| The objective of this thesis was to provide a comprehensive understanding of the cellular mechanisms involved during acute heat stress and how aerobic fitness impacted heat tolerance. The research employed an uncompensable exertional heat stress (EHS) model, examining endurance-trained (TR) and sedentary-untrained group responses while walking at 4.5 km ·hr-1 with 2% elevation in a climatic chamber (40°C, 30% R.H.) wearing protective clothing until exhaustion. Venous blood samples at baseline and 0.5°C rectal temperature increments (38, 38.5, 39, 39.5 and 40°C/Exh) were analyzed for a variety of circulating (Manuscript I) and intracellular (Manuscript II) immunological markers. In addition, various physiological, perceptual and immunological determinants contributing to Tre tolerated, independent of training-induced hypervolemia (Manuscript III) and the return to a non-conditioned state for sedentary individuals, were also examined (Manuscript IV). Study findings included that the threshold for endotoxemia and inflammatory activation during EHS were observed at a lower temperature in UT compared with TR, linking training-induced hypervolemia, endotoxin tolerance and heat tolerance (I). Circulating inflammatory, but not classical monocytes, contributed to the proinflammatory cytokine profiles observed during EHS, and also, an enhanced HSP72 response in TR may confer an improved heat tolerance through both anti-inflammatory and anti-apoptotic mechanisms (II). Links between endotoxemia, dehydration and volitional fatigue (III) and a cytoprotective effect lasting up to two weeks from acute EHS were identified (IV). Combined, these findings demonstrated for the first time that increases in circulating endotoxin correspond to NF-kappaB translocation and inflammatory cytokine production at T re values below 40°C, supporting the endotoxin translocation hypothesis of exertional heat stroke and a heat illness continuum contributing to EHI during EHS. In addition, it was concluded that one of the keys to the immuno-inflammatory pathways lies with intracellular HSP expression and its release into the circulation. As well, there appears to be a link between an improved LPS tolerance and heat tolerance. Furthermore, findings suggests that during uncompensable EHS, volitional fatigue is not solely related to an absolute temperature, but is a multifaceted phenomenon with complex interactions between peripheral and central mediators encompassing physiological, immunological and neuroendocrine systems. |
