October (Final Notebook)

temperature within a very narrow temperature range. Therefore, when body temperature rises above its normally regulated range, because of either environmental factors or excess metabolic heat production, irreversible thermoregulatory failure may rapidly develop. Operating at a very “high gain,” the thermoregulatory system works in concert with a set of coded behavioral functions to prevent/attenuate this hazardous outcome. A variety of factors affect thermal tolerance. Among these, only two responses are directly provoked to combat the deleterious consequences of heat stress: 1) the rapid heat shock response (HSR) and 2) heat acclimation. HSR is a rapid, short-acting molecular process associated with the synthesis of several families of heat shock proteins (HSPs) of different molecular weights. It is thought to protect cells from noxious stimuli and to accelerate their repair following short, sublethal heat injury. The time course of HSP accumulation and the family to which they belong vary in different cells, but, on average, the HSR in the intact body seems to operate several hours following the stress and retains its activity for a few days. In contrast, heat acclimation is switched on in response to persistent, moderate ambient heat and takes time to develop but is long acting (several weeks). The classical concept of heat acclimation is of an autonomically controlled array of integrative physiological processes working in concert to improve heat dissipation. Cumulative data from recent studies imply, however, that during the process of acclimation thermoregulatory control is modified through interplay among autonomic, cellular, and molecular responses, each of different intensities, time courses, and even direction. Whether HSPs play a role in the latter mechanism is still an open question. In contrast to poikilotherms, in which acclimation responses are evoked by a wide range of changes in body temperature and therefore can be easily detected individually, homeotherms undergo only very small shifts in their core temperature during acclimatization or acclimation (adaptation, under natural environmental stress vs. under artificial laboratory conditions, respectively). This raises the question, What are the nature and the magnitude of the strain required to elicit acclimation responses? Likewise, the marked acclimation response might result from the additive effects of many small, yet significant, changes at organ and cell levels. Because of the nature of this process, there are conceptual and methodological difficulties that prevent homeotherms from being the “first choice” model for studying cellular or molecular acclimation responses to hot environments. Our knowledge of the role of these processes in acclimating homeotherms is therefore sparse. Some aspects of the cellular heat acclimation responses in mammals, their dynamics during heat acclimation, and their contribution to shortand long-term thermoregulatory adaptive responses provide the central theme for this minireview. In this context, emphasis will be placed on processes associated with autonomic excitability, that is, effector organ feedback relationships. The role of HSP in acquiring thermal tolerance on acclimation will also be discussed.