Abstract

During normothermia, a reduction in near infrared spectroscopy (NIRS) derived muscle oxygen saturation (SmO2) is an indicator of central hypovolemia. Hyperthermia reduces tolerance to central hypovolemia. This study tested the hypothesis that reductions in NIRS derived SmO2 would be similar throughout normothermic and hyperthermic central hypovolemia to pre‐syncope. Ten healthy males (32 ± 5 y) underwent central hypovolemia via progressive lower‐body negative pressure (LBNP) to pre‐syncope during normothermia and hyperthermia (+1.2 ± 0.1°C increase in internal temperature). NIRS derived SmO2 (Reflectance Medical Inc.) was measured throughout and analyzed as the absolute change from pre‐LBNP. Hyperthermia reduced (P<0.001) LBNP tolerance by 38 ± 19%. Pre‐LBNP SmO2 was similar (P=0.654) between normothermia (74.1 ± 5.0%) and hyperthermia (72.6 ± 6.9%). SmO2 decreased (P<0.001) throughout LBNP, but the absolute reduction from pre‐LBNP to pre‐syncope was greater (P=0.018) during normothermia (‐10.0 ± 5.7%) than during hyperthermia (‐5.7 ± 4.5%). These data indicate that hyperthermia influences the magnitude of the reduction in NIRS derived SmO2 during central hypovolemia to pre‐syncope. However, a potentially confounding influence of hyperthermia‐induced increases in skin blood flow affecting the NIRS derived SmO2 signal cannot be discounted.Grant Funding Source: DOD Grant 110475007

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