Muscular Metabolism and Contraction in Exertional Heat Stroke

Abstract

A number of similarities have been observed between malignant hyperthermia (MH) and exertional heat stroke (EHS) syndromes. Malignant hyperthermia is a pharmacogenetic syndrome appearing in predisposed subjects characterized by rigidity and accelerated metabolism of skeletal muscles leading to a dramatic increase in core temperature. MH occurs in susceptible subjects after exposure to triggering agents such as inhalational fluorinated anesthetics and depolarizing muscle relaxants [1–3]. Exertional heat stroke (EHS), also called exercise hyperthermia, is characterized by hyperthermia above 40°C, neurological signs and rhabdomyolysis [1,4]. This syndrome occurs during intense, extended physical effort not only in hot and humid climatic conditions. Patients are healthy young adults who have no apparent clinical or biological deficit. Since the hypothesis of a preexisting muscular disorder was raised in EHS patients, our objective was to investigate the etiology of EHS and the possible link between EHS and malignant anaesthetic hyperthermia.