Predicting Cardiovascular Hemodynamics in Cold and Warm Environments at Rest with Skin and Core Temperature

Abstract

Many occupations require workers to be exposed to extreme heat or cold. During prolonged exposure to extreme environments, the cardiovascular system plays a critical role in thermal homeostasis, by adjusting blood flow in peripheral and central vascular beds. Importantly, exposure to either environment, and the concordant blood‐volume redistribution, increases morbidity and mortality from the additional [and often significant] stress on the cardiovascular system. To gain insight on how to predict cardiovascular stress during exposure to extreme environments at rest, this study attempted to build a regression model to examine the influence of progressive, whole‐body skin and core cooling and heating on cardiovascular hemodynamics. Seventeen participants (12 males, 22.9 ± 3.58 years, 174.2 cm ± 7.85 cm, 12.8 ± 6.20 kg fat mass, and 59.3 ± 9.49 kg fat free mass) wearing shorts and a t‐shirt participated in two laboratory sessions: i) progressive heating (22°C to 40°C); and ii) progressive cooling (22°C to 5°C); each aimed to independently influence skin and core temperatures. Cardiovascular hemodynamics data was collected via thoracic electrical bioimpedance, while metabolic and cardiorespiratory variables were assessed via indirect calorimetry. Mean weighted skin (Tsk) and core (Tc) temperature were measured via portable data loggers and a thermocouple, respectively. Mean weighted skin temperatures ranged from 22.7°C to 37.4°C and Tc ranged from 35.5°C to 37.9°C. A stepwise multiple linear regression analysis was conducted using Tsk, Tc, fat free mass, fat mass, sex and age as predictors for cardiovascular hemodynamics changes under thermal stress. The present model explained 24.4% of changes in stroke volume, 27.9% of heart rate, 15.9% of cardiac output and 49.5% of oxygen consumption. Although changes in Tsk and Tc temperature induced by whole‐body cooling and heating at rest accounted for changes in cardiovascular hemodynamics in the model, a significant portion of the variation remained unexplained. Further research is needed to develop a more accurate model to represent changes in cardiovascular hemodynamics under thermal stress.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.