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2��C. Once the target core and mean skin temperatures were attained, hyperthermic baseline values were measured. Thereafter, subjects underwent a simulated haemorrhagic challenge, using graded 3 min stages of LBNP at 10 mmHg per stage (beginning with 20 mmHg LBNP), until the development of syncopal symptoms. The termination of LBNP was based upon the subject self-reporting feeling faint and/or nauseous, a rapid and progressive decrease in blood pressure resulting in sustained systolic blood pressure being response Osimertinib mouse to LBNP are reported GPX4 relative to heat-stress values obtained prior to the onset of LBNP. Temperature and haemodynamic data were collected via a data-acquisition system (Biopac Systems Inc., Santa Barbara, CA, USA). Data were averaged over 60 s at the normothermic baseline as well as after a ?1.2��C increase in core temperature. During LBNP, data were averaged over the final 90 s prior to the termination of LBNP due to syncopal symptoms. Data were statistically analysed using either a one-way or a two-way ANOVA (time �� site) with repeated measures, depending on the variable in question. When a main effect was found, pairwise comparisons were made between conditions using Tukey's post hoc test. Statistical significance was set at P�� 0.05. Data are reported as means �� SD. Heat stress increased core (from 36.7 �� 0.3 to 37.9 �� 0.5��C) and weighted mean skin temperatures (from 33.8 �� 0.5 to 38.2 �� 0.7��C) from the normothermic baseline (both P P 0.05). Forearm skin temperature was not different between sites during normothermic baseline measures (Fig. 1). However, during whole-body heat stress the local skin temperatures were different between the mild (35.2 �� 0.6��C) and moderate sites (38.2 �� 0.6��C; P check details this difference persisted throughout LBNP to presyncope (mild, 35.1 �� 0.8��C; moderate, 38.3 �� 0.3��C; P