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Exertional Heatstroke in American Football: Persistent Battles, Research Frontiers

Armstrong, Lawrence E.

Current Sports Medicine Reports: May-June 2010 - Volume 9 - Issue 3 - p 126-127
doi: 10.1249/JSR.0b013e3181de7d7f
Invited Commentary

University of Connecticut, Human Performance Laboratory, Department of Kinesiology, Storrs, CT

Address for correspondence: Lawrence E. Armstrong, Ph.D., FACSM, University of Connecticut, Human Performance Laboratory, Department of Kinesiology, U-1110, Storrs, CT 06269-1110 (E-mail:

Exertional heatstroke (EHS) is one of the few conditions that results in sudden death among healthy athletes. The extreme whole-body hyperthermia, central nervous system impairment, hypotension, and shock can damage all organs of the human body. Unfortunately, during the past three decades, the incidence of EHS among high school and collegiate American football players has increased (5). This is tragic because death due to EHS can be prevented when diagnosis and treatment by cold water immersion are prompt. Therefore, this invited commentary describes present efforts to reduce EHS deaths, as well as scientific research that may improve our ability to identify and monitor athletes who are at risk for EHS.

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Clinical and scientific investigations consistently show that rapid recognition and diagnosis are essential, cold water or ice water immersion saves lives, and heat acclimatization reduces the risk of EHS. But engrained habits and opinions die hard. Many clinicians, coaches, and athletic associations have not yet embraced the following four concepts.

  1. Skin and ear canal temperatures do not represent heat storage in internal organs. Despite this fact, numerous commercial devices claim to measure "core body temperature" via direct contact with the forehead, or by measuring infrared radiation from the ear canal. Such claims have not been validated in controlled experiments involving athletes and are potentially dangerous; such measurements (i.e., aural temperature) have been shown to be inaccurate at very high rectal temperatures. As stated in the 2007 ACSM Position Stand regarding exertional heat illnesses, a definitive diagnosis of EHS requires a rectal temperature of ≥40°C (1).
  2. Several field and laboratory studies have compared the effectiveness of cooling modalities, administered to both EHS patients and healthy hyperthermic test subjects. Their findings are consistent. Cold water and ice water immersion provide superior cooling rates (i.e., rectal temperature decreases 5-14 times faster than packing with ice) (2). This fact raises an ethical and legal question: How can the use of inferior therapeutic modalities be justified during a medical emergency? This question especially is significant in light of cooling efforts administered to more than 2000 patients with EHS during mass participation running events and military training exercises; cold water and ice water immersion were 100% effective in preventing death (Casa, D.J., unpublished observations, 2010).
  3. The physiological adaptations which occur during 8-14 d of exercise-heat exposure include reduced rectal temperature, cardiovascular strain, and perceived exertion, as well as increased plasma volume. These adaptations are essential to the well-being of football players and explain why virtually all EHS deaths occur among nonacclimatized players during the initial 3 d of summer practices. Understanding this, the National Collegiate Athletic Association enacted guidelines in 2003 that prescribe the number and duration of football practice sessions, as well as the uniform items that should be worn, during the initial days of summer training. In 2008, a task force involving ACSM, the National Athletic Trainers Association, and five other sports medicine organizations published heat acclimatization guidelines for secondary school athletics (3). Such procedures provide football players with the most effective nonmedical means to reduce the risk of EHS.
  4. EHS deaths among football players occur almost exclusively on the football practice field, when athletes are pushed beyond the point at which they otherwise would stop to rest, rehydrate, and cool the body. Thus, coaches are responsible for removing a player from practice when he or she exhibits signs and symptoms of EHS such as disorientation, irrational behavior, vomiting, nausea, dizziness, or unexpected exhaustion. However, some coaches do not understand or accept this responsibility. It is alarming that 29 high school and collegiate EHS deaths occurred during the decade beginning with 2000, whereas 15 EHS deaths occurred during the 1990s, and 14 occurred during the 1980s (5). I conclude that education, increased awareness, and perhaps legislation are required. Local, state, and national coaching organizations should proactively train and require coaches to act always in the best interest of student-athletes. When done properly, this will not repress the coaching principle of developing every athlete to his full potential.
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With regard to scientific-medical research, five areas offer great promise in our quest to understand EHS and reduce its incidence among American football players. Human genetic analysis is the first frontier. Advancements in the use of gene chip technology have identified nearly 700 genes that are activated or suppressed by exercise-heat stress, in prior EHS patients (7). And when the $100 genome analysis becomes commonplace, as one high-tech company predicted recently, genome profiles will be possible for all athletes. Then it only will be a matter of time before we can identify those who are at great risk for EHS.

The second and third research frontiers involve specific genotypes. We desperately need to clarify the interactions of sickle cell trait (inheritance of one abnormal gene and one normal gene) and sickle cell disease (two abnormal genes are inherited) with exercise-heat stress. A sickling collapse is a medical emergency that, unlike heat acclimatization, cannot be reversed by physical training. In fact, since 2000, football players have collapsed and died more often with sickle cell disease than with any other condition (6). Further investigations also should clarify if (a) collapse and death are possible in athletes with sickle cell trait, as suggested by some case reports, (b) the ways in which both sickle cell genotypes influence heat storage and the development of EHS, and (c) whether screening for sickle cell disease or trait saves lives.

Another genotype involves cellular metabolism; it has been observed in animals and theoretically occurs in humans. Physiologists have long understood that heat production and mitochondrial adenosine triphosphate (ATP) synthesis are interconnected. However, uncoupling proteins (UCP1, UCP2, UCP3), which reside within the inner mitochondrial membrane, may cause respiration to be dissociated from ATP production, converting chemical energy only to heat (4). Future research should focus on specific gene variants of uncoupling proteins in humans, to learn whether some individuals generate an abnormally large amount of heat during exercise. If this is discovered, like sickle cell trait, genome screening someday could identify individuals who are at risk of life-threatening hyperthermia.

The fourth frontier involves the interactions between clothing and body morphology. Our research group recently conducted a series of controlled, randomized laboratory experiments involving experienced football players (body mass, 117.4 kg; height, 183.9 cm; body fat, 30.1%). They completed three experiments involving repetitive box lifting and treadmill walking in a hot environment (70 min at 33°C). These experiments differed in the amount of football gear that was worn (shorts with no shirt, a full uniform, or a partial uniform without helmet and shoulder pads). Interestingly, a strong positive correlation (R 2 = 0.71, P = 0.002) existed between the increase of rectal temperature and lean body mass, when subjects wore the full uniform; also, a strong negative correlation existed between treadmill exercise time (i.e., to the point of volitional exhaustion) and total fat mass (kg) when subjects wore shorts (R 2 = −0.90, P < 0.01) and the partial uniform (R 2 = −0.69, P = 0.003). These findings are consistent with EHS deaths among football linemen, who have large fat and lean body masses, and demonstrate that much about football uniforms remains to be learned.

The final research frontier, the consumption of nutritional and controlled substances, is vast. It also is insidious in that such compounds, legal and banned, have differential effects on rectal temperature and physiological function depending on the dose, exercise intensity-duration, clothing, and environmental conditions. The consumption of herbal products (bitter orange) and prescription medications (ecstasy) concurrent with exercise in the heat have not been studied adequately.

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As long as athletes, laborers, and soldiers exist, EHS will occur among healthy individuals who are pushed to physiological limits by competition, organizational demands, or intrinsic motivation. Physicians, emergency medical technicians, and athletic trainers should recognize that diagnosis via rectal temperature and treatment via cold or ice water immersion are best practices. Secondary schools, colleges, and professional football leagues should promote heat acclimatization, limit uniform items during initial summer workouts, and require coaches to take responsibility for athletes who exhibit signs and symptoms of EHS. In the future, we should expand our use of gene chips and genomic analyses, improve the design of uniforms and gear, and clarify the effects of nutritional supplements and medications on hyperthermia. I am confident that such a comprehensive approach will reduce the incidence of EHS in American football and eliminate deaths.

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1. Armstrong LE, Johnson EC, Casa DJ, et al. The American football uniform: Uncompensable heat stress and hyperthermic exhaustion. J. Athl. Train. 2010; 45:117-27.
2. Casa DJ, Armstrong LE, Ganio MS, Yeargin SW. Exertional heat stroke in competitive athletes. Curr. Sports Med. Rep. 2005; 4:309-17.
3. Casa DJ, Csillan D. Preseason heat-acclimatization guidelines for secondary school athletics. J. Athl. Train. 2009; 44:332-3.
4. Garvey WT. The role of uncoupling protein 3 in human physiology. J. Clin. Invest. 2003; 111:438-41.
5. Mueller F, Colgate B. Annual Survey of Football Injury Research, 1931-2009. National Center for Catastrophic Injury Research [Internet]. February 2009 [cited 22 February 2010]. Available from:
6. National Collegiate Athletic Association. The student-athlete with sickle cell trait. In: NCAA 2009-2010 Sports Medicine Handbook, Indianapolis, IN: National Collegiate Athletic Association; 2008, p. 86-8.
7. Sonna LA, Wenger CB, Flinn S, et al. Exertional heat injury and gene expression changes: a DNA microarray analysis study. J. Appl. Physiol. 2004; 96:1943-53.
© 2010 American College of Sports Medicine