3.9 Article

Variability in Orthostatic Tolerance During Heat Stress: Cerebrovascular Reactivity to Arterial Carbon Dioxide

Journal

AVIATION SPACE AND ENVIRONMENTAL MEDICINE
Volume 85, Issue 6, Pages 624-630

Publisher

AEROSPACE MEDICAL ASSOC
DOI: 10.3357/ASEM.3878.2014

Keywords

hyperthermia; simulated hemorrhage; inter-individual variability; hypocapnia

Funding

  1. University of Texas at Austin

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Introduction: A high degree of interindividual variability exists in the magnitude of heat stress (HS)-induced reductions in orthostatic tolerance relative to normothermia (NT). This variability may be associated with HS-mediated reductions in cerebral perfusion (indexed as middle cerebral artery blood velocity; MCAV(mean)) and altered cerebrovascular regulation. Methods: We tested the hypothesis that cerebrovascular reactivity to hypocapnia would be positively correlated with differences in tolerance to lower body negative pressure (LBNP) [assessed with a cumulative stress index (CSI)] between HS and NT (CSIdiff). Subjects (N = 13) underwent LBNP twice (NT and HS) separated by > 72 h to assess CSI. On a third day, cerebrovascular reactivity [changes in cerebral vascular conductance (CVCi) during hyperventilation-induced hypocapnia (indexed by end tidal carbon dioxide; PETCO2)] was assessed during NT, HS, and HS+LBNP (-20 mmHg; HSLBNP). Results: Tolerance to LBNP was reduced after a 1.5 +/- 0.1 degrees C increase in internal temperature and a high degree of variability was observed for CSIdiff (range: 122 to 1826 mmHg center dot min(-1)). The magnitude of reduction in CVCi during voluntary hyperventilation-induced hypocapnia (-16 +/- 5 Torr) was attenuated during HS and HSLBNP vs. NT (NT: -0.20 +/- 0.09 cm center dot s(-1) center dot mmHg(-1); HS: -0.12 +/- 0.09 cm center dot s(-1) mmHg(-1); HSLBNP: 0.11 +/- 0.11 cm center dot s(-1) center dot mmHg(-1)); however, no relationship existed between Delta CVCi/PETCO2 and CSIdiff in any condition. Conclusions: Cerebrovascular reactivity to hyperventilation-induced hypocapnia is attenuated when internal temperature is elevated, perhaps as a protective mechanism to protect against further reductions in the already diminished cerebral perfusion in this thermal state. However, individual differences in these responses do not appear to predict orthostatic tolerance during HS.

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