During normothermia, a reduction in near-infrared spectroscopy (NIRS)-derived tissue oxygen saturation (So2) is an
indicator of central
hypovolemia.
Hyperthermia increases skin blood flow and reduces tolerance to central
hypovolemia, both of which may alter the interpretation of tissue So2 during central
hypovolemia. This study tested the hypothesis that maximal reductions in tissue So2 would be similar throughout normothermic and hyperthermic central
hypovolemia to
presyncope. Ten healthy males (means ± SD; 32 ± 5 yr) underwent central
hypovolemia via progressive
lower-body negative pressure (
LBNP) to
presyncope during normothermia (skin temperature ≈34°C) and
hyperthermia (+1.2 ± 0.1°C increase in internal temperature via a water-perfused suit, skin temperature ≈39°C). NIRS-derived forearm (flexor digitorum profundus) tissue So2 was measured throughout and analyzed as the absolute change from pre-
LBNP.
Hyperthermia reduced (P < 0.001)
LBNP tolerance by 49 ± 33% (from 16.7 ± 7.9 to 7.2 ± 3.9 min). Pre-
LBNP, tissue So2 was similar (P = 0.654) between normothermia (74 ± 5%) and
hyperthermia (73 ± 7%). Tissue So2 decreased (P < 0.001) throughout
LBNP, but the reduction from pre-
LBNP to
presyncope was greater during normothermia (-10 ± 6%) than during
hyperthermia (-6 ± 5%; P = 0.041). Contrary to our hypothesis, these findings indicate that
hyperthermia is associated with a smaller maximal reduction in tissue So2 during central
hypovolemia to
presyncope.