Altered Responsiveness of Cold-Adapted Rats to Thermal Stress

Abstract

On cold-exposure an increase in the temperature difference between the body surface and the environment initiates an enhancement of heat loss of the organism. The fall of the temperature of the body sheU induced by such direct heat loss is further accentuated by effector mechanisms such as peripheral vasoconstriction which, in turn, help the whole body limit the rise in heat loss. Both the increase of heat conservation developing in the cold and the augmentation of heat production are thought to be induced by some central nervous system mechanisms, the intensity of this action being influenced by the thermal input from centrally and peripheraUy located cold receptors. The weight and/or contribution of central (CNS, other body core sites) as well as peripheral (skin) thermoreceptors in determining thermal information on the body as a whole is not known but is believed to come more intensely from the deep thermoreceptors than from their peripheral counterparts, the latter set of information having been regarded as quantitatively important only in cases of extremely strong thermal stimuli causing a dynamic change in receptor functioning (see 6). It seems only too logical to suppose that a strong reduction in heat loss at the very beginning of cold-exposure might even result in a paradoxical increase in heat conservation and deep body temperature would rise under such circumstances, a phenomenon placing an unnecessary burden on temperature regulation since the thermal gradient to be maintained (mostly by an exaggerated and costly heat production) would be even greater than that at thermoneutrality or in cold without a paradoxical overshoot.