Chapter 24
Nutrition, Metabolism, and Body Temperature Regulation
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24
Wearing light-colored, loose clothing that reflects radiant
energy. (Tis is actually cooler than being nude because bare
skin absorbs most of the radiant energy striking it.)
Homeostatic Imbalance 24.8
Overexposure to a hot and humid environment makes normal
heat-loss processes ineffective. Te resulting
hyperthermia
(elevated body temperature) depresses the hypothalamus. At a
core temperature of around 41°C (105°F), heat-control mecha-
nisms are suspended, creating a vicious
positive feedback cycle
.
Increasing temperatures increase the metabolic rate, which in-
creases heat production. Te skin becomes hot and dry and,
as the temperature continues to spiral upward, multiple organ
damage becomes a distinct possibility, including brain damage.
Tis condition, called
heat stroke
, can be fatal unless corrective
measures are initiated immediately (immersing the body in cool
water and administering fluids).
Te terms
heat exhaustion
and
exertion-induced heat ex-
haustion
are o±en used to describe the heat-associated extreme
sweating and collapse of an individual during or following vig-
orous physical activity. Tis condition, evidenced by elevated
body temperature and mental confusion and/or fainting, is due
to dehydration and consequent low blood pressure. In contrast
to heat stroke, heat-loss mechanisms are still functional in heat
exhaustion. However, heat exhaustion can rapidly progress to
heat stroke if the body is not cooled and rehydrated promptly.
Hypothermia
(hi
0
po-ther
9
me-ah) is low body temperature
resulting from prolonged uncontrolled exposure to cold. Vital
signs (respiratory rate, blood pressure, and heart rate) decrease
as cellular enzymes become sluggish. Drowsiness sets in and,
oddly, the person becomes comfortable even though previously
he or she felt extremely cold. Shivering stops at a core tem-
perature of 30–32°C (87–90°F) when the body has exhausted
its heat-generating capabilities. Uncorrected, hypothermia
progresses to coma and finally death (by cardiac arrest), when
body temperatures approach 21°C (70°F).
Fever
Fever is
controlled hyperthermia
. Most o±en, it results from in-
fection somewhere in the body, but it may be caused by cancer,
allergic reactions, or CNS injuries.
Whatever the cause, macrophages and other cells release
cytokines, originally called
pyrogens
(literally, “fire starters”),
at least two of which are now known to be interleukins. Tese
chemicals act on the hypothalamus, causing release of prosta-
glandins which reset the hypothalamic thermostat to a higher-
than-normal temperature, so that heat-promoting mechanisms
kick in. As a result of vasoconstriction, heat loss from the body
surface declines, the skin cools, and shivering begins to generate
heat. Tese “chills” are a sure sign body temperature is rising.
Te temperature rises until it reaches the new setting, and
then is maintained at that setting until natural body defenses
or medications reverse the disease process. Chemical mes-
sengers called
cryogens
(vasopressin and others) prevent fever
from becoming excessive and reset the thermostat to a lower (or
normal) level. Ten, heat-loss mechanisms swing into action.
metabolic rate and enhancing heat production. Tis
mechanism, called
chemical (nonshivering)
thermogen-
esis
, occurs in infants. Recently, deposits of brown adipose
tissue, a special kind of adipose tissue that dissipates en-
ergy by producing heat by this mechanism, have also been
demonstrated in adult humans.
4.
Enhanced thyroxine release.
When environmental tem-
perature decreases gradually, as in the transition from
summer to winter, the hypothalamus of infants releases
thyrotropin-releasing hormone
. Tis hormone activates the
anterior pituitary to release
thyroid-stimulating hormone
,
which induces the thyroid to liberate more thyroid hor-
mone to the blood. Because thyroid hormone raises meta-
bolic rate, body heat production rises. Adults do not show
a similar ²SH response to cold exposure.
Besides these involuntary adjustments, we humans make a
number of
behavioral modifications
to prevent overcooling of
our body core:
Putting on more or warmer clothing to restrict heat loss (hat,
gloves, and “insulated” outer garments)
Drinking hot fluids
Changing posture to reduce exposed body surface area
(hunching over or clasping the arms across the chest)
Increasing physical activity to generate more heat (jumping
up and down, clapping the hands)
Heat-Loss Mechanisms
Heat-loss mechanisms protect the body from excessively high
temperatures. Most heat loss occurs through the skin via radia-
tion, conduction, convection, and evaporation.
How do heat-exchange mechanisms help us lose heat? Te
answer is quite simple. Whenever core body temperature rises
above normal, it inhibits the hypothalamic heat-promoting
center. At the same time, it activates the heat-loss center and
triggers one or both of the following (Figure 24.26, top):
1.
Dilation of cutaneous blood vessels.
Inhibiting the vasomo-
tor fibers serving blood vessels of the skin allows the vessels
to dilate. As the blood vessels swell with warm blood, the
shell loses heat by radiation, conduction, and convection.
2.
Enhanced sweating.
If the body is extremely overheated
or if the environment is so hot—over 33°C (about 92°F)—
that heat cannot be lost by other means, evaporation be-
comes necessary. Sympathetic fibers activate the sweat
glands to spew out large amounts of perspiration. Evapo-
ration of perspiration is an efficient means of ridding the
body of surplus heat as long as the air is dry.
However, when the relative humidity is high, evaporation oc-
curs much more slowly. In such cases, the heat-liberating mech-
anisms cannot work well, and we feel miserable and irritable.
Behavioral or voluntary measures commonly taken to reduce
body heat in such circumstances include
Reducing activity (“laying low”)
Seeking a cooler environment (a shady spot) or using a device
to increase convection (a fan) or cooling (an air conditioner)
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