Temperature regulation during exercise: old concepts, new ideas.

In Figure 13 we have tried to summarize the interactions of thermal and nonthermal control of effector responses, the effects these responses have on the body during exercise, and the ways the changing state of the body feeds back on the central control systems. These systems were depicted in Figure 3 and are included in condensed form in Figure 13. Exercise affects thermoregulatory responses not only by increasing heat production, but also through a number of other mechanisms. For example, the thermoregulatory responses tend to reduce central venous pressure, and sweating without fluid replacement will increase plasma osmolality. The secondary effects of these changes on the control of the thermoregulatory responses may themselves have an important effect on the rise in Tc during prolonged exercise or exercise in the heat. In concluding, it is appropriate to briefly answer the questions raised in the introduction. In our view, the concept of shifting the set point is not different from the concept of resetting the "thermostat," and the temperature regulatory system is governed by only one set point, which does not change during exercise. Tsk does not change the set point as we have defined it. Rather it combines with thermal information from the core and other deep body thermo-detectors to produce a thermoregulatory command signal Tws distributed to all effector responses. To demonstrate a set point shift, one must show that the Tws thresholds for initiating all heat-dissipating responses shift in the same direction. Although this does not occur with exercise, it does occur with time of day, heat acclimation, endurance training, and fever. A hyperosmolar state also can raise the threshold for sweating and vasodilation uniformly, and therefore may also raise the set point. However, a change in posture, for example, which alters the threshold for vasodilation but not for sweating, does not alter the set point. We believe that a shift in threshold for a given effector may be produced by either a central or a peripheral mechanism. For example, an ion-osmotic influence on the sweating: Tc threshold may be at the level of the central nervous system or the sweat gland itself. However, a set point shift must be a central event, since it influences all effector responses uniformly. Is the set point governed by the ratio of sodium to calcium ions in the posterior hypothalamus? This is unlikely. Shifts in ion concentration can influence effector responses, but they do not appear to shift all effectors uniformly.