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 (CSI(diff)). 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; P(ET)CO2)] was assessed during NT, HS, and HS+LBNP (-20 mmHg; HS(LBNP)).
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 CSI(diff) (range: 122 to 1826 mmHg x min(-1)). The magnitude of reduction in CVCi during voluntary hyperventilation-induced hypocapnia (-16 +/- 5 Torr) was attenuated during HS and HS(LBNP) VS. NT (NT: -0.20 +/- 0.09 cm x s(-1) x mmHg(-1); HS: -0.12 +/- 0.09 cm x s(-1) x mmHg(-1); HS(LBNP): -0.11 +/- 0.11 cm x s(-1). mmHg(-1)); however, no relationship existed between deltaCVCi/ P(ET)CO2 and CSI(diff) 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.