title: Elevated skin and core temperatures both contribute to reductions in tolerance to a simulated haemorrhagic challenge.
abstract: What is the central question of this study? Combined increases in skin and core temperatures reduce tolerance to a simulated haemorrhagic challenge. The aim of this study was to examine the separate and combined influences of increased skin and core temperatures upon tolerance to a simulated haemorrhagic challenge. What is the main finding and its importance? Skin and core temperatures increase during many occupational settings, including military procedures, in hot environments. The study findings demonstrate that both increased skin temperature and increased core temperature can impair tolerance to a simulated haemorrhagic challenge; therefore, a soldier's tolerance to haemorrhagic injury is likely to be impaired during any military activity that results in increased skin and/or core temperatures. Tolerance to a simulated haemorrhagic insult, such as lower-body negative pressure (LBNP), is profoundly reduced when accompanied by whole-body heat stress. The aim of this study was to investigate the separate and combined influence of elevated skin (Tskin) and core temperatures (Tcore) on LBNP tolerance. We hypothesized that elevations in Tskinas well as Tcorewould both contribute to reductions in LBNP tolerance and that the reduction in LBNP tolerance would be greatest when both Tskinand Tcorewere elevated. Nine participants underwent progressive LBNP to presyncope on four occasions, as follows: (i) control, with neutral Tskin(34.3 ± 0.5°C) and Tcore(36.8 ± 0.2°C); (ii) primarily skin hyperthermia, with high Tskin(37.6 ± 0.2°C) and neutral Tcore(37.1 ± 0.2°C); (iii) primarily core hyperthermia, with neutral Tskin(35.0 ± 0.5°C) and high Tcore(38.3 ± 0.2°C); and (iv) combined skin and core hyperthermia, with high Tskin(38.8 ± 0.6°C) and high Tcore(38.1 ± 0.2°C). The LBNP tolerance was quantified via the cumulative stress index (in millimetres of mercury × minutes). The LBNP tolerance was reduced during the skin hyperthermia (569 ± 151 mmHg min) and core hyperthermia trials (563 ± 194 mmHg min) relative to control conditions (1010 ± 246 mmHg min; both P < 0.05). However, LBNP tolerance did not differ between skin hyperthermia and core hyperthermia trials (P = 0.92). The lowest LBNP tolerance was observed during combined skin and core hyperthermia (257 ± 106 mmHg min; P < 0.05 relative to all other trials). These data indicate that elevated skin temperature, as well as elevated core temperature, can both contribute to reductions in LBNP tolerance in heat-stressed individuals. However, heat stress-induced reductions in LBNP tolerance are greatest in conditions when both skin and core temperatures are elevated.
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas and Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.|Department of Biology, University of Colorado at Colorado Springs, Colorado, USA.
authors.forename: James
authors.initials: J
authors.lastname: Pearson
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas and Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.|School of Sport, Exercise and Rehabilitation Sciences, The University of Birmingham, Edgbaston, Birmingham, UK.
authors.forename: Rebekah A I
authors.initials: RA
authors.lastname: Lucas
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas and Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.|Department of Exercise and Nutrition Sciences, University at Buffalo, Buffalo, New York, USA.
authors.forename: Zachary J
authors.initials: ZJ
authors.lastname: Schlader
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas and Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
authors.forename: Daniel
authors.initials: D
authors.lastname: Gagnon
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas and Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
authors.forename: Craig G
authors.identifier: 0000-0001-7792-9713
authors.initials: CG
authors.lastname: Crandall
mesh_terms: D000328:Adult; D001831:Body Temperature / Q000502:physiology*; D005260:Female; D005334:Fever / Q000503:physiopathology*; D018882:Heat Stress Disorders / Q000503:physiopathology; D018869:Heat-Shock Response / Q000502:physiology; D006470:Hemorrhage / Q000503:physiopathology; D006801:Humans; D006979:Hyperthermia, Induced / Q000379:methods; D008150:Lower Body Negative Pressure / Q000379:methods; D008297:Male; D012867:Skin / Q000503:physiopathology*; D013575:Syncope / Q000503:physiopathology
keywords: cutaneous vascular conductance; hyperthermia; simulated hemmorhagic tolerance