Following exertional heat stroke (EHS), the American College of Sports Medicine recommends removal from training, frequent medical evaluations, and a slow return to exercise in the heat (1,5). It also suggests the use of a heat tolerance test (HTT) if return to activity is problematic. Following the laboratory test, the athlete is defined as either heat tolerant, (i.e., having the ability to sustain heat without a sharp rise in heart rate (HR)) or heat intolerant (7). The application of a traditional military-based HTT has been questioned in reference to elite triathletes due to the differences in normal exercise intensity and duration between these populations. In addition, the role of heat acclimation, which is a complex of physiological adaptations that reduce the physiological strain and improve an athlete’s ability to exercise in a hot environment while reducing the incidence of some forms of heat illness (3), has been suggested as a possible manner through which to further gauge an individual’s ability to adapt to exercise in the heat. The following case study illustrates the benefit of including an acclimation period into the determination of an athlete’s ability to return to play following EHS.
The Israeli Defense Force (IDF) developed the HTT to evaluate if military members who had experienced exertional heat illness (EHI) are able to return to duty including exercise in the heat (7,14). The IDF protocol involves walking on a treadmill (5 km·h−1, 2% grade) for 120 min in 40°C, 40% relative humidity (rh). Patients are considered heat tolerant if rectal temperature remains below 38.5°C and HR remains below 145 bpm (19). A pronounced plateau in both rectal temperature and HR during the test is a definitive sign of heat tolerance (15). Despite great success within the IDF, the value of an HTT in determining return to play or duty has been debated (9).
The contrary viewpoint is that the IDF HTT protocol does not relate to organ function (11), nor does it allow observation of an individual’s heat acclimation that describes an adaptation rather than an acute response (3). The U.S. military does not use the HTT after all cases of EHS. Each case is followed by reviewing laboratory blood tests and clinical signs and symptoms for normality. Patients are classified as without sequelae, with sequelae, or complex and observed over months. In some cases, a HTT will be ordered. All cases are reviewed individually, and the time course to return to duty can vary within the categories (5,16). This is more time consuming yet offers a potentially more comprehensive evaluation.
Currently, the efficacy of the IDF HTT as a predictor of safe return to sport is unknown. Therefore, the need exists for the development of a return-to-play protocol for athletes following EHS. Although in both elite athletes and military members, predisposing factors exist (17), EHI is due to uncompensable heat stress, which is influenced by the duration and intensity of exercise. Olympic triathletes typically race for shorter durations and at higher intensities (10) than military personnel where EHS occurs most commonly during lower intensity marching rather than during run training (8). Therefore, the rate of heat production and core temperature (Tc) rise differs between these populations. Recently, limitations in the IDF HTT have been observed in a female population (6), which introduces the possibility of limitations in the criteria for heat tolerance for other populations such as elite triathletes.
Separately, it is known that an individual’s heat acclimation status plays a role in heat tolerance (7). Although the classical HTT is designed to be performed prior to acclimation as a precursor to heat exposure, this may not be optimal for high-level athletes seeking to exercise at their highest capacity. In this venue, it is important to witness the physiological adaptations and if those adaptations have an effect on an individual’s heat tolerance. Therefore, we propose that an ideal return-to-play protocol should 1) closely approximate the stresses (environmental and exertional) incurred during competition and 2) evaluate if an individual is capable of adapting to exercise in the heat. The goal of the following case study was not to create a test that could determine heat tolerance/intolerance but to gather as much information about the athlete’s exercise heat capacity prior to, during, and after heat acclimation so that medical professionals overseeing the athlete could make the best decision for that athlete’s safety.
In February of 2010, a 27-year-old elite triathlete presented after 2 separate cases of presumptive EHS. The first EHS occurred in March 2009 during a race in 33°C and 80% rh. The athlete recovered and resumed training shortly thereafter. He successfully completed a race in 23°C and 70% rh 6 wk later in April 2009. However, 4 wk later, in May 2009, while competing in 31°C and 70% rh conditions, the athlete experienced a second EHS. No body temperature was taken after either EHS. However, based on a loss of consciousness for >90 min on each occasion, an altered mental status prior to collapse that was recognized by teammates he was racing with, and elevated liver enzyme presence upon return to the U.S. Olympic Training Center (Table), the medical team diagnosed the athlete as experiencing EHS (13).
Due to the lack of body temperature, it is impossible to rule out other potential diagnoses. After physician review of the medical examination and laboratory results, it was felt that the most likely differential diagnoses — exertional rhabdomyolysis, exertional hyponatremia, exercise-associated collapse, or cardiac abnormalities — were unlikely. The athlete had only minimal creatine kinase (CK) elevations on repeat testing, more consistent with his normal training load than with exertional rhabdomyolysis. Hyponatremia is seen more commonly in longer endurance races such as marathons (42.2 km) or Ironman-distance triathlons (3.9-km swim, 180-km bike, and 42.2-km run) and is associated with slower athletes that drink more water, (12) and it is unlikely based on the shorter disstance of the Olympic-distance triathlon. Exercise-associated collapse typically occurs when the athlete stops running after the finish. The cessation of lower leg muscle contraction causes a transient drop in blood pressure that may cause the athlete to become faint and collapse but almost always is resolved quickly with laying the athlete down and elevating the legs to increase their core circulatory pressure. In these cases, the collapses occurred prior to the finish line, and movement to the recovery position did not immediately return consciousness. Finally, the athlete had no prior or subsequent cardiac complaints such as chest pain or palpations with other high-intensity efforts. The athlete was questioned also by medical staff about any family history of cardiac or medical conditions that may have predisposed him to exertional collapse with no remarkable result. Therefore, EHS was decided to be the most likely diagnosis.
After the second EHS, the coaches and medical staff overseeing the athlete’s training and racing ordered that he was not to train intensely or race in a hot environment until a more concrete understanding of his exercise heat capacity was determined.
The athlete completed a 15-d exercise and heat exposure intervention to determine his physiological responses and adaptations to exercise in the heat. The complete protocol received approval by the Institutional Review Board of San Diego State University.
On day 1, the athlete underwent a cycling maximal exercise test to determine V˙O2max. Next, on day 2, the cycling wattage that corresponded to 70% of V˙O2max was determined using incremental 5-min exercise bouts.
On day 4, the athlete reported to the laboratory for an exercise heat stress test, cycling at 70% of V˙O2max in an environmental chamber (36°C, 50% rh) for 90 min or until gastrointestinal temperature (Tgi) reached the laboratory-mandated safety cut-off of 39.5°C. Before, during, and at the conclusion of testing Tgi (Fig. 1A), HR (Fig. 1B), sweat rate, fluid consumption, psychophysiological responses to scales based on the signs and symptoms of heat exhaustion (2) (Fig. 2), and rating of perceived exertion (RPE) (4) were measured. An aggregate EHI-related perceptual score was calculated by adding together each sign/symptom score (out of a possible 800 mm). Water and a carbohydrate beverage were provided ad libitum during testing.
On days 6 to 14, exercise heat acclimation occurred in an environmental chamber (36°C, 50% rh). Tgi and HR were recorded every 5 min. The acclimation sessions consisted of cycling and running separated by 6 min. Duration and intensity of the acclimation sessions increased from days 6 through 13. The intensity and duration on day 14 were reduced to match that of day 6. Throughout the 9 d of heat acclimation, the athlete continued his triathlon training outdoors in the afternoons, although the durations and paces of the outdoor workouts were reduced. The goal of the outdoor workouts was to maintain, not improve, cardiovascular fitness. Therefore, changes in the final exercise heat stress test would be attributable to changes in the exercise heat capacity and not fitness.
On day 15, the athlete performed a second exercise heat stress test. The exercise intensity and environment were replicated from day 6 of the protocol.
The preacclimation exercise heat stress test (day 4) was terminated at 45 min when Tgi exceeded 39.50°C. Mean work rate was 252 W. Sweat rate was calculated as 1.7 L·h−1. The athlete was noticeably upset after due to his perceived “poor” performance, and he did not exercise on the following day.
During the postacclimation exercise heat stress test (day 15), the athlete was able to complete 70 min of cycling before Tgi exceeded 39.50°C (Fig. 1A) at a mean intensity of 248 W. Exercise time increased 56%. Tgi rate of rise decreased to 3.0 from 3.6°C·h−1. At 45 min, Tgi and HR were lower: 38.52°C, 152 bpm, versus 39.72°C, 170 bpm. Sweat rate increased to 2.2 L·h−1. All perceptual ratings of EHI signs and symptoms were reduced (Fig. 2). The aggregate EHI-related perceptual scale score decreased from 402 to 145 mm, a 64% reduction. RPE at the end of the exercise decreased from 17 to 14.
Following all laboratory testing, the medical team evaluated the athlete’s responses and adaptations to make a decision on his training and competition status. Given that both of the previous EHS occurrences occurred during the final stretches of the athlete’s races, even a small improvement in exercise heat capacity could have made the difference between completion without incident and collapse. Therefore, they determined that the athlete’s improved exercise duration after heat acclimation warranted return to full training and competition.
In September of 2010, the athlete successfully raced in the heat (35°C), placing sixth. The athlete immediately was cooled via cold water immersion following the race as a precautionary measure, although he was otherwise asymptomatic for EHI. Following this race, the athlete continued to race successfully for the rest of the season without incurring an additional EHS.
Discussion and conclusions
The current evaluation of a triathlete’s exercise heat capacity using a novel exercise heat stress testing protocol yielded information about his ability to exercise in and adapt to exercise in the heat following two incidents of EHS. Because the HTT protocols that exist in the literature are not specific to an endurance athlete’s return to play. Moreover, a singular HTT does not allow for the assessment of adaptations to exercise in the heat.
The athlete was only able to tolerate cycling for 45 min during initial testing. However, the athlete exhibited classical heat acclimation responses including a decrease in exercise HR, initial Tgi, rate of Tgi rise, RPE, an increase in sweat rate, and potentially increased plasma volume (inferred due to 1-kg increase in morning body mass) (3). More importantly, after heat acclimation, the athlete was able to cycle longer before reaching the Tgi safety limit, and regardless of the increased duration, he reported lower signs and symptoms of EHI. The acclimation period and follow-up exercise heat stress test provided further insight of this athlete’s ability to become exercise heat tolerant.
It is important to note that although exercise duration improved, he did not complete the proposed 90 min of cycling at the exercise intensity close to his racing pace, nor did he reach a Tgi plateau as would be seen during compensable exercise heat stress. Two factors may explain these findings. First, the laboratory-mandated Tgi safety limit may not have allowed the athlete to display a true Tgi plateau. Elite endurance runners have regularly crossed the finish line of races safely while registering rectal temperatures above 40.0°C (18). Also, it is not known if elite triathletes ever experience a plateau in body temperature during a race. Second, air flow in the environmental chamber was limited to ~1 m·s−1, which does not replicate the convective and evaporative cooling of outdoor cycling. Thus, regardless of heat tolerance status or adaptations, a Tgi plateau may have been rendered impossible given the exercise intensity combined with the environmental conditions.
This unique case applies to the debate in reference to the use of the single HTT to determine an individual’s return to play or duty. It cannot yet be stated that successful heat acclimation excludes heat intolerance. Although heat acclimation was obvious in the present case report, we do not know if undiscovered organ damage or dysfunction places this triathlete at increased risk for future EHS. This is a question that will continue to be difficult to answer until additional markers for EHS recovery are discovered (16).
This case report supports utilizing return-to-play procedures that are specific to future exercise and environmental conditions that will be encountered for each patient/athlete. Forthcoming research should incorporate the given findings into field-based methods. Hopefully, it will be possible to monitor acclimatization adaptations without the necessity of an environmental physiology laboratory, allowing physicians to make informed and specific decisions about return to play.
The authors declare no conflicts of interest and do not have any financial disclosures.
1. American College of Sports Medicine, Armstrong LE, Casa DJ, Millard-Stafford M, et al.. American College of Sports Medicine position stand. Exertional heat illness during training and competition. Med. Sci. Sports Exerc. 2007; 39: 556–72.
2. Armstrong LE, Hubbard RW, Kraemer WJ, et al.. Signs and symptoms of heat exhaustion during strenuous exercise. Annals Sports Med. 1987; 3: 182.
3. Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med. 1991; 12: 302–12.
4. Borg G. Perceived exertion as an indicator of somatic stress. Scand. J. Rehabil. Med. 1970; 2: 92–8.
5. Casa DJ, Armstrong LE, Kenny GP, et al.. Exertional heat stroke: new concepts regarding cause and care. Curr. Sports Med. Rep. 2012; 11: 115–23.
6. Druyan A, Makranz C, Moran D, et al.. Heat tolerance in women — reconsidering the criteria. Aviat. Space Environ. Med. 2012; 83: 58–60.
7. Epstein Y. Heat intolerance: predisposing factor or residual injury? Med. Sci. Sports Exerc. 1990; 22: 29–35.
8. Epstein Y, Moran DS, Shapiro Y, et al.. Exertional heat stroke: a case series. Med. Sci. Sports Exerc. 1999; 31: 224–8.
9. Heled Y, Sawka MN. Point/Counterpoint: What is the Value of Heat Tolerance Testing for Determining Readiness for Return to Duty/Play Following Exertional Heat Stroke? Presented at: American College of Sports Medicine Annual Meeting, June 4, 2010.
11. Leon LR, Blaha MD, DuBose DA. Time course of cytokine, corticosterone, and tissue injury responses in mice during heat strain recovery. J. Appl. Physiol. 2006; 100: 1400–9.
12. Martinez JM, Laird R. Managing triathlon competition. Curr. Sports Med. Rep. 2003; 2: 142–6.
13. McDermott BP, Casa DJ, Yeargin SW, et al.. Recovery and return to activity following exertional heat stroke: considerations for the sports medicine staff. J. Sport. Rehabil. 2007; 16: 163–81.
14. Moran DS, Erlich T, Epstein Y. The heat tolerance test: an efficient screening tool for evaluating susceptibility to heat. J. Sport. Rehabil. 2007; 16: 215–21.
15. Moran DS, Heled Y, Still L, et al.. Assessment of heat tolerance for post exertional heat stroke individuals. Med. Sci. Monit. 2004; 10: CR252–7.
16. O’Connor FG, Casa DJ, Bergeron MF, et al.. American College of Sports Medicine Roundtable on exertional heat stroke — return to duty/return to play: conference proceedings. Curr. Sports Med. Rep. 2010; 9: 314–21.
17. Rav-Acha M, Hadad E, Epstein Y, et al.. Fatal exertional heat stroke: a case series. Am. J. Med. Sci. 2004; 328: 84–7.
18. Roberts WO. Exercise-associated collapse in endurance events: a classification system. Phys Sportsmed. 1989; 17: 49.
© 2013 American College of Sports Medicine
19. Shapiro Y. Pathophysiology of Hyperthermia and Heat Intolerance. Presented at: World Conference on Heat Stress, Physical Exertion and Environment, Sydney, AU: April 27–May 1, 1987.