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ACSM Expert Consensus Statement: Injury
Prevention and Exercise Performance during
Cold-Weather Exercise
John W. Castellani, PhD;
1
Clare M. Eglin, PhD;
2
Tiina M. Ikäheimo, PhD;
3,4
Hugh Montgomery, MBBS, BSc, MD;
5
Peter Paal, MD, PD, MBA;
6
and Michael J. Tipton, PhD
2
Abstract
Cold injury can result from exercising at low temperatures and can impair
exercise performance or cause lifelong debility or death. This consensus
statement provides up-to-date information on the pathogenesis, nature,
impacts, prevention, and treatment of the most common cold injuries.
Introduction
American College of Sports Medicine (ACSM) Expert
Consensus Statements are created by a small group of recog-
nized leaders in a field. They highlight knowledge gaps, pres-
ent existing knowledge, and provide recommendations for
clinical practice. The new, shorter format is intended to make
the text more focused and accessible.
This statement addresses the deleterious aspects of expo-
sure to cold. The use of cold in injury prevention, treatment,
or recovery is beyond its scope and is dealt with elsewhere
(1). As well, the reader is referred to review articles on the de-
tailed physiological responses to acute and chronic cold expo-
sure and effects of cold acclimatization (2,3). This statement
updates and replaces the ACSM position statement published
in 2006, entitled “Prevention of Cold Injuries during Exer-
cise”(4). As an official pronouncement of the college, it re-
flects the college's position on the scientific and clinical aspects
of cold injury during exercise.
Many people work or exercise in or
near a cold environment, be that cold
air or cold water. Cooling can impair
performance and threaten life, and cold
is a leading cause of death among people
engaged in sports (5). The breadth and
seriousness of the challenge represented
by cold are reflected in the topics covered in this statement
and include frostbite, nonfreezing cold injury (NFCI), hypo-
thermia, avalanche burial, snow blindness, drowning, and
sudden cardiac death. In addition, cold can constitute part of
a combined environmental threat, for example in combination
with hypoxia in high mountains. It follows that an under-
standing of the impact of cold environments and approaches
to mitigate these threats is essential for those hoping to per-
form in cold conditions.
Cold Air (Frostbite)
Frostbite is a direct freezing injury occurring when the skin
surface freezes in saltwater at ~ −0.55°C (31°F) (6) and in air
below −3°C (26.6°F) (7–9). Exposed tissues with poor perfu-
sion are most commonly affected (hands, feet, head) (10–12).
Exposure times for injury vary from seconds to hours, depend-
ing on the type and intensity of cold exposure, degree of phys-
ical activity, protective clothing, and various individual factors
(Table 1) (47). At subfreezing tissue temperatures, extracellular
ice crystals form in susceptible tissue, leading to cellular mechani-
cal damage and increased osmotic pressure, causing inflammation,
microvascular thrombosis, ischemia, and hypoxia. Formation of
intracellular ice crystals may then occur. Thawing increases tissue
edema and provokes an inflammatory response and reperfusion
injury (11). Frostbite is classified as described in Table 2.
Skin numbness is a sign of a heightened cold injury risk. A
pale spot on the skin indicates superficial cold injury, which
is characterized by partial skin freezing and mild edema (50).
The injured area should be rewarmed by contact with warm
skin (their own, or someone else's) and further cooling avoided.
With more severe frostbite, the injured area is cold to the touch,
andpatientsoftencomplainthatitfeels“like a block of wood”
(11). If possible, the frozen part or area should not be rewarmed
unless refreezing can be avoided (51).
SPECIAL COMMUNICATION
1
United States Army Research Institute of Environmental Medicine, Thermal
and Mountain Medicine Division, Natick, MA;
2
University of Portsmouth,
School of Sport, Health and Exercise Science, Portsmouth, United Kingdom;
3
University of Oulu, Oulu, Finland;
4
Department of Community Medicine,
UiT-The Arctic University of Norway, Tromsø, Norway;
5
University College
London, Centre for Human Health and Performance, London, United
Kingdom; and
6
Hospitallers Brothers Hospital, Anaesthesiology and
Intensive Care Medicine, Salzburg, Austria
Address for correspondence: John W. Castellani, PhD, United States Army
Research Institute of Environmental Medicine, 10 General Greene Avenue,
Building 42, Natick, MA; E-mail: john.w.castellani.civ@mail.mil.
1537-890X/2011/594–607
Current Sports Medicine Reports
Copyright © 2021 by the American College of Sports Medicine
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Frostbite occurrence ranges from 7% to 11% among the
general population in Scandinavian countries (10,13,14,52).
It also occurs in military training (15,53,54). It is more com-
mon in rural, northern climates (13,16), in occupations in-
volving high physical strain and extended cold exposure
(14); and in leisure/sporting activities, such as mountaineering
(17,18,55,56), cold climate hiking (57), use of all-terrain vehi-
cles in the cold or of snowmobiles (16); and sports activities
generating high wind speed, such as alpine skiing or sledding
(58), or associated with prolonged stationary posture, such
as kite skiing and hang gliding (59,60). A recent study con-
cluded that the incidence of frostbite injuries in the Austrian
Alps is low (56), mainly due to better awareness and clothing.
Age (19), sex (10,13,14,16,50,56), and ethnic background
(20,21) affect frostbite risk (Table 1). Diseases affecting neural,
vascular, and metabolic functions and related tissue perfusion
and microvascular function, as well as metabolic heat produc-
tion also may increase frostbite risk. Autonomic and peripheral
neuropathies (e.g., diabetes) impair neural control and thermal
sensations (22), central neurological disease (e.g.,multiplescle-
rosis, spinal cord injury) can impair mobility, thermoregula-
tion, cardiac and vascular control; and vascular disease can im-
pair tissue perfusion and responsiveness. Endocrine conditions
(e.g., hypothyroidism, hypopituitarism, adrenal insufficiency)
can decrease metabolic heat production in the cold. Psychiatric
illnesses can predispose to frostbite through increased risk be-
havior (14,22). Various medications that affect the circulation,
metabolism, and fluid balance may predispose to frostbite (22).
Impaired peripheral cold-induced vasodilation (CIVD) and
rewarming responses may predict frostbite risk, but the findings
are inconclusive (23,24,61–63).
Prevention
The primary strategy to reduce frostbite risk is to assess risk,
and to respond to it with appropriate mitigation strategies. The
wind chill temperature (WCT) index, which integrates temper-
ature and wind speed (64) provides an estimation of face
cooling and cheek frostbite risk (Fig. 1). Exposed fingers will
freeze at a warmer WCT than the cheek (65). Wind markedly
increases convective heat loss, decreases clothing insulation ca-
pacity, and increases evaporative heat loss (66). Frostbite risk
can be based on the WCT index and the period in which ex-
posed skin will freeze in more susceptible persons in the popu-
lation. The risk of frostbite on bare skin is less than 5% when
Table 1.
Factors predisposing to frostbite and NFCI.
Climate Individual Characteristics and Physiology
Wind
Wetness, Immersion in Cold Water
Contact with Cold Materials
High Altitude
Hypoxia
Long Duration or High Amount of Cold Exposure
African-American or Afro-Caribbean Ethnic Background
Male
Children
Elderly
Previous Cold Injury
Poor CIVD Response
Homeless
Behavioral Individual/clinical
Smoking
Alcohol use
Drug use
Inappropriate or constrictive clothing
Prolonged stationary situation, immobility
Fatigue, dehydration, malnutrition
Use of emollients
Military rank/task
Poor calorie intake
Coronary artery disease/ischemic heart disease, cardiac insufficiency, stroke
Peripheral vascular disease
Peripheral neuropathy
Cold sensitivity
Raynaud’s phenomenon, white fingers
Hand-arm-vibration syndrome, vibration
Diabetes
Hypothyroidism, hypopituitarism
Depression, schizophrenia, dementia
Neurovascular diseases
Sweating or hyperhidrosis
Previous cold injury
Medication (vasoconstrictors)
References: (7,10–46).
Table 2.
Traditional historical classification of frostbite adapted from Fudge (48).
Frostbite Degree Physical Findings
1st Degree Numbness, central white or yellow, waxy discoloration, surrounded by erythema
and edema, desquamation, dysesthesia
2nd Degree Surface blisters containing clear or opalescent fluid surrounded by erythema and edema
3rd Degree May initially present as 2nd degree, but hemorrhagic blisters appear within 24 h,
tissue loss involving entire thickness of skin
4th Degree Injury is through the dermis, into subcutaneous tissue, muscle, and bone
For field use, a simpler two-tier classification may be more appropriate (superficial —no or minimal anticipated tissue loss, corresponding to 1st- and
2nd-degree injury: deep —anticipated tissue loss, corresponding to 3rd- and 4th-degree injury (49).
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the ambient temperature is above −15°C (5°F), but increased
safety surveillance is warranted when the WCT index falls be-
low −27°C (−17°F), when frostbite can occur in 30 min or less
(4). Wet skin cools more rapidly and may increase risk (67). Ex-
posure to volatile liquids (which evaporate easily —such as
light liquid fuels) is of even greater risk. Exercise of sufficient in-
tensity increases skin perfusion and reduces skin cooling and
cold injury risk (25,67).
Touching or gripping cold material elicits contact cooling
and can cause a frostbite injury within a few seconds (26).
The degree of skin cooling depends on the surface tempera-
ture, type of material, contact duration, and several individual
factors. Human tissue in saltwater freezes at −0.55°C (31°F),
whereas seawater freezes at −1.9°C (28.6°F), so frostbite can
occur in very cold seas. Altitudes above 5000 m (18) increase
frostbite risk with the risk potentiated by wind and possibly by
factors, such as dehydration. Many factors may contribute to
this, with low environmental temperatures perhaps combining
with hypobaric hypoxia (27).
In all circumstances, frostbite risk is mitigated through the
maintenance of core body temperature, by reducing risk of con-
tact freezing (rapid heat loss through a conductor at a temper-
ature below zero), and through a general approach aimed at re-
ducing heat loss with clothing. Thus, skin exposure should be
avoided, windproof external layers used, excellent thermal in-
sulation (trapping warmed air, and limiting conduction from
Figure 1: WCT Index in°F (A) and °C (B). Frostbite time indicated onboth charts is the risk of cheek frostbite in the most susceptible 5% of the
population. From (64).
596 Vol u m e 20 Number 11 November 2021 Special Communication
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the skin) used. Where appropriate, multiple layers can help
(e.g., thinner gloves worn under mitts offer dexterity for short
periods when the hands are removed from those thicker mitts).
In extreme conditions, portable heating devices (whether chem-
ical or powered pads) can offer value. In freezing conditions,
liquid should be rapidly removed from exposed skin. This is es-
pecially important where the liquid might evaporate fast or
conduct easily (e.g., some liquid fuels).
Treatment
If frostbite is suspected, any further cold exposure should be
avoided with the casualty placed in a warm, dry environment.
Wet clothing should be removed and the injured region protected
from direct mechanical injury (e.g., no weight bearing if lower
limb affected). If hypothermia is present, this should be treated
first, with systemic hydration restored and maintained. Routine
antibiotic administration should be avoided, as should spon-
taneous thawing or rewarming through friction or via heat
sources (e.g., flame, vehicle engine) (68). The region should
only be thawed if refreezing can be prevented (69). Thawing
may initially use the body heat of the casualty or rescuers (e.g.,
placing the affected region in the axilla). When available, a 37°C
to 39°C (98.6°F to 102.2°F) waterbath should be used until the
skin has softened and is reddening (11). Once dried, loose dress-
ings and bandages can be applied. Swelling can lead to bandages
tightening and restricting blood flow. Thawing can be painful; ad-
ministration of analgesics (non-steroidal anti-inflammatory drugs,
paracetamol, sometimes opioids) may be required. Blister integrity
should be preserved, and efforts made to prevent secondary infec-
tion. Expert medical evaluation is required (70).
Nonfreezing Cold Injury
Nonfreezing cold injury (previously referred to as trenchfoot)
often results from exposure to cold-wet conditions causing tissue
temperatures to fall below 15°C (59°F) for a prolonged period.
The periphery is more commonly affected (not only fingers/toes
but also nose/ears). Unlike frostbite, the tissues do not freeze; in-
stead, protracted intense vasoconstriction and associated ische-
mia and/or reperfusion cause neurovascular damage (71).
Chilblains, a mild form of NFCI, occur following 1 to 5 h of
cold-wet exposure (above freezing) and predominantly affect
finger and toe skin (72). They are small, swollen, itchy, ery-
thematous papules, which may be tender or painful (73). A
hyperemic response to rewarming is characterized by red,
hot, and swollen skin accompanied by an itching or burning
sensation that may persist for several hours. Long-lasting effects
are rare (73). More severe NFCI has not only long affected the
military (28) but also occurs among athletes, such as ice skaters
(74), cyclists (75), divers (76), and long-distance Polar rowers
(77) and is a potential risk for hikers and mountaineers who be-
come incapacitated (78).
The “dose”of cold (temperature and duration) required to
cause NFCI is not known and varies between and, possibly,
within individuals. Most reports of NFCI have involved sev-
eral days to weeks of cold exposure (28,75,77,79); however,
exposures <24 h can cause NFCI (76,80). Short cold expo-
sures may result in NFCI if there is inadequate rewarming
and, therefore, prolonged low tissue temperature. The affected
area is pale, cold, and numb during cold exposure. On
rewarming, it becomes cyanotic while remaining cold and
numb; it may swell in severe cases. In very mild cases, recovery
occurs within a few days with nolasting symptoms (81,82). In
others, a subsequent hyperemic phase lasts between 2 wk and
3 months and is characterized by hot, red, and dry skin with
some paresthesia and, in severe cases, blistering (50,81). The
extent of tissue damage can only be assessed after this hyper-
emic phase. Chronic symptoms may then occur, lasting from
a few months tomany years, and include (in varying combina-
tions and severity): cold sensitivity, sensory neuropathy, pain,
and hyperhidrosis.
Cold sensitivity is characterized by cool skin temperatures
even in a warm environment and slow rewarming (due to re-
duced skin blood flow) following local cooling (83,84). In
combination with hyperhidrosis, which will increase evapora-
tive cooling, cold sensitivity increases the risk of subsequent
cold injury (29,85). Responses to peripheral cooling are di-
verse (86); a large proportion of the general population are
cold sensitive, some perhaps having subclinical forms of NFCI
(84,87–89). Athletes, such as windsurfers (90) and cold-water
swimmers, may develop cold sensitivity through cold expo-
sure, although altered sensory thermal sensation or endothe-
lial dysfunction is not generally observed (89).
Individuals from African-Caribbean backgrounds are more
susceptible to NFCI (21,82) as are those with previous cold in-
jury (29). Women also may be at greater risk due to their
greater rate of hand and foot cooling in the cold (91). The ev-
idence for either dehydration (28,71,77,82,92,93) or smoking
(28,30,82,94) increasing the risk of NFCI is equivocal.
Prevention
NFCI prevention should focus on keeping the body warm
by remaining active; feeling generally cold and being static
are NFCI risk factors (82). It also is essential that risk be
assessed in the manner suggested for frostbite and, likewise,
that tissues are protected from heat loss through conduction,
convection, radiation, and evaporation (see above). Of partic-
ular note is that wet or damp conditions greatly increase risk,
because of the enhanced ability of water to conduct heat, and
to drive cooling through evaporation. Appropriate clothing
(waterproof, windproof, breathable, and able to maintain its
insulation even in wet windy conditions) is essential, as is pro-
tection of the hands and feet. Waterproof boots and gloves
with breathable membranes to prevent sweat accumulation
during periods of high activity and subsequent cooling
through evaporation and conduction during periods of rest
are required (31). In cold-wet conditions, socks and gloves
should be changed frequentlyto ensure the feet and hands stay
dry. Restrictive footwear reduces blood flow and increases
foot cooling rates and should be avoided (31).
Interindividual NFCI susceptibility varies greatly, even when
clothing, environment, and tasking are identical (28,77). There-
fore, risk mitigation needs to be on an individual basis, with
anyone reporting feeling cold, complaining of cold extremities
being closely monitored or withdrawn from the event. If NFCI
is suspected, individuals should be removed from the cold-wet
environment to prevent further cooling and enable core
rewarming if the individual is hypothermic. The affected
feet/hands should be rewarmed slowly (11,50).
Accidental Hypothermia
Accidental hypothermia is defined as a drop in deep body
(core) temperature (T
deep
) to <35°C (95°F) (95,96). Primary
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hypothermia (commonest type of hypothermia in sports settings
among young and healthy athletes) results from environmental
cold exposure, and secondary hypothermia from factors, such
as exhaustion, trauma, insufficient home heating/insulation, dis-
ease and intoxication, advanced age, or multimorbidity (97). The
signs and symptoms of hypothermia are presented in Table 3.
In primary accidental hypothermia, body heat loss exceeds heat
production. The rate of cooling depends on factors, including
clothing worn, environmental conditions (e.g., water exposure,
temperature, wind), and exercise intensity. Cooling during seden-
tary cold water (10°C to 16°C) immersion in normothermic indi-
viduals ranges from ~1.0 to 1.8°C·h
−1
(1.8 to 3.2°F·h
−1
)(99–101).
It has been measured as high as 9°C·h
−1
(16.2°F·h
−1
) when buried
in avalanche snow (102,103). In air, physical activity attenuates
T
deep
cooling due to significantly increased heat production com-
pared with resting (4). Other factors also impact T
deep
cooling;
for example, shivering heat production is substantially impaired
by a central mechanism if hypoglycemia occurs (104). In cold
air, hypothermia is most likely to occur if an individual be-
comes injured or exhausted and is no longer able to exercise.
Prevention
When combined with exercise-induced heat production,
appropriate clothing provides the greatest protection against
hypothermia by reducing convective and evaporative heat loss
through windproofing and waterproofing, and insulation pro-
vided by air trapping (105). Clothing requirements vary with
changes in ambient air temperature, rainfall, and exercise inten-
sity (105,106). In the case of water immersion, the depth of im-
mersion (surface area of body exposed, compressive impact on
clothing insulation), water temperature, and movement also
will determine clothing requirements. Thermal models estimat-
ing whole-body cooling and needed clothing insulation, such as
the Insulation Required (107) and Cold-Weather Ensemble De-
cision Aid (108,109) predict the amount of clothing needed for
individuals to maintain T
deep
based on ambient temperatures
andexerciseintensities.Athigherexerciseworkloads,less
clothing is needed to protect against a fall in T
deep
.
Typical cold-weather clothing consists of three layers: an in-
ner layer, which is in direct contact with the skin and does not
readily absorb moisture, but wicks moisture to the outer layers
where it can evaporate; a middle layer, which provides the pri-
mary insulation; and an outer layer, which is designed to al-
low moisture transfer to the air while repelling wind and rain.
Sweating can easily exceed the vapor transfer rate of the outer
shell layer, causing moisture to accumulate on the inside, even
if the outer layer has substantial venting (e.g., zippers in
armpits) to allow moisture to escape. The outer layer should
typically not be worn during exercise (unless it is raining or
very windy) but should be donned during subsequent rest pe-
riods. In group settings, individuals should adjust clothing to
their own physiological responses (e.g., sweating) and not
wear a standard amount of clothing. A common problem is
that people begin exercising while still wearing clothing layers
appropriate for resting conditions, and thus are “overdressed”
after initiating exercise. If the combination of environmental
conditions, work intensity, and available clothing suggest that
body heat content cannot be maintained (e.g., low exercise in-
tensity in rainy conditions), then supervision or use of the
buddy system should be encouraged. Remaining dry, especially
for those exercising in remote regions, is extremely important
and carrying extra clothing that is waterproof, and dry cloth-
ing to change into, is important.
Treatment
Vital signs diminish as cooling progresses (Table 4, [95]).
Accurate T
deep
measurement using rectal or esophageal probes
is difficult in a field situation. In such a situation, accidental
hypothermia should be diagnosed by measuring tympanic tem-
perature with an insulated thermistor-based probe, allowing
readings of <32°C (89.6°F) (113). This can later be confirmed
with a rectal temperature using a low reading thermometer,
where and when practical.
Without accurate temperature measurements, the diagnosis
and classification of hypothermia must rely on medical history
and clinical findings (e.g., trunk feels cold, quality of vital
signs; Table 4). A revised hypothermia staging/classification
has been proposed (96), which correlates the level of con-
sciousness with the risk of hypothermia-induced cardiac arrest
(Table 5). Young and healthy casualties may have vital signs
still present at T
deep
< 24°C (75.2°F) (115). Signs of breathing
or cardiac activity (and/or respiratory and pulse rate) should
be sought for at least 1 min because respiratory rates may be
as low as 3 to 4 min, pulse rates as low as 10 to 15 bpm,
and pulse volume low and breaths shallow (95,96,115).
Treatment algorithms have been published for patients with
accidental hypothermia (Fig. 2) (95,96,116). Out-of-hospital
treatment consists of limiting further cooling. Patients should
be removed from wind and water. In a warm shelter, remove
wet and cold clothing. Out-of-hospital rewarming is almost
impossible with limited technical equipment; transport to a
hospital should take precedence (see below). In many patients,
T
deep
will continue to fall after rescue (i.e.,“afterdrop”). The
risk of hypothermia-induced cardiac arrest commences once
Tab l e 3 .
Signs and symptoms of hypothermia at different levels (98).
Mild (32–35°C; 89.6–95°F) Moderate (28–31°C; 82.4–88°F) Severe (<28°C; <82.4°F)
Cold extremities Apathy, poor judgment Inappropriate behavior
Shivering Reduced shivering Total loss of shivering
Tachycardia Weakness and drowsiness Cardiac arrhythmias
Tachypnea Slurred speech and amnesia Pulmonary edema
Urinary urgency Dehydration Hypotension and bradycardia
Mild incoordination Decreased coordination or clumsiness Reduced level of consciousness
Fatigue Muscle rigidity
598 Vol u m e 20 Number 11 November 2021 Special Communication
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T
deep
is <30°C (86°F) in young and healthy casualties; in the
elderly and multimorbid the risk increases at T
deep
< 32°C
(89.6°F) (96).
For mildly hypothermic patients in a field environment,
warm clothing and drinks with sugar should be given with su-
pervision and active rewarming encouraged. In mild hypo-
thermia cases that recover fully and risk factors are mitigated,
there is no need to evacuate. For moderate and severe hypo-
thermia and the critically ill, patients need to be handled very
gently (as mechanical impact can trigger cardiac arrest), kept
insulated, passively rewarmed slowly (0.75 to 1.0°C·h
−1
)
and evacuated.
Table 4.
The two main clinical classification systems for accidental hypothermia: The original Swiss system (110) and the wilderness medical society
classification (111).
Swiss System (110) WMS (111)
Category Clinical Findings
Estimated Core
Temperature (°C, °F) Category Clinical Findings
Estimated Core
Temperature (°C; °F)
Stage 1 Clear consciousness
with shivering
35°C to 32°C Mild Normal mental status,
shivering, but not
functioning normally/
able to care for self
35°C to 32°C
95°F to 89.6°F 95°F to 89.6°F
Stage 2 Impaired consciousness
without shivering
<32°C to 28°C Moderate Abnormal mental
status with shivering,
or abnormal mental
status without
shivering, but
conscious
32°C to 28°C
<89.6°F to 82.4°F <89.6°F to 82.4°F
Stage 3 Unconsciousness <28°C to 24°C Severe/profound Unconscious <28°C
<82.4°F to 75.2°F <82.4°F
Stage 4 Apparent death 24°C to 11.8°C
75.2°F to 53.2°F
Stage 5 Death due to irreversible
hypothermia
<11.8°C
<53.2°F
Core temperature data from stages 4 and 5 from Mroczek et al. (112).
WMS, Wilderness Medical Society.
Table 5.
Revised Swiss system for staging of accidental hypothermia (114).
AVPU denotes Alert, Verbal, Painful and Unconscious, respectively.
a
In the Revised Swiss System, “Alert”corresponds to a GCS score of 15; “Verbal”corresponds to a GCS score of 9 to 14, including confused patients;
“Painful”and “Unconscious”correspond to a GCS score <9. While shivering is not used as a stage-defining sign in the Revised Swiss System, its presence
usually means that the temperature is >30°C (86°F), a temperature at which hypothermic CA is unlikely to occur.
b
No respiration, no palpable carotid or femoral pulse, no measurable blood pressure. Check for signs of life (pulse and, especially, respiration) for up to
1min.
c
The transition of colors between stages represents the overlap of patients within groups. The estimated risk of cardiac arrest is based on accidental hy-
pothermia being the only cause of the clinical findings. If other conditions impair consciousness, such as asphyxia, intoxication, high altitude cerebral edema
or trauma, the revised Swiss System may falsely predict a higher risk of cardiac arrest due to hypothermia. Caution should be taken if a patient remains
“alert”or“verbal”showing signs of hemodynamic or respiratory instability like bradycardia, bradypnea,hypotension because this maysuggest transition to
a stage with higher risk of cardiac arrest.
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Figure 2: Treatment algorithm for patients with accidental hypothermia, from (96). Definitions of parenthetical numbers are: (1) decapitation,
truncal transection, whole body decomposed, or whole body frozen solid (chest wall not compressible); (2) SBP < 90 mm Hg is a reasonable
prehospital estimate of cardiocirculatory instability but for in-hospital decisions, the minimum sufficient circulation for a deeply hypothermicpa-
tient (e.g., <28°C) has not been defined; (3) Swiss staging of accidental hypothermia; (4) direct transport to an ECMO center is recommended
in an arrested hypothermic patient. In remote areas, transport decisions should balance the risk of increased transport time with the potential ben-
efit of treatment in an ECLS center (e.g., 6 h). (5) Warm environment, chemical, electrical, or forced air heating packs or blankets, and warm IV
fluids (38°C to 42°C). In case of cardiac instability refractory to medical management, consider rewarming with ECLS.(6) If the decision is made
to stop at an intermediate hospital to measure serum potassium, a hospital en route to an ECLS center should be chosen. HOPE and ICE scores
should not be used in children; instead consider expert consultation. DNR, do not resuscitate HT, hypothermia, MD, medical doctor, ROSC, return
of spontaneous circulation, SBP, systolic blood pressure.
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Out-of-hospital, casualties with stage 1 hypothermia (Table 5)
should be transported to a hospital able to deal with concomitant
illnesses or injuries (95,96). With colder patients, the risk of im-
minent cardiac arrest has to be evaluated (i.e.,systolicbloodpres-
sure <90 mm Hg, ventricular arrhythmia, T
deep
<30°C(86°F);
Fig. 2). If only one risk factor is present, the patient should be
transported to a hospital with the possibility to rewarm them
with extracorporeal life support (ECLS). Without any risk fac-
tor of imminent cardiac arrest, the patient can be carefully and
gently transported to the closest appropriate hospital and
rewarmed actively (e.g., forced warm air). If a patient has suf-
fered a hypothermia-induced cardiac arrest (stage 4), cardiopul-
monary resuscitation (CPR) should be initiated immediately.
Modifications to CPR have been proposed for hypothermia-
induced cardiac arrest patients, for example, at a T
deep
<30°C
(86°F), no epinephrine and a maximum of three shocks should
be attempted (95,96). Transport of a hypothermic patient in
cardiac arrest should be directly to a hospital with ECLS
rewarming capability.
In the hospital, prognostication of outcome after ECLS
rewarming should be performed with specific scores (Hypo-
thermia outcome prediction after extra-corporeal life support
(HOPE) or International accidental hypothermia extracorpo-
real life support (ICE)) (117–119), which are more reliable
than the traditional potassium triage (120,121).
Avalanche Burial
During avalanche burial, smaller people lose heat more rap-
idly than larger individuals because of a higher surface-area
ratio and smaller muscle mass (122). Regarding cooling rate,
the amount of subcutaneous adipose tissue and insulation
provided by clothing also are important. For example, while
wearing a thin monolayer garment, commonly used by back-
country skiing athletes during ascent, body core cooling can
approach 9°C·h
−1
during an avalanche burial. With thick
multilayer clothing ensembles, including helmet and gloves,
used in downhill skiing, cooling is slower (123).
Of all avalanche-buried persons, 10% to 20% die in the
first 30 min from trauma to the head, cervical and thoracic
spine, or from multiple trauma (124). More than 60% die
from asphyxia (i.e., lack of oxygen), most commonly within
the first 35 min of burial because either the airways are
obstructed or snow in front of the mouth and nose inhibits
air inhalation. The longer someone is buried following an
avalanche, the less chance of survival (124,125). Data in
European skiers from 1981 to 1991 (126,127) suggest three
phases of avalanche burial (survival, asphyxiation, waiting)
before rescue. For survival, 93% of avalanche victims are still
alive in the first 15 to 20 min and with asphyxiation, 65% die
during the next 15 min due to freezing snow caused by breath-
ing leading to a limited oxygen availability. Survival to 45 min
and beyond suggests an open-air pocket exists (i.e.,patentair-
ways with space in front of mouth and nose with access to
open air). These casualties will survive until an avalanche-
specific combination of hypothermia, hypoxia, and hypercap-
nia sets in (128). Less than 20% survive for more than 2 h
(129). Climate and topography affect the survival from ava-
lanche burial (126). In humid climates (e.g.,maritimecoast),
snow is denser, and asphyxia has an earlier onset than in the
Swiss Alps with a continental climate. Skiing in slightly for-
ested or rocky terrain results in more fatalities due to trauma.
Reduced burial depth is positively correlated with survival.
Only 4.4% of partially buried casualties (i.e.,headandchest
outside of the snow) compared with 51.3% of fully buried
casualties (i.e., head and chest below the snow) die (130).
An avalanche airbag reduces the risk of full burial and also
may reduce burial depth. The reduction in mortality is less
when the airbag does not inflate: in one study, noninflation oc-
curred in 20% of use, 60% of which was attributed to a de-
ployment failure by the user (131). With risk of avalanches,
winter sport athletes who are outside protected slopes should
be equipped with, and trained in the use of, an avalanche
airbag, an avalanche transceiver, a probe, and a metal-headed
shovel. Companions should quickly track the location with
an avalanche transceiver, probe the exact location and depth,
and excavate the buried casualty. Using digital instead of ana-
log avalanche transceivers, attending avalanche rescue courses
on correct tracking and probing, as well as regular training in
deploying an avalanche airbag and working in coordinated
groups will allow faster extrication. In mountain regions close
to urban centers, helicopter rescue has revolutionized avalanche
rescue because of fast transport times. Still, professional rescue
should not be expected on scene within the first 20 min. Thus,
rescue by peers on-site is of utmost importance to increase
survival chances.
Once extricated, patients are treated according to specific
avalanche resuscitation guidelines (96,118,119). In normo-
thermic patients, asphyxia triggered cardiac arrest can only
be survived for a few minutes and has a poor outcome. In hy-
pothermia triggered cardiac arrest (usually <30°C; 86°F), out-
come is substantially better (96,132,133).
Snow Blindness
The structures of the eye are vulnerable to damage from ex-
posure to ultraviolet (UV) light, with risk increasing at high al-
titudes (rising 4% per 300 m ascent). Being protected by the
brow, nose, and upper lid, the eye is mainly exposed to UV-
light that is reflected (emphasizing a need for lateral eye pro-
tection). The reflective incidence of water and snow are two-
fold and eightfold greater than grass. In a snowy environment
at 2000 m, UV exposure is doubled (134,135).
“Snow blindness”results from acute UV ocular injury. The
degree of conjunctival and corneal injury (“ultraviolet keratitis”)
depends on energy intensity and exposure duration. Limbic in-
jury causes pain when trying to focus the lens. Symptoms begin
4to10hafterexposureandrangefroma“gritty”sensation to
severe pain, blurred vision, uncontrolled blinking, eye-watering,
photophobia, and blepharospasm. Symptoms last <48 h, or
several days if severe. Injury can be compounded by corneal
swelling, which results from altitude-and wind-related hyp-
oxia and corneal evaporative drying, with hypoxia worsened
by contact lens use (135,136). A fluorescein eye stain test can
locate corneal injuries.
Prevention
Sunglasses or goggles with side protection, which absorb
>95% of all UV light, should be worn. Soft contact lenses,
which block UV-light and cover the pupil and limbus, offer
good protection. Brimmed hats offer additional shade.
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Tr e a t m e n t
Close eyes and rest until pain eases. In a first step, cool gently
through the closed eyelid (135). In a next step use oral analgesics
(e.g., paracetamol 1 g, four time a day). If available, administer a
topical lubricant (e.g., antioxidant artificial tears), and apply
nonsteroidal anti-inflammatory eyedrops (e.g., diclofenac
0.1%). Topical anesthetics slow corneal recovery and should
not be used outside emergency situations (e.g., descent from
high altitude). Consider topical antibiotics in severe cases to
prevent infection. Cycloplegic eye-drops (cyclopentolate 1%)
may relieve pain but impair vision (135,136).
Cold Water
The great cooling power of water means that some of the re-
sponses described for cold air (e.g., hypothermia) also occur in
cold water, but sooner. Humans cool four to five times faster
in cold water than in air at the same temperature (137).
There are four stages of immersion in cold water, each asso-
ciated with specific hazards and each related to the cooling of
different body tissues. Rapid skin cooling on initial immersion
stimulates the cutaneous cold receptors; their dynamic re-
sponse elicits the “cold shock,”a response not evoked by the
slower rates of skin cooling in air. Cold shock is regarded as
the most dangerous response caused by cold water immersion
and affects men and women to a similar extent (138,139). The
greatest responses are observed at water temperatures between
10°C and 15°C (50°F to 59°F) for lightly clothed (swim-suited)
individuals and include a “gasp”response, hyperventilation,
hypertension, and increased cardiac workload (140). These
can be precursors to drowning and cardiovascular issues. The
initial gasp response is 2 to 3 L (141,142), larger than the lethal
volume of seawater for drowning (1.5 L, [143]). The cold shock
response peaks in the first 30 s of immersion and usually abates
over the next 90 s as the peripheral cold receptors adapt to the
new skin temperature. There is a significant possibility of aspi-
rating water during initial immersion when conscious control
of breathing has been lost. In situations where the face also is
immersed on initial immersion, coactivation of sympathetic
and parasympathetic inputs to the heart can produce “auto-
nomic conflict,”resulting in potentially fatal arrhythmias in a
variety of sporting situations (e.g., open water swimming, tri-
athlon [144]).
After skin, the next body tissues to be affected by cooling are
the superficial nerves and muscle. The arms are particularly sus-
ceptible to cooling due to their anthropometry (thin cylinders),
anatomy (superficial nerves and muscles), and physiology (reli-
ance on blood flow for warming) (122). Within about 20 min
of immersion in water of 12°C (54°F) peripheral neuromuscular
cooling can significantly impair manual dexterity, grip strength
and coordination, impacting swimming ability (122,145).
Approximately 60% of cold-water immersion deaths occur
within the first minutes of immersion, long before hypother-
mia occurs (144). Under normal circumstances, adult humans
will not become hypothermic in under 30 min in even the
coldest water.
Prevention/Protection/Treatment
The cold shock response demonstrates temporal summa-
tion, with a greater response being observed with faster rates
of entry into cold water (146). Those entering cold water are
advised to rest with their airway clear of the water until they
have regained control of their breathing (“float first”). Pro-
longed head-in breath holding should be avoided oninitial im-
mersion. For open cold water swimming events, swimmers
should adapt to the water just before commencing the swim
(or have in-water starts); this reduces the chance of aspirating
water and makes the coordination of the swim stroke and
breathing easier.
Protection can be physiological or technological. Physiolog-
ical protection against cold shock can be achieved by cold ha-
bituation, with as few as six 2-min head-out cold water im-
mersions over 3 d reducing the cold shock response by 50%
by the last immersion (147). A reduction of 25% is still appar-
ent 14 months later (148). Although habituation will reduce
the ventilatory response on immersion, this may not translate
to an improved swimming capacity (149).
Importantly, repeated immersion in cold water does not
protect against neuromuscular incapacitation from peripheral
cooling; protection for this response can only be achieved by
limiting exposure or technological protection with protective
clothing. In terms of swim failure, it appears that the upper
arms (triceps region) are the most important region to protect
(145,150). However, insulation of the upper arms during a
simulated survival swim in 10°C water maintained warmer
arm skin temperature and swimming technique but did not
improve swimming duration or distance (151). Most sports
persons use wet suits rather than dry suits. The primary deter-
minants of the protection provided by a wet suit are its fit and
thickness. The fit should be as tight as possible commensurate
with sporting performance, and the thickness varies between
the torso and the arms, depending on the sport and require-
ments for regional flexibility. The minimum recommended
water temperature for triathlon racing is 12°C (54°F) in
wetsuits and 16°C (61°F) without wetsuits (152,153). It is rec-
ommended that water temperatures below 18°C (64°F) are
too cold for elite marathon swim racing without wet suit pro-
tection (154). Fédération Internationale de Natation rules
were changed in 2017 to make wetsuits compulsory below
18°C (64°F) and optional below 20°C (68°F) (155).
Protection also can be afforded by appropriate event orga-
nization. Swimming events, including mass starts, can be orga-
nized and supervised to minimize the chances of cardiac and
respiratory-related problems (156). Those providing safety
cover should be aware of the increased likelihood of cold-
related problems in the first (due to cold shock response)
and last (due to fatigue) minutes of an event and should be
trained to recognize impending swim failure (145).
Basic life support compressions and ventilations (2 rescue
breaths then CPR at 30:2 ratio) should be used and for drown-
ing victims, high concentrations of inspired oxygen given as
soon as possible. All those suspected of aspirating water should
be evacuated to hospital. For hypothermic casualties, follow the
advice given in the section on “Accidental Hypothermia.”
Cold and Performance
Cold air and water exposure can potentially have deleteri-
ous effects on aerobic and strength performance (157–163).
Interested readers are referred to previous reviews of the im-
pact of cold exposure on exercise performance and the physi-
ological mechanisms responsible for cold-related changes in
performance (122,164,165).
602 Vol u m e 20 Number 11 November 2021 Special Communication
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Decreased muscle temperatures (T
muscle
)lowerV
̇
O
2max
,ex-
ercise time, and power/sprint ability. For every 1°C fall in
muscle temperature, there is a 4% to 6% decline in these
markers of performance (166–168). For example, an 8°C de-
crease in T
muscle
decreases power output by 31% and maximal
voluntary contraction by 19% (169). Low T
muscle
(28°C to
29°C) also cause higher muscle lactate levels in both type 1
and type 2 muscle fibers (170,171), and overall, blood lactate
levels increase during exercise to a greater extent in cold com-
pared with temperate environments (157,172–177) suggest-
ing a greater reliance on anaerobic metabolism. Maximal
heart rate is lower by 10 to 30 bpm when T
deep
is lowered
by 0.5°C to 2.0°C (178) and cold water decreases leg muscle
blood flow during exercise (173,179).
In cold air, where there is little change in T
deep
or T
muscle
,
there is a lack of consensus on whether aerobic performance
declines: studies have demonstrated impairment (158–161),
improvement (180,181), or no change (182,183). Two studies
have examined, systematically, whether air temperature af-
fects performance. Cycling time to exhaustion at 70%
V
̇
O
2max
was longest at an ambient temperature (T
amb
)of
11°C while wearing shorts/t-shirt (158) with decrements seen
at 4°C and 31°C. While wearing cross-country ski uniforms,
Sandsund et al. (160) observed maximal running performance
at T
amb
between −4°C (24.8°F) and 1°C (33.8°F), with perfor-
mance reduced at −14°C (6.8°F) and warmer T
amb
. The lower
T
amb
in the running study can perhaps be attributed to the ski
uniform conferring greater thermal protection and the higher
exercise intensity. However, it should be noted that if more
clothing is needed to protect against environmental cold expo-
sure, this could reduce performance due to increased energy de-
mands caused by heavy clothing, resistance to movement, and
other equipment (4,184). Upper-body performance in cross-
country skiers also is reduced at colder T
amb
(185,186). Cold
temperatures also can impact biomechanics and gait, increasing
the energy demands of exercise (187). Furthermore, athletes
need to be cognizant of terrain factors (i.e., ice, snow cover) that
can cause slipping and coordination issues. Proper nutrition
and hydration are important for maintaining performance in
cold-weather environments. Practical recommendations in-
clude maintaining adequate carbohydrate stores and monitor-
ing fluid intake/output by tracking body mass changes and
urine output/color (188).
Combined Stressors
In the natural world, it is rare for stressors, such as heat and
humidity, cold and altitude, and cold and hyperbaric stress,
not to be combined or experienced sequentially. However,
largely because of the way subject areas are organized, the im-
pact of combined stressors on human responses has received
much less attention than the impact of isolated stressors. Be-
tween 1948 and 2012, there were only 14 studies examining
these areas with human participants (189). Since 2012, the num-
ber of studies has increased dramatically and the importance
of this area of research for human performance, health, and
disease is beginning to be realized (190). The areas of com-
bined stressors not only include the beneficial or detrimental ef-
fects of combined stressors, such as cold and hypoxia, but also
include cross-adaptation and cross-tolerance between such
stressors (Fig. 3), at both the systemic and cellular levels
1
.
Focusing on the combination of cold and altitude (hypoxia)
(191), cold-induced thermogenesis is reduced in hypoxia (192),
and T
deep
falls faster (193). During cooling and warming, the
vasoconstrictor response can occur earlier and be released later
if hypoxia is combined with cold, thereby increasing the “dose”
of cold experienced and the likelihood of cold injuries
(193,194), although this remains a matter for debate (195).
Adaptation to the initial responses to cold water immersion
reduces the subsequent responses to a hypoxic exposure (196)
including plasma epinephrine and norepinephrine, sympa-
thetic nervous system response, heart rate, ventilation, oxygen
consumption, and carbon dioxide production, as well as
symptoms of hypoxia and their severity (196).
In contrast to the clear interaction between cold and hyp-
oxia, it has been reported that cold acclimation does not alter
the physiological or perceptual responses during subsequent
exercise in the heat (197). The area of combined stressors is
clearly fertile ground for further investigation with regard to
the avoidance of injuries in the cold.
Figure 3: Theoretical overview of cross-adaptation(CA). CA1, adaptation to one stimulus providescross-tolerance to another. CA2, adaptation
to one stressor enhances adaptation to another stressor. CA3, combined adaptive effects of two stimuli providing beneficial responses to a third
variable. The cross-adaptive effect may “general”via some common pathway involving for example the autonomic nervous system or pathways
involved in cellular tolerance, or “specific”involving a more specific response to a stimulus such as shivering or vasoconstriction.
1
Cross-adaptation: “Adaptations made in response to one environmental
stressor are beneficial in another”Cross-acclimatization: “Adaptation de-
rived from a natural/terrestrial environment”Cross-acclimation: “Adapta-
tion derived from a simulated environment”Cross-tolerance: single or re-
peated exposures to a stressor eliciting a positive adaptive response in cel-
lular and molecular pathways during a subsequent exposure to a different
stressor (Gibson, 2017).
www.acsm-csmr.org Current Sports Medicine Reports 603
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Conclusions
Coaches, athletes, medical personnel, and officials need to
understand the physiology, pathophysiology, prevention,
protection, and treatment of cold-related impacts on perfor-
mance. From this understanding come optimal interventions
for the maintenance of performance and avoidance of frost-
bite, nonfreezing cold injuries, hypothermia, drowning, and
other medical events.
Click here (SDC link needed to PowerPoint file, http://links.
lww.com/CSMR/A122) to download a slide deck that summa-
rizes this ACSM Expert Consensus Statement on Injury Preven-
tion and Exercise Performance during Cold-Weather Exercise.
The authors declare no conflict of interest and do not have
any financial disclosures.
J.W.C. and M.J.T. are co-chairs.
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