Page 113 - JSOM Summer 2019

FIGURE 2 Incidence of heat stroke in the United States military by with high BMI increased exertional heat injury risk even more
demographic factors. A, gender; B, age; C, military service, D, race/ than each single factor alone. 32,33 More specifically with re-
ethnicity; MC, Marine Corps; AF, Air Force.
gard to EHS, a study of US Army recruits, found that those
43
with higher body fat (i.e., failed both the weight for height and
body fat screenings on entry to service, but were provided a
waiver) were 21.4 (95% CI 3.9–116.9) times more likely to
experience heat stroke in basic training compared to trainees
with lower body fat. In a series of EHS cases in the IDF, 50%
of fatal EHS cases (3 of 6) and 65% nonfatal cases (68 of 105)
were overweight or obese, defined as a BMI >25kg/m .
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Sleep Loss
It has also been suggested that sleep loss could increase sus-
ceptibility to EHS. Laboratory studies conducted for short pe-
riods of time (about 1 hour) in the heat at exercise intensities
of 50–60% VO max found small impairments in sweating and
2
vasodilation following 1 night without sleep or several nights
of limited sleep; however, rectal temperature remained un-
changed suggesting no effect on overall effect on thermoregu-
lation under these conditions. 44–46 One unique study compared
normal sleep (7–8 hours) to partial sleep restriction (4 hours of
sleep). Subjects performed exercise (walking on a treadmill at
Low Physical Fitness 2.2 miles/h) in the heat (35°C [95°F], 40% relative humidity)
When individuals are physically active at similar exercise under these two sleep conditions: 80 minutes in the morning
intensities (e.g., foot march in formation or formation run) and 80 minutes in the afternoon. Participants had higher rec-
lesser fit individuals will be exercising at a higher relative ac- tal temperatures in the afternoon (but not in the morning) in
tivity intensity (%VO max) than more fit individuals and his/ the partial sleep condition. / Thus, current evidence suggests
47
2
her core temperature will rise at a faster rate. 30,31 Thus, a lesser partial sleep restriction can raise the core temperature in very
fit individual could reach the critical EHS temperature sooner prolonged exercise and this could affect susceptibility to EHS.
than his/her more fit counterpart in hot environments.
Illnesses
Marine recruits who had slower 3-mile run times (>23 minutes It is logical to assume that conditions that raise the hypotha-
or >7.7 min/mile) on their final physical fitness test were 9.5 lamic balance point above 37°C (99°F) (e.g., fevers) would
(95% CI 5.2–17.0) times more likely to suffer an exertional increase an individual’s susceptibility to EHS because an in-
heat injury during training compared to faster recruits (<20 dividual would begin physical activity at a higher initial body
minutes or <6.7 min/mile). Similarly, Army personnel who temperature. However, the evidence for this assumption is lim-
32
demonstrated lower entry-level fitness on a Harvard Step Test ited. Several observational, case series, and case reports sug-
(5-minute test, 120 steps/min, step height 12 in.) were 2.0 gest that individuals with “illnesses” were at increased risk of
(95% CI 1.1–3.6) times more likely to suffer an exertional EHS, although the nature of these illnesses are generally not
heat injury in their first 6 months of service. In a series of well characterized. 34,48–52 Until more evidence is available, it is
33
EHS cases in the Israeli Defense Force (IDF), 83% of fatal best to err on the side of caution and individuals with illnesses
EHS cases (5 of 6) and 71% nonfatal cases (66 of 93) had low should be alerted to this possible danger when performing
aerobic physical fitness, defined as a 1.5-mile run time of >12 high intensity exercise in hot environments.
minutes (8 min/mile). 34
Certain infections can raise the hypothalamic balance point
Overweight and Obesity above 37°C (99°F) and create fevers. The mechanism whereby
Several studies have shown that obese or overweight indi- this occurs involves both humoral and neural pathways. In the
viduals have lower heat tolerance and slower acclimation to humoral pathway, prostaglandin E2 (PGE2) is released as a
heat. 35–37 There are several possible reasons for this. Obese in- direct result of the infectious agent and binds to specific recep-
dividuals have a lower skin surface:body mass ratio, which tors in the anterior hypothalamus to raise the hypothalamic
reduces the rate of heat exchange with the environment and balance point. Also in response to infection, neutrophils, mac-
results in faster accumulation of body heat. 38,39 Obese or over- rophages, and other cells produce endogenous pyrogens (e.g.,
weight individuals also have fewer sweat glands per body sur- interleukin 1, tumor necrosis factors) in an effort to contain
face area, 40,41 which likely reduces evaporative cooling ability. and destroy the infecting agent. These pyrogens further stimu-
Other factors may be involved. 7,37 late the release of PGE2. The neural pathways include cutane-
ous sensory nerves and the vagus nerve and involve the release
Data from the Singapore Defense Force indicated that over- of norepinephrine and PGE2 that also raise the hypothalamic
weight or obese military trainees (body mass index [BMI] balance point. 53
≥27kg/m ) had a 3.5 (95% CI 1.9–6.6) times higher likelihood
2
of experiencing a heat-related injury compared to those of
lower BMI. In Marine Corps basic training at Parris Island, Diagnosis
42
those with a BMI >26kg/m were found to have 3.6 (95% CI Especially in hot-humid environments medical personnel,
2
2.5–5.0) times the risk of exertional heat injury compared to trainers, and Operators should be on the lookout for signs
those <22kg/m . A combination of low initial aerobic fitness and symptoms of EHS because recognition is critical to the
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