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Human physiological responses to cold exposure: Acute responses and acclimatization to prolonged exposure

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Cold exposure in humans causes specific acute and chronic physiological responses. This paper will review both the acute and long-term physiological responses and external factors that impact these physiological responses. Acute physiological responses to cold exposure include cutaneous vasoconstriction and shivering thermogenesis which, respectively, decrease heat loss and increase metabolic heat production. Vasoconstriction is elicited through reflex and local cooling. In combination, vasoconstriction and shivering operate to maintain thermal balance when the body is losing heat. Factors (anthropometry, sex, race, fitness, thermoregulatory fatigue) that influence the acute physiological responses to cold exposure are also reviewed. The physiological responses to chronic cold exposure, also known as cold acclimation/acclimatization, are also presented. Three primary patterns of cold acclimatization have been observed, a) habituation, b) metabolic adjustment, and c) insulative adjustment. Habituation is characterized by physiological adjustments in which the response is attenuated compared to an unacclimatized state. Metabolic acclimatization is characterized by an increased thermogenesis, whereas insulative acclimatization is characterized by enhancing the mechanisms that conserve body heat. The pattern of acclimatization is dependent on changes in skin and core temperature and the exposure duration.
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Human physiological responses to cold exposure: Acute responses and
acclimatization to prolonged exposure
John W. Castellani , Andrew J. Young
U.S. Army Research Institute of Environmental Medicine,Natick, MA 01760-5007, United States
abstractarticle info
Article history:
Received 26 October 2015
Received in revised form 3 February 2016
Accepted 17 February 2016
Available online xxxx
Cold exposure in humans causes specic acute and chronic physiological responses. This paper will review both
the acute and long-term physiological responses and external factors that impact these physiological responses.
Acute physiological responses to cold exposure include cutaneous vasoconstriction and shivering thermogenesis
which, respectively, decrease heat loss and increase metabolic heat production. Vasoconstriction is elicited
through reex and localcooling. In combination, vasoconstriction and shivering operate to maintain thermalbal-
ance when the body is losing heat. Factors (anthropometry, sex, race, tness, thermoregulatory fatigue) that in-
uence the acute physiological responses to cold exposure are also reviewed. The physiological responses to
chronic cold exposure, also known as cold acclimation/acclimatization, are also presented. Three primary pat-
terns of cold acclimatization have been observed, a) habituation, b) metabolic adjustment, and c) insulative ad-
justment. Habituation is characterized by physiological adjustments in which the response is attenuated
compared to an unacclimatized state. Metabolic acclimatization is characterized by an increased thermogenesis,
whereas insulative acclimatization is characterized by enhancing the mechanisms that conserve body heat. The
pattern of acclimatization is dependent on changes in skin and core temperature and the exposure duration.
Published by Elsevier B.V.
Keywords:
Habituation, hypothermia
Insulative acclimatization
Shivering
Temperature regulation
Vasoconstriction
Contents
1. Introduction .............................................................. 0
2. Biophysicsofcoldexposure ....................................................... 0
3. Acutephysiologicalresponses ...................................................... 0
3.1. Modiersofthermoregulatoryeffectorresponsestocold ....................................... 0
3.2. Anthropometry/BodyComposition ................................................. 0
3.3. Sex ............................................................... 0
3.4. Age ............................................................... 0
3.5. Exertionalfatigue......................................................... 0
4. Physiologicaladjustmentstoprolongedorrepeatedcoldexposure ...................................... 0
4.1. Habituation ........................................................... 0
4.2. MetabolicAcclimatization ..................................................... 0
4.3. WhatDeterminesWhichPatternofColdAcclimatizationDevelops? .................................. 0
5. Summary................................................................ 0
Acknowledgments .............................................................. 0
References.................................................................. 0
1. Introduction
Human beings work and play in many cold-weather environments
(low temperature, high winds, low solar radiation, rain/water expo-
sure), and cold stress is rarely a limiting factor. For the most part,
human beings utilize behavioral thermoregulation in the cold. These
Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Corresponding author at: Thermal and Mountain Medicine Division, U.S. Army
Research Institute of Environmental Medicine, 10 Gene ral Greene Avenue, Natick, MA
01760-5007, United States.
E-mail address: john.w.castellani.civ@mail.mil (J.W. Castellani).
AUTNEU-01823; No of Pages 12
http://dx.doi.org/10.1016/j.autneu.2016.02.009
1566-0702/Published by Elsevier B.V.
Contents lists available at ScienceDirect
Autonomic Neuroscience: Basic and Clinical
journal homepage: www.elsevier.com/locate/autneu
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
behaviors include migration, building shelter, wearing high-insulation
clothing, and physical activity, and David Bass, the noted environmental
physiologist, once stated that man in the cold is not necessarily a cold
man.(Bass, 1958). However, there are situations where these
behaviors are not adequate, and physiological responses are required
to maintain thermal balance and protect against cold-weather injury.
Furthermore, there are also scenarios where chronic cold exposure is
experienced and adaptationsoccur. This paper will reviewhuman phys-
iological responses to cold, focusing on both acute and long-term
responses that cause cold acclimatization.
2. Biophysics of cold exposure
Changes in core temperature are caused by either a positive or neg-
ative change in heat storage. If the body produces more heat than it dis-
sipates,body tissue storage is positive, and deep body temperaturerises.
Conversely, if heat production is less than that lost to the external envi-
ronment,then heat storage will be negative and deep bodytemperature
will fall. We can present these relationships between production and
loss mathematically as follows (Gagge and Gonzalez, 1996):
S¼MþWorkðÞERCKs
where: S = heatstorage, M = metabolic heat production, E = evapora-
tion, R = radiation, C = convection, and K = conduction. Positive num-
bers indicate heat gain and negative values, heat loss. E, R, C, and K are
the heat exchange pathways (Gonzalez and Sawka, 1988). All units
are in W·m
2
. When environmental temperature and water vapor
pressure are lower than the skin temperature and vapor pressure of
water at the skin, heat loss results.
Humans cool two to ve times more quickly during immersion in
cold water, compared to when they are exposed to air at the same tem-
perature (Hong, 1984); this is due to higher conductive and convective
heat loss in water. This is further demonstrated by comparing the tem-
peratures where humans remain in heat balance or thermoneutral con-
ditions. In water, the thermoneutral temperature is about 35 °C (Costill
et al., 1967; Craig and Dvorak, 1966). In comparison heat balance is
achieved during air exposure at an ambient temperature of about
26 °C (Craig and Dvorak, 1966). Therefore, a resting person will be un-
able to maintain their deep body temperature when immersed in
water at a temperature regarded as thermoneutral in air. The reason
for these differences lies in the physical properties of air and water;
the thermal conductivity of water is 25 times that of air (Toner and
McArdle, 1996). Therefore cooling is extremely effective, even in mod-
erately cool water and results in rapid dissipation of the heat which is
delivered to the skin by conduction and convection (blood circulation)
from the deeper tissues.
3. Acute physiological responses
A decrease in peripheral temperatures, primarily skin, and core tem-
perature elicits the primary cold thermoregulatory responses (vasocon-
striction and shivering), also called thermoeffector responses. For
example, afferent signals from the skin are sensed in the preoptic area
of the anterior hypothalamus, from which efferent signals arise causing
cutaneous vasoconstriction and/or shivering thermogenesis. The con-
trol of these efferent responses during changing mean body tempera-
ture (integration of core and skin temperature) is depicted in Fig. 1.
The threshold is dened as the temperature point where the effector re-
sponse is initially activated, whereas the sensitivity of the response is
denoted by the slope of the mean body temperature-effector response.
Upon cold exposure, the initialphysiological response is a peripheral
skin vasoconstriction and a reduction in skin blood ow. This reduces
convective heat transfer between thebody's core and shell (skin,subcu-
taneous fat, and skeletal muscle), effectively increasing insulation by the
body's shell. However, heat is still lost from the exposed body surface
faster than it is replaced; therefore, skin temperature declines. Vasocon-
striction begins when skin temperature falls below about 35 °C and be-
comes maximal when skin temperature is 31 °C or less (Veicsteinas
et al., 1982). Thus, the vasoconstrictor response to cold exposure helps
retard heat loss and defend core temperature but at the expense of a
decline in peripheral tissue temperature.
There are three primary ways that vasoconstriction occurs (reex
and local cooling and a decrease in deep body temperature), each
with separate physiological mechanisms. This review will focus on the
skin temperature responses as these are most common. The rst is a re-
ex response, caused with whole-body cooling, or when one area of the
body is cooled, causing other areas to reexively vasoconstrict (e.g., face
cooling elicits a reex vasoconstriction to the ngers (Brown et al.,
2003)). The afferent and efferent neural pathways for reex vasocon-
striction have been determined (see Morrison paper in this series,
Figure XX will be added by journal). Cold exposure on the skin triggers
a receptor-mediated neural signaling pathway that traverses through
the dorsal horn of the spinal cord to the lateral brachial nucleus and
then on to the preoptic area of the hypothalamus, with efferent signals
travelling from the brain through the interomediolateral cell column of
the spinal cord and to sympathetic nerves innervating cutaneous blood
vessels. Norepinephrine is the primary neurotransmitter that accounts
for ~60% of the reex cold-induced vasoconstriction in skin vasculature
(Charkoudian, 2010), while neuropeptide Y is responsible for ~2030%
(Stephens et al., 2001, 2004).
Vasoconstriction is also caused by local cooling of skin blood vessels.
Early in the local cooling response (rst 10 min with no reex cooling oc-
curring from other areas), vasoconstriction is primarily mediated by nor-
epinephrine and the α
2
-adrenergic receptor (Thompson-Torgerson et al.,
2008). However as cooling continues, non-adrenergic and non-neuronal
mechanisms are responsible for the reduction in cutaneous blood ow.
Skin cooling results in an increase in mitochondrial reactive oxygen spe-
cies, which causes an increase in Rho kinase (Thompson-Torgerson et al.,
2007a, 2007b, 2008). Increased Rho kinase causes an inhibition of myosin
light chain phosphatase allowing the myosin light chain to be phosphor-
ylated leading to cutaneous vasoconstriction. As well, local cooling
Fig. 1. Representation of the thermal effector response (vasoconstriction, shivering) to a
change in mean body temperature (ΔMBT) relationship. As m ean body temperature
decreases a thermal effector response is elicited and increases (line A). The inection
point where this increase occurs is the threshold. The slope of the effector-ΔMBT
relationship represents the sensitivity of the response. Line B denotes a response where
the threshold is shifted, such that a thermal effect or response does not occur until a
larger ΔMBT occurs. In Line C, there is no threshold shift, but a change in the sensitivity
of the response. For this example, line C denotes a greater sensitivity to a ΔMBT, that is,
there is a greater effector for a given ΔMBT. Line D denotes both a th reshold and
sensitivity change.
2J.W. Castellani, A.J. Young / Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
induced increases in Rho kinase causes a translocation of α
2C
receptors
from the Golgi to the plasma membrane enhancing α
2
receptor sensitiv-
ity to norepinephrine (Chotani et al., 2000, 2004; Johnson, 2007). Fig. 2
schematically presents the mechanisms responsible for cutaneous vaso-
constriction following local cold exposure. Increases in RhoA/Rho kinase
also lead to a decrease in nitric oxide by down-regulating endothelial ni-
tric oxide synthase (Thompson-Torgerson et al., 2008).
Cold signals are transduced through the transient receptor potential
melastatin 8 (TRPM8) receptor. This receptor is a temperature sensitive,
calcium-permeable, cationic ion channel that also responds to chemical
stimuli such as menthol (Johnson et al., 2009). It is found in the dorsal
root ganglion sensory neurons that innervate the skin and also in tri-
geminal ganglion sensory neurons (Wang and Siemens, 2015) and is
expressed in vascular smooth muscle (Johnson et al., 2009). Fig. 3 pre-
sents the molecular mechanisms that cause a physiological response
upon cold exposure. Pharmacologically blocking the TRPM8 receptors
deleteriously impacts autonomic responses to cold exposure. Almeida
et al. (Almeida et al., 2012) found that in wild-type mice, use of the
TRPM8 receptor blocker M8-B caused a decline in core body tempera-
ture. This change in core temperature was caused by both an attenuated
vasoconstrictor and thermogenic response, leading to greater heat loss
and a decline in metabolic heat production, respectively.
Cold-induced vasoconstriction has pronounced effects in acral skin
regions (e.g., ngers, toes) making them particularly susceptible to
cold injury and loss of manual dexterity (Brajkovic et al., 1998). In
these areas, another vasomotor response, cold-induced vasodilation
(CIVD), modulates the effects of vasoconstriction. First described by
Lewis and also known as the hunting reex (Lewis, 1930), CIVD is a pe-
riodic uctuation of blood ow and skin temperature following an ini-
tial decline in these variables during cold exposure. A similar cold-
induced vasodilation in the forearm appears to reect vasodilation of
muscle as well as cutaneous vasculature (Ducharme et al., 1991a). Orig-
inally thought to just be a local cooling effect, evidence suggests that a
central nervous system mechanism mediates CIVD (Lindblad et al.,
1990). CIVD responses are more pronounced when the body core and
skin temperatures are warm (hyperthermic state) and suppressed
when theyare cold (hypothermic state), when compared to normother-
mia (Daanen and Ducharme, 1999; Daanen et al., 1997; O'Brien et al.,
2000). Exercise training (50% peak power; 5 days·week-1; 4 weeks)
may also improve the CIVD response (Keramidas et al., 2010).
Cold exposure also elicits increased metabolic heat production in
humans, which can help offset heat loss. In humans, most cold-
induced thermogenesis is attributable to skeletal muscle contractile ac-
tivity. Humans initiate this thermogenesis by voluntarily modifying be-
havior, that is, increasing physical activity (e.g., exercise, increased
dgeting) or by shivering. Shivering, which consists of involuntary re-
peated rhythmic muscle contractions during which most of the meta-
bolic energy expended is liberated as heat and little external work is
performed, may start immediately or after severalminutes of cold expo-
sure, and is initiated by a decrease in skin temperature. The fall in core
temperature provides the greatest stimulus for shivering, with the
ratio of the T
core
/T
skin
contribution to shivering being 3.6:1 (Frank
et al., 1999). Shivering becomes maximal at a core temperature of
~3435 °C and ceases at ~31 °C (Castellani et al., 2006). Shivering usu-
ally begins in the torso muscles, then spreads to the limbs (Bell et al.,
1992). The intensityand extent of shivering vary according to the sever-
ity of cold stress (e.g., air or water exposure, change in core tempera-
ture). As shivering intensity increases and more muscles are recruited
to shiver, whole-body metabolic rate increases, typically reaching
about 200250 W during resting exposure to cold air but often exceed-
ing 350 W during resting immersion in cold water. Shivering metabo-
lism as high as 763 W has been recorded during immersion in 12 °C
water (Golden et al., 1979).
It has been well established that rodents increase metabolic heat
production in brown adipose tissue (BAT) in response to cold exposure,
and it was thought for many years that adult humans lackedthis mech-
anism. However a series of papers (Saito et al., 2009; van Marken
Lichtenbelt et al., 2009; Virtanen et al., 2009) using positron emission
tomography (PET) and computed tomography (CT) scans along with
the tracer 18F-uorodeoxyglucose has discovered that adult humans
do indeed have active BAT that becomes active upon cold exposure.
Highest BAT levels are found in the neck, supraclavicular tissue, and tho-
racic and abdominal paraspinal sites (Cypess et al., 2009). BAT activa-
tion is negatively correlated with body mass index and % body fat
(Saito et al., 2009; van Marken Lichtenbelt et al., 2009) and women
appear to have more BAT than men (Cypess et al., 2009). However
there is no evidence that BAT thermogenesis can increase high enough
Fig. 2. Representation of the mechanisms involved in vasoconstriction following local cold
exposure. Local cooling of cutaneous blood vessels causes an increase inreactive oxygen
species (O
2
) within the mitochondria. This in turn activates RhoA and Rho kinase, which
can induce vasoc onstriction th rough 2 pathways. In pathway 1, Rh o kinase causes
translocation of alpha-2
C
adrenoceptors (α2
c
) receptors to move from the Golgi to the
plasma membrane. These α2
c
receptors bind norepinephrine (NE), leading to calcium
(Ca
2+
)inux and phosphorylation of myosin light chain (MLC) by the MLC kinase. In
the second pathway, increased Rho kinase inhibits myosin light chain phosphatase,
which allows MLC to remain phosp horylated and cutaneous blood vessels to remain
constricted. Printed with permission from Thompson-Torgerson et al. (2008).
Fig. 3. Representation of cold signal transduction through the transient potential
melastatin 8 (TR PM8) receptor, eliciting a dow nstream increase in metabolic heat
production and vasoconstriction. The response is modiable by other signaling
pathways. PIP
2
, phosphatidylinositol bisphosphate; PDGFR , platelet-de rived growth
factor receptor; AA, arachidonic acid; LPL, lysophospholipids; iPLA2, Ca
2+
-independent
subtype of phospholipase A2; PKA, protein kinase A; α
2
AR, alpha-2 adrenergic receptor;
PKA, protein kinase A; βAR, beta-adrenergic receptor.
3J.W. Castellani, A.J. Young / Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
to defend core temperature during acute whole body cold exposures
that require a robust metabolic response.
3.1. Modiers of thermoregulatory effector responses to cold
Individual characteristics are the primary source of variability in the
physiological response to cold exposure. Primary among these charac-
teristics is body anthropometry, but other sources of individual differ-
ences include sex, age, and prior cold/exercise fatigue.
3.2. Anthropometry/Body Composition
Most variability between individuals in their thermoregulatory re-
sponses and capability to maintain normal body temperature during
cold exposure is attributable to anthropometric and body composition
differences. Large individuals lose more body heat in the cold than
smaller individuals because they havelarger body surface areas. In gen-
eral, persons with a large ratio of surface area to mass have greater de-
clines in body temperature during cold exposure than those with a
smaller ratio (Gagge and Gonzalez, 1996; Toner and McArdle, 1996).
All body tissues provide thermal resistance to heat conduction
(i.e., insulation) from within the body. Inresting individuals, unperfused
muscle tissue provides a signicant contribution to the body's total in-
sulation (Ducharme et al., 1991b). However, during exercise or other
physical activity that contribution declines because increased blood
ow through muscles facilitates convective heat transfer from core to
the body's shell. Fat has the highest thermal resistivity of all the body's
tissues. Therefore, individuals with high subcutaneous fat levels are
protected against heat loss and subsequent declines in core tempera-
ture, and the fall in core temperature during cold exposure is inversely
related to subcutaneous fat thickness (Toner and McArdle, 1996). The
mechanism for this protective effect of subcutaneousfat thickness is pri-
marily a biophysical one. More subcutaneous fat, hence more insulation,
reduces conductive heat loss from underlying tissue. Thus skin temper-
ature falls more as subcutaneous fat thickness increases. A reduced skin
temperature lowers the thermal gradient between skin and the ambient
environment, and since the rate of body heat loss depends on the mag-
nitude of that gradient, a lower skin temperature effectively lowers
whole body heat loss and attenuates the fall in core temperature
(Buskirk et al., 1963; Cannon and Keatinge, 1960).
3.3. Sex
Sex-associated differences in thermoregulatory responses and ther-
mal balance during whole-body cold exposure appear almost entirely
attributable to anthropometric and body composition characteristics
(Toner and McArdle, 1996), as shivering sensitivity (Glickman-Weiss
et al., 2000a, 2000b) are similar between men and women. For example,
in men and women having equivalent total body masses, surface areas
are similar, but the women typically have a greater fat content which
enhances insulation. However, in women and men of equivalentsubcu-
taneous fat thickness, the women have a greater surface area but small-
er total body mass (and lower total body heat content) than men. Thus,
while insulation is equivalent, total heat loss during resting cold expo-
sure wouldbe greater in the women, because they have a larger surface
area for convective heat ux, and body temperature would tend to fall
more rapidly for any given thermal gradient, unless shivering thermo-
genesis compensated with a more pronounced increment than in the
men. This compensation may be possible when heat ux is low (mild
cold conditions), but women's smaller lean body mass limits their max-
imal capacity for thermogenic response; therefore, a more rapid core
temperature decline might occur under severely cold conditions than
in men of comparable body mass (McArdle et al., 1984a, 1984b). How-
ever, during exercise in cold-water, men and women whohave equiva-
lent body fat percentages exhibit similar thermoregulatory responses,
due to the women having a more favorable fat distribution over the
exercising limbs, compared to the men (McArdle et al., 1984b).
Peripheral responses to cold exposure are different between women
and men. Bartelink et al. (1993) observed during local cold exposure
that women had a lower nger skin temperature and blood perfusion
compared to men and this persisted into recovery. These ndings corre-
late with clinical observations that demonstrate that women have a
higher incidence of Raynaud's phenomenon (Grisanti, 1990). Mechanis-
tically, this may be related to estrogen increasing expression of cold-
sensitive α
2C
-adrenoceptors (Eid et al., 2007).
The thermoeffector responses to cold vary within a women's men-
strual cycle. During the luteal phase, the sensitivity of the shivering
response is lower, compared to the follicular phase, i.e., the slope of
the mean body temperature-metabolic heat production relationship is
attenuated (Gonzalez and Blanchard, 1998). Furthermore, there are
differences in nger skin temperature and cutaneous blood ow within
a menstrual cycle following nger cooling, with the lowest values ob-
served during the mid-luteal phase, compared to the pre-ovulatory peri-
od (Bartelink et al., 1990). Oral contraceptive use also affects the
thermoregulatory effector responses to cold exposure. Charkoudian
and Johnson Charkoudian and Johnson (1999) found that skin vasocon-
striction occurred at a higher core temperature during the high hormone
phase of oral contraceptive use (elevated estrogen and progestin), com-
pared to the low-hormone phase. Changes in reproductive hormone
levels caused by oral contraceptive use also impact the neurotransmit-
ters that modulate reex vasoconstriction. During the high hormone
phase of oral contraceptive use, there is a non-adrenergic component,
likely another sympathetic co-transmitter, responsible for reex vaso-
constriction (up to 40%), in addition to the alpha-adrenergic mediated
vasoconstriction (Stephens et al., 2002). However, this non-adrenergic
component was absent during the low reproductive phase of contracep-
tive use. Although it has never been denitively demonstrated, it is likely
this non-adrenergic sympathetic co-transmitter is neuropepetide Y
(NPY) (Stephens et al., 2004). In contrast to women taking contracep-
tives, normally menstruating women do not exhibit a difference in the
neurotransmitters modulating cutaneous vasoconstriction during high-
(luteal phase) and low-hormone (follicular) status (Thompson and
Kenney, 2004).
3.4. Age
People who are older than 60 years may be less cold tolerant than
younger persons, due to reduced vasoconstriction and heat conservation
in comparison to their younger counterparts (DeGroot and Kenney,
2007; Falk et al., 1994; Frank et al., 2000; Kenney and Armstrong,
1996; Smolander, 2002; Young and Lee, 1997). As shown earlier, NE
and NPY are the primary sympathetic neurotransmitters responsible
for reex vasoconstriction in the young. However, in the elderly, the
co-transmitter NPY does not mediate vasoconstriction. Furthermore,
NE-mediated vasoconstriction is attenuated with aging, likely through
a decrease in synthesis or release of that neurotransmitter (Holowatz
et al., 2010). In addition, the skin vasculature does not respond as robust-
ly to exogenous administration of NE, (Thompson and Kenney, 2004),
suggesting a blunted end-organ responsiveness (Holowatz et al., 2010).
Local cold induced vasoconstriction of cutaneous arteries, through
alpha-adrenergic and Rho kinase/Rho, changes with aging. Compared
to younger individuals, there is a shift away from an adrenergic re-
sponse (NE) to a non-adrenergic mechanism, i.e., Rho kinase. However,
despite this shift in the mechanism, there is no change in the overall
vasoconstrictor response to local cooling (Thompson et al., 2005;
Thompson-Torgerson et al., 2007b).
People generally experience a decline in physical tness with aging.
If older people exercise at the same absolute metabolic rates as younger
individuals, the older person will be working at a higher %VO
2max
,and
will fatigue sooner. Fatigue leads to a decrease in absolute heat produc-
tion increasing the likelihood of a reduction in core temperature. Older
4J.W. Castellani, A.J. Young / Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
individuals also appear to have a blunted thermal sensitivity to cold. For
example, in studies where subjects have control of setting a thermostat
as the ambient temperature uctuates, older individuals will allow the
air temperature to fall to lower levels before re-adjustingthe thermostat
(Ohnaka et al., 1993; Taylor et al., 1995). Aging also appears to reduce
the deep body temperature threshold for the onset of shivering and
cutaneous vasoconstriction (Frank et al., 2000). Collectively, the age-
related changes could increase susceptibility to hypothermia in older
persons.
Children, in comparison to adults, typically have a higher body sur-
face area-to-mass ratio and lower subcutaneous fat amounts and this
leads to substantial falls in core temperature when swimming in cold
(20 °C, 68 °F) water (Sloan and Keatinge, 1973). Interestingly, in 11
12 year old boys who had similar amounts of subcutaneous fat as
adult men (1934 years), core temperature was the same in 5 °C air
both at rest and during exercise, but the mechanism for achieving this
was different. The boys exhibited a more pronounced vasoconstrictor
and metabolic response compared to the men (Smolander et al.,
1992). Pre-menarcheal girls do not defend core temperature as well as
eumenorrheic girls during exercise-cold stress, due to a diminished va-
soconstrictor response (Klentrou et al., 2004).
3.5. Exertional fatigue
An association between exertional fatigue and susceptibility to hypo-
thermia was rst reported by Pugh (1966, 1967). He analyzed reports of
23 separate occasions that had led to numerous cases of hypothermia and
25 deaths. In his analysis of these incidences, Pugh identied physical ex-
haustion as a contributing factor for hypothermia. More recently exhaus-
tion and hypothermia were again linked as causal factors for a large
number of serious hypothermia casualties and four deaths during cold
exposure following a grueling 60-day military training course in which
soldiers are underfed, sleep deprived, and physically exhausted (Young
et al., 1998). Degraded thermoregulatory effector responses (shivering
and vasoconstriction) during/following physical exertion may potentially
increase the risk of hypothermia. This degraded effector response was
termed thermoregulatory fatigue(Castellani et al., 1999).
Shivering fatigue has been documented in two studies. Quantitative
evidence for shivering fatigue was reported by Bell et al. (1992). They
found that over a 2-h resting exposure to 10 °C air, the central frequency
of the EMG recording in the shivering pectoralis major decreased with
time, suggesting fatigue of this muscle group. Thompson and Hayward
(Thompson and Hayward, 1996) reported that during a 5-h walk at a
constant pace in cold, rainy conditions, one participant maintained a
stable metabolic rate and deep body temperature for the rst three
hours of exposure, but then exhibited a progressive decline inmetabolic
rate and deep body temperature over the nal 2 h, despite the fact that
walking pace remained unchanged throughout (Thompson and
Hayward, 1996). Another important factor to consider is that shivering
may be blunted due to hypoglycemia. Two studies clearly show that
very low glucose levels (b~ 3 mM) impair metabolic heat production
(Gale et al., 1981; Passias et al., 1996), with the effect most likely
centrally-mediated (Gale et al., 1981).
Follow-up studies were conducted to specicallyexamine if thermo-
regulatory fatigue would occur in different scenarios, including multi-
stressor (physical exhaustion, underfeeding, sleep loss) and multiple
cold-water immersion. In the multiple-stressor studies, shivering
responses were found to be delayed during a cold-exposure trial
performed immediately after completing either an exhaustive 9-week
training course (Young et al., 1998) or 84-h of exertional fatigue, nega-
tive energy balance and sleep loss (Castellani et al., 2003). Fig. 4 shows
the mean body temperature-metabolic heat production response before
and after the 84-h multi-stress period, clearly demonstrating a shift in
the onset/threshold of shivering thermogenesis.
The multiple stressor studies provided insight into possible mecha-
nisms of shivering fatigue, but did not directly answer the question of
whether a muscle that is shivering for long durations fatigues. To deter-
mine whether shivering responses to cold exhibited fatigue, metabolic
heat production was measured during 2-h cold-water immersions
(20 °C) repeated three times, serially in a single day (2-hour rewarming
intervening). Those shivering responses were then compared to meta-
bolic heat production measured during a single immersion completed
at the same time of day (Castellani et al., 1998). Cold-water immersion
produces more rapid core and peripheral cooling and induces higher
shivering rates than cold air, potentially causing fatigue. Similar to the
ndings in the multi-stressor studies, metabolic heat production was
lower during the serial immersions (REPEAT), than when only a single
immersion was completed at that same time of day (CONTROL). The
blunted thermogenic response in REPEAT appeared to be due to a
delay in the shivering onset, i.e. the intercept for the mean body
temperature-change in metabolic heat production relationship shifted
such that the increase in metabolic heat production during the 1100
and 1500 REPEAT exposures was not observed until the subjects
achieved a lower mean body temperature. These data, like the shift in
shivering onset observed in the multiple stressor studies suggests a
centrally-mediated change in the recruitment of muscle for shivering
thermogenesis, and a greater susceptibility to hypothermia.
Follow-on work examined the role of both acute and chronic exer-
cise, without the accompanying stressors of underfeeding and sleep
loss. These studies found that the vasoconstrictor responses to cold ex-
posure were blunted following a short bout (Castellani et al., 1999)or
several days (Castellani et al., 2001) of exercise.
4. Physiological adjustments to prolonged or repeated cold exposure
Humans chronically exposed to cold, either prolonged cold-
exposure periods or a series of repeated, intermittent cold-exposure
periods, experience adjustments
1
in the physiological responses to
cold compared to responses exhibited during acute or initial cold expo-
sure. Chronic heat exposure induces a fairly uniform pattern of physio-
logical adjustments in humans that provide a distinct thermoregulatory
advantage in terms of protecting from heat injury/illness and preserving
physical performance capability. In contrast, depending on the specic
Fig. 4. Metabolic heat production vs. mean body temperature during sedentary exposure
to 10 °C air following 84-h of exertional fatigue, sleep deprivation, and negative energy
balance (SUSOPS) vs. rested conditions (Control). SUSOPS demonstrated a signicant
shift for the onset of s hivering thermo genesis. From Castellani et al. (Cannon and
Keatinge, 1960).
1
The changes in physiological responses experienced by an individual as a result of
chronic or repeated cold exposures are properly termed adjustments. The differences in
physiological responses to cold exhibited by people in population groups who have lived
in cold climates formany generations as compared to people from population groups liv-
ing in warm climate, are termed adaptations.
5J.W. Castellani, A.J. Young / Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
conditions experienced and the degree to which thermal balance is
disrupted, chronic cold exposure can produce three different patterns
of physiological adjustments: 1) habituation, 2) metabolic adjustments,
and 3) insulative adjustments. These three patterns vary considerably,
both qualitatively in terms of the specic nature of the physiological ad-
justments developed, and quantitatively in terms of the thermoregula-
tory advantages conferred by those adjustments. Further, whereas
chronic heat stress typically involves whole-body heating, and the
resulting adjustments produced usually affect the whole-body re-
sponse, cold-exposure can often involve cooling of very limited regions
of the body (e.g., the ngers or nose), while the remainder of the body
(i.e. skin surface and deep body core) are protected from the environ-
mental stress and do not experience signicant cooling. Thus, local or
regional adjustments in physiological responses may be more readily
experienced with chronic cold exposure than with chronic heat expo-
sure. Therefore, the remainder of this paper will review the physiologi-
cal characteristics of different patterns of adjustments exhibited by
humans chronically exposedto cold, and considerthe underlying mech-
anisms thought responsible for their development.
4.1. Habituation
The most commonly observed pattern of thermoregulatory adjust-
ments observed in response to chronic or repeated cold exposure is
habituation. As habituation develops, physiological responses to cold
become less pronounced (blunted shivering, blunted cutaneous vaso-
constrictor response or both) than in the unacclimatized state (Young,
1996). Indigenous circumpolar residents such as the Inuits (Andersen
et al., 1960; Hart et al., 1962; Hildes, 1963), other Native North
Americans from the Arctic (Elsner et al., 1960; Irving et al., 1960) and
Norwegian Saami (Andersen et al., 1960) appear to respond to whole-
body cold exposure in the same general manner as persons indigenous
to temperate climates, that is metabolic heat production increases due
to shivering, and skin temperature and peripheral heat loss decrease
due to vasoconstriction of peripheral blood vessels. However, when
comparedto people from temperate climates, the increase in metabolic
heat production associated with shivering (as reected by the increase
in VO
2
) and the vasoconstriction of peripheral blood vessels (as
reected by the decline in skin temperature) appear less pronounced
in circumpolar residents, as demonstrated in studies of Norwegian
Saami shown in Fig. 5 (Andersen et al., 1963).
Habituation can be produced even if cold exposure is limited to rel-
atively small regions of the body as opposed to whole-body exposures.
For example, shermen and sh lleters work long hours every day
with one or both hands immersed in cold water, and these people
have been shown to maintain higher nger and hand temperatures
and lower systemic blood pressures during hand immersion in cold
water compared to control subjects (LeBlanc, 1988; LeBlanc et al.,
1960; Nelms and Soper, 1962). Slaughterhouse workers who handle
cold meat tend to show similar effects, although the effects are not as
pronounced (Enander et al., 1980). This suggests that repeated localized
cold exposure can produce localized habituation of vasoconstrictor re-
sponses. There is also evidence that repeated localized cold exposures
can induce habituation of the whole-body vasoconstrictor response to
cold (Savourey et al., 1996).
Genetic adaptations could conceivably account for differences in the
shivering and vasoconstrictor responses to cold observed in cross-
sectional comparisons of people indigenous to circumpolar regions
and people from temperate conditions, and in comparisons of people
from different occupations. However, longitudinal acclimatization stud-
ies have shown that habituation can also be induced in varying degrees
in people from temperate climate regions who experience repeated,
intermittent periods of cold exposure (Armstrong and Thomas, 1991;
Hesslink et al., 1992; Marino et al., 1998; Mathew et al., 1981; Silami-
Garcia and Haymes, 1989). The variation in the degree of habituation
developed in response to cold exposure appears related to the severity
of stress, i.e., duration of cold exposure, suggesting that physiological
mechanisms rather than genetic adaptations are responsible for devel-
opment of habituation. For example, in studies acclimating subjects to
fairly brief cold exposures, habituation effects are usually limited to
blunting of shivering (Armstrong and Thomas, 1991; Hesslink et al.,
1992; Silami-Garcia and Haymes, 1989), whereas in studies employing
longer exposure durations and/or a longer acclimatization periods,
more pronounced habituation of both shivering and vasoconstrictor re-
sponses to cold are seen (Marino et al., 1998; Mathew et al., 1981). The
blunting of shivering and vasoconstrictor responses that develop with
habituation, whether produced by livingin cold climates or by acclimat-
ing to repeated, intermittent cold exposure, can be sufciently pro-
nounced so as to allow a greater fall in core temperature during cold
exposure than experienced by non-habituated people (i.e., a hypother-
mic pattern of habituation, as shown in the responses of the Saami
shown in Fig. 1)(Andersen et al., 1960; Davis, 1961; Keatinge, 1961;
Kreider et al., 1959; Marino et al., 1998). Data also suggest that in-
creased physical tness may also blunt the vasoconstrictor response as
evidenced by higher overall mean skin and peripheral temperatures
(Adams and Heberling, 1958; Heberling and Adams, 1961). The specic
physiological mechanisms underlying the blunting of shivering and va-
soconstrictor responses to cold are not clearly dened, but some studies
provide evidence suggesting that following chronic or repeated cold ex-
posures, habituation is accompanied by reduced sympathetic nervous
activation and enhanced parasympathetic activation during exposure
to cold (Harinath et al., 2005; Makinen et al., 2008). For example,
Fig. 5. Oxygenuptake, and skin and rectaltemperature responses duringan overnight cold
exposure (0 °C) between Norwegain Saami and European controls. Data demonstrate a
cold habituation response, i.e., thermal effector responses are blunted (lower metabolic
heat production, less vasoconstriction) in the indigenous circumpolar residents. Drawn
from data reported by Andersen et al. (Andersen et al., 1960).
6J.W. Castellani, A.J. Young / Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
Leppaluoto et al. (Leppäluoto et al., 2001) demonstrated after 11days of
cold air exposure (2 h·d
1
; 10 °C), the norepinephrine response to cold
was reduced by 20%.
4.2. Metabolic Acclimatization
Some researchers have suggested that chronic cold exposures can
result in development of a more pronounced thermogenic response to
cold (Young, 1996). This pattern of cold adjustment has been termed
metabolic acclimatization.Either exaggerated shiveringor development
of nonshivering thermogenesis could account for a more pronounced
thermogenic response to cold during metabolic acclimatization.
Circumpolar residents (e.g., Alaskan Inuits and other Native
Americans) reportedly maintain higher resting metabolic rates than
subjects from temperate climates, enabling them to maintain warmer
skin temperatures with less shivering during cold exposure (Young,
1996). However, the increased metabolic rate of circumpolar residents
was also apparent in warm conditions, not just during cold exposures,
suggesting that this adjustment was not specic to chronic cold expo-
sure, but perhaps attributable to other factors such as diet (Leonard
et al., 2014; Leonard et al., 2002; Rennie et al., 1962; Rodahl, 1952;
Snodgrass et al., 2005). Similarly increased metabolic rates during cold
exposures were observed by Hammel (1960) in Alacaluf people com-
pared to unacclimatized European subjects. The Alacaluf were nomadic
Native Americans who at the time that Hammel did these studies
(Hammel, 1960) were living in fairly primitive conditions (unheated
dwellings and minimal clothing) on coastal islands off the southern
tip of South America in constantly rainy and cold weather, but here
again, whether the higher metabolic rate of the Alacaluf was really an
adjustment to chronic cold exposure or the effects of diet and lifestyle
cannot be determined. Finally, the Ama diving women of Korea, report-
edly experienced a substantial increase in basal metabolic rate between
summer and winter (Kang et al., 1963). At the time that these studies
were conducted, the Ama divers dove daily without protective wet
suits in water ranging in temperature from 27 °C in summer to as low
as 10 °C in winter (Kang et al., 1963). Non-diving women from the
same communities as the diving women were observed to maintain a
constant basal metabolic rate throughout the year, strongly suggesting
the seasonal elevation in metabolic rate of diving women was an effect
of chronic cold, and not an effect of diet or other lifestyle factors (Kang
et al., 1963). Regardless of what stimulated these adjustments, there
was no apparent thermoregulatory benet of the higher basal metabolic
rates. For example, the body temperatures of the Ama women fell much
lower during winter diving and they were unable to continue working
as long compared to summer diving (Kang et al., 1963).
Those aforementioned studies all employed cross-sectional compar-
isons of persons chronically exposed to cold to control subjects lacking
that chronic cold-exposure experience, making it difcult to determine
whether differences observed reect the effects of chronic cold or other
factors. However, there have also been some longitudinal studies
(i.e., employing subjects repeatedly measured throughout a series of
cold exposures) suggesting that a metabolic pattern of cold acclimatiza-
tion can develop in people who normally live in temperate climates. In
one of the oldest and most often cited such studies, Davis (1961) report-
ed that men who were acclimatized for 31 days by spending eight hours
per day exposed in a chamber to mild cold air (12 °C) conditions, dem-
onstrated an enhanced non-shivering thermogenesis in response to
cold exposure. Davis observed that (see upper panel of Fig. 6), while
both metabolic heat production (measured by open-circuit respirome-
try) and shivering intensity (measured from EMG activity of the upper
arm and thigh) during cold exposure declined over the course of the
cold acclimatization program, the decrease in shivering (EMG activity)
appeared to be more pronounced than the decrease in metabolic heat
production, therefore he concluded that non-shivering thermogenesis
must have developed to offset the decline in shivering. However,
when Davis' data are replotted (see lower panel of Fig. 6), it can be
seen that, in fact, the decline in metabolic heat production during cold
acclimatization was, in fact, closely correlated with the decline in shiv-
ering EMG activity. Further, the assumption that decreases in the EMG
activity of the arm and thigh muscles are representative of a decline in
whole-body shivering is probably unjustied, since shivering activity
of other muscle groups could have increased. Thus, the ndings report-
ed by Davis (1961) should not be interpreted as conclusively demon-
strating development of non-shivering thermogenesis during cold
acclimatization.
A similar approach was used in a more recent study claiming to
demonstrate the development of non-shivering thermogenesis as a re-
sult of cold acclimatization during winter (Nishimura et al., 2012).
These investigators measured metabolic rate using indirect calorimetry,
and shivering by EMG activity of the pectoralis major in 17 young men
during 80-min cold chamber exposures (16 °C) performed once in the
summer again during the following winter. The authors reported that
metabolic rate averaged about 0.15 kcal/min higher during the cold ex-
posures performed during the winter compared to those performed
during summer, but EMG activity of the pectoralis major was the
same in both exposures, leading them to conclude that a non-
shivering thermogenic response to cold had developed as a result of
chronic cold exposure during winter. However, the difference in meta-
bolic heat production between winter and summer was quite small,
equivalent to about 30 ml/min of oxygen consumption, which is very
close to the limit of resolution for human metabolic rate measured
using indirect calorimetry with most metabolic carts. Further, as men-
tioned above, assuming that EMG activity of a single muscle group
Fig. 6. Effect of 31 days of cold acclimatization on the metabolic and shivering
electromyogram (EMG) responses (Davis, 1961). Top panel shows that over the course
of acclimatizati on, the decrease in shivering activity was greater than the decline in
metabolic rate, which was interpreted as an enhancement of non-s hivering
thermogenesis. However, when Davis' data are replotted (lower panel), the decline in
metabolic heat production during cold acclimatization was closely correlated with the
decline in shivering EMG activity.
7J.W. Castellani, A.J. Young / Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
adequately quanties whole-body shivering activity is a faulty assump-
tion, since many other muscle groups can be recruited during shivering.
In another recent study (van der Lans et al., 2013), a cold chamber
acclimatization program (10 consecutive days, 6 h/day, 15 °C air) re-
portedly increased non-shivering thermogenesis in brown fat stores of
17 healthy, unacclimatized young men and women. During a standard-
ized 50-min exposure to mild cold conditions in a water-perfused
cooling suit before acclimatization, metabolic heat production (mea-
sured using indirect calorimetry) of the subjects increased from
1.123 kcal/min in thermoneutral conditions to 1.266 kcal/min, and the
authors calculated that about 11% of the 0.143 kcal/min increment (i.e.
about 0.016 kcal/min) in metabolic heatproduction duringbody cooling
was attributable to non-shivering thermogenesis (measured by cold-
induced uptake of tracer labeled glucose by the subjects' brown adipose
tissue). After acclimatization, metabolic heat production increased from
1.123 kcal/min during thermoneutral conditions to 1.314 kcal/min dur-
ing cooling, and the non-shivering component was calculated to ac-
count for about 18% of the 0.191 kcal/min increment (i.e. about
0.021 kcal/min) in metabolic heat production during cooling. The au-
thors contended that this cold-acclimation enhancement of non-
shivering thermogenesis was important from the standpoint of whole-
body energy balance, and they suggested that intermittently reducing
indoor temperatures to induce human cold acclimatization could be
an effective strategy for body weight management and obesity preven-
tion. However, their data indicate that even if cold-induced non-
shivering thermogenesis were sustained for 24 h per day, it would
only generate an additional 30 kcal/day of metabolic heat production,
and whether such an increment in metabolic rate would have implica-
tions for body weight loss is debatable.
Regardless, even if the cold-induced increments in metabolic heat
production that Nishimura et al. (2012) and van der Lans et al. (2013)
observed associated with cold acclimatization are attributable to non-
shivering thermogenesis, the magnitude of this non-shivering thermo-
genesis is probably inconsequential for thermoregulation. Metabolic
rate typically reaches 35 kcal/min during cold-induced shivering
(Sawka et al., 2012), and in one study, shiveringwas observed to elevate
metabolic rate to about 11 kcal/min (Golden et al., 1979). Therefore, on
whole, there is currently little evidence that cold acclimatization pro-
duces sufcient enhancement of the thermogenic response to cold
(shivering or non-shivering) to provide any meaningful thermoregula-
tory benet for cold-exposed humans.
The third major pattern of human cold acclimatization, referred to as
insulative acclimatization, is characterized by enhanced heat conserva-
tion mechanisms (Young, 1996). With insulative acclimatization, ther-
mal conductance at the skin is lower during cold exposure than
observed in the unacclimatized state. Typically but not always, with
this pattern of acclimatization, cold-exposure elicits a more rapid and
more pronounced cutaneous vasoconstrictor response. As a result, the
decline in skin temperature during cold exposure is greater in the accli-
matized than unacclimatized state.
Evidence for this pattern of acclimatization was rst observed in
older studies in which thermoregulatory responses of Aborigines living
in the central Australian desert were measured while they slept naked
outdoors in 5 °C cold air, and compared to responses of unacclimatized
European control subjects exposed to similar conditions. At the time
when these studies were completed, the central Australian Aborigines
were nomadic people who lived out of doors, wore no clothing, and at
night they slept on bare ground with little or no protection from the
cold. Whereas the metabolic rate of unadapted European subjects
sleeping in the cold increased, the Aborigine's metabolic rate remained
unchanged as ambient temperature fell, and their deep body core and
skin temperatures fell more than in the Europeans, thus thermal con-
ductance (metabolic heat production divided by the core to skin tem-
perature gradient) was less in the Aborigine than unacclimatized
Europeans (Hammel et al., 1959; Hicks, 1964; Scholander et al., 1958;
Stanton Hicks and O'Connor, 1938). A lower thermal conductance
could reect greater insulation in the body's peripheral shell due to a
more pronounced cutaneous vasoconstrictor response to cold as a result
of cold acclimatization, or it might simply reect the lower metabolic
heat production (i.e., habituated shivering) in the acclimatized Aborig-
ines compared to unacclimatized control subjects.
More denitive evidence for development of an insulative pattern of
cold acclimatization was observed in studies of the Ama diving women
of Korea, whose chronic cold exposure experiences were described in
the previous section of this paper. Hong (1973) measured maximal tis-
sue insulation (the reciprocal of thermal conductance) of divers and
non-diving Koreans from the same community while they were im-
mersed in water cool enough to elicit maximal vasoconstriction, but
without shivering. Maximal tissue insulation is a measure of the
individual's ability to resist body heat loss during cold exposure. Even
after accounting for variations in subcutaneous fat thickness (which
also inuences maximal tissue insulation as described earlier in this ar-
ticle), the Ama divers exhibited greater insulation than non-divers. In-
terestingly, the enhanced insulation of the diving women did not
appear to be the result of a more pronounced vasoconstrictor response
to cold. Hong et al. (1969) measured forearm blood ow and forearm
heat loss of diving and non-diving Koreans during immersion in three,
progressively cooler water temperatures. Forearm blood ow decreased
in both divers and non-divers as water temperature declined, but as
shown in Fig. 7, the diving women actually maintained higher forearm
blood ow than non-divers ateach water temperature. Even more nota-
ble, in each of the water temperature conditions, forearm heat loss was
less in divers than non-divers, despite the higher blood ow. Thus, this
pattern of acclimatization enabled the divers to resist heat loss, while
better maintaining blood ow to metabolically active tissue during
their work in the water. Hong et al. (1969) speculated that the insulative
acclimatization exhibited by the Ama divers represented development
of an improved counter-current heat exchange mechanism in the
peripheral circulatory system. However, studies to conrm that specu-
lation are not available. Since 1977, the Ama divers have worked
Fig. 7. Forearm blood ow and forearm heat ow during 3 cold water exposures (30, 31,
33 °C) in Ama diver s and controls. Fo rearm blood ow d ecreased in both divers and
non-divers as wate r temperature declined, but the Ama maintained higher for earm
blood ow than non-divers at each water temperature , suggesting a blunted
vasoconstrictor response, without the accompanying increase in heat loss. Data redrawn
from Hong et al. (Hong et al., 1969)
8J.W. Castellani, A.J. Young / Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
wearing wet suits, lessening the cold stress experienced during the div-
ing periods, and in more recent studies of the Ama divers, the insulative
pattern of cold acclimatization was no longer apparent (Park et al.,
1983).
Studies in which unacclimatized people undergobrief immersions in
mild to moderately cold water repeated for a few days or a week, dem-
onstrate that those cold exposure conditions can produce habituation,
but are not severe enough to causethe insulative pattern of acclimatiza-
tion to develop (Lapp and Gee, 1967; Radomski and Boutelier, 1982). On
the other hand, longer acclimatization periods employing more
prolonged and colder water immersions may produce insulative accli-
matization. In a study reported by Young et al. (1986, 1987), healthy
young men lacking signicant prior cold exposures completed a cold
acclimatization program consisting of 90 min of immersion in 18 °C
water, repeated ve days per week for eight weeks, and developed
some physiological adjustments consistent with hypothermic habitua-
tion (i.e., blunted thermogenic response to cold), but otheradjustments
were more consistent with the development of an insulative type of
cold acclimatization. For example, following repeated cold-water im-
mersion,cold-air exposure caused a more pronounced rise in blood nor-
epinephrine concentrations and a greater decline in skin temperature
than before acclimatization, suggesting that a more pronounced cutane-
ous vasoconstrictor response to cold had developed. In addition, a
smaller increment in blood pressure during cold exposure was observed
after acclimatization, while cardiac output responses to cold were unaf-
fected (Muza et al., 1988). The blunting of the systemic pressure re-
sponse to cold despite pronounced cutaneous vasoconstriction
indicated that subcutaneous vascular beds were better perfused follow-
ing acclimatization. Subsequent studies of the effects of prolonged, daily
cold water immersions repeated over several weeks provide similar
ndings conrming the development of enhanced vasoconstrictor re-
sponses to cold under these severe exposure conditions (Bittel, 1987;
Jansky et al., 1996a, 1996b; Skreslet and Aarefjord, 1968). An insulative
adaptation has also been observed in cold-water swimmers. Golden
et al (Golden et al., 1980) showed that swimmers who regularly trained
in cold water were better able to maintain core temperature, apparently
from an enhanced vasoconstrictor response. More recently, insulative
adaptations have also been demonstrated in adult and young children
who regularly swim in cold water (Bird et al., 2012; Hingley et al.,
2011). Interestingly, during sedentary immersion in cold-water,
acclimatized swimmers respond with a decline in core temperature
(Hingley et al., 2011), whereas during exercise on cold-water, no de-
cline in core temperature is observed along with a concomitant increase
in vasoconstrictor tone. Thus, as was suggested to have occurred in the
Korean diving women, acclimatization by prolonged cold-water immer-
sion, repeated over long periods may cause development of mecha-
nisms enabling better heat conservation by improved insulation at the
body surface, while perfusion of the subcutaneous shell is more opti-
mally maintained than before acclimatization.
Several studies have examined the role of reductions in skin and/or
core temperature in inducing physiological adaptations. O'Brien et al.
(2000) had two groups of subjects immersed in cold water (20 °C;
5 d·wk
1
; 60 min·d
1
); one group exercised so they experienced a
fall in skin temperature but not core, whereas the other group rested
during immersion and experienced a decline in both skin and core tem-
perature. A standardized cold-air test was used before and after accli-
mation to determine physiological changes. Their data show that
lowering skin temperature alone (exercise group) caused an insulative
or enhanced vasoconstrictor response, but to effect a change in sympa-
thetic nervous activity, both core and skin temperatures (resting
group). More recently, Tipton et al. (2013) used a similar experimental
design where one group experienced core and skin cooling (45-min im-
mersion in 12 °C water), whereas the other group only experienced skin
cooling (5-min immersion). Their ndings demonstrated a habituation
of the metabolic response during the initial (cold-shock, rst 5-min)
and middle stages (from 6-min to a 1.2 °C decrease in core tempera-
ture) of immersion in the group that had a reduction in both core and
skin temperature, with no changes observed in the skin-cooling-only
group. These recent ndings are in agreement with an earlier study by
Golden and Tipton (1988) that demonstrated resting cold-water expo-
sure elicits a blunting of the metabolic response to cold.
4.3. What Determines Which Pattern of Cold Acclimatization Develops?
A theoretical model, shown in Fig. 8, has been proposed (Young,
1996) to explain how the pattern of physiological adjustments that de-
velop with cold acclimatization is determined by the specicnatureof
the cold exposure and the associated physiological strain experienced.
The model's central premise isthat the key determinant for whether ha-
bituation, metabolic acclimatization or insulative acclimatization de-
velops is the degree to which cold exposure results in signicant
body-heat loss (Young, 1996). In this construct, repeated short cold
Fig. 8. Flowchart demonstrating a theoretical model of different patterns of human cold acclimatization.
9J.W. Castellani, A.J. Young / Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
exposures involving only limited parts of the body andproducingtrivial
whole body heat losses will promote development of habituation. In
contrast, repeated cold exposures that are prolonged and/or severe
enough to preclude body heat loss being balanced by increased thermo-
genesis (i.e., deep body temperature declines signicantly during expo-
sures) will promote development of insulative thermoregulatory
adjustments. The model also incorporates the possibility that the body's
thermogenic capability (either shivering or non-shivering) could be im-
proved if repeated exposure to cold conditions produces signicant
body heat loss, but concomitant increases in thermogenesis are suf-
ciently to balance body heat loss and prevent signicant core tempera-
ture declines. Thus, metabolic adjustments would most likely result
from chronic exposure to mild or moderatecold environments, whereas
insulative adjustments would result from more severe cold exposures.
Another possibility, which could be consistent with the model, is that
habituation, metabolic acclimatization and insulative acclimatization
are not really different types of cold acclimatization, but rather different
phases in a progressive development of complete cold acclimatization.
5. Summary
In cold environments, humans maintain thermal balance through
behavioral and physiological changes. When behavioral thermoregula-
tory strategies are inadequate, two primary effector responses are
acutely elicited to defend body temperature, cutaneous vasoconstric-
tion and shivering thermogenesis. Cutaneous vasoconstriction de-
creases heat loss to the environment by reducing the skin-to-
environment thermal gradient and is elicited through reex and local
cooling by adrenergic and non-adrenergic mechanisms. Shivering is ini-
tiated by decreases in skin temperature, with the intensity affected by
the magnitude of changes in core temperature. Maximal shivering in-
creases metabolic heat production ~ 34 times above resting levels.
Chronic cold exposure induces three distinct patterns of physiological
adjustments: habituation, metabolic adjustments, and insulative adjust-
ments. Habituation causes an attenuated vasoconstrictor and shivering
response; a metabolic acclimatization leads to an increase in metabolic
heat production, and insulative adjustments cause an enhanced vaso-
constrictor response to cold exposure. The type of acclimatization re-
sponse is dependent on the type and severity of chronic cold exposure.
Acknowledgments
Approved for public release; distribution is unlimited.
The opinions or assertions contained herein are the private views of
the author(s) and are not to be construed as ofcial or reecting the
views of the Army or the Department of Defense.
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12 J.W. Castellani, A.J. Young / Autonomic Neuroscience: Basic and Clinical xxx (2016) xxxxxx
Please cite this article as: Castellani, J.W., Young, A.J., Human physiological responses to cold exposure: Acute responses and acclimatization to
prolonged exposure, Auton. Neurosci. (2016), http://dx.doi.org/10.1016/j.autneu.2016.02.009
... The risk ratios were lower in the 1997-cohort, and mainly due to a higher number of persons without cold-related symptoms. Among ostensibly healthy persons, cardiac symptoms in cold weather may relate to activation of the autonomic nervous system induced by body cooling (Castellani and Young, 2016). The increased sympathetic activity elicits vasoconstriction of the superficial vasculature, thus augmenting blood pressure and cardiac work (Ikäheimo, 2018). ...
... Especially age and gender weakened the unadjusted associations between cold-related symptoms and health outcomes. Ageing involves varying effects on nervous, metabolic and circulatory functions related to progressive deterioration of thermoregulation (Castellani and Young, 2016;Greaney et al., 2016;Degroot and Kenney, 2007). Women usually report more symptoms than men, also shown in our previous studies Näyhä et al., 2002;Harju et al., 2010). ...
... Women usually report more symptoms than men, also shown in our previous studies Näyhä et al., 2002;Harju et al., 2010). This can be due to the higher heat loss and lowered bodily heat production in the cold, which increases their susceptibility (Castellani and Young, 2016). Women also tend to report more symptoms in general (Degroot and Kenney, 2007;Barsky et al., 2001;Kroenke and Spitzer, 1998). ...
Article
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Background Symptoms perceived in cold weather reflect physiological responses to body cooling and may worsen the course of a pre-existing disease or precipitate disease events in ostensibly healthy individuals. However, the associations between cold-related symptoms and their health effects have remained unknown. We examined whether cold-related cardiac and respiratory symptoms perceived in cold weather predict future morbidity and mortality. Methods: Cold related symptoms were inquired in four national FINRISK surveys conducted in 1997, 2002, 2007, 2012 in Finland including altogether 17 040 respondents. A record linkage was made to national hospital discharge and cause-of-death registers. The participants were followed up until the first hospital admission due to a cardiovascular or respiratory disease or death, or until the end of 2015. The individual follow-up times ranged from 0-18 years (mean 11 years). The association of cold-related symptoms with morbidity and mortality was examined by Kaplan-Meyer and Cox-regression analyses. Results: Cold-related cardiac [hazard ratio (HR), 1.76 and its 95% confidence interval (95% CI), 1.44-2.15] and combined cardiac and respiratory symptoms [1.50 (1.29-1.73)] were associated with hospitalization due to cardiovascular causes. The respective HRs for admissions due to respiratory causes were elevated for cold-related respiratory [1.22 (1.07-1.40)], cardiac [1.24 (0.88-1.75)] and cardiorespiratory [1.82 (1.50-2.22)] symptoms. Cold-related cardiorespiratory symptoms were associated with deaths from all natural [1.38 (1.11-1.72)], cardiovascular [1.77 (1.28-2.44)] and respiratory [2.19 (0.95-5.06)] causes. Interpretation: Cold weather-related symptoms predict a higher occurrence of hospital admissions and mortality. The information may prove useful in planning measures to reduce cold-related adverse health effects.
... Cold exposure, e.g., under climatic conditions of the North, has a significant impact on human health; it modifies clinical parameters in healthy people [1] and constitutes a risk factor for the development of various pathologies [2]. This is especially true for residents of temperate climatic zones moving to the North for various reasons: they adapt to cold by any of the possible mechanisms suitable for particular individuals [3,4]. ...
... At the same time, in the context of the expanding area of human presence, it should be noted that the range of cold temperatures acceptable for adaptation is significantly wider than the range of heat temperatures, due to physical and chemical properties of proteins in the human body. Importantly, the processes of adaptation to both cold and heat are accompanied by changes in the cardiovascular system [1][2][3]29] and in its autonomic regulation, which can be registered in the analysis of HR and BP variability [30]. ...
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Objectives: A method of continuous heart rate (HR) and blood pressure (BP) recording was used for the evaluation of the cardiovascular system parameters in participants of short-term (<1 month) high-latitude expeditions, in comparison with the parameters of residents of Central Russia and the Arctic region. Material and methods: A dynamic examination of participants of Arctic expeditions (30 men, residents of middle-latitude regions, aged 46.7±1.7 years), workers permanently living in Central Russia (the Moscow region, 44 men, aged 46.7±1.0 years) and residents of the North (the Murmansk region, 35 men, aged 46.6±1.3 years) was performed. The authors used a spiroartheriocardiorythmograph allowing the parallel recording of HR, BP, spectral characteristics of HR variability (HRV) and the variability of systolic BP (sBP) and diastolic BP (dBP), cardiac performance parameters, and spontaneous baroreflex sensitivity (BRS). The parameters were recorded at rest, in a sitting position, over 2 min. Results: The basic clinical parameters (HR, BP and cardiac performance) did not differ in the workers living in different climatic zones. However, the residents of the North demonstrated a lower total power (TP) of the dBP variability spectrum and a lower relative power of the high-frequency (HF) range in both the sBP and dBP variability spectra. The participants of expeditions to the North had a lower TP of the HRV spectrum (in comparison with both control groups) that did not change during the expeditions; BRS was reduced, while the TP of the sBP spectrum was increased in comparison with the corresponding parameters obtained from the residents of circumpolar regions, and decreased during the expedition in parallel with a decrease in the sBP values. The TP of both the sBP and dBP variability spectra, as well as the power of the HF range in these spectra, were similar in the participants of expeditions to those obtained from the residents of Central Russia, and they considerably surpassed the corresponding parameters in the northerners surveyed. Conclusions: The revealed peculiarities of the cardiovascular system in the participants of high-latitude expeditions can be considered as correlates of positive, and adequate in terms of the physiological value, adaptive shifts in the autonomous regulation of the cardiovascular system.
... Hygienic requirements presuppose working at low temperatures, ranging from approximately 0°C to 15°C in production halls to − 20°C in cold storages [2]. Low temperatures combined with physical loading factors may precipitate respiratory [3], cardiovascular [4], and musculoskeletal symptoms, as well as peripheral circulation disturbances, particularly in fingers and hands [5][6][7][8][9]. Low temperatures also negatively affect physical and mental performance [10,11] and lead to decreased work ability and productivity. ...
... Decreased lung function has been reported among cold storage workers [13]. However, people living in cold climates have adapted to low temperatures and are less sensitive to occupational cold exposure [7]. ...
Article
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Background: Few studies have examined cold-related symptoms among cold workplace workers in Thailand. This study aimed to determine the prevalence of cold-related cardiorespiratory, circulatory, and general symptoms and performance degradation among Thai chicken industry workers and identify vulnerable groups. Methods: Overall, 422 workers aged from 18 to 57 years at four chicken meat factories in Thailand were interviewed for cold-related symptoms and complaints. The results were expressed in terms of model-based adjusted prevalence and prevalence differences (PDs) in percentage points (pp) with 95% confidence intervals (CIs). Results: In total, 76.1% of the respondents reported cold-related respiratory symptoms, 24.6% reported cardiac symptoms, 68.6% reported circulatory symptoms, and 72.1% reported general symptoms. In addition, 82.7% of the respondents reported performance degradation. Cold-related respiratory symptoms increased by PD 29.0 pp. (95% CI 23.4-34.6) from the lowest to the highest educational group, with a similar pattern observed in performance degradation. Forklift drivers and storage and manufacturing workers complained of cold-related respiratory symptoms more than office staff (PD 22.1 pp., 95% CI 12.8-31.3; 12.0 pp., 95% CI 2.4-21.6; and 17.5 pp., 95% CI 11.5-23.6, respectively); they also reported more performance degradation (PD 24.1 pp., 95% CI 17.0-31.2; 19.8 pp., 95% CI 14.1-25.6; and 14.8 pp., 95% CI 8.0-22.6, respectively). Weekly alcohol consumers reported more performance problems owing to cold (PD 18.2 pp., 95% CI 13.9-22.6) than non-consumers of alcohol. Cardiac and circulation symptoms were more common in women than men (PD 10.0 pp., 95% CI 1.1-18.9; and 8.4 pp., 95% CI 0.5-16.4, respectively). The age trend in performance issues was curved, with the highest prevalence among those aged 35-44 years, while the oldest workers (45-57 years) perceived less cold-related symptoms, particularly thirst. Conclusions: Cold-related symptoms and performance degradation were found to be common in this industry, with vulnerable groups comprising of highly educated workers, forklift drivers, storage and manufacturing workers, weekly alcohol consumers, aging workers, and women. The results demonstrate a need for further research on the adequacy of protection provided against the cold, particularly given that global warming will increase the contrast between cold workplaces and outdoor heat.
... In fact, males presented 8.4% more cases of fatigue than females. This difference may be explained by the higher percentage of muscle mass in males (Castellani & Young, 2016). The lower muscle mass in females limits their thermogenic response capacity although this lower adaptation to thermal change is not a limitation but rather makes females more thermally competent when using this type of PPE (Mantooth, Mehta, Rhee, & Cavuoto, 2018). ...
Article
Background More recently, due to the coronavirus disease 2019 pandemic, health care workers have to deal with clinical situations wearing personal protective equipment (PPE); however, there is a question of whether everybody will tolerate PPE equally. The main objective of this study was to develop a risk model to predict whether health care workers will tolerate wearing PPE, C category, 4B/5B/6B type, during a 30-minute simulation. Methods A nonexperimental simulation study was conducted at the Advanced Simulation Center, Faculty of Medicine, Valladolid University (Spain) from April 3rd to 28th, 2017. Health care students and professionals were equipped with PPE and performed a 30-minute simulation. Anthropometric, physiological, and analytical variables and anxiety levels were measured before and after simulation. A scoring model was constructed. Results Ninety-six volunteers participated in the study. Half the sample presented metabolic fatigue in the 20 minutes after finishing the simulation. The predictive model included female sex, height, muscle and bone mass, and moderate level of physical activity. The validity of the main model using all the variables presented an area under the curve of 0.86 (95% confidence interval: 0.786–0.935), and the validity of the model had an area under the curve of 0.725 (95% confidence interval: 0.559–0.89). Conclusions Decision-making in biohazard incidents is a challenge for emergency team leaders. Knowledge of health care workers' physiological tolerance of PPE could improve their performance.
... Adaptive changes in the body's thermoregulatory system include such functional modifications as a change in the capacity of effector systems, a decrease in the energy cost of maintaining temperature homeostasis, an increase in the physiological efficiency of heat generation, and a change in regulatory characteristics. [1,2,3]. ...
... a Adjusted for multiple cofounders, including infant sex, maternal age, race, marital status, parity, pre-pregnancy BMI, hypertensive disorders of pregnancy, gestational diabetes, insurance status, alcohol and smoking use during pregnancy, humidity, particulate matter with diameter <2.5 μm, ozone, and season of conception. (Lian et al., 2017;Castellani and Young, 2016;Poston, 1997). As such, it is possible that even small changes in temperature may affect thermoregulatory capabilities, and therefore health outcomes in pregnancy, although further research on these mechanisms related to stillbirth is needed. ...
Article
Background Ambient temperature events are increasing in frequency and intensity. Our prior work in a U.S. nationwide study suggests a strong association between both chronic and acute temperature extremes and stillbirth risk. Objective We attempted to replicate our prior study by assessing stillbirth risk associated with average whole-pregnancy temperatures and acute ambient temperature changes in a low-risk U.S. population. Methods Singleton deliveries in the NICHD Consecutive Pregnancies Study (Utah, 2002-2010; n=111,505) were identified using electronic medical records. Ambient temperature was derived from the Weather Research and Forecasting model. Binary logistic regression determined the adjusted odds ratio (aOR) and 95% confidence interval (95% CI) for stillbirth associated with whole-pregnancy exposure to extreme cold (<10th percentile) and hot (>90th percentile) versus moderate (10th-90th percentiles) average temperature, adjusting for maternal demographics, season of conception, hypertensive disorders of pregnancy, and gestational diabetes. In a case-crossover analysis, we estimated the stillbirth adjusted odds ratio (aOR) and 95% CI for each 1° Celsius increase during the week prior to delivery using conditional logistic regression. In both models, we adjusted for relative humidity, ozone, and fine particulates. Results We observed 500 stillbirth cases among 498 mothers. Compared to moderate temperatures, whole-pregnancy exposure to extreme cold (aOR: 4.42, 95% CI:3.43, 5.69) and hot (aOR: 5.06, 95% CI: 3.34, 7.68) temperatures were associated with stillbirth risk. Case-crossover models observed a 7% increased odds (95% CI: 1.04, 1.10) associated with each 1° Celsius increase during the week prior to delivery. Discussion Both chronic and acute ambient temperature were associated with odds of stillbirth in this low-risk population, similar to our prior nationwide findings. Future increases in temperature extremes are likely and the observed risk in a low-risk population suggests this association merits attention.
... Environment International 142 (2020) 105851 were defined as workers in the present study, women working as farmers tend to take part in agricultural activity, which may increase their exposure to cold-weather environments (e.g., high winds, rain/ water exposure and low temperature). Chronic cold exposures can produce metabolic adjustments to keep thermal balance, which is also called as cold acclimatization (Castellani et al. 2016). For example, residents in cold climates reportedly maintain higher resting metabolic rates than subjects from temperate climates, enabling them to maintain warmer skin temperatures with less shivering during cold exposure (Young, 2011). ...
Article
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Background Little is known about the effect of ambient temperature on preterm birth, especially for the trimester-specific effects. Objective To evaluate whether exposure to relatively low or high temperature during pregnancy is associated with increasing risk of preterm birth or not. Method We analysed the data of a birth cohort with 1,281,859 singleton pregnancies during 2013–2014 and matched the home address of each pregnant women to the model based daily meteorological and air pollution data. Then we used the Cox proportional hazard regression models with random effect to estimate the non-linear associations between exposure to relatively low or high temperature at each trimester of pregnancy and the risk of preterm birth, after controlling for air pollution and individual-level covariates. Finding The overall preterm birth rate was 8.1% (104,493 preterm births). Exposure to relatively low or high temperatures during the entire pregnancy significantly increase the risk of preterm birth, with hazard ratios (HRs) [95% confidence intervals (CIs)] of 1.03 (95%CI: 1.02, 1.04) for relatively low (9.1 ℃, the 5th percentile) temperature and 1.55 (95%CI: 1.48, 1.61) for relatively high (23.0 ℃, the 95th percentile) temperature in comparison with the thresholds (12.0 ℃). Pregnant women at the early pregnancy (the 1st and 2nd trimester) are more susceptible to high temperatures while pregnant women at the late pregnancy (the 3rd trimester) are more susceptible to low temperatures. Conclusion These findings provide new evidence that exposure to relatively low or high temperatures during pregnancy increases the risk of preterm birth, which can serve as scientific evidence for prevention of preterm birth.
... Initially, we have to describe a phenomenon known as coldinduced vasodilation (CIVD) or the hunting reflex. This refers to a paradoxical vasodilatation that often occurs in the acral areas to modulate the effects of vasoconstriction, which is, in its turn, the first body response to cold [13,14]. Indeed, people living in cold regions often have a stronger CIVD reaction in the peripheral vessels, in comparison to those living in warm or tropical countries. ...
Article
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Rosacea is a chronic inflammatory cutaneous condition, characterized by facial redness in the first stages, followed by papules, pustules and deformities later on the course. The pathogenesis of the disease involves several factors, such as immunologic, infectious and environmental triggers. Genetic predisposing factors are also postulated due to the remarkably positive family history often found. Through a detailed literature review, we aim to qualify and quantify the impact of climatic versus genetic factors on rosacea epidemiology worldwide. Possible associations are here considered, including the higher prevalence of rosacea in fair-skinned individuals of Northern European descent, the influence of the latitude, cold weather, and the diagnostic inaccuracy in people with skin of color. Further, we discuss the roles of cold-induced vasodilation, the skin colonization by Demodex mites, and the findings from the most recent genetic studies in this field.
Thesis
Endurance athletes typically spend the large majority of training (> 70%) at low intensities (i.e. below lactate threshold) coupled with short and intermittent bouts of high-intensity exercise or interval training (HIIT). Despite HIIT being a relatively small part of training in terms of duration, it has a substantial effect on the adaptations to endurance training. While it is well-established endurance exercise performance is affected in both hot and cold environmental conditions, the effect ambient temperature (TA; frequently referred to as environmental temperature) has on HIIT as performed by an endurance athlete population is not well understood. Therefore, the overall purpose of this thesis was to investigate the effects TA has on HIIT in an endurance trained population. Specifically, this thesis aimed to increase the understanding of how TA acutely affects performance and physiological responses during high-intensity intervals (Study 1); how repeated exposure to TA manipulates physiological responses during high-intensity intervals (Study 2), and how TA affects performance outcomes of a HIIT intervention (Study 3). In Study 1, eleven well-trained cyclists completed 4 interval sessions at 5°C, 13°C, 22°C, and 35°C (55 ± 13% RH) in a randomised order. Each session involved 5 x 4-minute intervals interspersed with 5 minutes of recovery. During the intervals, power output, core temperature (TC), oxygen consumption (VO2), and heart rate (HR) were recorded. It was hypothesized that the 13°C condition would have the highest mean power output compared to the other TA conditions. However, mean session power output for 13°C (366 ± 32 W) was not significantly different than 5°C (363 ± 32 W), 22°C (364 ± 36 W), or 35°C (352 ± 31 W). Power output was lower in the 5th interval of the 35°C condition, compared with all other TA. TC was higher in 22°C compared with both 5°C and 13°C (P= .001). VO2 was not different across TA. HR was higher in the 4th and 5th intervals of 35°C compared with 5°C and 13°C. It was concluded well-trained cyclists performing maximal high-intensity aerobic intervals can achieve near optimal power output over a broader range of TA than previous literature may indicate. Study 1 indicated TA had acute effects on performance and physiological responses during high-intensity aerobic intervals, especially in terms of cardiovascular stress. However, whether acute cardiorespiratory and thermoregulatory responses during high-intensity intervals change as a result of repeated TA exposures (i.e. during HIIT) was unknown. In Study 2, 20 trained cyclists and triathletes completed a 4-week (8 session) HIIT intervention in either cool (13°C) or hot (35°C) conditions. The HIIT intervention utilized the interval protocol from Study 1 and recorded cardiopulmonary and thermoregulatory measures during the first (INT8) and last (INT8) sessions. It was observed that time spent at or near maximal oxygen consumption (VO2max) during HIIT was greater in 13°C (877 ± 297 seconds) than 35°C (421 ± 395 seconds), but did not change for either TA condition between INT1 and INT8. HR was not significantly different between 13°C (164 ± 9 bpm) and 35°C HIIT (164 ± 12 bpm). TC significantly decreased in 35°C HIIT between INT1 and INT8. These results potentially indicate the relationship between time spent at or near VO2max and cardiovascular strain during HIIT is influenced by TA. Additionally, HIIT performed intermittently (~2x per week) at 35°C resulted in demonstrated evidence for heat acclimation in endurance athletes. Study 1 and Study 2 provided findings for performance, cardiorespiratory, and thermoregulatory responses during acute high-intensity interval sessions and after repeated exposure to TA. In particular, differences in time spent at or near VO2max between 13°C and 35°C HIIT, and changes in thermoregulatory responses over the course of a HIIT intervention both have the potential to affect endurance performance outcomes and coinciding physiological responses. In order to investigate this, Study 3 evaluated submaximal warm-ups and 20 km time-trials in temperate conditions (22°C) before (TT1) and after (TT2) the HIIT interventions from Study 2. Gross mechanical efficiency (GME) was measured during the warm-up (at 50% peak power output), whilst power output and HR were measured during the 20 km TT. Rate of perceived exertion (RPE) and body temperature (TB) were measured through the warm-up and time-trial. It was demonstrated that time-trial power output was increased after HIIT interventions in both the 13°C (3%; HIIT13) and 35°C (7%; HIIT35), yet no differences between groups for power output, HR, or RPE were noted. Within subject increases for HR and RPE during the 20 km time-trial were noted in HIIT13, but not in HIIT35. GME approached a significant decrease (P= .051) in HIIT13. A significant interaction in TB was observed between groups and TT1 and TT2 during both the 20 km time-trial and submaximal warm-up. These findings indicate that HIIT performed in hot and cool conditions result in similar temperate time-trial performance outcomes. However, changes in cardiorespiratory, thermoregulatory, and subjective responses during aerobic exercise after a HIIT intervention appear to be dependent on the TA HIIT is performed in. The results of this thesis demonstrate TA acutely affects performance, and cardiorespiratory and thermoregulatory responses during high-intensity intervals; repeated exposures to TA during HIIT can stimulate changes in thermoregulatory responses; and TA exposure during HIIT has limited effect on temperate endurance performance, yet affects coinciding cardiorespiratory, thermoregulatory, and subjective responses. These findings will assist coaches and athletes to make better informed decisions relating to HIIT prescription and acclimating endurance athletes to TA.
Chapter
Geriatric Forensic Medicine and Pathology - edited by Kim A. Collins September 2020
Literature Review
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Habituation of the cold shock response and adaptation in deep body cooling with prolonged cold water immersion is well documented in adults. This study aimed to determine whether children exhibit similar adaptive responses. Eight children aged 10–11 years underwent a 5 min static immersion in 15 °C (59 °F) water, five then swam for up to 40 min, before and after a year of regular cold water swim training. Following acclimatization, no differences were found in heart rates or respiratory frequencies on initial immersion, despite a smaller relative V ˙ O 2. Children reported feeling warmer (p < .01) and more comfortable (p < .05), implying acclimatization of subjective perception of cold. No difference was found in cooling rates while swimming. On comparison with data of adults swimming in 12 °C (53.6 °F) water, no difference was found in cooling rates, but the trend in both acclimatized groups to a slower rate of cooling was significant (p ≤ .026) when the data were pooled. These data may support a theory of insulative adaptation.
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