Heat stress response and inflammation in acute temperature stresses

Inflammatory factors, both centrally produced and released from adipocytes (fat cells), have been shown to affect metabolism and to contribute to the pathogenesis and development of many chronic diseases such as heart disease, type 2 diabetes and cancer. Inflammatory response has been shown to be affected by environmental stresses such as heat and cold exposure. The aim of this thesis was to study the effects of heat and cold stresses on inflammatory response over the course of 3 experiments which exposed healthy subjects to one of two heat intensities or to cold stress. This thesis is presented in the classical format and is composed of the following: Chapter 1 introduces the main concepts of inflammation and summarizes the existing literature on temperature stress and inflammation; Chapter 2 describes the methodologies used; Chapter 3 presents the results from the three studies; Chapter 4 discusses the relevance of our results in terms of the pre-existing research in this area and Chapter 5 provides some speculation into the underlying causes of the observed changes, suggests further studies to investigate the speculations and ends with some concluding remarks.;Results showed that, during the higher intensity heat exposure, plasma IL-6 increased by 440% while no statistical change were observed for adiponectin and TNFa levels. No changes were noted in inflammatory markers during the lesser intensity heating. With cold exposure, plasma IL-6 and adiponectin increased over time, falling short of statistical significance. No change in TNFalpha was noted at any point. Increases in plasma IL-6 and adiponectin are positively correlated with increases in core temperature.;This thesis supports the notion that temperature stress influences inflammatory response. The novelty of this work lies in the use of two different heat exposure intensities, both lower than the majority of heating intensities used in previous literature, the study of cold stress in human subjects without the confounding effect of other co-existing stresses and the quantification of adiponectin levels in human subjects during temperature stress.;Subjects were exposed to either moderate intensity heating (Experiment 1: three hours in chamber set at 42°C, 1.1+/-0.01°C core temperature increase), low intensity heating (Experiment 2: two hours in liquid perfusion suit with circulating water temperature set at 48°C, 0.4+/-0.02°C core temperature increase) or cold exposure (Experiment 3: two hours in liquid perfusion suit with circulating water temperature set at 5°C, no change in core temperature). Fasting blood samples were taken before and during the temperature stress. Plasma levels of pro-inflammatory factors, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) were measured along with the adipocyte-derived anti-inflammatory factor, adiponectin.