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Exercising in hot and cold conditions poses one of the greatest challenges to human homeostasis. Popular belief is that cold exposure increases susceptibility to upper respiratory tract infections, however, evidence to support a link between cold exposure, impaired immune function and increased incidence of infection is not well defined. On the other hand, if heat production during exercise is not effectively dissipated, core body temperature can rise to dangerous levels, thereby placing the individual at risk of developing exertional heat-illness (EHI), or the more serious, and potentially fatal, condition of exertional heat stroke (EHS). In addition to exercising in hot and humid environments, a number of risk factors for EHI/EHS have been identified. Other potential risk factors, which are less well supported, include the circulating inflammatory response that follows a muscle-damaging exercise bout. All together, these conditions might potentially affect athletes and military personnel, which are expected to perform arduous physical activity, often in extreme environments. Hypothermia is common in trauma victims and is associated with an increase in mortality. Its causes are still not well understood. We found (Chapter 4) that after mildhypothermia (Body rectal temperature (Tre) 35.17 ± 0.33 °C) vaccine-stimulated IFN-γ production significantly decreased by 44% suggesting temporary immune suppression. Moreover, despite rewarming and feeding, vaccine-stimulated IFN-γ production did not return to control values within 3-hour, suggesting more prolonged immune suppression, specifically, impaired antimicrobial capacity and increased risk of infection. This might partially explain the increased mortality reported after mild-hypothermia. During exercise heat stress (HS) (Chapter 5), ΔTre was significantly greater following EIMD than in CON (0.52 ºC). Therefore, HS was increased during endurance exercise in the heat conducted 30min trial after, and to a much lesser extent, 24h after muscledamaging exercise. These data indicate that EIMD is a likely risk factor for EHI particularly during exercise-heat stress. After a repeated bout of muscle-damaging exercise (EIMD trial 2) (Chapter 6), final Tre during HS was lower (39.25 ± 0.47 ºC) than in EIMD trial 1 (39.59 ± 0.49 ºC), whilst no differences between repeat trials were observed in control trials (CON). Thus, incorporating a muscle-damaging bout into training is a strategy to reduce the risk of EHI in individuals undertaking heavy exercise with an eccentric heat component. Further research is required clarify the role of thermo-genic activity on innate immune markers during cold exposure needs clarification. In addition, future studies would need to examine the supposed contribution of pyrogenic pathways after muscle damage upon exercise heat strain in more depth.