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SPECIAL COMMUNICATION
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ACSM Expert Consensus Statement on Exertional
Heat Illness: Recognition, Management, and
Return to Activity
William O. Roberts, MD, MS, FACSM;1 Lawrence E. Armstrong, PhD, FACSM;2
Michael N. Sawka, PhD, FACSM, FAPS;3 Susan W. Yeargin, PhD, ATC;4
Yuval Heled, PhD, FACSM;5 and Francis G. O’Connor, MD, MPH, FACSM, FAMSSM6
as low as 15°C (1). Based on data from
the National Center for Catastrophic
Sport Injury Research at the University
of North Carolina at Chapel Hill,
deaths in athletes from exertional heat
stroke (EHS) have averaged three per
year since 1995, mainly in high school
football players (2). Despite educational
and preventive efforts to lessen EHS
morbidity and mortality, recent literature
reveals little to no change in the annual
number of EHS deaths among athletes
(3). The prevalence of exertional heat
illness across all sports is not known (4).
The difficulty assessing the data and
trends surrounding the epidemiology of
exertional heat illness is partly explained
by the number of cases that are not
treated and documented in medical care facilities, and the
inconsistent terminology and case definitions (5).
The incidence rate of exertional heat illness increases as ambient temperature and relative humidity rise during the
warmer months of the year (6–10); this rate is predicted to increase as average world temperature and relative humidity continue to escalate with climate change (11). The increased
prevalence of obesity, physical inactivity, low physical fitness,
and lack of heat acclimatization may contribute to the increase
incidence rate. However, other factors such as more frequent
heat waves and suboptimal prevention strategies may be responsible (7,12–14). Many medical management issues related
to the recognition, treatment, and recovery of exertional heat
illnesses remain controversial (15,16).
A systematic review of 62 epidemiological studies reported
the highest incidence of exertional heat illness in American
football, running, cycling, and adventure races (5). Marathon
running and triathlons report the highest number of hospitalizations due to the extended duration of vigorous exercise (5).
Few sports are immune from exertional heat illness and examples of rates (per 100,000 athlete exposures) during training
and competition in National Collegiate Athletic Association
Abstract
Exertional heat stroke (EHS) is a true medical emergency with potential for
organ injury and death. This consensus statement emphasizes that optimal
exertional heat illness management is promoted by a synchronized chain of
survival that promotes rapid recognition and management, as well as communication between care teams. Health care providers should be confident in the
definitions, etiologies, and nuances of exertional heat exhaustion, exertional
heat injury, and EHS. Identifying the athlete with suspected EHS early in the
course, stopping activity (body heat generation), and providing rapid total
body cooling are essential for survival, and like any critical life-threatening situation (cardiac arrest, brain stroke, sepsis), time is tissue. Recovery from EHS is
variable, and outcomes are likely related to the duration of severe hyperthermia. Most exertional heat illnesses can be prevented with the recognition and modification of well-described risk factors ideally addressed through
leadership, policy, and on-site health care.
What Is the Clinical Problem?
Athletes, elite, recreational and tactical, and occupational
laborers, regularly perform stressful physical activities in warm
to hot environments, sometimes wearing heavy equipment
(e.g., football player), protective clothing (e.g., firefighter), or
both (e.g., warfighters). Heat stress impairs exercise performance
and causes physiological strain that may evolve into exertional
heat illness in a wide range of temperature conditions starting
1
Department of Family Medicine and Community Health, University of
Minnesota Medical School, Minneapolis, MN; 2Human Performance
Laboratory, University of Connecticut, Storrs, CT; 3School of Biological
Sciences, Georgia Institute of Technology, Atlanta, GA; 4Department of
Exercise Science, University of South Carolina, Columbia, SC; 5Clinical and
Integrative Physiology Unit, Heller Institute of Medical Research, Sheba
Medical Center, ISRAEL; and 6Consortium for Health and Military Performance,
Uniformed Services University of the Health Sciences, Bethesda, MD.
Address for correspondence: William O. Roberts, MD, MS, FACSM,
University of Minnesota Medical School, Minneapolis, 1414 Maryland Ave E,
St Paul MN, 55115, MN; E-mail: rober037@umn.edu.
1537-890X/2009/470–484
Current Sports Medicine Reports
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sports are: men’s American rules football (15.5), wrestling
(2.9), cross-country (4.8), basketball (4.1), soccer (3.1), and
women’s cross country (3.5), outdoor track & field (5.9), tennis
(4.3), field hockey (0.20), and soccer (3.0) (9). High school rates
also vary by sport (17), some examples include girl’s field
hockey (3.9), lacrosse (0.6), volleyball (0.3), soccer (1.1),
cross-county (2.8); and boy’s baseball (0.57) and soccer (0.51)
(7,18). Boy’s American rules football consistently has the
highest rate of exertional heat illness, with Kerr et al. (7,18)
reporting 11 times the rate (4.42 to 5.2) of all other high
school sports combined. In military and occupational settings,
Army and Marine Corps personnel and laborers in occupations with heat-exposed physical activity consistently have
the highest rates of exertional heat illness (19–21).
This American College of Sports Medicine (ACSM) consensus statement replaces the position statement published in
2007 (22) with emerging practices for recognition, prevention,
and management of exertional heat illness (15,16) and focuses
on exertional heat exhaustion (EHE), exertional heat injury (EHI),
and EHS. Additional conditions, such as exercise-associated
muscle cramps, exertional rhabdomyolysis, exercise collapse
associated with sickle cell trait, and exercise-associated
hyponatremia, are not included in this statement, although
they are important to consider in the initial evaluation of a collapsed athlete. The consensus statement will identify evidencebased strategies to reduce morbidity and mortality of exertional heat illness, including introducing a staged return to
activity (RTA) for athletes recovering from an EHS event.
What Is Serious Exertional Heat Illness?
Serious exertional heat illness includes EHS, EHI, and EHE;
whether these entities occur independently or on a spectrum has
not been determined. Exertional heat illness related to strenuous exercise and elevated body temperatures often presents
with athlete collapse and can range from self-limited EHE to
potentially life-threatening EHS (23–27). Any athlete or laborer
presenting with a clinical picture, suggesting a potentially
life-threating exertional heat illness, should be cooled until a
more thorough evaluation can be completed.
EHE is defined as the inability to sustain the required cardiac
output and blood pressure to continue physical activity because
of high skin blood flow requirements and/or dehydration related
to heat stress. Body temperature is elevated by the metabolic heat
produced during exercise but is usually 40°C rectal temperature. The term “heat stroke” reflects the presence of focal “stroke-like” symptoms associated
with warm environments and hyperthermia, although the
symptoms in most victims are more global (encephalopathy)
than focal (stroke syndrome). CNS changes associated with
EHS vary from mild personality deviations to the continuum
of confusion, delirium, stupor, or unconsciousness. Altered
mental status with loss of orientation to person, place, or time
is common. Severe agitation with florid psychosis can occur,
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Table 1.
Signs and symptoms of exertional heat illness that often resolve with
rapid cooling.
Common Signs and
Symptoms of Exertional
Signs and Symptoms
Suggesting EHS
Heat illness
Persistent mental status changes
Dizziness
Personality changes (frontal lobe)
Headache
Inappropriate behavior or
aggressiveness
Nausea
Delirium
Unsteady walk
High rectal temperature, >40°C
(104°F)
Generalized weakness
Loss of ambulatory function
(ataxia)
Muscle cramps
Flaccid muscles or persistent
rigidity
Fatigue
Stool incontinence
Chills
Seizure
Eyes closed
Coma
Missing assigned tasks
(cognitive function)
Recurrent vomiting
Sweaty skin (not dry), warm
or cool to touch
Skin color varies from
pale to flushed
Weak or rapid pulse
Tachycardia
Systolic hypotension
and some victims are verbally and physically aggressive with
potential to injure caregivers. In addition to CNS dysfunction,
EHS is usually associated with body temperature >40°C,
along with signs and symptoms of cardiovascular and other
organ system distress (see Table 1). Organ and tissue damage
occur with prolonged hyperthermia, sometimes due to delayed
recognition and cooling, but the damage may not be clinically
evident until later in the disease process. Clinical management
following EHS may require critical care interventions for organ
and tissue damage induced by hyperthermia and sequelae, including systemic inflammatory response syndrome (SIRS) and
disseminated intravascular coagulopathy (DIC) (24–26).
A presenting core temperature ≥40°C alone is not sufficient
to establish the diagnosis of EHS (15,24,25,27). Core temperature values ≥40°C (exertional hyperthermia) have been documented during high-intensity physical activity in both warm
and hot weather with no apparent adverse effects on performance or health (31–33).
EHI is characterized by evidence of organ (e.g., gastrointestinal, kidney, liver, muscle) damage and dysfunction in the presence of hyperthermia without CNS changes seen in EHS and
requires laboratory testing to establish the diagnosis (24–26).
In an exercise setting, EHI also can be a consequence of delayed
recognition and/or inadequate cooling of EHS. The exact clinical pathway to tissue or organ injury is unknown but may be
a result of dehydration and reduced blood flow during a more
severe EHE episode or a direct thermal injury during an EHS
episode in which CNS dysfunction was minor or missed. EHI
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Figure 1: The impact of heat stress on physiological strain resulting in either adaptation or exertional heat illness.
may or may not be on a continuum as an intermediate condition between EHE and EHS. EHI typically causes tissue and
organ dysfunction that may persist for several weeks (30), including acute kidney injury, transient diarrhea (gut injury),
and/or transaminitis associated with liver injury. More severe
EHI-associated EHS can result in liver or kidney failure requiring organ transplantation for patient survival.
What Is the Pathophysiology of Exertional Heat Illness?
During exercise in the heat, the primary physiological challenge is an increase in cardiac output to support both high skin
blood flow for heat dissipation and high muscle blood flow for
metabolism at the expense of compensatory reductions in renal
and splanchnic blood flow (27,34). When these compensatory
responses are insufficient, skin, muscle, and even brain blood
flow are compromised affecting tissue metabolism and heat exchange (25,27,34). In addition, as ambient temperature increases, sweating increases, and sweat evaporation become the
primary heat transfer mechanism (35). If the high rates of sweating fluid loss are not replaced, the reduced plasma volume (from
dehydration) further elevates physiological strain, impairing
work capabilities and increasing the risk of exertional heat
illness (25,27,34).
Figure 1 diagrams progression from exercise heat stress to
exertional heat illness. The greater the heat stress the greater the
physiological strain as evidenced by hyperthermia, blood pressure
regulation challenges, reduced tissue perfusion, ischemia, and both
elevated oxidative and nitrosative stress (27,34).
If the physiological strain is not excessive, multiple heat exposures will stimulate adaptations, such as heat acclimation
(35) and acquired thermal (heat) tolerance (36), which help
to improve performance in the heat and protect from exertional
heat illness (27). The adaptive changes will induce molecular
adaptions, including heat shock protein (HSP) expression,
which improve tissue/organ protection or thermal tolerance. If
the physiological strain is excessive, it will induce pathological
events, including increased gut permeability, endotoxemia, exaggerated acute phase response and SIRS, coagulopathy, and
cell death (25,27,37). In addition, reduced cerebral blood flow,
combined with abnormal local metabolism and coagulopathy,
can lead to dysfunction of the CNS. These perturbations induce
changes are associated with EHS and EHI. There is no evidence
that EHI or EHS will induce abnormalities to hypothalamic regions, but thermoregulatory feedback loops may be damaged
(15). Of particular concern is intestinal barrier damage accentuating endotoxin leakage and potentiating liver damage,
endotoxemia, SIRS, and sepsis (25,37). The composition of
an athlete’s gut microbiome may predispose an EHS or EHI
victim to endotoxemia and SIRS (38).
Preliminary research indicates there may be an association
with EHS/EHI and long-term health issues. For example,
EHS/EHI victims were reported to have a 3.9 times higher incidence of major cardiovascular events, a 5.5 times greater incidence of ischemic stroke, and a 15 times greater incidence of
atrial fibrillation during a 14-year follow-up period (39,40).
Similarly, a cohort mortality study of male and female U.S.
Army personnel hospitalized for exertional heat illness with
Figure 2: The exertional heat illness chain of survival promotes better outcomes and increases communication between care teams (43).
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an unknown duration of hyperthermia prior to cooling demonstrated a 40% increased long-term mortality risk when
compared with hospital admissions for appendicitis as reference cases (39). Recent evidence from an animal model suggests that 30-d post-EHS epigenetic memory changes can
suppress the immune system and alter HSP responses (41). In
heat-tolerant athletes believed to be fully recovered from a prior
EHS/EHI episode (ranging from 6 wk to 10 years), after a bout
of exercise-heat stress, the lymphocyte HSP72 level was lower
and in vitro lymphocyte HSP70 induction tended to be lower
in post-EHI patients suggesting potential for reduced acquired
cellular tolerance (42). There were no differences between control and post-EHS groups for core temperature or heart rate
(HR), emphasizing the ability to have similar physiological
strain responses during a modest heat exposure and the need
for more detailed molecular biomarkers (42). These findings
suggest that future research is needed to examine the relationship between residual tissue damage from EHS/EHI and
long-term morbidity and mortality.
How Is Exertional Heat Illness Optimally Managed?
Evaluating and managing an athlete or laborer with exertional heat illness requires an effective “chain of survival” comparable to the American Heart Association’s paradigm for out
of hospital cardiac arrest. The “chain of survival” for exertional
heat illness includes four linked steps: prehospital management;
emergency medical service (EMS); advanced clinical management in a medical treatment facility; and finally, guiding the
RTA (See Fig. 2). The first three links in clinical care are detailed
in this section on optimal management; the final step of
Figure 3: The evaluation and field care of an athlete with suspected exertional heat illness. Initiate immediate cooling measures based on the
best and most practical cooling strategy for the site. If both rectal temperature measurement and cooling strategy are readily available, getting a
rectal temperature is the best first step for clinical management decision making. Body cooling should take priority if a rectal temperature cannot
be measured immediately, but a temperature measurement will be needed eventually determine an end point for active cooling. In some settings
with a heat illness care team on site, a recovered athlete may be released to family rather than transported to an emergency facility. Not all EHS
casualties are unconscious, and it is important to look at the full clinical presentation. Based on field experience, the first three boxes in this cascade
can take too much time and aggressive cooling should be started within minutes of collapse. Time sensitivity is obvious in cardiac arrest and acute
stroke syndrome, but not necessarily engrained in those evaluating and managing heat stroke for the first time.
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473
facilitating a RTA with attention to precipitating risk factors
is discussed in sections V and VI.
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Prehospital Management
Exertional heat illness clinical management depends on early
recognition, immediate cooling, and transport to a medical facility for advanced care (see Fig. 3). The observation that the
best outcomes are achieved with rapid reversal of body hyperthermia through early aggressive cooling is supported by robust
literature (43–45); accordingly, prehospital management is the
most critical element of limiting the morbidity and mortality
of an exertional heat illness event. A recent consensus statement
proposed several key steps in the paradigm of prehospital EHS
victim care, including rapid recognition, rapid assessment, and
rapid cooling (43).
Rapid recognition
An evaluation for EHS is usually triggered by the collapse or
near collapse of an athlete or laborer during or immediately following physical activity with heat stress. The differential diagnosis in a collapsed athlete is extensive, but most often due to
sudden cardiac arrest, exertional heat illness, sports-related
concussion, exercise-associated hyponatremia, hypoglycemia,
hypothermia, or exercise-associated postural hypotension
(exercise-associated collapse). Many of these diagnoses have
overlapping clinical presentations and a systematic approach
incorporating vital signs and a brief cognitive assessment will
expedite recognition and initial management, especially for
providers in a field setting (Table 1). In all weather conditions,
self-limiting postexercise collapse is usually due to sudden discontinuation of skeletal muscle pump activity causing venous
pooling and postural hypotension rather than heat illness or
dehydration, and the associated orthostatic instability usually
resolves in less than 30 min with leg elevation and rest (46,47).
A missed EHS diagnosis or delayed whole-body cooling may
lead to single or multiple organ failure or death (14). The entire
clinical picture, including the history of events leading up to the
collapse, mental status changes, vital signs, including rectal temperature, available point of care on site laboratory results, and
regular reassessment, should be considered to optimally establish
a diagnosis and manage the athlete with exertional collapse (24).
Rapid assessment
An unconscious athlete with spontaneous respirations or a
conscious athlete with CNS changes should be assessed for
EHS with an onsite core (rectal) temperature measurement.
However, whole-body cooling should not be delayed for a
core temperature measurement when EHS is suspected based
on clinical circumstances and working diagnosis. Rectal temperature measurement is the best estimate of core body temperature in the field (48–50). Shell temperature measured in
the aural canal or tympanic measures, oral sublingual, temporal artery or forehead, and axilla sites correlate poorly with
rectal temperature and should not be used for clinical decision
making for heat-related problems (48–52).
Rapid cooling
The best outcomes for EHS and EHI require rapid on-site
whole-body cooling. On-site cooling prevents treatment delays
and cooling interruptions associated with transportation to
medical facilities and emergency department (ED) evaluation
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Volume 20 Number 9 September 2021
protocols for encephalopathy. Body cooling serves two purposes:
1) reducing organ and tissue temperatures and 2) supporting
tissue perfusion by vasoconstricting skin and superficial tissue
vessels moving blood volume from the peripheral to the central circulation. Cooling rates >0.15°C·min−1 are best for survival without medical complications. Insufficient or delayed
cooling can result in the medical complications of EHI or
death (45).
Reducing body temperature by any means possible is essential to decrease the morbidity and mortality associated with
EHS, and conductive heat exchange methods are the most effective in the field. The thermal conductivity of water is 32
times that of air and using circulating cold water to facilitate
convective heat exchange at the skin level is the best means
of rapidly reducing core body temperature (51,53,54). Ice water
tub immersion is very effective for whole body cooling in hot, humid conditions (55,56). At the Falmouth Road Race (11.4 km),
there have been no fatalities and limited hospitalizations in 274
consecutive runners, aged 11 to 70 years, rapidly cooled on-site
with ice water tub immersion (56).
Other whole-body cooling methods like rotating ice watersoaked towels on the trunk, extremities, and head augmented
with ice packs in the neck, axilla, and groin; repeatedly dousing
the body with ice water; or spraying with tap water can effectively cool hyperthermic patients (see Table 2). Evaporative
cooling methods are more effective in airconditioned spaces or
low relative humidity environments and often not effective in
the field as high relative humidity limits evaporative heat transfer.
Placing ice packs over major blood vessels in the groin, axilla,
and neck can be combined with other cooling strategies, but is
not recommended as a lone treatment modality. However, in a
“first aid” situation ice packs over the major vessels may be a lifesaving start to therapy.
Initiating whole-body cooling as soon as possible is essential, and Table 2 lists potential methods for use in the field.
The method used will be site-dependent and a blend of several
elements, including clinical experience of the providers, site
assets and limitations, water and ice access, patient size and
body type, and the incidence rate of EHS at the site (57). Victims
with low body mass and with high surface area to mass ratio
(such as children or thin endurance athletes) may cool more
rapidly than victims with large body mass and relatively low
surface area (football linemen) who can store more heat in the
tissues (58). While cold water immersion is very effective, in
some situations the use of 40-gallon tubs and 20 lbs to 30 lbs
of ice may be impractical, and more portable methods may be
an alternative to rapidly initiate whole-body cooling (59).
The primary goal of prehospital cooling is to lower the body
temperature, prioritizing core temperature reduction to below
39°C within 30 min to 60 min of collapse to protect the critical organs. Athletes with indwelling rectal thermistors can
be monitored continuously without interrupting body
cooling. Repeatedly measuring rectal temperature every
10 min, when an indwelling thermistor is not available, interrupts body cooling and reduces the overall cooling rate. The
recommendation to stop active cooling at ~38°C (101°F) to
prevent hypothermic overshoot is empirical and not based
on data showing adverse outcomes. There are no known disadvantages or adverse outcomes from cooling below 38°C
and most “overcooled” athletes will be in the 35°C to 37°C
(95°F to 97°F) range, which has no adverse physiological effect
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Table 2.
Onsite whole-body cooling strategies for EHS casualties that are effective in the field.
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Body Cooling Strategies
Treatment Notes
Ice water (~2°C) or cold water (~20°C)
immersion with stirring: whole body
Immerse body to neck, circulate or stir the water to increase heat
transfer, add ice during cooling, support head above water level.
Continuous supervision.
Ice water immersion: half body
Immerse the torso and pelvic region
Rotating ice water-soaked towels applied to the limbs,
trunk, and head with ice packs in the groin, axilla, and
neck; whole body
2 people, 6–8 towels, change rapidly, wring towels after soaking in
bucket of ice water
Tarp-assisted water immersion: partial body
6–8 people to hold the sides of the tarp. Ensure as much of the
torso and groin are immersed as possible
Cold water dousing: whole body
Free flowing hose or bucket with cool tap water
Ice water-soaked sheets only or with fanning: whole body
Frequently re-wet sheets with cold water
High powered spray misters: whole body
1–2 people to supervise
Water spray and fans: whole body
1 person to spray
Cold water immersion in portable water-impermeable bag:
whole body with head out.
1–2 people, add ice and water as needed
Cooling blanket — cold air (Bair Hugger)
Available in EMS vehicles
The approximate cooling rates will vary with body mass, body fat, surface area, blood flow, and other factors. The strategy must be practical and achievable at the site. Starting whole body cooling immediately is critical to achieve the best outcomes and should not be delayed by starting IV fluids or transfer to
an emergency medical facility.
(24). Simply continuing uninterrupted cooling until the victim
“wakes up” (eyes open, normal behavior, and conversational) is the more effective cooling strategy in this clinical
scenario. Checking a rectal temperature at the point of waking
up will confirm cooling to the goal level and cooling can be
discontinued. If a victim does not wake up in 30 min to
40 min, clinical reassessment is indicated.
Intravenous fluid replacement requirements vary based
on the duration of physical activity and individual sweating
rates. The need for intravenous (IV) fluid replacement is often
clinically apparent following cooling and the return of peripheral blood volume to the central circulation. Peripheral IV
sites complicate cooling procedures, and initiating IV fluids
can be delayed if the patient is responding well to cooling measures (60–63). Oral fluids are preferred to IV fluid replacement
and should be started when the patient can tolerate oral intake.
Emergency Medical Transport
An EHS victim cooled on-site should be transported, as soon
as possible, to a hospital ED that is equipped to evaluate and
manage the complications of EHS and EHI. In road race settings
that manage many exertional heat illness-related problems, casualties with EHS who are promptly recognized, treated, wake up
easily, and clinically stable are often discharged to home with
family. In other settings not accustomed to exertional heat illness
and EHS field management, ED evaluation is strongly recommended following on-site cooling.
If on-site cooling was not started or completed, a suspected
EHS casualty is best managed at the nearest medical facility
with the capability for cooling and medical management of
exertional heat illness complications. EMS vehicles in areas
with high exertional heat illness incidence rate should be equipped
to begin or continue cooling therapy treatment en route (chilled IV
fluids, ice packs, cooling blankets [Bair Hugger™], fans) and use
the vehicle air conditioning at high settings when EHS is suspected.
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Many EMS vehicles now carry refrigerated IV fluid chilled to
4°C (39°F) to augment induction of therapeutic hypothermia
in cardiovascular emergencies.
Advanced Medical Treatment Facility Management
The third phase of clinical management involves advanced
care using an ED and hospital with inpatient critical care capability. When an individual with suspected exertional heat illness is transported to the hospital, the EMS dispatcher should
ideally direct the patient to a facility with known experience
and familiarity with heat casualties and notify the ED medical
team in advance to allow preparation for immediate treatment
upon arrival. The diagnosis of EHI and/or EHS can be challenging, as the patient may present with a temperature 3 d of >32°C (90°F)
Wearing heavy clothes, equipment, or uniforms
Individual factors
Age (infants, older adults)
Overweight, high body mass index
Poor physical fitness
Inappropriate work to rest ratios
Predisposing Factors
Exertional heat illness can occur in both healthy and “highrisk” individuals when performing vigorous activity in warm
or hot conditions. Risk factors for exertional heat illness listed
in Table 6 can be unique to a particular exertional event or a
given individual, and often, more than one risk factor is present in an individual victim. While EHS is not completely understood and is challenging to predict, numerous risk factors
associated with EHS have been identified by epidemiologic
data that include environmental, physiological, drug use, and
compromised health factors (25,26). For athletes, the most
common risk factors are low physical fitness, lack of heat acclimatization, obesity, and heat waves or unexpectedly hot
weather (14,25,89). Risk factors outlined in Table 6 can help
identify individuals who should be more closely monitored by
the sports medicine team and staff stakeholders during participation or have a “buddy” assigned to report any signs or symptoms (24,26). The most physically fit, heat acclimated, and
motivated individuals tend to sustain high rates of metabolic
heat production during intense physical activity and are highly
motivated to continue activity even when experiencing excessive fatigue or symptoms of exertional heat illness (see Fig. 4).
In addition, the presence of a predisposing factor (e.g., recent
viral illness or fever) on a particular day increases the risk of
heat stroke in subsequent days and sets up the “multiple-hit
hypothesis” (25,27), which may account for athletes who have
completed the same exercise-heat stress task many times in the
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Inadequate heat acclimatization for current conditions
Heat stress in the previous 1 d to 3 d
Hypohydration
Medications and drugs
Diuretics
Anticholinergics
B-adrenergic blockers
Antihistamines
Antidepressants
Stimulants (amphetamines, cocaine, ecstasy, ephedra)
Health conditions
Viral or bacterial infections
Fever
Diarrhea or vomiting
Skin disorders (rash, large area of burned skin)
Diabetes mellitus
Cystic fibrosis/trait
Cardiovascular disease
Behavioral
Self-imposed motivation to excel
Leadership or organizational structure
Peer or coach pressure to excel
Special Communication
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