The validity of the heat tolerance test in prediction of recurrent exertional heat illness events

Schermann, Haggai; Heled, Yuval; Fleischmann, Chen; Ketko, Itay; Schiffmann, Nathan; Epstein, Yoram; Yanovich, Ran

doi:10.1016/j.jsams.2017.10.001

Cited by 24 publications

(27 citation statements)

References 10 publications

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“…For example, in the French military, 15.4% of the patients experiencing EHS reported a previous EHS episode (Abriat et al 2014). More recently, another study reported an incidence of 4.1% of recurrent exertional heat illness episodes in a cohort of 145 patients (Schermann et al 2018). Likewise, US active military personnel, who experienced EHS in the previous year, had a 7.3 times greater chance of getting a second EHS episode (Mayer TA, King MA, Bedno SA, Ward MD, Leon LR, unpublished observations).…”

Section: Introductionmentioning

confidence: 99%

Delayed metabolic dysfunction in myocardium following exertional heat stroke in mice

Laitano

Garcia

Mattingly

et al. 2020

The Journal of Physiology

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Key points Exposure to exertional heat stroke (EHS) is associated with increased risk of long‐term cardiovascular disorders in humans. We demonstrate that in female mice, severe EHS results in metabolic changes in the myocardium, emerging only after 9–14 days. This was not observed in males that were symptom‐limited at much lower exercise levels and heat loads compared to females. At 14 days of recovery in females, there were marked elevations in myocardial free fatty acids, ceramides and diacylglycerols, consistent with development of underlying cardiac abnormalities. Glycolysis shifted towards the pentose phosphate and glycerol‐3‐phosphate dehydrogenase pathways. There was evidence for oxidative stress, tissue injury and microscopic interstitial inflammation. The tricarboxylic acid cycle and nucleic acid metabolism pathways were also negatively affected. We conclude that exposure to EHS in female mice has the capacity to cause delayed metabolic disorders in the heart that could influence long‐term health. Abstract Exposure to exertional heat stroke (EHS) is associated with a higher risk of long‐term cardiovascular disease in humans. Whether this is a cause‐and‐effect relationship remains unknown. We studied the potential of EHS to contribute to the development of a ‘silent’ form of cardiovascular disease using a preclinical mouse model of EHS. Plasma and ventricular myocardial samples were collected over 14 days of recovery. Male and female C57bl/6J mice underwent forced wheel running for 1.5–3 h in a 37.5°C/40% relative humidity until symptom limitation, characterized by CNS dysfunction. They reached peak core temperatures of 42.2 ± 0.3°C. Females ran ∼40% longer, reaching ∼51% greater heat load. Myocardial and plasma samples (n = 8 per group) were obtained between 30 min and 14 days of recovery, analysed using metabolomics/lipidomics platforms and compared to exercise controls. The immediate recovery period revealed an acute energy substrate crisis from which both sexes recovered within 24 h. However, at 9–14 days, the myocardium of female mice developed marked elevations in free fatty acids, ceramides and diacylglycerols. Glycolytic and tricarboxylic acid cycle metabolites revealed bottlenecks in substrate flow, with build‐up of intermediate metabolites consistent with oxidative stress and damage. Males exhibited only late stage reductions in acylcarnitines and elevations in acetylcarnitine. Histopathology at 14 days showed interstitial inflammation in the female hearts only. The results demonstrate that the myocardium of female mice is vulnerable to a slowly emerging metabolic disorder following EHS that may harbinger long‐term cardiovascular complications. Lack of similar findings in males may reflect their lower heat exposure.

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Section: Introductionmentioning

confidence: 99%

Delayed metabolic dysfunction in myocardium following exertional heat stroke in mice

Laitano

Garcia

Mattingly

et al. 2020

The Journal of Physiology

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“…Whether it has long-term impacts on epigenetics or health is not entirely clear. Epidemiological data suggest that heat stroke exposure is associated with increased susceptibility to a second heat stroke (Abriat et al 2014;Schermann et al 2018) and a higher incidence of cardiovascular disease, renal failure or other severe health disorders later in life (Wallace et al 2007;Wang et al 2019;Laitano et al 2020;Tseng et al 2020). Furthermore, in athletes previously exposed to heat illness, heat shock protein responsiveness of blood leukocytes is blunted, when evaluated at least 6 months after exposure (Ruell et al 2014).…”

Section: Introductionmentioning

confidence: 99%

Exertional heat stroke leads to concurrent long‐term epigenetic memory, immunosuppression and altered heat shock response in female mice

Murray

Brant

Iwaniec

et al. 2020

The Journal of Physiology

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Exposure to exertional heat stroke (EHS) has been linked to increased long-term decrements of health. Epigenetic reprogramming is involved in the response to heat acclimation; however, whether the long-term effects of EHS are mediated by epigenetic reprogramming is unknown. r In female mice, we observed DNA methylation reprogramming in bone marrow-derived (BMD) monocytes as early as 4 days of recovery from EHS and as late as 30 days compared with sham exercise controls. r Whole blood, collected after 30 days of recovery from EHS, exhibited an immunosuppressive phenotype when challenged in vitro by lipopolysaccharide. r After 30 days of recovery from EHS, BMD monocytes exhibited an altered in vitro heat shock response. r The location of differentially methylated CpGs are predictive of both the immunosuppressive phenotype and altered heat shock responses.

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“…However, this relatively long recovery period remained unchanged until recently for 2 main reasons. First, the protocol served for many years as a safety tool in RTD decisions, 16 preventing a premature RTD. Second, although most clinical guidelines recommended return to gradual activity only 7 to 21 days after clinical recovery, 9,10,14 no evidence has shown that clinical recovery is an accurate indicator of the function of the thermoregulatory mechanism.…”

Section: Discussionmentioning

confidence: 99%

“…The IDF has used this test for the last 4 decades because it is simple, safe, and reliable (98.2% of participants who had had a negative HTT did not experience a repeat EHI). 4 The raw data obtained during the test were analyzed for many years by an experienced physiologist or physician. This requirement was a major disadvantage, which has recently been addressed by applying computational methods for the objective interpretation of results.…”

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confidence: 99%

When Should a Heat-Tolerance Test Be Scheduled After Clinical Recovery From an Exertional Heat Illness?

Schermann

Hazut-Krauthammer

Weksler

et al. 2020

Journal of Athletic Training

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Objective Researchers have produced a hypothesis of transient heat intolerance (HI) after exertional heat stroke (EHS). Based on this hypothesis, heat-tolerance testing (HTT) has been postponed until weeks 6 to 8 after EHS and other types of exertional heat illness (EHI). We compared the HTT results of participants after either EHS or other EHI who were tested earlier (≤6-week group) versus those who were tested later (>6-week group) to verify the hypothesis. Design Cohort study. Setting Data obtained from records of military athletes who experienced EHS or EHI. Patients or Other Participants All participants who underwent HTT after EHI or EHS experienced between 2014 and 2018 and for whom complete data regarding the severity of the event (rectal temperature, neurologic symptoms, and laboratory results) and HTT results were available were included. Participants with suspected EHS and those with other EHIs were evaluated separately. Main Outcome Measure(s) The percentages of participants with HI and mean probability of heat tolerance were compared between those tested within 6 weeks of the event and those tested later. Results A total of 186 participants were included in this study (EHS: 12 in the <6-week group, 9 in the >6-week group; EHI: 94 in the <6-week group, 71 in the >6-week group). In the EHS group, the percentages with HI (33% versus 44%, P = .67) and mean probability of heat tolerance (0.82 versus 0.82, P = .98) did not differ. In the EHI group, participants who were tested after 6 weeks had a greater chance of being diagnosed with HI (38% versus 21.3%, P < .02) Conclusions The HTT results were similar between participants with EHS who were tested early (<6 weeks) and those tested late (>6 weeks). Further investigation of heat-tolerance changes in larger cohorts of patients after EHS is required to verify the theory of transient HI.

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The validity of the heat tolerance test in prediction of recurrent exertional heat illness events

Cited by 24 publications

References 10 publications

Delayed metabolic dysfunction in myocardium following exertional heat stroke in mice

Delayed metabolic dysfunction in myocardium following exertional heat stroke in mice

Exertional heat stroke leads to concurrent long‐term epigenetic memory, immunosuppression and altered heat shock response in female mice

When Should a Heat-Tolerance Test Be Scheduled After Clinical Recovery From an Exertional Heat Illness?

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