Endocrine and thermoregulatory responses to acute thermal exposures in 6-month-old pigs reared in different neonatal environments

J

PII: SO306-4565(96)0003f%S

rkwn.

Biol. Vol. 22. No. 2. pp. 87-93. 1997 c 1997 Elsevier Science Ltd All rights reserved. Printed in Great Britain 0306-4565197 $17.00 + 0.00

ENDOCRINE AND THERMOREGULATORY RESPONSES TO ACUTE THERMAL EXPOSURES IN 6-MONTH-OLD PIGS REARED IN DIFFERENT NEONATAL ENVIRONMENTS* B. ANN

BECKER,‘?

JOHN

MARK

J. KLIR,’

ROBERT

L. MATTERI,’

and MICHAEL

ELLERSIEK’

DONALD

E. SPIERS,’

L. MISFELDT’

of Animal ‘Animal Physiology Unit, USDA, Agricultural Research Service. ‘Department ‘Department of Molecular Microbiology and Immunology, School of Medicine, University Columbia, MO 65211, U.S.A.

(Receiwd

27 October 1995; accepted

in rerised,fbmr

23 Noremher

Sciences and of Missouri,

1996)

Abstract-l. Endocrine and thermoregulatory responses to acute heat (34’C) and cold (10°C) exposures were determined in eight pigs at 6 months of age. Half of the pigs had been reared in a cycling upper thermal environment (27-32-C) for the first 28 days of life, while the others had been reared in a lower thermal environment (21 C). 2. Concentrations of cortisol increased significantly during both acute heat and cold thermal exposures (P = 0.0001) although the response was greater in the heat than in the cold (P = 0.003). A prolactin response occurred during acute heat exposure (P = 0.004). Growth hormone secretion increased during acute cold exposure (P = 0.001). There was a strong tendency for increased epinephrine secretion during both acute heat and cold exposures (P = 0.06). No significant effects of either exposure were found on plasma norepinephrine (P = 0.9). or triiodothyronine (P = 0.11). 3. Neonatal environment did not affect daily core body temperature (T,) before acute heat or cold exposures, but did alter amplitude of the 24-h T, cycle. The amplitude was significantly greater in animals reared in the lower thermal environment (P < 0.001). 4. Acute heat exposure resulted in significant increases in T, (P < 0.001) and heat production (P < 0.01). Neonatal thermal environment had no significant effect on T, and heat production responses to acute heat and cold thermal exposures. 0 1997 Elsevier Science Ltd

Key Word Index: Neonatal

environment;

thermal

stress; hormones;

which

INTRODUCTION

exert

thermoregulation;

biological

thermoregulation Numerous

studies

have

stressors

during

response

to those stressors

and Maslova, GonzPlez

the

shown

neonatal

that period

(Ader,

1985; Hamamura

et al., 1990; Milenkovic

1990; Meaney

exposure alters

to

Faichney

adult

1970; Naumenko and Onaka,

1989;

and Martinovic,

et al., 1991; FernBndez-Teruel

variety

of hormones

sequent

physiological

Meyerson Moldow

et al.,

information

whether

temperatures

were handling

thermoregulatory alterations of

were characterized hormones

such

stressors,

by behavior as cortisol

and

and responses

and stress-sensitive prolactin

and

that

during

may

1986). Neonatal can

influence

Joksimovic,

function

exposure a critical

1991;

exposure

to a

alter

sub-

permanently (Chowen

et al., 1991; Zadina and et al., 1981). However,

1993). In many of these studies the selected stressors and restraint

effects

(Tomic

and Barry,

swine

et al., 1996; Kastin, 1986; there is no

to different neonatal

ambient period

of

development results in long-term endocrine and thermoregulatory

responses to acute thermal exposures. The thermoregulatory system of the pig is not

(PRL),

completely

*Mention of a trade name, proprietary product or vendor does not constitute a guarantee or warranty of the product by USDA or imply its approval to the exclusion

mature

at birth.

In swine

production

systems supplemental heat is provided for piglets, which at birth have a narrow thermoneutral zone of 3&34”C (Simmons, 1976; Holmes and Close, 1977).

of other products or vendors that may also be suitable. tTo whom correspondence should be addressed. 87

88

B. Ann Becker CI trl

The zone shifts to 25530’ C by weaning (334 weeks of

acute

For

thermal

exposures,

age) (Simmons, 1976). Young pigs (i.e. 2+ weeks of age) maintained for 3-6 weeks in a cold (IO<(Z)

were placed

in calorimetry

boxes

(see below)

maintained

at

environment

environmental

chambers.

than those reared at thermoneutrality (23 ‘C) (Herpin et al., 1987) or in warm (35°C) environments (Heath

the calorimetry

boxes before the experiment

and

response.

have a higher metabolic

Ingram,

exhibit

1981). Cold-reared

higher intensity

(NE) responsiveness. skin temperature

rate, in general.

(10°C)

of shivering,

pigs

also

than warm-reared

controls

and

(Heath

and Ingram, 1983). In addition, young pigs reared at an ambient temperature closer to thermoneutrality exhibit

a greater

magnitude

body temperature the

exposure

(Ingram

and

Mount,

earlier results

suggest

the early thermal

thermal

than

1965; Ingram,

the possibility

1977). These

can produce yet

no

of lasting

Accordingly,

was designed to determine relevant hormone responses thermal exposures

effects

in

Research

venipuncture

exposure. Samples were centrifuged and the plasma was harvested and frozen until further analysis. Peripheral

blood

triiodothyronine

concentrations (T,)

immunoassay

were

(RIA)

kits (Diagnostic

using

Products

CA). Concentrations determined

of

cortisol

determined

by

commercially

Corporation,

of epinephrine

using a commercially

and radio-

available

Los Angeles,

(E) and NE were

available extraction

MA). Briefly, the catecholamines

of early

the present

study

pigs that had been during the

eluted

with

analyzed

a diluted

by high

at a pH of 8.6, then

extraction

performance

acid,

and

liquid

finally

chromatog-

raphy with an electrochemical detector (ESA. Bedford, MA). Concentrations of PRL and growth hormone

(GH)

previously

described

were

determined

(Matteri

telemetric Mini-Mitter

by

RIA

as

cr al., 1994).

temperature

transmitters

Co., Inc., Sunriver,

OR) for

measurement of core body temperature (T,) were sterilized and implanted into the peritoneal cavity of

of age and averaging Brody Climatology Research (Animal

University

of the boxes in the stress

onto alumina

AND METHODS

Center,

to

to avoid

kit (ESA, Bedford,

I26 kg, were used in this study. All thermal exposures

Sciences

the

Pigs were conditioned

just prior to and at the end of each acute thermal

Calibrated

were conducted in the Samuel Laboratory for Environmental

and

in

the novelty and confinement

(VHF-T-l,

Eight adult pigs, ca 6 months

temperature

were first absorbed

period. MATERIALS

desired

have

body temperature and to acute hot and cold

in 6-months-old

the

pigs

shifts in

studies

reared in either a cool or hot environment neonatal

animals

that even small differences

ability,

environment.

in

at the end of

warm-reared

environment

thermoregulatory examined

and rate of increase

when heat challenged period

exposure.

Blood samples were taken by jugular

norepinephrine

tissue thermal conductance,

heat

of Missouri).

each

animal

through

a ventral

midline

incision.

Signals from each transmitter intervals (Telonics Receiver,

were received at IO-min Mini-Mitter Co.. Inc.,

Sunriver,

by an automated

data

5.0, Mini-Mitter,

Co.,

OR) and recorded

acquisition

system

(Datacol

Half of the pigs had been reared in a constant lower thermal environment (21 C) during the first 28 days

Inc., Sunriver, OR). Rectal temperature (Tee) was also measured at selected times using a thermistor probe

of life, while the others had been reared in a cycling

attached to a recorder (Digital Thermometer, Scientific, St Louis, MO).

upper

thermal

environment

(temperature

started

to

rise at 0600 h to reach 32 C at ca 1400 h, and started

Pigs were placed in calorimetry

to fall at 1800 h to reach 27 C at ca 0000 h). After the

to the environmental

early neonatal treatment period, pigs were housed individually in a controlled environment of 21 C

estimate

(thermoneutral

The

for mature

pigs) and

provided

ad

heat

ditioned

conditions

production.

to the calorimeters

system

was designed

boxes equilibrated of the chamber

All animals

described

acute thermal testing. temperature transmitters were surgically inserted into the peritoneal cavity (see

trations of oxygen (O?) (Servomex-Oxygen Model 54OA-Sybron, Taylor Instruments,

below). During testing, each animal was exposed to either acute heat (34 C) for 3 h or acute cold (10°C) for 4 h. Exposures were I week apart. The order of

ough,

exposure neonatal

was such that half of the animals from each group were first exposed to acute heat

followed by the acute cold exposure, and the other half was first exposed to acute cold followed by the

previously

Sussex,

U.K.)

were

to con-

prior to the experiment, for pigs and

libitunz access to a standard corn-soybean meal ration and water. The light:dark cycle was l4:lO throughout the whole study. Three weeks before

previously described analysis and data

Fisher

has been

(Becker et al., 1993). Gas acquisition have also been (Manalu

and

et al., 1991). Concen-

carbon

Analyzer, Crowbor-

dioxide

(COZ)

(Anarad Model AR 60, Anarad, Santa Barbara, CA) were measured simultaneously and heat production was estimated using an equation adapted from Kibler (1960) as modified for computer applications by Baeta (1985). Air temperature within each calorimeter was monitored

continuously

using thermocouples

Endocrine Table

I. Concentrations

and thermoregulatory

responses

in 6-month-old

pigs

89

blood hormones from pigs before and after acute cold (10 C) and hot (34°C)

of peripheral

exposures*

Acute cold (10°C) Neonatal environment Cortisol (ng/ml) T? (ngiml) Prolactin @g/ml) GH

Before

21°C 27-32’C 21 ‘C 27-32 ‘C 21 c 27-32 ‘C 21 c 27-32’ C 21 c 27-32’~C 21°C 27-32°C

Wml) Epinephrine (pg/ml) Norepinephrine (pgiml)

42.8 37.6 0.45 0.40 2.3 2.1 0.8 0.9 384 325 1474 1666

+ 6.3 k 8.2 a 0.09 * 0.03 If: 0.4 f 0.1 k 0. I + 0. I k I25 k 129 & 338 * 807

After

Before

70.0 * 5. I 64.3 k 8.9 0.47 + 0.06 0.48 * 0.04 I .8 + 0. I 2.5 + 0.5 I .4 L- 0.2t I .7 * 0.27 349 + 56 472 f I48 ll56+74 1855 * 274

51.5f 4.6

*Values are means + SEM; n = 4 ‘for each neonatal group. tsignilicant response to acute thermal exposure (P < 0.05). fResponse to acute heat greater than response to acute cold exposure

attached

to a datalogger

ger/Recorder, NY).

The

Sampling

production

occurred

was

exposure,

(Molytek

Partlow

measured

and

time of day. Average

3 h of acute heat exposure,

heat

thermoneutral and 4 h of acute

the General

Linear Models Procedure

Body temperature measures

data

analysis

using

of SAS (1988).

were analyzed

by repeated

RESULTS

responses are shown

of

exposure

cortisol

in

the

Concentrations exposure creased

to

acute

heat

and

I. Plasma

increased

with

than

of PRL

(P = 0.004).

cold

in Table

(P = O.OOOl), although

greater

T,

average

was 0.8”C

(39.8 f O.l”C)

for each animal

was analyzed

exposure

to determine

whether neonatal thermal treatments resulted in long-term shifts in 24-h rhythm. Temperature values to hourly values using an average

of the six IO-min values for each hour, followed

by

an average

to

across

a reliable

two consecutive

24-h periods

value for each hour of the 24-h

cycle.

Endocrine trations

temperature

for the identical

T, (40.5 f O.l’C)

prior to initial acute thermal

provide

Endocrinolog?

exposures

with T, transmission

were first reduced

of variance.

138.4 & 4.st $ 129.5 + 15.97 $ 0.33 * 0.02 0.41 f 0.05 7.2 &- 1.4t 6.3 _I l.8t 0.9 * 0.1 1.0 f 0.1 314 + 40 665 f 194 804k 116 1830 k 467

8.9 0.03 0.06 0.2 0.4 0.2 0.4 63 II0 I82 973

higher (P < 0.001) than under these conditions. Core

of variance

After

1.520-1620 h for 3 days at 21 ‘C

and compared

during

by analysis

between

DatalogHartford,

continuously

heat (34°C)

(P < 0.05).

New

cold exposure. Data were analyzed

64.4 k 0.37 f 0.46 + 2.4 f 2.7 * I .o * I .3 * I85 + 338& 778 + 3161 +

Portable

Corp.,

calculated

Acute

the

during cold exposure

GH

either

acute

the response cold

increased and

heat

concenwas

(P = 0.003).

with acute

heat

concentrations

in-

(P = 0.001). There was

A comparison of the two acute exposure showed no hourly difference routine groups (P > 0.05) in T,. Likewise, there were no significant hourly treatment

differences

daily change

between

neonatal

the amplitude

in T, was only O.S”C in animals

41.5 27.32wTa E

(P > 0.05)

groups (Fig. I). However,

PoCTa

of

reared

A .

.

a strong tendency for increased E secretion during both acute heat and cold exposures (P = 0.06). No significant

effects

of

either

acute

cold

or

exposure were found on plasma concentrations (P = 0.9), or TJ (P = 0.1 I). No significant

heat of NE effect

(P > 0.05) of neonatal thermal environment was found on any of the endocrine responses to the acute thermal

exposures

at 6 months

of age.

~.O’,‘..,‘..,“‘,...,.‘.,‘.‘l 4 8 0 Time

I.2

16

20

24

(Hour of day)

Thermoregzflation

The initial comparison a reasonable

analysis

temperature

was a

of 7’, and T, values to determine

if T,, is

estimate

of body

of T,. Rectal temperature

was

Fig. I, Normal core body temperature of pigs presknted as a function of time of day. Solid line shows the average for all animals. Vertical lines on the last points represent + SEM for all points in the figure

B. Ann Becker CI or/

90

heat exposure

produced

T,

across

response

no differences neonatal

(P > 0.05) in

treatment

groups

(Fig. 2). The acute cold exposure change produce

resulted

in no significant

(P > 0.05) in A, over time (Fig. 3) but did a 0.5 C decrease

exposure.

There

treatment

were

over the entire

no differences

group responses

240-min

in neonatal

to the acute cold exposure

(P > 0.05). The changes in body temperatures heat

exposure

were

associated

during the acute with

increase

(P < 0.01) in heat production

contrast,

heat production environment

(Table 2). In

did not significantly

in the cold. Heat production neonatal

a significant change

was not influenced

by

(P > 0.05).

DISCUSSION

L

IO

9

8

11

12

Time (Hour of day)

endocrine

Fig. 2. Difference between pre-exposure and acute heat exposure core body temperatures (AT,) as a function of time of day (upper graph) for pigs reared at 27-32 C and 21 C. Solid line shows the average for all animals. Vertical dashed lines indicate beginning and end of thermal exposure. Vertical solid lines on the last points represent k SEM. Mean ambient temperature during heat exposure is shown on the lower graph

at 27-32C

compared

to 0.8 C for animals

An animal’s stressor

ability to cope with an acute thermal

involves and

1968). Potential the animal’s Mount,

complex

interactions

prior

exposure

1965; Daniel&Severs

1974; Ingram.

interactions

thermoregulatory

systems

between (Mount,

on

may occur depending to stress

(Ingram

and

rf al., 1973; Heidmaier,

1977; De Souza and Van Loon.

1982;

from the

21 C group (P < 0.001). An analysis of daily change in T, was performed by averaging the pre-exposure values

for the eight

temperature 40.3“C

decreased

animals from

(Fig.

I). Core

40.5”C

at 0600 h (P i 0.05) with

body

at 0100 h to

nadir

(40.3’ C). At 1200 h, T, was not significantly

at 0900 h different

(P > 0.05) from the 0100 h level. A rapid increase in T, occurred after 1800 h and (40.9 ‘C), which was significantly than the 0100 h reading. All acute thermal exposure using lo-min interval values duration between identical

peaked higher

at 2100 h (P < 0.05)

data were analyzed collected over the

of each test. In addition, the differences exposure and pre-exposure T, values for times of day (i.e. AT, were used for all

analyses to eliminate any effect due to normal daily change in T,. An increase in AT, occurred over the first 30 min prior to each acute thermal exposure (Figs 2 and 3). possibly due to animal activity and body heat generated during movement to the calorimeters. Exposure to acute heat (34 ‘C) resulted in a 0.5’C increase (P < 0.05) at 30 min and a 2.l”C increment at 160 min (P < 0.001). The overall rate of increase was O.l’C/lO min (P < 0.001). The acute

a

9

10

11

lz

13

Time (Hour of day) Fig. 3. Difference between pre-exposure and acute cold exposure core body temperatures (AT,) as a function of time of day (upper graph) for pigs reared at 27-32’C and 21’s. Solid line shows the average for all animals. Vertical dashed lines indicate beginning and end of thermal exposure. Vertical lines on the last points represent _+ SEM. Mean ambient temperature during cold exposure is shown on the lower graph

Endocrine and thermoregulatory

responses in 6-month-old pigs

91

Table 2. Heat production in pigs in thermoneutral(21’ C), after acute cold (10°C) and hot (34’C) exposures* Acute thermal exposure

Neonatal constant low environment (2 I “C)

Neonatal cycling high environment (27-32°C)

7.4 L- 0.2t 6.3 + 0.77 II.3 f l.O$

7.4 * 0.3 7.0 f 0.5t II.0 f I.61

21 c IO’C 34’c

*Values are means + SEM; n = 4 for each neonatal group. t fNumbers with different superscripts are different (P < 0.01).

Macari et al., 1983; Herpin et al., 1987; Akana et aI.,

a/., 1994; Matteri

1992; Walker

and Dallman,

early neonatal

concentrations

of cortisol

1993). Using peripheral as an indicator

of acute

GH secretion

stress in pigs (Becker et al., 1985), the acute heat and

cold,

cold thermal

secretion.

defined

as stressors

intensity.

imposed

present

study

in this study can be

with quantifiable

The neonatal

significant tory

exposures

have repeatedly of neonatal

and

used in the

been shown

effects on the endocrine

systems

duration

thermal conditions

to have

and

Becker,

1993a. b; Matteri et al., 1994; Matteri and Becker, 1994, 1996). Although the amphtude of the 24-h T, cycle

was

infhrenced

environment,

long-term

thermoregulatory posures

by

early

neonatal

alterations

responses

thermal

in endocrine

to acute

and

thermal

ex-

The effects

of thermal PRL,

environment

on cortisol,

and GH secretion

heat,

our

observation.

In GH

1983; Goya

exposure

knowledge, most

et al.,

a pronounced

while lowering

ingestion

lowered

have been

27-32°C

in

among

acute increase

1983). Similarly,

observed

in the present

in GH by ice (Weeke

the NE response

elevates

produced

study

study. The thermal

rapid than those observed

at

cold

differences

challenges

serum GH concentrations

shown

pigs

to

Gundersen,

of body temperature

used in that

rearing

and

unique

factors in determining the GH subjects, intense heat exposure

secretion,

and Gundersen,

GH

is an

exposure

(Weeke

1995). Perhaps

studies are important response. In human (40°C) induced

increased

this

cases,

secretion

well-documented in pigs (Klemcke ef al., 1987; Kraeling et a/., 1987; Matteri et al., 1994). We have that

adult acute

to

severe acute thermal challenge which occurred in humans (Weeke and Gundersen, 1983) was not

were not detected.

catecholamines,

than

To

species and the degree of thermal

and thermoregula-

pigs (Spiers

1994). Consistently,

did not influence

in the present study. Interestingly,

rather

depresses

and Becker,

environment

changes

(Weeke

and

stressors

Gundersen,

1983)

in T, which were greater and more presently.

lactotroph secretory activity relative to that observed after rearing at 21°C. In each of these earlier studies,

Thermoregulatory responses of pigs to acute cold or heat exposures were not affected by early thermal

elevated

PRL secretion

in the amount The

present

pituitary

results

induced

early development

a lasting change

Depressed

that

thyrotroph

environment

in the present

for release.

shown

long-term

increase

ambient

of an increase

PRL available

indicate

PRL content

ment during confer

was reflective

of cellular

the

in

that

temperatures

study. Other studies have

exposure

of young

pigs to

above or below thermoneutral-

by a warm environ-

ity alters the response

apparently

and Ingram, 1983; Ingram and Mount, 1965; Ingram, 1977). Data from our laboratories are consistent with

in pituitary secretory

does not

function. ability

in piglets

to thermal

challenge

(Heath

these earlier studies (Spiers and Becker, 1993a, b). In

reared in a hot environment (Matteri and Becker, 1994) appears to be reversible, as there was no

the present study, there was a period of 5 months between termination of the neonatal treatment period

indication

and the acute thermal exposures.

of altered

thyroid

axis activity

between

neonatal treatment groups in the present study. Consistent with data obtained in humans (Weeke and Gundersen, alteration thermal

l983), we found in thyroid

exposure.

axis activity

However,

occur in the thyroid

no evidence

showed

function

Our results indicate

for a normalization

thermoregulatory responsiveness. The present study is the first to indicate of early

thermal

environment

on the

of

an impact 24-h

body

to acute thermal

temperature cycle. Neonatal exposure to 27-32°C reduced the amplitude of the 24-h body temperature

that rearing

cycle by almost half although long-term effects on absolute values of T, were not statistically detected.

elevated temperature (27-32°C) enhanced secretory ability in piglets, a similar somatotroph

the acute

species differences

axis response

stress (Goya er al., 1995). While our earlier studies

during

of a rapid

that such a delay is sufficient

was not observed

may

at

lactotroph effect on (Matteri

et

Mean core temperature

decreased

at 0100 h to a low

level at 060&1200 h and increased to a peak at 2100 h. Tympanic temperature for swine at ther-

B. Ann Becker or CI/

92

moneutrality

also reached a minimum

and peaked

around

midnight

(Hahn.

body

temperature

variation

in internal

correlated

with feeding

change

level at midday

in metabolic

activity

1989). Daily has

been

and a concomitant (Ingram

and

Legge. 1970: Van der Hel et ul., 1984; Nienaber

and

Hahn,

1991). In fact, removal

ad libirur?~ access 24-h cycle (Ingram

for

and

1985).

does

heat production

temperature Ingram

that

constant

T, rhythm,

the possibility

to selected

and

in pigs

access

but

acute

or the

Dauncey. to feed

we have

that feeding activity

be responsible for this cycle. In conclusion, endocrine and responses

activity

to obliterate

1973;

shown

eliminate

eliminated

body

internal Mount,

We have

not

of feeding

to feed is reported

not could

thermoregulatory

thermal

exposures

in

6-months-old

pigs were not affected by prior thermal

environment

in which the pigs were reared during the

neonatal change

period. However,

the amplitude

in T, was significantly

reared in the lower thermal Ackno,c/edgen2ents-The Paul Little and Peggy conducting this study.

greater

of the daily

in the animals

environment.

authors thank Kurt Holiman. Ann Eichen for their assistance in

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