The origin, significance and plasticity of the thermoeffector thresholds: Extrapolation between humans and laboratory rodents.

Abstract

In this review, there is an overarching emphasis on the extrapolation of knowledge from one physiological regulator to another, with a particular emphasis on autonomic thermoregulation in humans and rodents. Through mammalian phylogenetics, one finds evidence for the gradual acquisition of an ability to maintain whole-body thermal stability, with discrete autonomic mechanisms arising for the generation, retention and dissipation of thermal energy. The sequential attainment of those thermoeffectors, over aeons, makes it unlikely that they are controlled by a common central processor, so the presence of a single activation switch is perhaps inconceivable. Instead, effector activation is associated with the arrival at lower and upper critical (threshold) body temperatures, with regions between those points defining zones of mammalian thermoneutrality. As thermal energy content deviates from thermoneutrality, there is a progression from purely passive (physical) heat exchanges through to autonomic (thermoeffector) recruitment. That activation is morphologically dependent, with an obligatory greater basal metabolic heat production evident in smaller individuals within both hypo- and normothermic states. Indeed, a first-principles, morphological case is presented for the existence of an effector recruitment cascade, with human observations providing the empirical support. That sequential activation is consistent with the presence of multiple central controllers, and both animal and human experiments supporting that possibility are reviewed. Finally, the case is presented that mammals possess multiple thermoreceptive fields, thermoeffectors with discrete neural pathways and several central, but independent, controllers of thermoeffector function. Those concepts are summarised in updated conceptual and neuronal models for human thermoregulation.