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Central Control

Temperature is regulated by central structures (primarily the hypothalamus) that compare integrated thermal inputs from the skin surface, neuraxis, and deep tissues with threshold temperatures for each thermoregulatory response. Though integrated by the hypothalamus, most thermal information is "preprocessed" in the spinal cord and other parts of the central nervous system. This hierarchic arrangement presumably developed when the evolving thermoregulatory control system co-opted previously existing mechanisms (e.g., shivering from muscles previously used for posture and locomotion).[1] It is likely that some thermoregulatory responses can be mounted by the spinal cord alone.[4] For example, animals and patients with high spinal cord transections regulate temperature better than might be expected.

The slope of response intensity versus core temperature defines the gain of a thermoregulatory response. A response intensity no longer increasing with further deviation in core temperature identifies the maximum intensity. This system of thresholds and gains is a model for a thermoregulatory system that is further complicated by interactions between other regulatory responses (i.e., vascular volume control) and time-dependent effects.

How the body determines absolute threshold temperatures is unknown, but the mechanism appears to be mediated by norepinephrine, dopamine, 5-hydroxytryptamine, acetylcholine, prostaglandin E1 , and neuropeptides. Thresholds vary daily in both sexes (circadian rhythm) and monthly in women by approximately 0.5°C. Exercise, food intake, infection, hypothyroidism and hyperthyroidism, anesthetic and other drugs (including alcohol, sedatives, and nicotine), and cold and warm adaptation alter threshold temperatures.

Control of autonomic responses is approximately 80% determined by thermal input from core structures ( Fig. 40-1 ).[5] [6] In contrast, a large fraction of the input controlling behavioral responses is derived from the skin surface. The interthreshold range (core temperatures not triggering autonomic thermoregulatory responses) is only 0.2°C.[7] This range is bounded by the sweating threshold at its upper end and by vasoconstriction at the lower end. Because energy cost and nutrients are conserved without excessive autonomic control within this range, some animals such as camels and desert rats use this strategy extensively to allow core temperature changes of up to 10°C each day.

Both sweating and vasoconstriction thresholds are 0.3°C to 0.5°C higher in women than men, even during the follicular phase of the monthly cycle (first 10 days).[8] Differences are even greater during the luteal phase.[9] Central thermoregulatory control is apparently intact even in somewhat premature infants.[10] In contrast, thermoregulatory control is sometimes impaired in the elderly.[11]


Figure 40-1 There is a linear relationship between mean skin temperature and the core temperature triggering vasoconstriction and shivering. Skin temperature contributes about 20% to control of each thermoregulatory defense. (Redrawn from Cheng C, Matsukawa T, Sessler DI, et al: Increasing mean skin temperature linearly reduces the core-temperature thresholds for vasoconstriction and shivering in humans. Anesthesiology 82:1160–1168, 1995.)

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