This paper is concerned with the basis for thermoregulation under conditions of thermodynamic equilibrium. The thermoregulatory system can in principle only be understood through an appropriate integration of its physical, chemical, physiological and neurological aspects. The common description of thermoregulation simply as a hypothalamic “feedback” control of a servomechanical “set point” has not led to an adequate self-contained model. Review of steady-state data (nude, resting human, low wind and humidity, 5–45 deg C ambient temperature Ta) indicates that, at the very least, there are physical-physiological aspects of thermoregulation not explained by a hypothalamic set point model. Rather, we can point to a wide spectrum of cyclic “thermodynamic engine” processes which regulate the various subsystems of the body [1]. The cooperative orchestration of all these processes produces a dynamic regulation of temperature, essentially as a self-regulation. This dynamic regulation produces an overall thermal equilibrium for the entire body. To illustrate some unresolved equilibrium problems: Reported mean skin temperatures Ts versus Ta are incompatible with the physically determined skin-to-air transfer coefficient of about 7 kcal/m2/hr/deg C. At low Ta, either mean metabolism M must be higher or Ts must be lower, or the physical conductance must be rejected. One experimental test suggests that Ts is lower than commonly quoted (e.g., Ts = 26 deg C instead of 30 deg C at Ta = 20 deg (C). Such discrepancies may arise if free convective transfer is suppressed or if experiments are not carried on to equilibrium. Change in metabolism, heat storage, and tissue temperature may be significant for several hours, requiring at least 3 hours of sample data for accurate equilibrium temperature measurements. At low Ta, there is no solid evidence for metabolic regulation; in the cold, equilibrium M rises only 20–30 percent, not 200–300 percent as proposed by some workers. At high Ta, the usual definition of mean tissue conductance [C = M/(TcTs)] leads to nonphysically large C as Ts approaches deep body temperature Tc. This paper is restricted to the physiological-physical modeling of the regulation of a variety of coupled fluxes (e.g., oxidative metabolism, evaporative flux, free and forced convective flux, fluid heat exchange) and potentials (e.g., internal and surface temperatures, evaporative phase changes). To resolve the foregoing difficulties we offer two hypotheses: (a) the body autoregulates a vital core; peripheral regions cool, e.g., extremity Ts drops toward ambient, the regulated core “contracts” longitudinally; (b) a significant portion of the evaporative heat loss may occur below the skin’s surface. Adjustment of two parameters emerging from these hypotheses allows a consistent modeling of steady-state thermoregulation. We suggest that hypothalamic control is one component of regulation and operates at higher frequency (with 7-min period) than steady-state autoregulation (3-hr period).

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