Chapter 16
Temperature Acclimatization
Changes in sweating onset, volume, and composition deter-
mine people’s chronic adaptation to high temperatures. A
person newly arrived in a hot environment has poor ability
to do work; body temperature rises and severe weakness may
occur. After several days, there is a great improvement in
work tolerance, with much less increase in body temperature,
and the person is said to have acclimatized to the heat. Body
temperature does not rise as much because sweating begins
sooner and the volume of sweat produced is greater.
There is also an important change in the composition
of the sweat, namely, a marked reduction in its sodium con-
centration. This adaptation, which minimizes the loss of
sodium from the body via sweat, is due to increased secre-
tion of the adrenal mineralocorticoid hormone aldosterone.
The sweat gland secretory cells produce a solution with a
sodium concentration similar to that of plasma, but some of
the sodium is absorbed back into the blood as the secretion
fl ows along the sweat gland ducts toward the skin surface.
Aldosterone stimulates this absorption in a manner identi-
cal to its stimulation of sodium reabsorption in the renal
Cold acclimatization has been much less studied than
heat acclimatization because of the diffi culty of subjecting
people to total-body cold stress over long enough periods to
produce acclimatization. Moreover, people who live in cold
climates generally dress very warmly and so would not develop
acclimatization to the cold.
Table 16–9
Summary of Effector Mechanisms
in Temperature Regulation
Desired Effect
Stimulated by Cold
Decrease heat loss
1. Vasoconstriction of skin vessels
2. Reduction of surface area
(curling up, etc.)
3. Behavioral response (put
on warmer clothes, raise
thermostat setting, etc.)
Increase heat production
1. Increased muscle tone
2. Shivering and increased
voluntary activity
3. Increased secretion of
epinephrine (minimal in adults)
4. Increased food appetite
Stimulated by Heat
Increase heat loss
1. Vasodilation of skin vessels
2. Sweating
3. Behavioral response (put on
cooler clothes, turn on fan, etc.)
Decrease heat production
1. Decreased muscle tone and
voluntary activity
2. Decreased secretion of
epinephrine (minimal in adults)
3. Decreased food appetite
In addition to obesity, anorexia, bulimia, and temperature
acclimatization, several other features of energy usage and
thermoregulation are of great clinical interest.
Fever and Hyperthermia
is an elevation of body temperature due to a resetting of
the “thermostat” in the hypothalamus. A person with a fever
still regulates body temperature in response to heat or cold
but at a higher set point. The most common cause of fever is
infection, but physical trauma and stress can also induce fever.
The onset of fever during infection is often gradual, but
it is most striking when it occurs rapidly in the form of a chill.
The temperature setting of the brain thermostat is suddenly
raised. Because of this, the person feels cold, even though
his or her actual body temperature may be normal. Thus, the
typical actions that are used to increase body temperature,
such as vasoconstriction and shivering, occur. The person
also curls up and puts on more blankets. This combination
of decreased heat loss and increased heat production serves
to drive body temperature up to the new set point, where it
stabilizes. It will continue to be regulated at this new value
until the thermostat is reset to normal and the fever “breaks.”
The person then feels hot, throws off the covers, and
manifests profound vasodilation and sweating.
What is the basis for the thermostat resetting? Chemical
messengers collectively termed
endogenous pyrogen (EP)
are released from macrophages (as well as other cell types) in
the presence of infection or other fever-producing stimuli.
The next steps vary depending on the precise stimulus for
the release of EP. As illustrated in
Figure 16–19
, in some
cases EP probably circulates in the blood to act upon the
thermoreceptors in the hypothalamus (and perhaps other
brain areas), altering their input to the integrating centers. In
other cases, EP may be produced by macrophage-like cells in
the liver and stimulate neural receptors there that give rise to
afferent neural input to the hypothalamic thermoreceptors.
In both cases, the immediate cause of the resetting is a
local synthesis and release of prostaglandins within the
reduces fever by inhibiting this
prostaglandin synthesis.
The term
was coined at a time when the identity of
the chemical messenger(s) was not known. At least one peptide,
interleukin 1 (IL-1),
is now known to function as an EP,
but other peptides—for example,
interleukin 6 (IL-6)
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