Neuronal Effector Mechanisms That Decrease or Increase Body Temperature
When the hypothalamic temperature centers detect that the body temperature is either too high or too low, they institute appropriate temperature-decreasing or temperature-increasing procedures. The reader is probably familiar with most of these from personal experience, but special features are the following.
Temperature-Decreasing Mechanisms When the Body Is Too Hot
The temperature control system uses three important mechanisms to reduce body heat when the body tem-perature becomes too great:
1. Vasodilation of skin blood vessels. In almost allareas of the body, the skin blood vessels become intensely dilated. This is caused by inhibition of the sympathetic centers in the posterior hypothalamus that cause vasoconstriction. Full vasodilation can increase the rate of heat transfer to the skin as much as eightfold.
2. Sweating. The effect of increased bodytemperature to cause sweating is demonstrated by the blue curve in Figure 73–7, which shows a sharp increase in the rate of evaporative heat loss resulting from sweating when the body core temperature rises above the critical level of 37°C (98.6°F). An additional 1°C increase in body temperature causes enough sweating to remove 10 times the basal rate of body heat production.
3. Decrease in heat production. The mechanisms thatcause excess heat production, such as shivering and chemical thermogenesis, are strongly inhibited.
Temperature-Increasing Mechanisms When the Body Is Too Cold
When the body is too cold, the temperature control system institutes exactly opposite procedures. They are:
1. Skin vasoconstriction throughout the body.
This is caused by stimulation of the posterior hypothalamic sympathetic centers.
2. Piloerection. Piloerection means hairs “standingon end.” Sympathetic stimulation causes the arrector pili muscles attached to the hair follicles to contract, which brings the hairs to an upright stance. This is not important in human beings, but in lower animals, upright projection of the hairs allows them to entrap a thick layer of “insulator air” next to the skin, so that transfer of heat to the surroundings is greatly depressed.
3. Increase in thermogenesis (heat production). Heatproduction by the metabolic systems is increased by promoting shivering, sympathetic excitation of heat production, and thyroxine secretion. These methods of increasing heat require additional explanation, which follows.
Hypothalamic Stimulation of Shivering. Located in thedorsomedial portion of the posterior hypothalamus near the wall of the third ventricle is an area called the primary motor center for shivering. This area is normally inhibited by signals from the heat center in the anterior hypothalamic-preoptic area but is excited by cold signals from the skin and spinal cord. There-fore, as shown by the sudden increase in “heat pro-duction” (see the red curve in Figure 73–7), this center becomes activated when the body temperature falls even a fraction of a degree below a critical tempera-ture level. It then transmits signals that cause shiver-ing through bilateral tracts down the brain stem, into the lateral columns of the spinal cord, and finally to the anterior motor neurons. These signals are non-rhythmical and do not cause the actual muscle shaking. Instead, they increase the tone of the skeletal muscles throughout the body by facilitating the activity of the anterior motor neurons. When the tone rises above a certain critical level, shivering begins. This probably results from feedback oscillation of the muscle spindle stretch reflex mechanism. During maximum shivering, body heatproduction can rise to four to five times normal.
Sympathetic “Chemical” Excitation of Heat Production. As pointed out, an increase in either sym-pathetic stimulation or circulating norepinephrine and epinephrine in the blood can cause an immediate increase in the rate of cellular metabolism. This effect is calledchemical thermogenesis. It results at least par-tially from the ability of norepinephrine and epineph-rine to uncouple oxidative phosphorylation, which means that excess foodstuffs are oxidized and thereby release energy in the form of heat but do not cause adenosine triphosphate to be formed.
The degree of chemical thermogenesis that occurs in an animal is almost directly proportional to the amount of brown fat in the animal’s tissues. This is a type of fat that contains large numbers of special mitochondria where uncoupled oxidation occurs, these cells are supplied by strong sympathetic innervation.
Acclimatization greatly affects the intensity of chemical thermogenesis; some animals, such as rats, that have been exposed to a cold environment for several weeks exhibit a 100 to 500 per cent increase in heat production when acutely exposed to cold, in con-trast to the unacclimatized animal, which responds with an increase of perhaps one third as much. This increased thermogenesis also leads to a corresponding increase in food intake.
In adult human beings, who have almost no brown fat, it is rare for chemical thermogenesis to increase the rate of heat production more than 10 to 15 per cent. However, in infants, who do have a small amount of brown fat in the interscapular space, chemical ther-mogenesis can increase the rate of heat production 100 per cent, which is probably an important factor in maintaining normal body temperature in neonates.
Increased Thyroxine Output as a Long-Term Cause of Increased Heat Production. Cooling the anterior hypothalamic-preoptic area also increases production of the neu-rosecretory hormone thyrotropin-releasing hormone by the hypothalamus. This hormone is carried by way of the hypothalamic portal veins to the anterior pitu-itary gland, where it stimulates secretion of thyroid-stimulating hormone.
Thyroid-stimulating hormone in turn stimulates increased output of thyroxine by the thyroid gland. The increased thyroxine increases the rate of cellular metabolism throughout the body, which is yet another mechanism of chemicalthermogenesis. This increase in metabolism does notoccur immediately but requires several weeks’ expo-sure to cold to make the thyroid gland hypertrophy and reach its new level of thyroxine secretion.
Exposure of animals to extreme cold for several weeks can cause their thyroid glands to increase in size 20 to 40 per cent. However, human beings seldom allow themselves to be exposed to the same degree of cold as that to which animals are often subjected. Therefore, we still do not know, quantitatively, how important the thyroid mechanism of adaptation to cold is in the human being.
Isolated measurements have shown that military personnel residing for several months in the arctic develop increased metabolic rates; some Inuit (Eskimos) also have abnormally high basal metabolic rates. Further, the continuous stimulatory effect of cold on the thyroid gland may explain the much higher incidence of toxic thyroid goiters in people who live in cold climates than in those who live in warm climates.
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