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Exercise in extreme environmental conditions places increased systemic stress on the body. Environmental conditions in which physical activity occurs (such as for athletic competition or occupational and military endeavours) include dry and humid heat, where internal body temperatures exceeding 40.6°C can be fatal, and at altitude where ascents above 2,500m can lead to illness, particularly when combined with physical activity. In these extreme environments, the difference from typical habitual normothermic, normoxic conditions presents a significant physiological challenge to regulate temperature and reduce systemic hypoxia resulting from reductions in inspired oxygen content.

The human body has a unique ability to adapt both physiologically and behaviourally, in order to tolerate the increases in physiological and cellular strain induced by changes in environmental conditions. Altitude acclimation/acclimatization defines adaptive responses occurring in simulated (low oxygen concentration) or actual (low barometric pressure) environments. Physiological adaptations to this altitude training paradigm include red blood cell proliferation following erythropoiesis , angiogenesis, and mitochondrial biogenesis. These adaptations improve oxygen delivery and utilisation, thus reducing anaerobic contributions to physical work at a given intensity translating to an increased ability to perform physical activity requiring aerobic metabolism. Provision of altitude training facilities is problematic for some individuals, as is the ability to reside within the environment for extended periods within a day, and for consecutive days for up to four weeks.

Heat adaptations are attainable in periods ranging from four to ten consecutive days, with daily exposure requirements optimised at a maximum of 100 minutes, with as little of 30 minutes of moderate intensity exercise required in hot, humid conditions (≥30°C and ≥40% relative humidity). Thus, heat acclimation/acclimatization may be more attainable than altitude acclimation/acclimatization, and may be equally effective at reducing the physiological strain of these unfamiliar conditions. In contrast to the primarily haematological adaptations elicited at altitude, heat derived adaptations are multisystemic with homeostatic reductions in basal body temperature, improved sweat responses to facilitate heat dissipation via evaporation and blood plasma expansion improving cardiovascular function. Each of these contributes to a favourable attenuation in physiological strain at rest and during physical activity in both the hot, and cool conditions.

Numerous data evidence acclimation or acclimatization to environmental stress in isolation, using repeated actual or simulated exposures, as an effective intervention which allows an individual to maintain physical activity, and/or attenuate physiological strain. At present, it is unknown whether acclimation to one environmental stressor might offer protection in a different environmental condition sharing similar physiological consequences, though this phenomenon has been proposed in a number of recent reviews.

Animal models, and a small number of human studies have begun to experimentally elucidate mechanisms associated with cross adaptation. Cross adaptation proposes that acclimation or acclimatization to one environmental extreme, for example, heat stress or hypoxia, will facilitate maintenance of physical activity and/or attenuate physiological strain in a different environment. Mechanisms for cross adaptation can be subdivided into physiological adaptations (cross acclimation) and cellular adaptation (cross tolerance). Cross acclimation describes the maintenance of equal absolute rate of oxygen delivery for metabolism in extreme environments as in normothermic, normoxic conditions. This is typically achieved by reducing basal heat stored, increasing heat dissipation, maintaining central blood volume, and increasing the relative oxygen carrying capacity of the blood. These cross acclimation adaptations reduce the increases in the relative cost of metabolism at a given workload under environmental stress. Cross tolerance describes cytoprotective adaptations that become acutely, and chronically induced given repeated environmental stimuli. Cross tolerance is largely facilitated by changes in basal heat shock proteins. Heat shock proteins are molecular chaperones which increase cellular resistance to apoptosis and maintain cellular and molecular function, for instance, the cascade of adaptation which follow changes in gene expression.