Elevated skin and core temperatures both contribute to reductions in tolerance to a simulated haemorrhagic challenge. Issue 2 (13th January 2017)

• Record Type: Journal Article
• Authors: Pearson, James; Lucas, Rebekah A. I.; Schlader, Zachary J.; Gagnon, Daniel; Crandall, Craig G.
• Is Part Of: Experimental physiology. Volume 102:Issue 2(2017:Feb.)
• Page Start: 255
• Page End: 264
• Publication Date: 2017-01-13
• Subjects: cutaneous vascular conductance -- hyperthermia -- simulated hemmorhagic tolerance; Physiology, Experimental -- Periodicals; 571.0724
• DOI: 10.1113/EP085896
• Languages: English
• ISSNs: 0958-0670

Abstract

Abstract : New Findings: 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 ( T skin ) and core temperatures ( T core ) on LBNP tolerance. We hypothesized that elevations in T skin as well as T core would both contribute to reductions in LBNP tolerance and that the reduction in LBNP tolerance would be greatest when both T skin and T core were elevated. Nine participants underwent progressive LBNP to presyncope on four occasions, as follows: (i) control, with neutral T skin (34.3 ± 0.5°C) and T core (36.8 ± 0.2°C); (ii) primarily skin hyperthermia, with high T skin (37.6 ± 0.2°C) and neutral T core (37.1 ± 0.2°C); (iii) primarily core hyperthermia, with neutral T skin (35.0 ± 0.5°C) and high T core (38.3 ± 0.2°C); and (iv) combined skin and core hyperthermia, with high T skin (38.8 ± 0.6°C) and high T core (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. Abstract :