Core temperature responses during passive heat exposure differentiate mice previously exposed to exertional heat stroke and endotoxemia.

Exertional heat stroke (EHS) induces thermoregulatory and inflammatory disturbances, yet whether core temperature (Tcore) responses are altered during subsequent passive heat exposure (PHE) remains unknown. Our purpose was to determine whether prior exposure to EHS or lipopolysaccharide (LPS)-induced systemic inflammation alters Tcore response during a subsequent PHE in mice. Receiver operating characteristic (ROC) curve assessment was performed as a secondary analysis to establish the ability of the Tcore response to discriminate animals previously exposed to EHS or LPS. Thirty-one female mice were assigned to three groups: control (CON), LPS, or EHS. Animals were implanted with a Tcore telemetry sensor. Three hours before the PHE, mice in the LPS group received a single intraperitoneal injection of LPS (100 µg·kg-1), whereas 24 h before the PHE, EHS mice underwent an EHS protocol at 37.5°C and 40% relative humidity. CON animals received no intervention. The PHE test consisted of 40 min exposure to a 40°C environment with Tcore continuously recorded. During PHE, EHS mice exhibited higher Tcore than CON and LPS mice at 10 min (CON: 39.7 ± 0.2°C; LPS: 39.4 ± 0.4°C; EHS: 40.6 ± 0.3°C; P < 0.001) and 20 min (P < 0.001). After 30 min, both EHS and LPS groups displayed higher Tcore relative to CON. ROC curve analysis demonstrated that a Tcore threshold of 40.8°C at 10 min yielded 69% sensitivity and 94% specificity for identifying prior EHS (P < 0.001). These findings demonstrate that prior EHS and LPS alter the Tcore response during subsequent PHE in mice.NEW & NOTEWORTHY Prior exertional heat stroke (EHS) altered core temperature (Tcore) responses during subsequent passive heat exposure (PHE) in mice. Systemic inflammatory stress induced by lipopolysaccharide (LPS) also altered Tcore, although with a distinct temporal profile compared with EHS. These findings demonstrate that both serious heat illness and inflammatory stress can disrupt Tcore responses during environmental heat exposure and establish a foundation for future mechanistic studies investigating recovery following physiological stress in mice.