Influence of progressive skin heating upon arterial blood pressure and tolerance to a simulated hemorrhage challenge following exercise in a cold environment
Authors: Tracy Phillip , Hill Joel , Liester Jai , Sullivan Kevin , Pearson James 
Published: May 2024

Purpose: Our aim was to examine the role of graded skin heating on blood pressure and tolerance to a simulated hemorrhage (lower body negative pressure, LBNP) in individuals who have exercised in a cold environment. We hypothesized that arterial blood pressure and tolerance would be lower during LBNP at higher skin temperatures. Methods: Following completion of a maximal exercise test, 7 participants (181±7 cm, 88.7±14 kg and 25±6 yrs) four exercise cold stress trials, comprising high intensity interval exercise on a cycle ergometer: 5 min at 60% VO2 max (1.9±0.4 L.O2.min) followed by 15 intervals of 60 sec at 88% peak power output (Wmax) (239±51 W) and 60 sec at 10% Wmax (27±6 W) in an environmental chamber (0°C 70% RH, Can-Trol International). Upon completion participants remained in the environmental chamber and underwent LBNP to pre syncope. Rectal (Tcore; °C) and mean skin (8 site average, Tskin; °C) temperatures, arterial blood pressure (Brachial Artery Auscultation, Suntech Tango; MAP; mmHg) and cutaneous vascular conductance (Laser Doppler Flowmetry, Perimed, CVC; AU/mmHg) were measured throughout. After the onset of LBNP, skin temperature was either kept cold (Cold), increased back to baseline (Normothermic), mildly heated (Warm) or severely heated (Hot) using a water perfused suit. LBNP tolerance was calculated via cumulative strain index (CSI). MAP, CVC, Tcore and Tskin were analyzed using a two-way ANOVA with repeated measures. CSI was compared between trials using a one-way ANOVA with repeated measures. Results: After exercise and immediately prior to LBNP, Tcore had increased from baseline 1.0±0.2°C and was not different between trials (P = 0.67), while Tskin was reduced from 33.2±0.5°C to 28.3±1.9°C (P = 0.001). MAP was elevated following exercise and immediately prior to LBNP in all trials relative to baseline, from 82±6 to 89±8mmHg. During LBNP, Tskin remained low in the Cold trial (27.6±1.2 °C) but was increased in all other trials (Normothermic: 32.3±0.8°C, Warm: 34.8±0.5°C and Hot: 36.4±0.7°C, all P < 0.05). MAP was different between trials (Trial Effect P = 0.022). MAP was lowest in the Hot trial whether expressed 3 min after the onset of LBNP or at 60% CSI (81±9mmHg and 78±7 mmHg, respectively) relative to the Cold (89±10 and 84±9 mmHg) Normothermic (86±8 and 82±6 mmHg) and Warm trials (86±7 and 80±6 mmHg), respectively. MAP was reduced at pre syncope in all trials (59±9mmHg). CVC was different between trials (Trial Effect, P < 0.0001). At 60% CSI, CVC was lowest in the Cold trial (0.17±0.11 AU/mmHg) but increased in the Normothermic (0.27±0.08 AU/mmHg) Warm (0.43±0.40 AU/mmHg) and Hot trials (0.60±0.43 AU/mmHg). LBNP tolerance was different between trials (Main Effect: P < 0.01). LBNP tolerance was lowest in the Cold trial (700 ± 346 mmHg*min) and was increased in Normothermic (856±399 mmHg*min) Warm (821±345 mmHg*min) and Hot trials (990±328mmHg*min). Conclusion: These preliminary findings suggest that skin warming >32°C increases tolerance to a simulated hemorrhagic challenge while further heating to ~36°C lowers arterial blood pressure without compromising LBNP tolerance in exercise cold stressed individuals.

Supported by a RMACSM Grant.

This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.