Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, 1864 Stadium Road, Room 100, Gainesville, FL, USA.
Thermal and Mountain Medicine Division, US Army Research Institute for Environmental Medicine, Natick, MA, USA.
Sports Med. 2020 Sep;50(9):1581-1592. doi: 10.1007/s40279-020-01318-4.
Exertional heat stroke (EHS) and malignant hyperthermia (MH) are life-threatening conditions, triggered by different environmental stimuli that share several clinical symptoms and pathophysiological features. EHS manifests during physical activity normally, but not always, in hot and humid environments. MH manifests during exposure to haloalkane anesthetics or succinylcholine, which leads to a rapid, unregulated release of calcium (Ca) within the skeletal muscles inducing a positive-feedback loop within the excitation-contraction coupling mechanism that culminates in heat stroke-like symptoms, if not rapidly recognized and treated. Rare cases of awake MH, independent of anesthesia exposure, occur during exercise and heat stress. It has been suggested that EHS and MH are mediated by similar mechanisms, including mutations in Ca regulatory channels within the skeletal muscle. Rapid cooling, which is the most effective treatment for EHS, is ineffective as an MH treatment; rather, a ryanodine receptor antagonist drug, dantrolene sodium (DS), is administered to the victim to prevent further muscle contractions and hyperthermia. Whether DS can be an effective treatment for EHS victims remains uncertain. In the last decade, multiple reports have suggested a number of mechanistic links between EHS and MH. Here, we discuss aspects related to the pathophysiology, incidence, diagnosis and treatment. Furthermore, we present evidence regarding potential overlapping mechanisms between EHS and MH and explore current knowledge to establish what is supported by evidence or a lack thereof (i.e. conjecture).
运动性热射病（EHS）和恶性高热（MH）是危及生命的疾病，由不同的环境刺激引发，它们具有一些共同的临床症状和病理生理特征。EHS 在正常的体力活动中，但并非总是在炎热和潮湿的环境中发生。MH 在接触卤烷麻醉剂或琥珀酰胆碱时发生，这会导致骨骼肌内钙离子（Ca）的快速、不受调节释放，从而在兴奋-收缩耦联机制内引发正反馈环，最终导致类似热射病的症状，如果不能迅速识别和治疗。在运动和热应激期间，即使没有麻醉暴露，也会发生罕见的清醒 MH 病例。据推测，EHS 和 MH 由类似的机制介导，包括骨骼肌内 Ca 调节通道的突变。EHS 最有效的治疗方法——快速降温，对 MH 无效；相反，向患者给予肌浆网钙释放通道抑制剂药物，即硝苯呋海因（DHCA），以防止进一步的肌肉收缩和体温过高。DHCA 是否可以成为 EHS 患者的有效治疗方法仍不确定。在过去的十年中，多项报告表明 EHS 和 MH 之间存在多种机制联系。在这里，我们讨论与病理生理学、发病率、诊断和治疗相关的方面。此外，我们还提供了关于 EHS 和 MH 之间潜在重叠机制的证据，并探讨了当前的知识，以确定哪些证据支持或缺乏证据（即推测）。
