Physiology 5th Ed.


Humans maintain a normal body temperature at a set point of 37° C (98.6° F). Because environmental temperatures vary greatly, the body has mechanisms, coordinated in the anterior hypothalamus, for both heat generation and heat loss to keep body temperature constant. When the environmental temperature decreases, the body generates and conserves heat. When the environmental temperature increases, the body reduces heat production and dissipates heat.

Mechanisms for Generating Heat

When environmental temperature is less than body temperature, mechanisms are activated that increase heat production and reduce heat loss. These mechanisms include stimulation of thyroid hormone production, activation of the sympathetic nervous system, and shivering. Behavioral components also may contribute by reducing the exposure of skin to the cold (e.g., wrapping arms around oneself, curling up in a ball, adding more clothing).

Thyroid Hormones

Thyroid hormones are thermogenic: Their actions on target tissues result in heat production. Major actions of thyroid hormone are stimulation of Na+-K+ ATPase, increased O2 consumption, increased metabolic rate, and increased heat production. Therefore, it is logical that exposure to cold temperatures activates thyroid hormones. The mechanism for this activation is not entirely clear, but it includes increased conversion of thyroxine (T4) to the active form, triiodothyronine (T3), in target tissues.

Because thyroid hormones are thermogenic, it follows that an excess or deficit of thyroid hormones would cause disturbances in the regulation of body temperature. In hyperthyroidism (e.g., Graves disease, thyroid tumor), metabolic rate increases, O2 consumption increases, and heat production increases. In hypothyroidism (e.g., thyroiditis, surgical removal of the thyroid, iodine deficiency), there is a decreased metabolic rate, decreased O2consumption, decreased heat production, and extreme sensitivity to cold. (For a complete discussion of this topic, refer to Chapter 9.)

Sympathetic Nervous System

Cold environmental temperatures activate the sympathetic nervous system. One consequence of this activation is stimulation of β receptors in brown fat, which increases metabolic rate and heat production. This action of the sympathetic nervous system is synergistic with the actions of thyroid hormones: For thyroid hormones to produce maximal thermogenesis, the sympathetic nervous system must be simultaneously activated by cold temperatures.

A second consequence of activation of the sympathetic nervous system is stimulation of α1 receptors in vascular smooth muscle of skin blood vessels, producing vasoconstriction. Vasoconstriction reduces blood flow to the surface of the skin and, consequently, reduces heat loss.


Shivering, which involves rhythmic contraction of skeletal muscle, is the most potent mechanism for increasing heat production in the body. Cold environmental temperatures activate centers in the posterior hypothalamus, which then activate the α and γ motoneurons innervating skeletal muscle. The skeletal muscle contracts rhythmically, generating heat and raising body temperature.

Mechanisms for Dissipating Heat

When the environmental temperature increases, mechanisms are activated that result in increased heat loss from the body by radiation and convection. Since heat is a normal byproduct of metabolism, the body must dissipate this heat just to maintain body temperature at the set point. When the environmental temperature is increased, more heat than usual must be dissipated.

Mechanisms for dissipating heat are coordinated in the anterior hypothalamus. Increased body temperature decreases sympathetic activity in skin blood vessels. This decrease in sympathetic tone results in increased blood flow through skin arterioles and greater arteriovenous shunting of blood to venous plexuses near the surface of skin. In effect, warm blood from the body core is shunted to the body surface, and heat is then lost by radiation and convection. Shunting of blood to the surface is evidenced by redness and warmth of the skin. There also is increased activity of the sympathetic cholinergic fibers innervating thermoregulatory sweat glands to produce increased sweating (cooling). The behavioral components to dissipate heat include increasing the exposure of skin to the air (e.g., removing clothing, fanning).

Regulation of Body Temperature

The temperature-regulating center is located in the anterior hypothalamus. This center receives information about environmental temperature from thermoreceptors in the skin and about core temperature from thermoreceptors in the anterior hypothalamus itself. The anterior hypothalamus then orchestrates the appropriate responses, which may involve heat-generating or heat-dissipating mechanisms.

If core temperature is below the set-point temperature, then heat-generating and heat-retaining mechanisms are activated. As previously discussed, these mechanisms include increased metabolic rate (thyroid hormones, sympathetic nervous system), shivering, and vasoconstriction of blood vessels of the skin (increased sympathetic tone).

If core temperature is above the set-point temperature, then heat-dissipating mechanisms are activated. These mechanisms include vasodilation of blood vessels of the skin (decreased sympathetic tone) and increased activity of sympathetic cholinergic fibers to sweat glands.


Fever is an abnormal elevation of body temperature. Pyrogens produce fever by increasing the hypothalamic set-point temperature. The result of such a change in set point is that a normal core temperature is “seen” by the hypothalamic center as too low relative to the new set point. The anterior hypothalamus then activates heat-generating mechanisms (e.g., shivering) to raise body temperature to the new set point.

At the cellular level, the mechanism of pyrogen action is increased production of interleukin-1 (IL-1) in phagocytic cells. IL-1 then acts on the anterior hypothalamus to increase local production of prostaglandins, which increase the set-point temperature.

Fever can be reduced by aspirin, which inhibits the cyclooxygenase enzyme, necessary for the synthesis of prostaglandins. By inhibiting the production of prostaglandins, aspirin (and other cyclooxygenase inhibitors) interrupts the pathway that pyrogens utilize to raise the set-point temperature. When fever is treated with aspirin, the temperature sensors in the anterior hypothalamus now “see” body temperature as too high relative to the set-point temperature and set in motion the mechanisms for dissipating heat including vasodilation and sweating.

Disturbances of Temperature Regulation

Heat exhaustion can occur as a consequence of the body’s responses to elevated environmental temperature. Normally, the response to increased temperature includes vasodilation and sweating in order to dissipate heat. However, if the sweating is excessive, it can result in decreased ECF volume, decreased blood volume, decreased arterial pressure, and fainting.

Heat stroke occurs when body temperature increases to the point of tissue damage. If the normal response to elevated environmental temperature is impaired (e.g., if sweating does not occur), then heat cannot be appropriately dissipated and core temperature increases to dangerous levels.

Malignant hyperthermia is characterized by a massive increase in metabolic rate, increased O2 consumption, and increased heat production in skeletal muscle. The heat-dissipating mechanisms are unable to keep pace with the excessive heat production, and if the hyperthermia is not treated, body temperature may increase to dangerously high, or even fatal, levels. In susceptible individuals, malignant hyperthermia can be caused by inhalation anesthetics.