Assessment of various mechanisms involved in heat-stress induced reductions in orthostatic tolerance
MetadataShow full item record
Purpose: This study aimed to expand our knowledge of the underlying mechanisms of orthostatic tolerance. First, cerebral perfusion was compared with reductions in orthostatic tolerance between normal thermic and heated conditions. The researchers' hypothesized that subjects with the greatest reduction in orthostatic tolerance will experience the largest drop in cerebral blood flow. Additionally, ANG II was measured in order to identify if during passive heating, the elevation in plasma ANG II is negatively correlated with heat-stress induced reductions in orthostatic tolerance. Lastly, orthostatic tolerance changes during the simulated hemorrhage between heat stress and normal thermic conditions will be compared to fitness level, measured by VO2 max. Results and Conclusion: Cerebral perfusion, as indexed by middle cerebral artery blood velocity, was reduced during heat stress compared with normothermia (P [less than] 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 PCO2 were lower; whereas, heart rate was higher in the large difference group compared with small difference group (P [less than] 0.05 for all). In opposition to the hypotheses, the large differences in tolerance to a simulated hemorrhage during normothermic and heat stress conditions are not solely related to the degree of heat stress-induced reduction in cerebral perfusion. Also, an individual's level of cardiorespiratory capacity (fitness) and/or the degree of heat stress-induced increase in plasma ANG II does not reliably predict the level of reduction in tolerance to a simulated hemorrhage challenge when heat stressed.