International Journal of Sports Physiology and Performance, 2014, 9, 744-750

http://dx.doi.org/10.1123/ijspp.2014-0232
© 2014 Human Kinetics, Inc.
www.IJSPP-Journal.com
BRIEF REVIEW

Managing Heat and Immune Stress

in Athletes With Evidence-Based Strategies
David B. Pyne, Joshua H. Guy, and Andrew M. Edwards

Heat and immune stress can affect athletes in a wide range of sports and environmental conditions. The classical thermoregula-
tory model of heat stress has been well characterized, as has a wide range of practical strategies largely centered on cooling and
heat-acclimation training. In the last decade evidence has emerged of an inflammatory pathway that can also contribute to heat
stress. Studies are now addressing the complex and dynamic interplay between hyperthermia, the coagulation cascade, and a
systemic inflammatory response occurring after transient damage to the gastrointestinal tract. Damage to the intestinal mucosal
membrane increases permeability, resulting in leakage of endotoxins into the circulation. Practical strategies that target both
thermoregulatory and inflammatory causes of heat stress include precooling; short-term heat-acclimation training; nutritional
countermeasures including hydration, energy replacement, and probiotic supplementation; pacing strategies during events; and
postevent cooling measures. Cooperation between international, national, and local sporting organizations is required to ensure
that heat-management policies and strategies are implemented effectively to promote athletes’ well-being and performance.

Keywords: immune function, athlete, practical strategies

Athletes in a variety of sports train and compete in environments
that potentially pose a risk to health and performance. In particular,
athletes competing in outdoor sports in the summer months can be
exposed to conditions of high heat and humidity during training and
competition. The international federations responsible for the conduct
of these sports are aware of the underlying risks to health and have
implemented measures to help protect the health and well-being of
their athletes.1 The International Olympic Committee (IOC) Medical
Commission has reviewed the relevant scientific evidence, developed
practical safety guidelines, and identified research priorities on the
environmental challenges faced by Olympic and other international-
level athletes. Much of this work is focused on the traditional thermo-
regulatory model of heat stress. However, in the last decade evidence
has emerged of an inflammatory pathway that can also contribute to
heat stress, mediated principally via release of endotoxins from the
gastrointestinal tract. While understanding of the complex physi-
ological regulation of heat stress continues to evolve, it is timely to
review the causes, management, and treatment of heat illnesses. The
IOC Medical Commission and international sport federations have
implemented new guidelines and taken additional steps to mitigate
risks of heat illness even further.2 The aim of this review is to describe
new insights into the thermoregulatory and inflammatory models of
heat stress, explore the interaction between heat stress and immune
responses, and summarize evidenced-based practical strategies for
minimizing risks to health and exercise performance.
Physiological Models of Heat Stress
Classical Thermoregulatory Model of Heat Stress
Uncompensable heat stress can have substantial effects on thermo-
regulatory control, health, and exercise performance. The classical
Pyne is with the Physiology Dept, Australian Institute of Sport, Canberra,
Australia. Guy and Edwards are with the Inst of Sport and Exercise Science,
James Cook University, Cairns, Australia. Address author correspondence
to David Pyne at david.pyne@ausport.gov.au.
744
thermoregulatory model of stress centers on the heat-balance equa-
tion relating heat production during exercise or physical activity with
various mechanisms of heat dissipation (ie, evaporation, conduction,
convection, and radiation). The magnitude of the hyperthermic
response (driven by ambient conditions and/or exercise) has long
been considered the primary determinant of exertional heat illnesses
including heat syncope, heat exhaustion, and, in rare cases, heat
stroke.3,4 Heat stroke is characterized by central nervous system
dysfunction and initiation of the coagulation cascade, which can
culminate in multiorgan failure and death.5 Heat therefore effects
a broad range of thermoregulatory, immune, inflammatory, and
neuromuscular systems down to the tissue and molecular level.
In the context of exercise and sport, the exertional factors that
influence heat stress include the volume and intensity of acute
bouts of exercise, the cumulative stress of training over an extended
period, the competitive demands of different events and sports,
and the underlying environmental conditions, particularly ambient
temperature and relative humidity. In addition to these exertional
factors, the degree of passive exposure to heat and humidity in
everyday living is a consideration. Hyperthermia appears to involve
both intrinsic and extrinsic modulators.6 Intrinsic factors include
genetics, fitness level, degree of heat acclimatization, diet, current
medications, and sleep quality.3 Extrinsic factors include exercise
intensity and duration, ambient temperature and relative humidity,
and the degree of solar radiation. A complete understanding of the
causes and factors regulating heat illness is needed to facilitate
design of more efficient prevention and treatment strategies.
In addition to classical thermoregulatory factors, recent
studies indicate that heat stress can affect neuromuscular func-
tion, skills, and technique that underpin sports performance. For
example, neuromuscular-system integrity of the lower limbs was
compromised immediately after tennis match play in hot and cool
conditions as a consequence of the development of peripheral
fatigue.7 The larger and persistent strength losses observed under
heat stress were associated with greater levels of central fatigue,
especially during sustained contractions. In another study, skill
performance in field hockey was decreased after intermittent high-

intensity shuttle running, with the magnitude of decrease greater
in hot environmental conditions. The exact mechanism for this
decrement in performance is unclear but was deemed unlikely to
be related to classical physiological indicators of low glycogen
concentration or dehydration.8 It may be more plausible that this
is a feature of complex brain regulatory control, mediated through
reductions to neural drive.9
Inflammatory Models of Heat Stress
Several researchers have pointed to a more contemporary inter-
pretation of an integrated thermoregulatory/inflammatory model
of heat illnesses. In the last decade there has been accumulating
evidence that heat stress can also occur when thermoregulation
is compromised by circulatory and metabolic demands leading
to systemic inflammation.3,10 The redistribution of cardiac output
from internal organs to peripheral tissues increases hypoxia and
oxidative stress and disturbs the gastrointestinal epithelium. Gram-
negative bacteria present in the gut form the human intestinal
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microbiome, and their release into the circulation is considered
one of the primary intrinsic modulators of hyperthermia. This
disturbance can damage the intestinal mucosal membrane, increas-
ing permeability and resulting in leakage of endotoxins into the
circulation. Exercise-induced endotoxemia has been attributed
to translocation of lipopolysaccharides (LPS) from the intestine
to the portal circulation. When the rate of LPS clearance by the
liver is overwhelmed by LPS leakage from the gut and there
are insufficient levels of anti-LPS antibodies, endotoxemia will
ensue.11 Anti-LPS antibody capacity might be reduced because
of a preexisting illness or inflammatory process or some other
unknown exercise- or training-related cause. In severe cases, the
resulting endotoxemia is a major contributing factor to multiple
organ failure associated with exertional heat stroke. Production
of inflammatory mediators, primarily muscle-derived pyrogenic
cytokines, is a major contributing factor to the onset of heat-stroke-
related morbidity and mortality. In mild cases, the endotoxemia
might be the cause of subclinical fatigue resulting in impaired
thermoregulation and possibly exercise performance and recovery.
It appears that a complex and dynamic interplay between heat
cytotoxicity, coagulation, and a systemic inflammatory response
occurs after damage to the gut and other organs.10,12
The so-called tight junctions between the epithelial cells
lining the gastrointestinal tract play an important role in main-
taining gut permeability. The stress of heat and oxidative damage
during exercise causes disruption to the intestinal epithelial cells’
tight-junction proteins, resulting in increased permeability to
luminal endotoxins. The endotoxin moves into the blood stream,
leading to a systemic immune response. Tight-junction integrity
is altered by the phosphorylation state of the proteins occludin
and claudin and could be influenced by the type of exercise per-
formed.11 Prolonged and high-intensity exercise could lead to an
increase in key phosphorylation enzymes that ultimately cause
tight-junction dysfunction, but different mechanisms might be
involved.11 Protein markers of gut permeability can be quantified
in blood, urine, or stool samples, which largely precludes simple
field-based monitoring of athletes.
There are several lines of evidence supporting the involvement
of both the classic thermoregulatory and inflammatory pathways in
regulation of heat stress and heat stroke. Some athletes, and indi-
viduals in occupational or military settings, can perform adequately
with a core temperature exceeding 40°C.13 In contrast, other reports
indicate that athletes can suffer the effects of heat stress at more
Managing Heat and Immune Stress   745
moderate core temperatures below 40°C. The inference drawn here
is that it is not solely hyperthermia that drives heat stress. Other
field-based observations of individual variability to heat stress
point to more complex regulation involving both thermoregulatory
and inflammatory processes. Anecdotal reports indicate that some
individuals have succumbed to heat stress in environmental condi-
tions similar to those where previously they successfully tolerated
the thermal load.
Other evidence for an inflammatory process in heat stress comes
from animal models. Sedated animals protected from the effects of
heat load in the absence of endotoxemia survived, whereas animals
with endotoxemia died under exactly the same environmental condi-
tions.14 Administration of medication to reduce the heat-induced rise
in plasma LPS therefore appears to reduce morbidity and mortality
in primates. In human subjects, endotoxemia has been detected
in heat-stroke patients15 and in healthy runners after endurance
races.15–17 Mild endotoxemia during exercise can occur at core
temperatures around 38°C.18 During the late 1990s and early 2000s
the view emerged that heat stroke is triggered by hyperthermia but
driven by endotoxemia characterized by an acute-phase response
and systemic inflammation.19 A preexisting inflammatory state can
exacerbate heat stress in both animals20 and humans. A 12-year
clinical study of soldiers presenting with heat stroke in a military
hospital in Thailand indicated that 95% of cases were preceded by a
bout of low-grade fever or upper respiratory tract infection.21 Illness
accompanied by a fever in the lead-up to exercising or competing
in thermally challenging environments also appears to be a risk
factor for heat stroke.
The combination or interaction of the dual pathways of classi-
cal thermoregulation and endotoxemia present an interesting chal-
lenge to the regulation of body temperature. A study of 60-minute
running at 70% VO2max in moderately trained individuals in either
hot (33°C, 50% relative humidity) or cool conditions (22°C, 62%
relative humidity) indicated that intestinal permeability is affected
primarily by exercise, whereas exercise-induced endotoxemia is
influenced more by environmental conditions.22 An increase in intes-
tinal permeability may not be sufficient to trigger exercise-induced
endotoxemia per se, while post-LPS translocation from the gut to
the portal circulation and beyond could be the primary mechanism
driving an increase in inflammatory processes. In any case, both
the demands of exercise and environmental conditions need to be
considered in the context of thermoregulatory and inflammatory
processes. A disturbed immune system, either preexisting or exercise
induced, may be a contributing factor. Future studies will address
issues around the complex interplay of classical and inflammatory
models to determine whether they operate independently or in an
integrated manner. Once key regulatory processes have been better
characterized, the effectiveness of practical interventions that target
gut health and status of the immune system, as well as traditional
physiological indicators of heat stress, can be evaluated.23
Heat Stress and the Immune System
The effects on the human system of heat stress during exercise in
hot conditions have been investigated using both experimental and
observational studies. Impacts are generally modest and athletes can
train and compete in warm to hot conditions with the confidence
that immune function is unlikely to be impaired, provided preven-
tive strategies are followed. Most of the available evidence does
not support the contention that exercising in the heat poses a great
threat to immune function.4 During exercise or physical activity the
hypothalamic set point remains the same, but mechanisms of heat
 746  Pyne, Guy, and Edwards
dissipation become compromised, causing body temperatures to
rise. This response is different from the increase in body temperature
associated with a fever mediated by an increase in the hypothalamic
set point. This difference has been confirmed experimentally using
incubation (passive heating) studies. In moderate to hot environ-
mental conditions there is a modest increase in the circulating
concentrations of leukocytes, stress hormones, catecholamines,
and immunoregulatory cytokines. In contrast there are only limited
effects of heat stress on functional activities of neutrophils, mono-
cytes, and natural killer (NK) cells.4 Some studies, however, show
that stimulated lymphocyte responses are lower after exercise in the
heat. More work is needed to clarify the sequence of events involving
prolonged and/or intensive exercise, high ambient temperatures and
humidity, and perturbations in the immune system that culminate
in up-regulation of inflammatory processes.
Cytokines are intracellular peptides that exert both proinflam-
matory and anti-inflammatory effects24 and can act as both mediators
and protectors in the resolution of inflammation. The interaction
between proinflammatory, anti-inflammatory, and immunoregula-
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tory cytokines is complex, situation specific, and likely dependent
on environmental conditions, demands of exercise, and individual
level of fitness. A strong inflammatory response after heat stress is
involved in both damage-generating processes and repair mecha-
nisms during the recovery phase in hours and days after strenuous
exercise. In normal circumstances, the inflammatory response is
transient and diminishes quickly as homeostasis is reestablished.
Uncoupling of the regulatory balance between proinflammatory and
anti-inflammatory cytokine responses is thought to exacerbate tissue
damage. One study explored the relationship between cytokine pro-
duction and release of LPS. LPS-dependent ex vivo cytokine release
was strongly influenced by exercise, and these changes could only
in part be attributed to changes in messenger RNA.25 Assessment of
interleukin (IL)-1ra, IL-6, and IL-10 pointed to a less pronounced
anti-inflammatory response in women than in men. Early production
of IL-10 by peripheral blood cells in response to exercise has also
been reported,25 although this effect may be blunted by repeated
exposures to exercise in the heat.26
NK cells also appear to be involved in up-regulation of an
immune response during exercise in the heat. Exercise in the heat
increased free plasma heat shock protein (HSP) concentration, and
HSP colocalized with CD94 on NK cells, highlighting links between
exercise and activation of the innate immune system.27 A study of 2
bouts of treadmill running 45 minutes apart indicated that leukocyte,
neutrophil, and basophil counts can increase substantially after
exercise in hot or cold environments, with a greater increase likely in
hot environments.28 Lymphocyte and neutrophil antioxidant enzyme
activities and carbonyl index increased or decreased substantially
after exercise only in the hot environment. The lymphocyte expres-
sion of catalase, HSP72, and superoxide dismutase was increased
in the hot environment. Taken together these results support the
notion that increased core body temperature during exercise can
elicit an acute-phase immune response and immune-cell adaptations
to counteract the oxidative stress.28
Antioxidant status is another factor that can influence the
inflammatory response to exercise. Adaptations to exercise and train-
ing include a higher level of antioxidants and lower concentration of
lipid peroxidation products. Physical exercise at an elevated ambient
temperature caused lower changes in oxidative-stress indices than
did sauna bathing.29 Exposure to the sauna bathing induced a shift
in pro-oxidant/antioxidant balance toward oxidation, although the
shift was lower in the athletes than in the untrained men. This leads
to the assertion that physical exercise increases tolerance to elevated
ambient temperature and oxidative stress.29 It has been known for
a long time that physical fitness confers some advantages in terms
of improved heat tolerance. Another explanation for this benefit
is possibly related to improvements in control of oxidative-stress
mechanisms.30
Practical Intervention Strategies
for Athletes
International federations and national sporting organizations have
the primary responsibility in implementing policies and procedures
for minimizing or reducing the risk of heat illness. While polices,
programs, and procedures are carefully developed, their implemen-
tation and effectiveness can be impaired as a consequence of limited
resources, poor communication, or inadequate engagement of local
authorities, officials, coaches, and athletes. For example, contempo-
rary guidelines appear to be inadequate for fully assessing the risk
of heat stress and are likely too conservative in informing safety
decisions in professional beach volleyball.31 Another study reported
only a low proportion of surveyed US high school football programs
complied fully with all 17 nationally and internationally mandated
guidelines. Fortunately, however, many heat-illness-prevention
strategies were voluntarily implemented. State-level-mandated
exertional-heat-illness prevention guidelines may increase compli-
ance with recognized best-practices recommendations. Ongoing
longitudinal monitoring of compliance is also recommended.32 A
summary of planning and policy recommendations for sporting
organizations and event managers to consider in preparation for
competitions is presented in Table 1.
Mass-participation events in distance running and triathlon
present challenges for organizers dealing with large numbers of
competitors with a wide range of fitness levels.33 It appears that
exercise intensity, in this case running velocity, can influence the
rate of increases in core body temperature. Analysis of 30,000
performances at the Chicago Marathon indicated that intermediate-
level women were consistently better pacers than intermediate-
level men, and this difference was magnified from cold to warm
race temperatures.34 In contrast, elite men and women runners had
similar pacing strategies. In hotter temperatures, novice runners are
advised to implement a slower initial velocity to maintain or increase
running velocity later in the race.34 Another study also showed that
running velocity was a good predictor of the likely elevation in core
temperature during a 21-km road race.13
The key preventive strategies for reducing the risk of heat ill-
ness and heat stroke center on undertaking an environment-specific
heat acclimation or acclimatization program before training and
competition and employing a range of cooling methods suitable
for the particular sport or activity undertaken (see Table 2). How-
ever, on the basis that heat stress is regulated by both classical and
inflammatory processes, it follows that prevention, management, and
treatment should also incorporate a combination of interventions.
On the classical thermoregulation side, athletes and coaches are
encouraged to attend to a range of practical issues including cloth-
ing, rehydration, training scheduling, preexercise and postexercise
cooling methods, and provision of appropriate sports-medicine
personnel.35 On the gut health and inflammatory side, athletes and
coaches should review training prescription and load management,
dietary practices, stress levels, and sleep quality and quantity, during
both training and competitions.
 Managing Heat and Immune Stress   747

Table 1  Planning and Policy Recommendations for Sporting Organizations and Event Managers to Consider in
Preparation for Competitions
Issue Details
Preevent planning International federations.
National and local sporting organizations.
Event organizers.
Adverse-weather policy.
Medical coverage Appoint medical personnel.
Provide postevent cooling modalities.
Provide emergency facilities and equipment.
Postseason and competition review of adverse events and future planning Review all adverse events.
Review effectiveness of medical coverage.
Obtain input from athletes, coaches and support personnel.
Summarize key points for future planning.
Note: Derived from material in references 1, 2, 31–33, 50, 59, 60.
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Table 2  Checklist of Evidence-Based Practical
Strategies for Limiting Heat and Immune Stress in
Athletes
Timing Recommendation
Preevent Health status.
Attend to hydration needs.
Precooling.
Probiotic supplementation.
Short-term heat-acclimation training. 40, 45, 46
During and
within events Attend to hydration needs.
Energy needs—carbohydrate.
Pacing strategies.
Postevent Implement postcooling strategies.
Precooling and Postcooling
Early intervention and rapid cooling are the key considerations for
managing heat illnesses in athletes. In recent years there has been
systematic investigation of precooling as a means of reducing the
impact of challenging environments on health and performance.36
The most effective options include application and ingestion of cold
drinks (water, ice, or ice slurries),37 separately or in combination,
immediately before exercise. Although many studies have observed
improvements in exercise capacity or performance after precooling,
some strategies are more logistically challenging than others and
often impractical for use in competition or field settings.
Rapid cooling by any means available can reduce the risk of
adverse effects, tissue damage, morbidity, and mortality. Cold-water
immersion is the most effective method38,39 but may not always
be available when needed in sporting venues, particularly during
training or traveling away. Pouring and/or spraying of cool or
cold water, hosing, and use of cold-soaked towels are other useful
options. Cooling is likely to benefit both the thermoregulation and
inflammatory processes that underpin heat stress. Tissue cooling
reduces intestinal permeability and whole-body cooling can reduce
References
circulating levels of LPS and the proinflammatory cytokines TNF-α
1, 2 and IL-1α.15 These immediate treatment strategies in situ are well
50–53 established. However, less is known about the subsequent manage-
ment in the days and weeks after an episode of heat illness.
36, 37
57, 61 Training Interventions
Heat-Acclimation Training.  Short-term tolerable increases
(~20%) in training load over a few weeks appear to offer some
50–53 protection against developing endotoxemia during exercise in
54, 55 the heat.40 Further work is needed to define how both short- and
long-term training can improve heat tolerance. Heat-tolerance
13, 47–49 testing has been proposed as a potential tool that, when combined
37, 38 with appropriate clinical information, may assist in return-to-play
decisions. However, currently no standard of care is available for
performing heat-tolerance testing. The Israeli Defense Forces
heat-tolerance-testing protocol, developed over decades of careful
research, has proven useful for military personnel and is used by
other militaries to assist in return-to-play (or duty) decisions.41 It
is likely that improvement of heat tolerance by physical fitness is
caused by a greater cardiovascular capacity that permits greater
LPS tolerance and not only enhanced perfusion of heat-loss
tissues but also via maintenance of a better gastrointestinal tract
blood supply, thereby better maintaining the normal barrier to
movement of endotoxins from gut lumen to plasma. Sedentary
and relatively inactive individuals, with their lower cardiovascular
capacity, redistribute more blood flow away from the gut during
environmentally induced hyperthermia, thus allowing endotoxin-
induced fever to aggravate hyperthermia.42
A rethinking of current heat-acclimation strategies has been
suggested, as most research and advice for improving physiological
strain in the heat include maintaining hydration using long-term
acclimation protocols (>10 d). These strategies have typically used
untrained or moderately trained subjects. As short as 4 or 5 days
of heat training can be effective in achieving partial acclimation in
 748  Pyne, Guy, and Edwards
sports such as cricket43 and field hockey.44 Meaningful physiological
and performance improvements occurred for highly trained ath-
letes using a short-term (5-d) heat acclimation under hyperthermia
control with dehydration.45 Adaptations may be more pronounced
after fluid regulatory strain from a dehydration-acclimation regi-
men. Furthermore, highly trained athletes may have physiological
gains similar to those who are less trained using short-term heat
training. However, research has tended to focus on untrained or
moderately trained participants, and more information is required
for highly trained athletes. HSP70 response is up-regulated with
short-term heat training, indicating that this marker could be useful
for monitoring thermoregulatory tolerance and protective adaptive
changes. Physiological adaptations after heat acclimation are rela-
tively short term and may vanish only a few days or weeks after
removal from heat exposure. Short-term heat training of 4 or 5 days
can be effective, less expensive, and less likely to disrupt the taper-
ing for competition in elite performers. More information on the
time course of acclimation decay would be valuable for teams and
athletes preparing for competition,45,46 particularly when combined
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with long-haul travel.
Pacing Strategies in the Heat.  Variables relating to fluid balance
were not associated with any core temperature parameters or
pacing.13 Hyperthermia, typically defined as core body temperature
exceeding 39.5°C, is common in trained individuals undertaking
outdoor distance running in environmental heat without evidence
of fatigue or heat illness. Most studies investigating pacing during
prolonged exercise in ambient temperatures have observed a fast
start, followed by an even pace strategy in the middle of the event,
with an end sprint in the final minutes of the race. A reduction in
pace observed at commencement of the event is often more evident
during exercise in hot environmental conditions. Furthermore,
reductions in power output and muscle activation occur before
critical core temperatures are reached, indicating that subjects can
anticipate the exercise intensity and heat stress they will be exposed
to, resulting in a tactical adjustment of power output. Both climatic
stress and pharmacological manipulation of the central nervous
system have the ability to elicit changes in endurance performance.47
Consideration should also be given to cognitive and perceptual
issues related to sports performance given, their likely impairment in
adverse environmental conditions.48 Pacing is also an issue in routine
training, particularly higher-intensity interval training common in
both individual and team sports. A combination of performance and
perceptual markers for athletes to self-determine both work and rest
in interval training in hot conditions is advisable.49
Nutritional Countermeasures
Fluids.  It is apparent that fluid replacement in the heat is not a
just a simple matter of hydration and electrolytes, although they
are key considerations.50 A range of other nutrients (principally
carbohydrate) and compounds are often included in fluid-
replacement beverages to augment physiological functions
unrelated to hydration, such as the provision of energy. The optimal
composition of a fluid-replacement beverage depends on the source
of the fluid loss, whether from sweat, urine, respiration, diarrhea,
or vomiting. The interaction of digestion of foodstuffs and fluids
with exercise can lead to gastrointestinal disturbance. A reduction
in perfusion of the gut can damage mucosal surfaces, and increase
allergen absorption, gut permeability, and release of LPS (or
endotoxemia). The goal of exercise rehydration is to take in more
fluid orally than the amount lost in sweat. Sports drinks provide
the replenishment of sodium and carbohydrates to assist with
intestinal absorption of water and muscle-glycogen replenishment.
Gastric emptying is proportionally slowed by carbohydrate-rich
(hyperosmolar) solutions, yet to prevent hyponatremia, avoiding
overhydration is recommended.51
It is also apparent that the optimal fluid-replacement beverage
should be customized according to specific physiological needs,
environmental conditions, intended benefits, and individual char-
acteristics and taste preferences.52 Hydration regimens should be
individualized, preplanned, and rehearsed well before competition.
In a study of tennis in hot conditions53 a preplanned hydration regi-
men and ad libitum fluid consumption restricted losses in body mass
to <1%. However, undertaking match play in a euhydrated state
attenuated thermal, physiological, and perceptual strain. Maximal
voluntary strength in the lower limbs and repeated-sprint ability
deteriorated similarly in both conditions but were restored within
24 hours.
Carbohydrate and Protein.  Heat stress might attenuate the effects
of carbohydrate on immunoendocrine responses to exercise by
increasing endogenous glucose production and reducing the rate of
exogenous carbohydrate oxidation. One study compared the efficacy
of carbohydrate consumption on immune responses to exercise
in temperate versus hot conditions.54 Carbohydrate ingestion
attenuated neutrophil counts during exercise in hot conditions,
whereas it had no substantial effect on any other immune variable
in either temperate or hot conditions.54 Protein ingestion could
be beneficial during recovery from stressful training55; however,
research is warranted to determine whether the benefits of protein
supplements for enhancing recovery of fluid balance after exercise
affect subsequent performance levels in the heat.
Probiotics.  New prophylactic approaches with probiotic supple­
mentation in individuals undertaking high-intensity physical activity
offer promise in promoting anti-inflammatory effects and enhancing
the intestinal mucosal barrier function.56 One study reported a
substantial enhancement in performance in a group of moderately
trained subjects after a course of probiotic supplementation.
Probiotic supplementation substantially improved run time to fatigue
compared with a placebo (37:44 ± 2:42 vs 33:00 ± 2:27 min:s).
However, mean core body temperature during exercise was similar
between trials (probiotic 38.1°C ± 0.2°C, placebo 38.1°C ± 0.1°C).57
Serum LPS concentration increased postexercise, while there was
a moderate to large reduction in preexercise and postexercise
concentration after probiotic supplementation. Although there is
evidence that numerous supplements can enhance immune function,
8 weeks of bovine colostrum supplementation saw a counterintuitive
increase in gut permeability in recreational runners training 3 times
a week. The increase in intestinal permeability with colostrum may
have been related to greater leakiness of tight junctions between
cells of the gastrointestinal tract or by increasing macromolecular
transport as it does in neonatal gut.58
Medical.  Much of the information on medical interventions
applies to the relatively infrequent cases of heat exhaustion or heat
stroke. A medically administered treatment plan involving blood
cultures, imaging, and vasopressor administration to modulate
hypotension has been suggested for more serious heat illnesses.6
Prescription of antibiotics is discouraged, given an increased risk of
disturbing the gut microbiota, as well as enterocolitis or candidiasis,
collectively outweighing the likely therapeutic benefit.24 There
is increasing interest in military settings in the effectiveness of
various behavioral and therapeutic approaches targeted at both

the individual and organizational level.59 Various pharmacological
and nonpharmacological strategies have been employed to manage
heat illnesses.5 Some of these approaches might be applicable to
exercise and sport settings, notwithstanding possible negative effects
on performance and full compliance with antidoping regulations.
Guidelines on return to full training and competition after heat
illness are somewhat limited in contrast to recovery from injury or
infectious illness. In terms of promoting gut health, prophylactic
administration of an LPS-suppressing corticosteroid is known to
reduce morbidity and mortality in primates. More work is required
to verify whether this approach is viable in human subjects and,
eventually, athletes.
Conclusions
Heat and immune stress are important considerations for athletes
training and competing in many sports in challenging environmental
conditions. The past decade has seen the emergence of new insights
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into thermoregulation during exercise and causes of heat illness. It
is now recognized that inflammatory pathways can also contribute
to heat illness in a variety of settings. Experimental research has
been conducted on many interventions including precooling, short-
term heat-acclimation training, nutritional countermeasures around
hydration, energy replacement and probiotics, pacing strategies
during events, and postevent cooling measures to promote the per-
formance and recovery of athletes. There has been much attention
placed on heat illnesses, from risk reduction to immediate treatment
and long-term management. Policy and planning guidelines for
international, national, and local sporting organizations have been
developed, although their implementation has not always been
timely and effective. Future work will clarify the management of
heat issues in athletes originating from both thermoregulatory and
inflammatory pathways.
References
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2. Bergeron M, Bahr R, Bärtsch P, et al. International Olympic Commit-
tee consensus statement on thermoregulatory and altitude challenges
for high-level athletes. Br J Sports Med. 2012;46(11):770–779.
doi:10.1136/bjsports-2012-091296
3. Epstein Y, Roberts W. The pathophysiology of heat stroke: an inte-
grative view of the final common pathway. Scand J Sci Med Sport.
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