Eur J Appl Physiol (2008) 104:491–499
DOI 10.1007/s00421-008-0798-3
O R I G I N A L A R T I CL E
EVect of body temperature on cold induced vasodilation
Andreas D. Flouris · David A. Westwood ·
Igor B. Mekjavic · Stephen S. Cheung
Accepted: 5 June 2008 / Published online: 21 June 2008
© Springer-Verlag 2008
Abstract Cold-induced vasodilation (CIVD) is an acute
increase in peripheral blood Xow observed during cold
exposures. It is hypothesized to protect against cold inju-
ries, yet despite continuous research it remains an unex-
plained phenomenon. Contrary to the traditionally held
view, we propose that CIVD is a thermoregulatory reXex
mechanism contributing to heat loss. Ten adults (4 females;
23.8 § 2.0 years) randomly underwent three 130-min expo-
sures to ¡20°C incorporating a 10-min moderate exercise
period at the 65th min, while wearing a liquid conditioning
garment (LCG) and military arctic clothing. In the pre-
warming condition, rectal temperature was increased by
0.5°C via the LCG before the cold exposure. In the warm-
ing condition, participants regulated the LCG throughout
the cold exposure to subjective comfort. In the control con-
dition, the LCG was worn but was not operated either
before or during the cold exposure. Results demonstrated
that the majority of CIVD occurred during the warming
condition when the thermometrically-estimated mean body
A. D. Flouris · D. A. Westwood · S. S. Cheung
School of Health and Human Performance,
Dalhousie University, Halifax, Canada
I. B. Mekjavic
Department of Automation, Biocybernetics and Robotics,
Institute Jozef Stefan, Ljubljana, Slovenia
S. S. Cheung
Department of Physical Education and Kinesiology,
Brock University, St Catharines, Canada
A. D. Flouris (&)
Institute of Human Performance and Rehabilitation,
Centre for Research and Technology-Thessaly,
32 Siggrou Street, Trikala 42100, Greece
e-mail: aXouris@cereteth.gr
temperature (Tb) was at its highest. A thermoregulatory pat-
tern was identiWed whereby CIVD occurred soon after Tb
increased past a threshold (»36.65°C in warming and pre-
warming; »36.4°C in control). When CIVD occurred, Tb
was reduced and CIVD ceased when Tb fell below the
threshold. These Wndings were independent of extremity
temperature since CIVD episodes occurred at a large range
of Wnger temperatures (7.2–33.5°C). These observations
were statistically conWrmed by auto-regressive integrated
moving average analysis (t = 9.602, P < 0.001). We con-
clude that CIVD is triggered by increased Tb supporting the
hypothesis that CIVD is a thermoregulatory mechanism
contributing to heat loss.
Keywords CIVD · Vasodilation · Vasoconstriction ·
Thermoregulation · Finger temperature
Introduction
Cold-induced vasodilation (CIVD) is a counterintuitive
acute increase in local cutaneous blood Xow that develops
during cold exposures resulting in increased local tissue
temperature which may protect the region from cold inju-
ries (Daanen and van der Struijs 2005). However, its
appearance has been described as non-systematic (Cheung
and Mekjavic 2007; Reynolds et al. 2007) and, therefore,
unexplainable.
The diYculty to hitherto elucidate the CIVD response
may be partly attributable to the currently incomplete
understanding of the physiology of the sympathetic vaso-
constrictor and vasodilator nerves that regulate cutaneous
circulation. CIVD is evident almost exclusively in areas of
glabrous skin (e.g., human palms and soles, Daanen 2003)
which are innervated solely by noradrenergic sympathetic
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vasoconstrictor nerves, compared to areas of nonglabrous
skin that are innervated by both branches of the sympa-
thetic nervous system (Charkoudian 2003; Kellogg 2006).
This distinction is fundamental to the present discussion
because arteriovenous anastomoses (AVA; thick-walled,
low-resistance blood vessels that allow high Xow rates
directly from arterioles to venules and play a major role in
CIVD, Daanen 2003) exist almost exclusively in glabrous
skin where they are innervated heavily and solely by sym-
pathetic vasoconstrictor nerves (Lossius et al. 1993). Con-
sequently, CIVD may be caused by inhibited (or decreased)
vasoconstriction rather than by active vasodilation. In addi-
tion, the synchronicity in the vasomotion of AVA carried in
the diVerent areas of the body (Lossius et al. 1993) and the
strong relationship of blood Xow Xuctuations through all
AVA with variations in heart rate and arterial blood pres-
sure (Lossius et al. 1994) suggest the involvement of supra-
spinal regions of the central nervous system in the control
of CIVD. Indeed, the notion of a central CIVD component
is supported in several experiments (Kunimoto 1987; Sen-
dowski et al. 1997, 2000; Werner 1977). These Wndings
provide support to the notion that thermal balance has a
strong impact on the CIVD reaction which seems to be
superimposed on the general vascular status of the periphe-
ral blood vessels.
With the assumption that survival of the whole organism
takes precedence over the survival of individual tissues in
the periphery, we propose that CIVD is but one aspect of a
co-ordinated thermoregulatory response to cold exposure
that is implemented via local and central mechanisms of
vasoconstrictor control, with the goal of regulating overall
thermal balance. According to our hypothesis, CIVD acts to
dissipate heat and thus lower mean body temperature (Tb)
when the latter is above ideal—a somewhat paradoxical
notion given that the observed phenomenon occurs in cold
environments. An increased Tb is not a rare event in
humans—even during cold exposures—since 70–100% of
the metabolic energy released for muscular work is con-
verted to heat (Flouris and Cheung 2006). In addition, heat
production is increased during cold exposure through
changes in metabolism (Haman et al. 2002) and shivering
thermogenesis (Eyolfson et al. 2001). Thus, when initially
exposed to cold, humans engage cutaneous vasoconstric-
tion to conserve heat. Increased heat production is then
adopted as a behavioral or reXexive chronic response that is
slower but more adaptive than peripheral vasoconstriction
(Caputa and Cabanac 1980; Wilson et al. 1991). Added to
cutaneous vasoconstriction, we propose that this increased
heat production may occasionally cause Tb to rise (over-
shoot) transiently above ideal, which causes CIVD to occur
in order to dissipate the excess heat. The notion that CIVD
pertains paradoxically to heat dissipation is supported in
several human (Daanen 2003; Daanen and Ducharme 1999;
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Eur J Appl Physiol (2008) 104:491–499
Daanen et al. 1997; Takano and Kotani 1989) and animal
(Grant and Bland 1931) investigations that reported higher
occurrence of the phenomenon at increased Tb. Yet these
experiments did not assess the link between CIVD and Tb in
real-time, but only through repeated-measures designs
incorporating conditions of hyper-, hypo-, and normo-ther-
mia. Therefore, the purpose of the present experiment was
to investigate the minute-by-minute association between
CIVD and Tb during a prolonged cold exposure.
Materials and methods
The experimental protocol conformed to the standards set
by the Declaration of Helsinki and was approved by the
appropriate ethical review board at Dalhousie University.
Volunteers were 10 healthy adults (males 6; females 4; 23.8
§ 2.0 years; height 1.8 § 0.1 m; weight 71.6 § 11.4 kg)
that had none or very limited previous experience with cold
exposure experiments. Female participants were tested dur-
ing the early follicular phase (days 1–6) of their cycle.
Written informed consent was obtained from all partici-
pants after full explanation of the procedures involved. Par-
ticipants were given a detailed verbal description of the
protocol, followed by extensive familiarization with all data
collection procedures and instruments during an initial
familiarization session performed at least 3 days prior to
testing. Anthropometrical measurements were also per-
formed at this time.
The study adopted a randomized crossover design with
participants visiting the laboratory on three diVerent occa-
sions to undergo a 130-min passive cold exposure. To test
the hypothesis that CIVD is related to Tb, we manipulated
body heat content passively (i.e., by applying heat to the
participants’ skin using a liquid conditioning garment sys-
tem, LCG (Flouris and Cheung 2006) either before or dur-
ing the cold exposure) and actively (i.e., through increased
endogenous heat release from exercise). In order to increase
the validity of our Wndings, we used a comparatively strict
(Purkayastha et al. 1992) CIVD deWnition of an uninter-
rupted sharp increase of ¸4°C in Wnger temperature (Tf).
Participants underwent the three 130-min cold exposures
in an environmentally controlled chamber while wearing a
LCG underneath arctic clothing. The 130-min duration was
selected in order to produce signiWcant changes in Tb and Tf
with no serious risk to the participants’ thermal integrity. In
the pre-warming condition, 50°C water was circulated in
the LCG prior to the cold exposure until core (i.e., rectal)
temperature was increased by 0.5°C, with no warming dur-
ing the exposure. In the warming condition, participants
regulated freely (increased or decreased) the LCG inlet water
temperature during cold exposure to subjective comfort,
with no warming prior to the cold exposure. In the control
Eur J Appl Physiol (2008) 104:491–499
condition, the LCG was worn but it was not operating
either before or during the cold exposure. All participants
underwent the three conditions in a random order through a
random allocation algorithm performed by SPSS statistical
package. Testing was conducted by the same investigators
between 0900 and 1400 h. Participants were extensively
familiarized with the LCG and the control of its inlet water
temperature during the familiarization session. They were
instructed to consume a light breakfast and adequate
amounts of water prior to arriving in the laboratory, having
abstained from alcohol and caVeine for 12 h. Ad libitum
water ingestion was permitted during data collection. Par-
ticipants were also advised to avoid physical activity and
excessive stressors such as exposure to extreme hot or cold
temperatures for 48 h prior to data collection and particu-
larly during the period between awakening and experimen-
tation and during transit from home to the laboratory.
Cold exposure and protective clothing
During cold exposure participants were seated at rest for 130
min, with a 10-min exercise period at half-time (i.e., 65–75
min), inside an environmentally controlled chamber (Convi-
ron GR96, Winnipeg, Canada) with air temperature main-
tained at ¡20°C (air velocity 0.05 m s¡1). Although the
typical procedure used to evoke CIVD in laboratory settings
is local cooling, it has been clearly demonstrated that CIVD
responses occur also during whole-body cold exposure (Sch-
winghamer and Adams 1969). Whole-body cooling was,
therefore, adopted in the current experiment because it pro-
vides a more realistic real-world scenario. In addition, the
cold stimulus to the hand was strong enough to evoke CIVD
given that Wnger skin temperature reached as low as 5°C in
certain subjects (see “Results” section). During their time
inside the chamber, participants wore—over top of the
LCG—commercially available clothing simulating all three
layers of the Improved Environmental Clothing System
Canadian Forces Arctic clothing ensemble (3.6 clo, 0.556 m2
K W¡1). The three-layer system included a Xeece garment
(Wrst layer), an uninsulated inner parka and pants (second
layer), and an insulated outer parka and pants (third layer). In
addition standard military mukluks, woollen socks, and a
balaclava were also worn, together with a thin pair of long,
cotton underwear worn under the Xeece pants [additional
overall clo value of 0.3 (0.05 m2 K W¡1)]. The hands were
insulated with thin gloves and Arctic mitts (1.2 clo, 0.185 m2
K W¡1). Therefore, only the areas around the eyes and the
mouth were directly exposed to the environment.
Liquid conditioning garment (LCG)
Participants wore a LCG (Med-Eng, Pembroke, ON, Canada)
consisting of 1/8⬙ diameter Tygon tubing sewn over a
493
close-Wtting stretchable hood (6.1 m of tubing), shirt cover-
ing the torso and arms (38.1 m of tubing), and pants (25.0
m of tubing). The face, hands, and feet were left uncovered.
To promote maximum heat transfer between the skin and
the garment, male participants wore only shorts while
females also wore a bra. Inlet water temperature of the gar-
ment, with a Xow rate of »1 L min¡1, was controlled by a
recirculating chiller/heater (Polyscience, Niles, IL, USA)
with a resolution of 0.5°C.
Exercise regimen
Given that the LCG allowed only for passive exogenous
changes in body heat content, participants were asked to
complete a short sub-maximal exercise protocol during
each cold exposure in order to incorporate the eVects of
increased body heat content via endogenous heat on CIVD.
This paradigm also provides a more realistic real-world
scenario given that individuals exposed to cold generally go
through periods of rest interspersed by periods of sub-max-
imal physical activity. In fact, several studies in the past
have investigated CIVD in individuals working with their
hands in a cold environment (Hellstrom and Andersen
1960; Krog et al. 1960; Leblanc et al. 1960; Nelms and
Soper 1962). At the 65th min of each cold exposure partici-
pants were seated on a stationary Monark bike situated
inside the environmental chamber and exercised for 10 min
at a workload requiring 60% of their age-predicted maxi-
mum heart rate (220-age).
Thermoregulatory variables
Core, skin, and Wnger temperatures were recorded through-
out all conditions at 8-s intervals using a data logger
(Smartreader 8 Plus, ACR, Vancouver, Canada) interfaced
with a computer to allow continuous monitoring. Esopha-
geal temperature was measured with a Xexible thermistor
(Mon-A-Therm Core, Mallinkrodt Medical, St Louis, USA)
placed through the nasal passage into the esophagus at a
distance equal to one-quarter of the standing height. Rectal
temperature was measured with a Xexible thermistor (Mon-
A-Therm Core, Mallinckrodt Medical, St Louis, USA)
inserted to a depth of 15 cm beyond the anal sphincter to
assess rectal temperature. The esophageal and rectal tem-
perature values were used to provide a mean core tempera-
ture [core temperature = (esophageal + rectal)/2)]. The
rational for averaging rectal and esophageal temperature
stems from the fact that the former is the core temperature
index used by most studies and allows for comparisons
between our data and those of others but, at the same time,
it is inherently limiting for our purposes due to its well-
known response delay (the reader is reminded that the aim
of the current analysis is to assess changes across time).
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Therefore, the average of rectal and esophageal temperature
provides us with an index that is an acceptable indicator of
core temperature with a fast response to changes in thermal
balance. Four ceramic chip skin thermistors (MA-100,
Thermometrics, Edison, NJ, USA) were attached to the
chest, upper arm, thigh, and calf to allow the measurement
of mean skin temperature using the area-weighting for-
mula: mean skin temperature = 0.3(chest + arm tempera-
ture) + 0.2(thigh + leg temperature) (Ramanathan 1964).
Mean body temperature (Tb) was calculated as the weighted
sum of core and skin temperatures using the previously
described and widely used formula (Hardy and DuBois
1938): 0.67(mean core temperature) + 0.33(mean skin tem-
perature). Finger temperature (Tf) was measured with a
thermistor placed on the pad of the fourth Wnger of the non-
dominant hand. All skin themistors were held in place
against the skin with surgical tape (3 M Transpore Tape, 3
M Canada).
Statistical analyses
Chi-square was used to detect diVerences in CIVD occur-
rence (i.e., number of CIVD events) among conditions (i.e.,
pre-warming, warming and control). Repeated measures
ANOVA were used to detect diVerences among conditions
with regards to the duration of CIVD [time (in s) between
the uninterrupted sharp Tf increase of ¸4°C and the return
of Tf to pre-CIVD levels]. The same statistical procedure
was used to detect possible diVerences in Tf and Tb at CIVD
start (i.e., point of the uninterrupted sharp Tf increase of
Fig. 1 CIVD occurrence and properties (mean § SD) in all condi-
tions. Note: All chi-square comparisons of ‘CIVD occurrence’ among
conditions were signiWcant at P < 0.05. * = repeated measures ANOVA
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Eur J Appl Physiol (2008) 104:491–499
¸4°C), CIVD maxima (i.e., highest Tf value during a
CIVD) and CIVD end (i.e., point of the return of Tf to pre-
CIVD levels). Thereafter, auto-regressive integrated mov-
ing average (Box and Jenkins 1976) (ARIMA) analysis was
used to investigate whether changes in Tf time series
(dependent variable) could be explained by changes in Tb
time series (independent variable). The purpose of using
ARIMA in the speciWc analysis is to determine if and when
Xuctuations in Tb were associated with similar Xuctuations
in Tf across time. All statistical analyses were performed
with SPSS (version 14.0.1, SPSS Inc., Chicago, Illinois)
statistical software package. The level of signiWcance was
set at P < 0.05.
Results
Results are presented as mean (SD). Statistically signiWcant
Tb diVerences were observed between conditions [pre-
warming 36.64(0.25)°C; warming: 36.73(0.50)°C; control:
36.31(0.50)°C] (P < 0.05). A total of 119 CIVD episodes
were observed using the adopted deWnition (i.e., an uninter-
rupted sharp increase of ¸4°C in Tf), 56 of which occurred
during the warming condition (Fig. 1), when Tb was at its
highest. Mean Tb and Tf at CIVD start were 36.4 and
17.2°C, respectively (Fig. 1). As illustrated in Figs. 2, 3 and
4, a thermoregulatory response pattern was apparent
whereby CIVD occurred soon after Tb surpassed a thresh-
old. Subsequent to the occurrence of all CIVD events, Tb
was reduced and the phenomenon ceased when Tb fell
comparisons of CIVD properties between conditions signiWcant at P <
0.05. The slight diVerence in Tf between occurrence and ending was
due to repeated CIVD events blocking Tf from reaching pre-CIVD levels
Eur J Appl Physiol (2008) 104:491–499
Fig. 2 Finger temperature (Tf, left y axis) and mean body temperature
(Tb, right y axis) in the three conditions for a male participant chosen
at random. To minimize noise, values are shown as three-point moving
averages from data collected every 8-s. The 10-min exercise period
performed between the 65th and 75th-min as well as the end of pre-
warming are indicated by dashed lines. All CIVD events (indicated by
below the threshold. In a few instances when Tb remained
above the threshold despite the occurrence of CIVD, addi-
tional CIVD events were observed (e.g., CIVD 10 in
Figs. 2 and 4). These Wndings were independent of extrem-
ity temperature since CIVD episodes were observed at a
comparatively vast range of Tf ranging from 7.2 to 33.5°C
(Fig. 1). The validity of the aforementioned patterns regard-
ing Tb and Tf was examined using ARIMA analysis. This is
because cold exposure, LCG-induced heating and exercise
in the present experiment represented disturbances (shocks)
that somehow aVected the level of a series (in this case Tb)
as well as the level of another series (in this case Tf). Based
on these disturbances, ARIMA can mathematically
describe the association between the two time series. A
detailed presentation of the ARIMA procedure can be
found in the Appendix. In summary, results from the
ARIMA analysis demonstrated that, across time, Xuctua-
tions in Tb were systematically followed (approximately
160 s later) by similar Xuctuations in Tf.
495
numbers) occurred when Tb increased past a threshold and were fol-
lowed by a decrease in Tb. With the exception of CIVD 10, all CIVD
events were preceded by an increase in Tb. The Tb threshold for the
control condition was at 36.3°C (CIVD 1–3) while the equivalent was
at 36.6°C when heating manipulations occurred (i.e., warming and pre-
warming conditions, CIVD 4–10)
Discussion
The current results support the proposed hypothesis that an
association exists between Tb and CIVD and that the trig-
gering mechanism of CIVD is an increase in Tb past a
threshold. Although the present design cannot fully estab-
lish causal relationships, based on deterministic models of
causality (Olsen 2003), our results reveal very strong longi-
tudinal associations because the independent variable (i.e.,
Tb) changed before the dependent variable (i.e., Tf) in time
in a consistent manner. The present data suggest substantial
loss of body heat during CIVD demonstrating its cooling
capacity, which conWrms previous Wndings (Cannon and
Keatinge 1960). The notion that CIVD is a heat-loss mech-
anism is supported in several investigations (Daanen 2003;
Daanen and Ducharme 1999; Daanen et al. 1997; Takano
and Kotani 1989) that reported increased CIVD prevalence
rates at higher levels of Tb. In addition, it is generally
agreed that there is a central component in CIVD given that
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Fig. 3 Finger temperature (Tf, left y axis) and mean body temperature
(Tb, right y axis) in the three conditions for a male participant chosen
at random. Graph properties are similar to Fig. 2. All CIVD events
were preceded by an increase in Tb past a threshold and were followed
normothermic and/or centrally warm humans demonstrate
accelerated CIVD responses (Daanen et al. 1997; Takano
and Kotani 1989), while those that are centrally cold reveal
CIVDs of delayed onset and lesser magnitude (Daanen
et al. 1997; Elsner et al. 1960; Keatinge 1957; Werner
1977). However, previous investigations did not arrive to
the conclusions of the present study, probably because they
did not assess the link between CIVD and Tb in real-time
but only through repeated-measures designs incorporating
conditions of hyper-, hypo-, and normo-thermia. In the
present experiment, by establishing the link between body
heat content and CIVD in real time minute-by-minute data,
the CIVD phenomenon becomes systematic and interpret-
able in terms of biological control processes.
Despite marked interindividual variation, the CIVD
response consistently occurred soon after—approximately
160 s—Tb surpassed a threshold, observed most often at
36.4°C in the control condition and at approximately
36.65°C in the warming and pre-warming conditions. This
diVerence in thresholds may be caused by hysterisis (a phe-
nomenon by which an eVect in a component depends not
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Eur J Appl Physiol (2008) 104:491–499
by a decrease in Tb. The Tb threshold for the control condition was at
36.3°C (CIVD 1) while the equivalent was at 36.75 and 36.5°C for the
warming (CIVD 2–8) and pre-warming (CIVD 9–10) condition,
respectively
only on the present stimulus, but also on the previous state
of the component), with the system’s Tb threshold being
shifted upwards because it has been approached from a
diVerent “direction” (i.e., Tb was above the threshold for the
majority of the time in warming and pre-warming, and
below the threshold in control). The existence of large
interindividual variation in the magnitude, the threshold
and the time course in the suppression and activation capa-
bility of the vasoconstrictor system (Michikami et al. 2001)
as well as the core temperature threshold for hand blood
Xow changes (Daanen and van der Struijs 2005) has been
previously established and was not an unexpected Wnding.
Local skin temperature did not appear to interfere with
the control of CIVD in our experiment since episodes were
observed with Tf at CIVD onset ranging from 7.2 to 33.5°C.
In conjunction with the lack of repetitive cyclical variation
(periodicity) in CIVD events despite that participants were
exposed to a stable environment, our results suggest that
CIVD events as well as the ‘hunting reaction’ intervals
were not associated with either environmental stimuli or
peripheral thermal integrity. These Wndings suggest the
Eur J Appl Physiol (2008) 104:491–499
Fig. 4 Finger temperature (Tf, left y axis) and mean body temperature
(Tb, right y axis) in the three conditions for a female participant chosen
at random. Graph properties are similar to Fig. 2. All CIVD events oc-
curred when Tb was above a threshold and were followed by a decrease
in Tb. With the exception of CIVD 10, all CIVD events were preceded
involvement of supraspinal regions of the central nervous
system in the control of CIVD. Indeed, the eVects of tem-
perature on Wnger constrictor tone depend primarily on the
integrity of the sympathetic nervous system, at least during
the early phases of localized cooling (Johnson et al. 2005;
Sendowski et al. 2000; Thompson-Torgerson et al. 2007).
However, local skin receptors appear to play a role by mod-
ifying the response of AVA to this central reXex (Johnson
and Park 1979; Roberts and Zygmunt 1984; Sendowski
et al. 2000; Tipton et al. 1993). Although our results dem-
onstrate clearly a central component to the control of
CIVD, we did not see any eVects of local factors possibly
because we did not examine local eVector components. The
inXuence of direct local cooling on vasomotor muscle may
be substantial, and one of the hypothesis of CIVD postu-
lates that it is caused by direct cold-induced paralysis of the
peripheral blood vessels (Keatinge 1980). In our view, this
hypothesis is limited in that it has been investigated only ex
situ eliminating any central inXuences and it has not been
conWrmed in real-time CIVD data. Cold-induced paralysis
497
by an increase in Tb. The Tb threshold for the control condition was at
36.4°C (CIVD 1) while the equivalent was at 36.8°C and 36.5°C for
the warming (CIVD 2–6) and pre-warming (CIVD 8, 9, 10) condition,
respectively. CIVD 8 occurred at 37°C
of the peripheral blood vessels may well contribute to
CIVD, yet our data and that of many others (Daanen et al.
1997; Elsner et al. 1960; Keatinge 1957; Kunimoto 1987;
Sendowski et al. 1997; 2000; Werner 1977) suggest a cen-
tral component to CIVD.
It should be noted that the current Tb values are the prod-
uct of thermometric calculations based on standard mean
core and skin temperature weighting coeYcients for an indi-
vidual exposed to cool steady-state conditions, a method that
is inferior in accuracy compared to calorimetry. However,
thermometric calculations are generally accepted as valid
and sensitive to change (Flouris et al. 2007) and it is impor-
tant to remember that the aim in the present experiment was
to investigate the changes in Tf and Tb across time as well as
the relationship between these changes, not cross-sectional
diVerences between the two variables. Therefore, the eVects
of thermometry, if any, were constant across time (since
coeYcients in all Tb formulas are constant) and, therefore,
did not inXuence our conclusions. We did not incorporate
separate analyses for skin and core temperatures, which may
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have a disparate eVect on CIVD since reXex constriction in
the cold is predominantly driven by skin temperature, while
reXex dilation in the heat is driven almost entirely by core
temperature. Therefore, the Tb estimate used herein may
have not completely accounted for the underlying thermo-
regulatory sensory inputs and eVerent outputs. Also, our
results would be further strengthened by measuring Wnger
blood Xow or forearm-Wnger temperature gradient. While the
present results are based only on absolute Wnger skin temper-
ature data, this parameter is the most commonly used mea-
sure for CIVD (Daanen 2003), while similar methods have
been extensively used to measure Wnger perfusion (Sessler
2003). In conclusion, the results from the present experiment
support that an association exists between Tb and CIVD and
that the triggering mechanism of CIVD is an increase in Tb
past a threshold. Ergo, CIVD appears to be the eventuality of
a thermoregulatory function based on the suppression and
activation of the sympathetic vasoconstrictor system. As
local eVects of cold as well as skin and core temperatures
may play diVerential roles in CIVD, future experiments
should aim in isolating the local and central components of
this response. In addition, further research on the role of
vasoconstrictor nerve activity in maintaining thermal balance
in humans should be projected in future studies.
Acknowledgments The authors wish to express their gratitude to the
subjects who participated in the experiments, to Peter Romkey and the
K.C. Irving Center at Acadia University for providing the environmen-
tal chamber and associated technical assistance, and to Dr. René J.L.
Murphy at Acadia University for providing the arctic clothing. The
project was supported by a Discovery Grant (S. S. Cheung and G. G.
Sleivert) from the Natural Sciences and Engineering Research Council
(NSERC). A. D. Flouris was supported by funding from the Natural
Sciences and Engineering Research Council of Canada and the Cana-
dian Space Agency.
Appendix
Plotting the Tf time series against the Tb time series for each
participant and condition separately (Figs. 2–4) yielded a
systematic pattern (relationship between Tf and Tb
described above) but no periodicity [i.e., regular repetition
in time (lack of periodicity is an essential ARIMA assump-
tion)] (Box and Jenkins 1976). Further analyses were con-
ducted using data from all participants and conditions
simultaneously. To statistically address the possibility that
the two time series (i.e., Tf and Tb) were not inherently
unpredictable [random-walk/white noise (another ARIMA
assumption)], the autocorrelation of the residuals from
exponential smoothing (Gardner 1985) was calculated for
each time series for a maximum of 38 lags/data points (i.e.,
»5 min, given that data were collected every 8 s), conWrm-
ing that neither of the two was random (Box-Ljung statistic
P < 0.001). The exponential smoothing technique is very
123
Eur J Appl Physiol (2008) 104:491–499
useful in time series analysis as it emphasizes the regularity
of a series by removing some of the random variation and
by giving extra weight to more recent observations. This
allows the researcher to capitalize on any pattern that is evi-
dent in the observed series and to use that pattern to draw
relevant conclusions. In the current analysis, the changes in
Tf were detected approximately 160 s (or 20 lags/data
points) following changes in Tb. Thus, the Tf series was
recalculated to incorporate 20 lags and further analyses
were conducted using this new variable.
ARIMA models combine as many as three types of pro-
cesses based on the concept of random disturbances or
shocks: autoregression (i.e., AR), integration/diVerencing
(i.e., I) and moving averages (i.e., MA). Between two obser-
vations in a time series, a disturbance (in this case cold expo-
sure/LCG heating) occurs that somehow aVects the level of
the series (in this case Tb) as well as the level of another
series (in this case Tf). These disturbances as well as the asso-
ciation between the two time series can be mathematically
described by ARIMA models. Using the appropriate model-
building procedure for the best possible series model (Box
and Jenkins 1976) the identiWcation of the processes underly-
ing the time series was conducted to determine the integers
for autoregression, diVerencing and moving average. Given
that the autoregression and moving average components
require stationary series (Box and Jenkins 1976), the autocor-
relations and partial autocorrelations of Tf and Tb time series
were calculated showing that neither was stationary. This
was also evident in all preliminary plots of Tf and Tb across
time (Figs. 2–4). Following diVerencing transformation at lag
2, stationarity was achieved with no spikes evident to the
38th lag (»5 min of data collection given that data were col-
lected every 8 s). As the series were diVerenced twice to
achieve stationarity, the ARIMA integration parameter was
set to ‘2’ (Box and Jenkins 1976). Further, given that both
series had one spike in the Wrst value of the autocorrelation
and exponentially declining values of the partial autocorrela-
tion, the appropriate order for autoregression and moving
average was ‘0’ and ‘1’, respectively (Box and Jenkins
1976). The resulting ARIMA [0, 2, 1 (i.e., 0 order of autore-
gression; 2 degree of diVerencing; 1 order of moving aver-
age)] was found to be parsimonious and adequate model with
no spikes evident to the 38th lag (Box-Ljung statistic P <
0.001) and Tb signiWcantly associated with Tf (t = 9.602, P <
0.001). These results demonstrate that, across time, Xuctua-
tions in Tb were systematically followed (approximately 160
s later) by similar Xuctuations in Tf.
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