A high degree of inter-individual variability exists in heat stress (HS) -induced reductions in orthostatic tolerance relative to normothermia (NT), which may be associated with HS-mediated reductions in cerebral perfusion, and thus mechanisms of cerebrovascular control during hypotensive challenges. This study tested two hypotheses; 1) the magnitude of increase in cerebral autoregulation (CA) would be negatively correlated with the difference in tolerance to graded lower body negative pressure (LBNP) 30 [assessed with a cumulative stress index (CSI)] during HS relative to NT (CSIdiff), and 2) cerebrovascular sensitivity to HS-induced hypocapnia would be positively correlated with CSIdiff. Subjects (N=13) were exposed to LBNP on two occasions (NT and HS) separated by >72h to assess CSI. On a third day, indices of CA were assessed during NT and HS by spectral and transfer function analyses, and cerebrovascular sensitivity to changes in PaCO2 was determined during NT, HS, and HS+LBNP (-20 mm Hg; HSLBNP). Estimates of CA were improved during HS compared to NT (P0.05). Hyperventilation-induced hypocapnia reduced cerebral vascular conductance (CVCi) during HS and HSLBNP relative to NT (P0.05 for all). In summary, HS augments mechanisms of cerebrovascular control to protect against orthostatic challenges; however, individual differences in these responses do not predict tolerance to a simulated hemorrhage when internal temperature is elevated.



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