnitude of reduction did not differ between groups (P = 0.51). In the initial stage of LBNP during heat stress (LBNP 20 mmHg), middle cerebral artery blood velocity and end-tidal PCO(2) were lower; whereas, heart rate was higher in the large difference group compared with small difference group (P < 0.05 for all). These data indicate that variability in heat stress-induced reductions in tolerance to a simulated hemorrhage is not related to reductions in cerebral perfusion in this thermal condition. However, responses affecting cerebral perfusion during LBNP may explain the interindividual variability in tolerance to a simulated hemorrhage when heat stressed.
authors.affiliation: Environmental and Autonomic Physiology Laboratory, Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas 78712, USA.
authors.forename: Joshua F
authors.initials: JF
authors.lastname: Lee
authors.forename: Michelle L
authors.initials: ML
authors.lastname: Harrison
authors.forename: Skyler R
authors.initials: SR
authors.lastname: Brown
authors.forename: R Matthew
authors.initials: RM
authors.lastname: Brothers
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000097:blood / Q000378:metabolism; D001783:Blood Flow Velocity / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001831:Body Temperature / Q000502:physiology; D002245:Carbon Dioxide / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000502:physiology*; D054022:Cerebrum / Q000098:blood supply* / Q000378:metabolism / Q000502:physiology; D005260:Female; D006339:Heart Rate / Q000502:physiology; D018882:Heat Stress Disorders / Q000378:metabolism / Q000503:physiopathology*; D006470:Hemorrhage / Q000503:physiopathology*; D006358:Hot Temperature; D006801:Humans; D008150:Lower Body Negative Pressure / Q000379:methods; D008297:Male; D020768:Middle Cerebral Artery / Q000378:metabolism / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D013312:Stress, Physiological / Q000502:physiology*; D013575:Syncope / Q000378:metabolism / Q000503:physiopathology
chemical_list: D000804:Angiotensin II; D002245:Carbon Dioxide