Tissue oxygen saturation during hyperthermic progressive central hypovolemia

During nor-mothermia, 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.