Exertional heat stroke (EHS) is among the leading causes of sudden death during sport and physical activity. However, previous research has shown that EHS is 100% survivable when rapidly recognized and appropriate treatment is provided. Establishing policies to address issues related to the prevention and treatment of EHS, including heat acclimatization, environment-based activity modification, body temperature assessment using rectal thermometry, and immediate, onsite treatment using cold-water immersion attenuates the risk of EHS mortality and morbidity. This article provides an overview of the current evidence regarding EHS prevention and management. The transfer of scientific knowledge to clinical practice has shown great success for saving EHS patients. Further efforts are needed to implement evidence-based policies to not only mitigate EHS fatality but also to reduce the overall incidence of EHS.
Preventing Death from Exertional Heat Stroke—The Long Road from Evidence to Policy
Douglas J. Casa, Yuri Hosokawa, Luke N. Belval, William M. Adams, and Rebecca L. Stearns
Evidence of the Exercise-Hypogonadal Male Condition at the 2011 Kona Ironman World Championships
David R. Hooper, William J. Kraemer, Rebecca L. Stearns, Brian R. Kupchak, Brittanie M. Volk, William H. DuPont, Carl M. Maresh, and Douglas J. Casa
Purpose: Prior research has illustrated that high volumes of aerobic exercise result in a reduction in basal concentrations of testosterone in men. Those studies were mostly conducted on recreational runners and identified reduced testosterone, but not concentrations low enough to be considered pathological. Therefore, the purpose of this study was to assess the basal concentrations of testosterone and cortisol in elite triathletes, as well as the impact of a World Championship race, on the acute responses of these hormones. Methods: A total of 22 men (age 40.6 [11.5] y, height 179  cm, weight 77.0 [7.0] kg) who participated in the 2011 Ironman World Championships served as subjects. Resting blood samples were taken 2–4 d prior to provide a baseline (BL), as well as immediately, 1 d, and 2 d after the event and were later analyzed for total testosterone and cortisol concentrations. Results: At BL, 9 men had a normal testosterone concentration, whereas 9 men fell within a “gray zone” and 4 other men demonstrated concentrations suggestive of deficiency. Testosterone was significantly lower than BL at 1 d (95% confidence interval [CI] 0.10–0.34, P < .001, ES = 0.53) and 2 d (95% CI 0.01–0.21, P = .034, ES = 0.35) after the event. Cortisol was significantly different from BL at immediate post (95% CI 1.07–0.83, P < .001, ES = 8.0). There were significant correlations between time and age (R = .68, P = .001), as well as BL testosterone and cortisol (R = .51, P = .015). Conclusion: Elite ultraendurance athletes may demonstrate not only reduced testosterone but also sometimes clinically low concentrations that could be indicative of androgen deficiency.