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Evidence for a Direct Role of Physical Effort in the Etiology of Heatstroke Injury and Mortality

Richard W. Hubbard, W. T. Matthew, R. E. Criss, Ingrid V. Sils, M. Mager

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Abstract

A total of 171 untrained, unacclimatized and unanesthetized rates were used to evaluate the effects of sedentary and work-induced hyperthermia on the incidence of mortality and cellular injury, 24 h post-exposure. Cellular injury was defined as serum transaminase activity (SGPT and SGOT) exceeding 1000 IU/L (heatstroke levels). Both the percent mortality and the percentage of 24 h survivors with transaminase levels above 1000 IU/L were plotted against maximum core temperatures. Exertion-induced hyperthermia produced a significantly higher incidence of cellular injury and heatstroke death at lower core temperatures than hyperthermia alone. With hyperthermia only, the SGPT and SGOT dose-response curves were identical. When work was combined with hyperthermia, there was a greater incidence of elevated SGOT at lower core temperatures. These curves bore a striking resemblance to curves reflecting heat and/or work induced mortality in humans. The results suggest a direct role of physical effort in causing heatstroke injury and mortality. (Author)

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A total of 171 untrained, unacclimatized and unanesthetized rates were used to evaluate the effects of sedentary and work-induced hyperthermia on the incidence of mortality and cellular injury, 24 h post-exposure. Cellular injury was defined as serum transaminase activity (SGPT and SGOT) exceeding 1000 IU/L (heatstroke levels). Both the percent mortality and the percentage of 24 h survivors with transaminase levels above 1000 IU/L were plotted against maximum core temperatures. Exertion-induced hyperthermia produced a significantly higher incidence of cellular injury and heatstroke death at lower core temperatures than hyperthermia alone. With hyperthermia only, the SGPT and SGOT dose-response curves were identical. When work was combined with hyperthermia, there was a greater incidence of elevated SGOT at lower core temperatures. These curves bore a striking resemblance to curves reflecting heat and/or work induced mortality in humans. The results suggest a direct role of physical effort in causing heatstroke injury and mortality. (Author)

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Available abstract

A total of 171 untrained, unacclimatized and unanesthetized rates were used to evaluate the effects of sedentary and work-induced hyperthermia on the incidence of mortality and cellular injury, 24 h post-exposure. Cellular injury was defined as serum transaminase activity (SGPT and SGOT) exceeding 1000 IU/L (heatstroke levels). Both the percent mortality and the percentage of 24 h survivors with transaminase levels above 1000 IU/L were plotted against maximum core temperatures. Exertion-induced hyperthermia produced a significantly higher incidence of cellular injury and heatstroke death at lower core temperatures than hyperthermia alone. With hyperthermia only, the SGPT and SGOT dose-response curves were identical. When work was combined with hyperthermia, there was a greater incidence of elevated SGOT at lower core temperatures. These curves bore a striking resemblance to curves reflecting heat and/or work induced mortality in humans. The results suggest a direct role of physical effort in causing heatstroke injury and mortality. (Author)

Key concepts: Heatstroke, Hyperthermia, Medicine, Incidence (geometry), Exertion, Transaminase, Etiology, Core temperature

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Evidence for a Direct Role of Physical Effort in the Etiology of Heatstroke Injury and Mortality — Research Paper | ScholarLens