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The Effect of Passive Heat Stress and Exercise-Induced Dehydration on the Compensatory Reserve During Simulated Hemorrhage

Gagnon, Daniel; Schlader, Zachary J.; Adams, Amy; Rivas, Eric; Mulligan, Jane; Grudic, Gregory Z.; Convertino, Victor A.; Howard, Jeffrey T.; Crandall, Craig G.

doi: 10.1097/SHK.0000000000000653
Clinical Aspects

ABSTRACT Compensatory reserve represents the proportion of physiological responses engaged to compensate for reductions in central blood volume before the onset of decompensation. We hypothesized that compensatory reserve would be reduced by hyperthermia and exercise-induced dehydration, conditions often encountered on the battlefield. Twenty healthy males volunteered for two separate protocols during which they underwent lower-body negative pressure (LBNP) to hemodynamic decompensation (systolic blood pressure <80 mm Hg). During protocol #1, LBNP was performed following a passive increase in core temperature of ∼1.2°C (HT) or a normothermic time-control period (NT). During protocol #2, LBNP was performed following exercise during which: fluid losses were replaced (hydrated), fluid intake was restricted and exercise ended at the same increase in core temperature as hydrated (isothermic dehydrated), or fluid intake was restricted and exercise duration was the same as hydrated (time-match dehydrated). Compensatory reserve was estimated with the compensatory reserve index (CRI), a machine-learning algorithm that extracts features from continuous photoplethysmograph signals. Prior to LBNP, CRI was reduced by passive heating [NT: 0.87 (SD 0.09) vs. HT: 0.42 (SD 0.19) units, P <0.01] and exercise-induced dehydration [hydrated: 0.67 (SD 0.19) vs. isothermic dehydrated: 0.52 (SD 0.21) vs. time-match dehydrated: 0.47 (SD 0.25) units; P <0.01 vs. hydrated]. During subsequent LBNP, CRI decreased further and its rate of change was similar between conditions. CRI values at decompensation did not differ between conditions. These results suggest that passive heating and exercise-induced dehydration limit the body's physiological reserve to compensate for further reductions in central blood volume.

*Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas and University of Texas Southwestern Medical Center, Dallas, Texas

Department of Exercise and Nutrition Sciences, University at Buffalo, Buffalo, New York

Institute for Clinical and Translational Science and Department of Pediatrics, University of California, Irvine, California

§Flashback Technologies Inc., Boulder, Colorado

||US Army Institute of Surgical Research, JBSA Fort Sam Houston, Texas

Address reprint requests to Dr Craig G. Crandall, Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, 7232 Greenville Ave, Dallas, TX 75231. E-mail:

Received 26 February, 2016

Revised 17 March, 2016

Accepted 10 May, 2016

GZG and JM are cofounders of Flashback Technologies Inc.

This project was supported by a grant from the Department of Defense (W81XWH-12-1-0152). DG was supported by a Postdoctoral Fellowship from the Natural Sciences and Engineering Research Council of Canada.

The authors report no conflicts of interest.

© 2016 by the Shock Society