Abstract

Orthostatic tolerance is reduced in the heat stressed human. PURPOSE: To test hypotheses that heat stress alters cerebral blood flow velocity (CBFV) responses to orthostatic stress. METHODS: 8 subjects were exposed to lower-body negative pressures (LBNP) of 10, 20, 30, and 40 mmHg during normothermia and whole-body heating. CBFV (transcranial ultras on ography), mean arterial blood pressure (MAP), cerebral vascular resistance (MAP CBFV−1), heart rate, and internal temperature were measured during the experimental trials. RESULTS: Whole-body heating increased internal temperature (from 36.9±0.1 to 37.7±0.1° C; P<0.01), heart rate (from 61±8 to 91±8 beats min−1; P<0.01) and cerebral vascular resistance (from 1.53±0.11 to 1.69±0.12 units; P<0.05), decreased CBFV (from 56±4 to 50±3 cm sec−1; P<0.05), but did not alter MAP. In normothermia, 30 mmHg LBNP (the highest level of LBNP achieved by the majority of subjects in both thermal conditions) did not significantly alter CBFV, cerebral vascular resistance, or MAP, but did increase heart rate. During whole-body heating, 30 mmHg LBNP decreased MAP (from 81±2 to 75±3 mmHg), decreased CBFV to 39±1 cm sec−1, increased cerebral vascular resistance to 1.92±0.12 units, and increased heart rate to 117±12 beats min−1, all P<0.05. Also, during heating 7 of 8 subjects could not complete the LBNP protocol without exhibiting presyncopal symptoms. CONCLUSION: Heat stress decreases CBFV and reduces CBFV for a given orthostatic challenge, thereby reducing the reserve by which CBFV can further decrease prior to the onset of syncopal symptoms. Moreover, increases in cerebral vascular resistance during heat stress, coupled with even greater increases in this variable during combined orthostasis and heat stress, likely further contribute to reduced orthostatic tolerance in this thermal condition.

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