Chapter 6

Control and integration of thermoregulatory processes

The animal 's heat balance has been represented by the formula, M.+ G = L + A C. As for the heat
gain and loss terms, physiological, anatomical, and behavioral processes by which the animal
increases or decreases the rate at which it exchanges heat with its surroundings have been
discussed in the preceding chapters. These are called physical thermoregulatory processes. An
animal also can change its metabolic rate in at-tempting to achieve heat balance with its
environment. This is called chemical thermoregulation, and it will be dis-cussed in a later chapter.
The means by which an animal controls physical and chemical thermoregulatory processes are the
subject of this chapter.

Control mechanisms

Thermoreceptors: the afferent step

Warm and cold receptors

Information on body temperature is sensed by spe-cial nervous receptors. Temperature-sensitive

neurons thermoreceptors — are located throughout the body. They are phasic/tonic receptors.
Some are sensitive to increasing temperature, others to decreasing. For example, a warm receptor
reacts upon an abrupt temperature rise in a tissue— by briefly increasing the frequency of its
afferent neural impulses by an amount corresponding to the rate-of-change in temperature, and
then assuming a new tonic discharge rate according to the new temperature. Similarly, cold
receptors are stimulated by a fall in temperature.

Locations

Thermoreceptors also can be classified by their loca-tion in the body. There are central-nervous
thermoreceptors in the hypothalamus; extrahypothalamic deep-body ther-moreceptors in the
spinal cord, the walls of major veins and of the gastrointestinal tract, and other structures; and
peri-pheral thermoreceptors in the body shell, especially the skin. Information from all of these
sites is channelled via afferent nerves to the hypothalamic thermoregulatory center. The question,
still largely unanswered, is: What is the relative importance of the various thermoreceptors to an
animal 's thermoregulation?

Hypothalamic thermoregulatory center: the integrative and response-decision step The

hypothalamus contains the animal' s thermo-regulatory center. This receives information from
other deep-body thermoreceptors and from peripheral thermo-receptors. In addition, the
hypothalamus itself is ther-mosensitive. Various bits of information on body tempera-tures are
integrated in the hypothalamus. How does the hypothalamic thermoregulatory center go about
deciding what thermoregulatory response —if any needed? There is still no clear answer to this
question. Several theo-ries have been proposed. Each has its strengths and its

Box 6-A

Fever in a pig: a case of serendipity

Astute researchers often learn things by accident. This is called serendipity: finding something not
sought. The key is to be prepared and in the proper frame of mind to recognize the importance of
certain accidental things when they happen. That is how D. L. Ingram, K. F. Legge, and L. E. Mount
came to know about the onset of spontaneous fever in a young pig (Brit. Vet. J. 129:xxxii, 1973).

These scientists had been monitoring a pig's carotid temperature continuously by means of a
telemetric apparatus for over a week in connection with an experi-ment on variation of body
temperature over time. All of a sudden, shortly after 0800 hours one morning, the record shows
carotid temperature in this pig rose very rapidly—by .08 C° per minute, for half an hour. This is
almost three times the rate of rise due to the heat increment after a meal.

When these authors reported this chance observation, they tied it together with previous
knowledge and a bit of speculation when they suggested that in fever, heat production might rise
at about the same rate as during the period following a meal, but during the orset of fever, heat
loss is impeded by peripheral vasoconstriction, whereas it is enhanced by vasodila-tion after an
eating bout.
60

weaknesses. Each is based on experimental observations nd inter reta-which in turn bear errors of
measurement ap tion. They are necessary steps to more accurate under standing of the
phenomena of thermoregulation, although none is probably accurate itself. Hammel ' s variable
set-point theory of thermoregulation According to H. T. Hammel, hypothalamic tempera-ture is
the controlled body temperature, and hypothalamic thermoregulatory responses are proportional
to the differ-ence (which can be as little as .1 C°) between actual hypo-thalamic temperature and a
certain hypothalamic set-point temperature. The thermoregulatory center is thus somewhat anal-
ogous to a room thermostat, which has a temperature set-point and a temperature sensor, and
compares these two temperatures. For instance, if actual hypothalamic tem-perature were lower
than set-point temperature, the hypo-thalamus might respond by calling for a decrease in heat
loss or an increase in heat production, and the processes invoked and their respective magnitudes
would be some-how proportional to the difference between actual and set-point temperatures.
Thus, according to this theory, central-nervous thermoreceptors are crucial to thermoregulation.
However, stimuli from extrahypothalamic thermore-ceptors are equally important according to
Hammel's theory. The hypothalamic set-point temperature is adjust-able. Its major adjusters are
inputs from other deep-body and peripheral thermoreceptors. Other adjusters are exer-cise,
sleep, pyrogens, and dehydration. Here's how the theory goes : If inputs from skin
thermoreceptors report an increase in skin temperature, hypothalamic set-point tern-perature
would decrease (analogously, the thermostat would be reset at a lower point). Consequently,
actual hypo-thalamic temperature would not need to increase as much before the
thermoregulatory center would respond by call-ing for increased heat loss or decreased heat
production. In effect, extrahypothalamic thermal inputs make the ther-moregulatory center more
sensitive to changes in hypothal-amic temperature. They warn the thermoregulatory center of an
imminent change in actual hypothalamic temperature. The response again would be proportional
to the difference between the actual temperature and the new set-point in the hypothalamus.
Thus, according to Hammel ' s theory, extrahypo-thalamic signals serve as fine tuners of the
hypothalamic thermoregulatory center. This view accordsgenerally with another thermoregulatory
theory.

Bligh 's two-tiered theory of thermoregulation

John Bligh has suggested that body temperature is regulated by a two-tiered control system. Fine
control of body temperature within 1 C° of the species mean is achieved in response to input from
hypothalamic, other deep-body, and peripheral thermoreceptors. According to this theory, the
relative influences of thermoreceptors in various sites on fine control of thermoregulatory
processes varies among classes and species of animals. In addition, Biigh postulated the existence
of a coarse-control, s stem that is activated outside a certain
Environmental management in animal agriculture

Box 6-B

Measuring body temperature

The rectum is a convenient place to insert a therrno_ meter, and rectal temperature is the most
common indicator of body temperature of an animal in both research and production. But this
method of thereto. metry has some shortcomings. In the first Place sampling error can occur if the
temperature-sensitivle element lies next to a blood vessel in the rectal wall instead of in the
lumen's feces. Second, the rectum is not the site of the thermoregulatory center, which itself is
thermosensitive. Also, the rectum's temperature response to a change in body heat content or
even blood temperature is relatively slow. Following some work by human physiologists, A. j.
Guidry and R. E. McDowell (j. Dairy Sci. 49:74, 1966) simply inserted a commercially available
temperature probe into a cow's ear canal to measure the tempera-ture near her tympanic
membrane. This structure is near the hypothalamus, and thus the thermoregulatory center. They
found that ear-drum temperature rose and fell more rapidly than did rectal temperature when ice
was put in the cow 's rumen or when she was exposed to an extremely hot environment.

Later, when M. M. Ahmad and F. B. Mather similarly installed a temporary temperature probe at a
chicken's tympanic membrane, they found this temperature to be a more reliable indicator of
rapid changes of body tem-perature in this species, too (Poul. Sci. 53:1616, 1974).

Of course, temperature probes also have been im-planted surgically in or near the hypothalamus
itself in cattle and chickens (j. D. Findlay and D. L. Ingram: J. Physiol. 155:72, 1961; N. R. Scott, A. T.
Johnson, and A. van Tienhoven: Trans. Am. Soc. Agr. Eng. 13:342, 1970), but traumatic
consequences of the opera-tion and the presence of the probe itself limit the con-clusions that can
be drawn from these measurements. Surgery has also been used to place thermometer probes
near the carotid artery, through which blood flows to the brain (D. L. Ingram and K. F. Legge: J.
Physiol. 210:989, 1970). The measurement is called carotid temperature, and its variations closely
parallel those in hypothalamic temperature.
critical body-temperature range for instance, more than 2 C° higher or lower than normal. Coarse-
control re-sponses are stimulated by large changes in actual hypo-thalamic temperature, and
serve as an emergency override mechanism to prevent large variations in body tempera-ture,
according to this theory.

Integration, response decisions, and efferent signals Nerves carrying thermal information from
various parts of the body synapse in the hypothalamic thermoregu-

.r.

ap°

Control and integration of thermoregulatory processes

latory center with those that carry thermoregulatory orders. These synapses represent sites of
integration and response decision. Serotonin and norepinephrine seem to be among the
neurotransmitters active at these synapses. Prostaglandins and acetylcholine might be, too.
Signals from the hypothalamic thermoregulatory center travel by direct nervous links to
thermoregulatory effectors. Alternatively, they travel neurally to another part of the central
nervous system where they synapse with an efferent nerve which in turn carries the signal to the
ef-fector. Another possibility is these signals can comprise the secretion of a releasing factor for an
adenohypophysial tropic hormone involved in chemical thermoregulation.

Neural or hormonal control: the efferent step Control of physical thermoregulation Tissue
insulation. Some thermoregulatory-center output affects the function of the vasomotor center in
the medulla oblongata. Resistance to blood flow in peripheral vessels is controlled primarily by
sympathetic nerves that originate in this part of the brain. Increased impulse frequency in these
nerves causes vasoconstriction; de-creased frequency leads to relaxation and ultimately vaso-
dilation. Circulating catecholarnines from the adrenal me-dullae also increase vasoconstrictor
tone. In food mammals, at least, an increase in skin tem-perature appears to be sufficient to
provoke an increase in blood flow to the skin, although an increase in hypothalamic temperature
leads to the same result. Cover insulation. Arrector pili and arrector plum-orum muscles —
responsible for piloerection and feather fluffing, respectively are also innervated by sympathetic
nerves. As heat stress becomes progressively more severe, peripheral vasodilation increases to a
maximum, at which point the animal actively increases its rate of evaporative heat loss. The
environmental temperature at which this occurs is also inversely related to minimal cover
insulation. Sweating. The control of thermal sweating in those food mammals in which it occurs is
poorly understood. As has been mentioned already, there is no nerve supply to the sweat glands
of food mammals. Nevertheless, sweat glands of cattle, sheep, and pigs are somehow stimulated
by epinephrine, and perhaps by norepinephrine. In cattle, at least, intact sympathetic innervation
of the skin is neces-sary before thermal sweating occurs, and catecholamines of adrenal-medullary
origin seemingly are not involved. The pig's sweat glands are not activated by heat stress. In both
cattle and sheep, a rise in skin tempera-ture — even without rising core temperature is sufficient
to elicit an increase in the rate of sweating. Hence, the animal can initiate sweating to combat
heat stress even before homeothermy has been upset. The skin-tempera-ture threshold for
sweating is about 32°C in European-type cattle and about 35°C in zebus, and sweating rate is
directly proportional to skin temperature for ranges of several de-grees above these critical points.
Sweating can also be stim-ulated by a rise in hypothalamic temperature. Panting. The output of
the thermoregulatory center also affects the function of respiratory centers in the pons and
medulla oblongata, which in turn control breath-ing. By this mechanism, panting and the
consequent in-

61

crease in respiratory-evaporation rate are invoked in re-sponse to heat stress. Panting starts
abruptly when skin and other extra-hypothalamic sites are warmed to a certain threshold even
without a change in body-core temperature, in cattle and sheep. Furthermore, there might even
be humidity recep-tors in the upper respiratory tract involved in respiratory control during stress
from a hot, humid environment. The pig, on the other hand, usually does not pant in re-sponse to
an increase in skin temperature in the absence of increased core temperature. Increasing
hypothalamic temperature causes pant-ing in all food mammals. In cattle, at least, the respiratory
reaction to warming the hypothalamus is directly propor-tional to environmental temperature,
and thus presumably to skin temperature, also. This observation accords with both Hammel' s and
Bligh' s thermoregulatory theories. The critical skin temperature for the onset of panting seems to
be one or two degrees higher than that for the on-set of sweating in cattle. Thus, in animals with a
relatively large sweating response, skin temperature is kept cooler by evaporation of sweat, so
there is a delay in peripheral stimuli to panting. Conversely, in poor sweaters, the skin warms to
the panting threshold more quickly.

Control of chemical thermoregulation

As cold stress becomes progressively more severe, physical thermoregulatory processes increase
to maximal effectiveness. If the environment becomes still colder, the animal invokes chemical
thermoregulatory responses in an attempt to achieve homeothermic heat balance. An animal
responds metabolically to cold stress by two general mechanisms. One involves skeletal muscle
con-traction—the shivering thermogenic reaction to cold. The other is increased metabolic rate in
virtually all of the body' s tissues — the nonshivering response. As will be dis-cussed later,
increased heat production in skeletal muscles via spasm or tonus is a response to acute cold stress,
while the general metabolic reaction develops more slowly during chronic stress. Skeletal-muscle
response. The thermoregulatory center can elicit involuntary increase in heat production in
skeletal muscles. Some of the center's output synapses with nerves in the primary motor center,
located in another part of the hypothalamus. Efferent nerves arising there travel via the spinal
cord and the somatic nervous sys-tem's peripheral motor nerves to skeletal muscles. The function
of the primary motor center in the hypothalamus is modified by the output of several secondary
motor centers in other parts of the brain. Proprioceptors and tension feed-back from skeletal
muscles also participate in regulating the involuntary skeletal-muscle response to cold stress.
General metabolic response. Several hormones thyroid hormone, the glucocorticoids, and growth
hor-mone —probably participate in certain ways in the control of the metabolic response to
chronic cold stress. Their respec-tive secretion rates are inversely related to environmental
temperature and, when injected into an animal, they all increase metabolic rate. The secretion of
growth hormone, thyrotropin, and adrenocorticotropin, respectively, is controlled by respec-tive
releasing and inhibiting factors that arise in the hypo-thalamus and travel to the adenohypophysis
via the hypo-

62

thalamo-hypophysial portal system. It is presumed that some of the thermoregulatory center's

output changes the hypothalamus's secretion of releasing factors for these hormones.
Sympathoadrenal function. Cold stress stimulates the sympathetic portion of the autonomic
nervous system and the adrenal medullae, which together comprise the svmpathoadrenal system.
Nerve fibers arising in the hypo-thalamic thermoregulatory center synapse just outside the spinal
cord with sympathetic efferent nerves leading to var-ious metabolic-fuel storage sites and the
adrenal glands. These fibers are stimulated when there is a need for an increase in heat
production. The result is an increased secretion of the catecholamines —norepinephrine and epi-
nephrine— by sympathetic postganglionic nerve endings and adrenal medullae in response to cold
stress. These hormones play a supportive role in the various thermogenic reactions to acute and
chronic cold stress. They mobilize metabolic fuels, such as fatty acids and glu-cose, from body
depots and increase cardiac output to facili-tate transport of substrates to, and reaction products
from, the sites of cold-induced thermogenesis. Catecholamines also synergize with thyroid
hormone to increase general metabolic rate during chronic cold stress. In general, the rates of
heat-production reactions just discussed are affected by the temperature of peri-pheral,
extrahypothalamic deep-body, and hypothalamic thermoreceptors. In specific experimental
situations, one class or another of thermoreceptors often dominates the control of cold-induced
thermogenesis.

Control of behavioral thermoregulation

An animal behaves, apparently involuntarily, in specific ways in order to alter its rate of heat
exchange with its environment. It may alter its posture, huddle with groupmates, avoid adverse
environmental elements, seek favorable features of the surround, or alter its micro-environment
to suit itself. These behavioral reactions to temperature stress thus can be considered to be part
of the animal 's repertory of physical-thermoregulatory processes. The animal also can increase
skeletal-muscle activity volun-

heat-production rate

maximal deathdeath

intolerably cold zone

absolute lower critical temp

s mmit

`Nifk. lower critica

Environmental management in animal. agriciat toe

tat ily to increase heat production rate, a chemi regulatory process. All of the behaviors mentioned
involve body ment. Such motor activity results from the coordinaPlovt forts of several skeletal
muscles. Control of the :iced et muscles responsible for a given motor activity is dt:letal complex of
mechanisms that involves many regions critto a central nervous system, as well as motor nerves
the of the somatic nervous system. The nature of these mechanisms is still poorly und

Ilerr14.

stood, but some of the hypothalamic thermore er

center's output presumably leads to the cerebraigucetrY which is a major participant in motor
control. Interneurrit: would potentiate the involvement of other parts of 71, brain, such as the
cerebellum, in the control of rnovernen"te as well. Motion is ultimately initiated and controlled bl
efferent signals that travel by motor nerves synapsing the spinal cord with peripheral motor
nerves of the somatic nervous system. Axons of these peripheral nerves serve effector skeletal
muscles.

Integrated reactions to cold

The various physical and chemical thermoregulatory processes in the homeothermic animal s
repertory of de_ fenses against cold stress have been described already. The particular complex of
reactions invoked depends on the nature of the stress and the animal's adaptive status when it
occurs.

Degrees of cold stress

Cold stress can be characterized in terms of its intern sity and duration.

Intensity: thermorekulatory zones in cold stress

Environmental heat demand and effective environ-mental temperature. Environmental heat

demand reflects the cooling power of the surroundings. It is equal to the heat flux from a given
animal to a particular environment. As environmental temperatures drop, the environment usually
increases its demand for heat. Of course, other fac-tors —such as air movement also influence
environmental heat demand. Effective environmental temperature is an index of an animal' s total
thermal environment in terms of environ-mental heat demand. Thus, for instance, when two cool
environments are comparable, except one has a higher rate of air movement, the one with the
higher air speed would have a lower effective environmental temperature. Effec-tive
environmental temperature will be discussed further in the next chapter. When environmental
heat demand becomes so great. that an animal must invoke one or more thermoregulatory
processes in order to maintain a normal body i temperature, the animal is undergoing cold stress.
Cold stresses vary in their degrees of intensity (Figure 6-1). Thermal-comfort zone. There is a
relatively nar-row zone of effective environmental temperature in which heat production at the
animal' s minimal or thermoneutral rate is offset by net heat loss to the environment without the

cold

zone

low

cool

zone

effective environmental temperature Figure 6-1. Relation between heat-production rate and lower
environ-mental temperatures.

therrnoneutral AC'

thermal-comfort zone

moderate

Noe, A44°

Control and integration of thermoregulatory processes

aid of special heat-conserving or -dissipating mechanisms. The animal is under neither cold stress
nor heat stress when its effective environmental temperature is within the thermal-comfort zone.
Cool zone. As effective environmental temperature falls below the lower limit of the thermal-
comfort zone, the animal is in the cool zone. In this region, the animal invokes physical-
thermoregulatory processes to conserve metabolic heat. As temperature decreases within the
cool zone, metabolic rate of the fed animal remains at the ther-moneutral level. But, because
heat-conserving mechanisms do require the expenditure of energy, the animal ' s main-tenance-
energy requirement does increase. The magnitudes of the various insulative and behav-ioral
responses to cold stress increase progressively as ef-fective environmental temperature falls in the
cool zone. They are at their maximal effectiveness in conserving heat at the lower limit of the cool
zone, which is called the lower critical temperature.

Box 6-C

Acclimation to cold

When animals have become acclimated to an extreme thermal environment, their thermal
responses differ from what they had been before acclimation occurred. J. Slee studied cold
acclimation in sheep and the time course of deacclimation (Anim. Prod. 19:201, 1974). To
determine an individual's initial resistance to a cold environment, each sheep was closely shorn
and sub-jected to an acutely cold environment: air tempera-ture was lowered from 28°C to —
20°C over a short period, and when it was below 0°C air velocity in the animal' s microenvironment
was raised to 1.8 m sec-1 Rectal temperature was monitored all the time, and the period from the
moment air temperature passed below 0°C to when the sheep 's rectal temperature had fallen
from the normal of around 39.5°C to 36.0°C was taken as an index of cold resistance.

Enhanced cold resistance "cold acclimation" in-duced in this way was known to be maximal
around two weeks after the first acute cold episode, at which time the index was at least half
again longer than initially. There was also evidence that acclimation following a single acute cold
episode was lost within eight weeks. But when a second cold exposure occurred two weeks after
the first, cold acclimation was largely retained in groups tested for a third time after an additional
two, four, or six weeks.

time (weeks) 0 2 4 6 8

mean index of cold resistance (minutes) grout 1 group 2 150 196 254 297 226

332

group 3 260 391

361

63

Cold zone. Below the lower critical temperature lies the cold zone. Since measures aimed at
limiting heat loss reach maximal efficacy in the cool zone, the only way an animal can maintain
homeothermy in the cold zone is to increase its rate of metabolic heat production. Of course,
heat-conserving processes continue at maximal effective-ness throughout the cold zone. As
effective environmental temperature continues to fall in the cold zone, metabolic rate must be
raised in parallel with environmental heat de-mand so the animal can maintain a normal body
tern-perature. The lower critical temperature is a very important environmental parameter in
animal production, as either an animal's rate of productivity or its efficiency of feed conver-sion
suffers at environmental temperatures below this point. The many factors that influence a given
animal' s lower critical temperature will be discussed later. These include level of feed intake,
maximal thermal insulation, time of day, and social thermoregulation via huddling. Summit
metabolic rate is the highest rate an animal 'with free access to feed can maintain over an
extended period. The effective environmental temperature at which summit metabolic rate
obtains is called the absolute lower critical temperature, which is also the lower limit of the cold
zone. Intolerably cold zone. below the cold zone. An animal can increase its heat-production rate
slightly above the summit level — to the maximal level— as the environment continues to demand
more and more heat in the intolerably cold zone. But maxi-mal metabolic rate can be maintained
for a short period only. Therefore, in the intolerably cold zone, heat-produc-tion rate cannot for
long compensate for the high rate of heat loss, so body temperature falls, and sooner or later the
animal dies. Thus, the absolute lower critical temperature is also called the homeothermic cold
limit.

The intolerably cold zone lies

Duration of cold stress

The nature of an animal' s homeothermic response to cold also depends on how long the stress
has been endured. In general, early responses rely more on increasing heat production. These
means are gradually replaced by those that increase insulation as the cold stress lasts longer. This
is an energy-conservative plan, since less energy is usually required to increase and maintain
insulation than to support an increased metabolic rate. Teleologically, this plan is less hazardous
for the foraging wild animal; it is less expensive for the fed domestic animal. Of course, as an
animal's insulation changes, so do the limits of its thermoregulatory zones (Chapter 8). In
particular, as insulation increases, less expenditure of energy is required for homeothermic
balance at agiven ef-fective environmental temperature. There are examples of early and later
responses to cold stress via cover insulation (piloerection versus in-creased pelage insulation due
to reduced shedding), tissue insulation (peripheral vasoconstriction versus increased
subcutaneous fat deposition), and cold-induced heat pro-duction (shivering versus general
increase in metabolic rate). Two terms are sometimes used often loosely to describe cold stress.
"Acute" usually refers to cold stress of abrupt or recent onset, and sometimes to cold stress that

64

is SrVri r in relation to the animal's adapi al ion status. "chi °laic", on the other hand, is used in
conne( don with cold stress of slower or earlier (inset , and to cold stress that the animal can cope
with mote lh
hysical thermoregulation in the cool tone An animal attempts to conserve metabolic heat in the
cool zone of effective environmental temperature in two major ways: by physiologically and
anatomically increas-ing insulation and by behaviorally reducing effective body surface area or
seeking shelter. in addition, it may gradu-ally lower its set-point temperature so body
temperature-- and thus body-to-environment thermal gradient —is reduced.

Insulative responses

Cover insulation. Insulative effects of piloerection and feather-fluffing have been described earlier.
These are initial responses to cold stress. in cattle, as the duration of cold stress lengthens, pelage
depth usually increases, thus increasing cover insulation. This effect seems to be due to the
influence of cold stress. Photoperiod largely controls hair growth (Chapter 15), but cold stress
apparently dis-rupts the follicle cycle and reduces the rate at which hair is shed. Tissue insulation.
An early response to cold stress is peripheral vasoconstriction, which increases tissue in-sulation,
as discussed previously. However, tissue insula-tion is related biphasically with environmental
tempera-ture. It increases as temperature decreases to a certain point, beyond which the cold-
induced vasodilation de-scribed earlier commences. Cyclical, cold vasodilation acts to reduce
average tissue insulation over time. Hence, below the environmental temperature at which cold
vaso-dilation ensues, tissue insulation actually decreases as environmental temperature falls
(Table 6-1). Of course, periodic vasodilation prevents the tissues from freezing. In the longer run,
animals with unlimited access to feed might increase the thickness of the subcutaneous fat depot
to increase tissue insulation. However, this result has not been found to occur generally as the
animals' need for metabolizable energy is so high in these circumstances that an insufficient
amount is left for extra fat deposition.

Chemical thermoregulation in the cold zone

Animals can increase heat-production rate above the thermoneutral level in three ways: by
increasing volun-tary skeletal-muscular activity, involuntary skeletal-muscu-lar contraction, or
general metabolic rate. The latter two are

Table 6-I Tissue insulation in the young pig as a function of environmental temperature
environmental temperature (0C) 35 30 25 10

a5

Source: DA L. Ingram. 1964, Res. Vet, Sci. 5:357,

tissue insulation (C° m2 hr kcal-1)

.063 .085 .113 .107 .101

Environmental management in animal agriculture

major means of chemical-thermoregulatory reaction to cold stress.

Sequence of cold wind uced thermogenic responses Tbersnogenic muscle spasm. The early
response t cold stress is spastic, involuntary skeletal-muscle contra: tion. Therrnogenic muscle
spasm usually causes the animal to shake, and this movement. is called ashivering. Thermo.. genic
muscles pasm is a relatively inefficient means of pro_ clueing heat useful in warming the body.
First, not all of the muscular-contraction energy goes to heat; some goes to produce shivering
movements. Further, thermogenic mus. de spasm occurs in the body's shell, so. some of the heat
produced is lost directly through the skin to the environ. mcnt, without passing through and.
warming the core. Finally, shivering movement can disrupt the animal's boundary layer, and thus
reduce thermal insulation. Thermogenic muscle tonus. True shivering is gradually replaced during
prolonged cold stress by therrnoe genic muscle tonus, which is involuntary skeletal-muscle
contraction that does not cause body movement. It is more efficient than shivering to the extent
shivering movements decrease the efficiency of heat production and enhance heat loss. General
metabolic rate. gradually gives way in turn to increased metabolic rate throughout the body,
which is sometimes called cold-induced nonshivering thermogenesis or true chemical
thermogenesis. This ultimate heat-production reaction oc-curs in both food mammals and birds,
and it is most effi-cient. It represents a partial shift of the site of cold-induced heat production to
the core. Of course, since skeletal muscle and fat in the body shell amount to on the order of half
of the body's metabolic mass, much of the general increase in heat production also occurs in the
body shell. The magnitudes of cold-induced thermogenic reac-t ions will he discussed later. rig

Thermogenic muscle tonus

Acclimatization and acclimation to cold stress

Acclimatization to cold stress refers to adaptive re-sponses to cold, complex environments that
occur over weeks and months. There is some evidence that food mam-mals and birds do
acclimatize and acclimate to cold. For instance, chickens subjected to a 5°C environment for sup to
nine months showed a steady increase in heat-production rate. This might have been due simply
to increased feed-intake rate, instead of increased effectiveness of thermo-genic mechanisms as in
true acclimation. This seems to explain the observations in cattle and pigs, for example.

Thermal insulation

Cover insulation. Some food mammals acclimatize. to cold stress by increasing cover insulation. It
is increased in cattle and pigs after they endure cold stress for weeks or months. Sheep, on the
other hand, have no cold-induced increase in cover insulation during chronic cold exposure. Tissue
insulation. As mentioned earlier, there 15 little evidence for an increase in tissue insulation as the
period of cold stress increases, regardless of the quantity of feed available. It thus appears that
insulative accliniati

ie Lrat irttai Itio‘ Pro, Ito "'eat ron, Dire.

110, Cie Ore nee

-uus ate cal oc-ffi. d. tale of .se

Lc-

vie P

Control and integration of thermoregulatory processes

Table 6-2 Effective surface area of the piglet as a function of air and wall temperatures

air temperature wall temperature effective surface area (°C) (°C) (m2) 30 30 .114 30 20 .108 20 20
.101 20 10 .095

Source: L. E Mount. 1964. J. Physiol. 173:96.

nation is limited to increased cover insulation, and this only in some species.

Effective surface area

Postural change is an important homeothermic reaction as it alters effective body-surface area.

When ef-fective environmental temperature falls, an animal ordi-narily reduces its effective
surface area (Table 6-2). This reaction also occurs as animals respond to increasing air speed in a
cool or cold environment (Table 6-3). When an animal is forced to lie on a cool floor, it may alter
its lying posture, and inc sodoing reduce its area of contact with the floor by about two-thirds
(Table 6-4).

Heat production

Table 6-4 Effect of lying posture on floor-contact area in 70-kg pigs

lying posture

flat on one side two legs under belly three legs under belly four legs under belly

65

floor-contact area (m2)

.22 .17 .14 .09

Source: F. J. Grommers et al. 1970. J. Anim. Sci. 31:1232. Metabolic changes. It has been suggested
that, during prolonged cold stress and after the general increase in metabolic rate has occurred,
the body burns one kind of substrate—for example, fats or proteins —preferentially and that this
is of adaptive significance. It now seems that during chronic cold stress animals burn
carbohydrates, fats, and proteins in the approximate proportions in which they occur in the diet,
after accounting for variable body deposition and use in product synthesis. There does appear to
be an increase in transaminase activity in the liver as cold stress progresses. This presum-ably
increases the potential rate at which certain amino acids could be burned. Of course, as feed
intake increases in reaction to cold stress, so does amino-acid intake, so the animal presumably
would have more amino acids left to catabolize. Results of studies of metabolism of acutely cold-
stressed steers suggests that both glucose and volatile fatty acids are catabolized during shivering
thermogenesis.

Cold habituation. Upon sudden subjection to a relatively severe cold stress, animals that have
been ex-periencing a milder cold stress for a long period sometimes delay for several hours their
thermogenic reaction to the acute stress, and their body temperature may actually fall for awhile.
This cold habituation is useful in that it permits the animals to withstand acute cold stresses of
short dura-tion—as often occur in nature (for example, each night) —without unnecessarily raising
metabolic rate. In this way they conserve feed energy. If the stress persists for longer than a few
hours, heat production rises to effect heat bal-ance at normal body temperature. Hormonal
changes and influences. The secretion rates of the various therrnogenic hormones—thyroid hors
more, glucocorticoids, catecholamines, and growth horw !none- are increased in response to cold
stress in food mammals and birds. However, there is as yet incomplete knowledge of their
participation in cold acclimatization. To be sure, they are associated with time changes in meta-
bolic response to cold stress, but they might not be the causes of these chanages.

Table 6-3 Effective zone*

surface area of the piglet as a

air speed (cm sect 1) 34 82 158

function of air speed in the cold

ratio of effective surface area to total surface area

.75 , 54. AS .41

*The environmental temperature at which these observations were made was 20t, well below the
min's lower critical temperature of around 34 C Therefore. the postural response changed even in
the cold zone, Source K Mourn 1966, matt., Exp„ Physiol, 51,18.

Integrated reactions to heat

The various thermoregulatory processes the homeo-thermic animal uses to combat heat stress
have been de-scribed already. The nature of the stress and of the ani-mal ' s adaptive status
determine the character of the par-ticular combination of reactions an animal calls into play in a
given instance of heat exposure.

Degrees of heat stress

Heat stress can be quantified in terms of its intensity and duration.

Intensity: thermoregulatory zones in heat stress When effective environmental temperature

becomes so high the animal must invoke one or more thermoregula-tory processes in order to
maintain homeothermy, the ani-mal is said to be undergoing heat stress. Just as there are
different intensities of cold stress, there are also different intensities of heat stress(Figure 6-2).
Thermal-comfort zone. The thermal-comfort zone was described earlier. The animal is under
neither heat stress nor cold stress when its effective environmental tem-perature is within these
relatively narrow limits. Metabolic rate is minimal and the animal needs to use neither heat-
dissipating nor -conserving mechanisms in the thermal-comfort zone. Warm zone. As effective
environmental tempera cure rises above the upper limit of the thermal.cornfort zone, the animal
is in the warm zone, where thermoregulaw tory reactions are limited to more woraless passive
facilitation

66

heat-production rate
thermoneutral

thermal-comfort zone

reduced —*- activity

IV V • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • * • • • • • • •
• • 4 • • • • • • • • • • • • • • • • • • •• • • • • • • • • • • • • • • • • • • • • • • •• • • • • • • • •
•• • • • • • • • • • • • • • • • • • • • • • • • • • • • IP • • • • • • • • • • • • • S • • • • 44 • • • • • •
• • • • • • • • • • • • • • • • • • • • • • • • • • • • I • • • • • ID • • S • ▪ • • • • • • • • • • • • • • •
•••••••••••••••••••••••••••••••••••••••••••••••••

heat death ■A„

upper critical temp

- j'I •

warm

zone

hot

zone

intolerably hot zone

moderate effective environmental temperature Figure 6-2. Relation between heat-production rate
and higher environ-mental temperatures. of heat loss. Decreasing tissue insulation by vasodilation
and increasing effective surface area by changing posture are the major adaptates. Birds also
move their wings away from their bodies to increase exposure of trunk skin to the environment
and dust themselves with cool litter. The mag-nitudes of these reactions increase as effective
environ-mental temperature increases in the warm zone. Tissue-insulation reduction is maximal at
the upper limit of the warm zone. These reactions require relatively little expenditure of energy.
Therefore, metabolic rate is practically at the minimal level throughout the warm zone of effective
envi-ronmental temperature. Hot zone. As effective environmental temperature continues to rise,
the homeothermic animal must call into play the active heat-dissipating mechanisms —sweating
and panting. As already mentioned, in sweating animals, sweating ordinarily commences at a
lower effective environ-mental temperature than does panting. Additional behav-ioral reactions to
heat stress are invoked in the hot zone. The active heat-dissipation processes require the
expenditure of considerable amounts of energy, hence in the hot zone the animal's heat-
production rate rises above the minimal level. This heat adds to the animal's metabolic heat load,
thus compounding the stress. As this happens, the animal sometimes adjusts its set-point
temperature upward so body temperature increases above normal. The animal technically
remains homeothermic, because it is still controlling body temperature, albeit at a higher level.
There is a point in the upper part of the hot zone where an animal may voluntarily reduce bodily
activity to a minimum, presumably in an attempt to reduce heat pro-duction. There is a narrow
region of effective environmental temperature just below the upper limit of the hot zone where
heat-production rate plateaus or even drops slightly as a result of this behavior. As effective
environmental temperature continues to rise, the point is finally reached where heat balance can
be maintained only when all of the animal's therm.oregulatory processes operate at maximal
effectiveness. Thispoint is called the upper critical temperature. Intolerably hot zone. Above the
hot zone lies the intolerably hot zone. When effective environmental tern-

high

I 4,

Environmental management in animal agri cuittoe

Box 6-D

Heat-tolerance indices

Because of the huge need in warm climatic regions of the world for human food of animal origin,
means of increasing animal productivity as rapidly as possible in those areas are being sought
intensely. One potential tool with which to hasten genetic improvement of ani-mals in the tropics
and subtropics would be some index of heat tolerance that accurately predicted an individ-ual's
subsequent performance in a hot environment. Even more useful would be a test performed on
males which would predict the tolerance of their respective offspring. Robert McDowell analyzed
many approaches to the evaluation of heat adaptability of cattle (Improvement of Livestock
Production in Warm Climates, Chapter 5, W. H. Freeman and Co., San Francisco, 1972). These
included a dozen field and laboratory tests which yielded various heat-tolerance indices, ranging
from A. 0. Rhoad's Iberia heat-tolerance test, through J. C. Bonsma 's hair-coat felting test and the
exercise and cooling efficiency test of D. F. Dowling, to M. S. Barrada 's line of equal effect.

McDowell pointed out the strengths and weaknesses of each method of assessment, concluding:
"In all the field and laboratory tests there were occasional cross-bred animals which showed a low
level of response and had a high milk yield. The same was true in the pure European breeds. It
appears that although, on the aver-age, the responses of the Zebu (Brahman and Red Sindhi)
crosses to the direct effects of high ambient temperatures were less the in for pure European
breeds, the degree of reaction in high yielding cows depended more on the individual than on the
breed group with the frequency for a combination of high heat tolerance and productivity not
being markedly improved by adding Zebu genes. The indices described are at best rather
nonspecific; they indicate primarily an animal 's lack of ability to maintain thermal balance or a
normal state of homeostasis, or characterize the general adjustments (e. g., short hair coat) the
animal has made to the total environment. "

perature rises above the upper critical temperature, the ani-mal can no longer control its body
temperature; the envi-ronment limits the ability of the maximally responding ani-mal to balance
its heat loss against internal and external heat loads. In the intolerably hot zone, body
temperature begins to rise uncontrollably. An increase in body temperature causes, due to the van
' t Hoff effect, an increase in meta-bolic rate, which causes an increase in heat-production rate,
which in turn results in a further increase in body tempera-ture, and so on. This positive-feedback
sequence is called spiralling hyperthermy. The upper lethal body temperature is reached quickly
when an animal exists in the intolerably hot zone.

Cont

ill a ho rei ac

Control and integration of thermoregulatory processes

Duration of heat stress

An animal ' s initial response to heat stress consists mainly of facilitating heat loss. As the stress
continues, however, the animal tends to rely progressively more on reducing metabolic heat load.
Other changes during heat acclimation and acclimatization will be discussed later.

Digression and further remarks

Environmental and skin temperatures Skin temperature is the major input in homeo-thermic
control loops concerned with reactions to heat stress, at least in mammals. It reflects the heat
content of the skin, which is determined by the rates at) which heat reaches and leaves this
structure. The relation between environmental temperature and skin temperature in cattle,
sheep, and pigs, respectively, is shown in Figure 6-3. Of course, the temperature of the pelage tips
even more closely resembles environmental temperature (Figure 6-4). The difference between
skin and pelage-tip tempera-ture becomes smaller as environmental temperature rises. In fact,
reversal can occur, and pelage-tip tempera-ture may exceed skin temperature in very hot
situations.

Sweating and panting

Thermal sweating. Data in Table 6-5 reiterate the species differences in maximal rate of thermal
sweating. These result in differences in the severity of deleterious side effects of sweating, which
would be gravest in cattle, of course. The threshold skin temperature for vasodilation in sheep is
around 34°C, while that for thermal sweating is around 32°C in European-type cattle and around
34°C in zebu cattle. Thermal panting. Respiration rate is also related to effective environmental
temperature. In general, respira-tion rate remains at a minimal level until some threshold
temperature is reached. The skin-temperature threshold for initiation of thermal panting in Bos
taurus and in sheep is around 36°C. The stimulus for second-phase breathing seems to be a
hypothalamic temperature over 40.5°C in both species. Pigs begin to pant in response to heat
stress when skin temperature rises above 35°C. In birds, on the other hand, core temperature,
rather than skin temperature,

trunk-skin temperature (0C)

40

38

36

34

32

30

28 •
26

24

••

••

MEMO MIND INIIMID •

• • • • • • 1 I t t I I I I I I II 1 I 2

=10

0 10 20 30 40 environmental temperature (0C)

67

dairy cows, RH 65% (Thompson et al., 1952) calves, .017 gm 1- 'humidity (Beakley and Findlay,
1954) pigs (Ingram, 1964) sheep, 5- to 10-cm fleece (Eyal, 1963) chickens (Wilson and Plaister,
1951) Figure 6-3. Relation between skin and environmental temperatures.

Table 6-5 Maximal rate of water evaporation during heat stress from skin of food mammals and
birds

species

maximal rate of water evaporation (gm hr 1m-2)

passive diffusion sweating total

active

European-type cattle zebu-type cattle sheep pig chicken

30 30 30 30 30
300 300 30

00

330 330 60 30 30

Sources: T. E. Allen. 1962. Aust. J. Agr. Res. 13:165. R. E. McDowell et al. 1961. J. Anim. Sci. 20:380.
A. H. Brook and B. F. Short. 1960. Aust. J. Agr. Res. 1L557. D. Engram. 1967. J. Comp. Path. 77:93.
M. VanKampen. Int. J. Biometeorol. 15:244.

surface temperature (°C)

40

35

25

15

10

-10

animal surface

0 10 20 30 40 environmental temperature (°C)

trunk skin

pelage tips

N ■ dairy cows (Thompson et al., 1952)

•11111111111111.

j 1 I I 1 I 1 It 1 I I I I

sheep (Eyal, 1963)

Figure 6-4. Relations among skin, pelage-tip, and environmental tem-peratures.

70

just as well be that these hormonal changes are secondary to or actually caused by primary
metabolic changes induced in some other way.

Energy cost of heat-stress responses Thermoregulatory reactions against heat stress re-quire the
expenditure of energy. Therefore, they increase an animal 's metabolic rate. Vasodilation and the
concomi-tant increase in blood flow apparently have negligible influ-ence on heat-production rate.
Sweating results in about a 10-percent increase. As for panting, in cattle, the initial re-action has a
low energy cost, but maximal thermal polypnea requires about 10 percent of a bovid' s total
energy expendi-ture, while maximal thermal hyperpnea accounts for up to 25 percent. In swine,
maximal thermal panting costs around 15 percent of total heat production. Hence, the ser-ies of
thermoregulatory mechanisms invoked in reaction to heat stress are increasingly costly in terms of
the internal heat load generated.

Heat death

Extremely hot environments can be lethal. The ulti-mate cause of death in an extremely hot
environment is the animal's inability to rid itself of metabolic and gained heat, with the
consequent rise in body heat content and tempera-ture. The usual immediate cause of death is
tissue hypoxia, although blood oxygen level is not decreased. At any rate, there appears to be a
shift from aerobic metabolism to anaerobic as heat death is approached. Upper lethal body
temperature is about 3 C° higher than normal body temperature. Hence, that of poultry is about
45°C, while that of cattle, sheep, and pigs is about 42°C. The threshold of lethally hot conditions is
deter-mined by many factors in addition to effective environmen-tal temperature. These include
species, age, body weight, reproductive status, level of performance, level of feed in-take, the
thermal-environmental conditions to which the animal is accustomed, the rate of increase in
environ-mental temperature, and the period of exposure to severe heat. The occurrence on
several days in succession of high maximal temperatures and narrow daily temperature cycles in
effect lengthens the exposure period. Abrupt in-creases in average daily temperature — as when
animals are moved from one shelter to a less protective facility during hot weather—increase the
chances of heat death. Heat death occurs more frequently in poultry than in livestock, but it does
occur in the mammals, as well. Broiler chickens fed high-energy diets are especially susceptible to
heat prostration and death.

Environmental management in animal agriculture responses by the animal. As the stress becomes
chronic changes occur in the animal's strains. Body temperatur ' e which may have been
elevated, tends to become normal, as do respiratory and heart rates. These changes are due pan.
ly to a compensatory decrease in food intake (and thus a decrease in heat-production rate), as
well as reduced thy. road activity and, sometimes, reduced cover insulation. These adaptates are
observed during an animal's seasonal acclimatization to heat, and are further substanti. ated by
the fact that rectal-temperature rise incattle during a standard acute heat-exposure test is less in
summer than in winter. Acclimation to either dry or humid heat has been observed in calves.
Reduction in metabolic rate is thought to be the major factor in this adjustment. Also, chickens
exposed to a 37°C environment four hours a day, six days a week, fOr four weeks, had
progressively lower rectal tern_ peratures during the daily heat-stress period. The chickens
became more heat-tolerant during the four-week acclima_ tion period. The acclimation was
apparently not due to increased respiratory-evaporative loss. It might have owed to several
factors, including decreased metabolic rate, decreased activity, decreased respiratory work,
improved circulatory convection, and postural adjustments. Acclima-tization of chickens to
seasonal environmental-temperature differences has also been found, and this is perhaps due to a
seasonal cycle in metabolic rate.

Concluding remarks

Acclimatization and acclimation to heat stress Acclimatization or acclimation to heat stress occurs
when an animal, in response to repeated or continuous ex-posure to an environment hotter than
formerly experienced, develops functional, structural, and behavioral traits that increase its ability
to live in a hot environment without distress. Acute heat stress elicits certain thermoregulatory

Animal sensitivity to hot surroundings

Effects of warm or hot environments on animals is greater than those of cool or cold ones. In the
first place, animals cannot survive for long periods effective environ-mental temperatures 5 C ° or
more higher than normal body temperature, but they can survive a long while at 20° to 60 C°
below normal.' Second, upper lethal body temperature is but a few degrees above normal body
temperature, whereas lower lethal body temperature is 20 C° or more below normal. It suffices to
say simply that animals can thermoregulate more effectively in cold environments than in hot
ones.

Diurnal temperature variation in hot environments

In most natural environments, diurnal variation in effective thermal environment is such that
maximal heat stress occurs for a relatively short period each day several hours at midday or
shortly thereafter. In Most cases, animals then have an opportunity to compensate for this
maximal stressful period by losing heat to relatively cool surroundings at night. This point must be
appreciated when assessing the heat stress caused by a given hot natural environment. Of course,
animals kept in a closed shelter usually experience less daily temperature variation than do those
in natural habitats. Shelters buffer the anle mil's effective microenvironment so that in summer,
for example, heat is kept in the building once it is inside, Just as it is prevented from escaping
rapidly to the macro-environment during cold weather.