The Effect of Passive Heat Stress and Exercise-Induced Dehydration on the Compensatory Reserve During Simulated Hemorrhage
Gagnon D, Schlader ZJ, Adams A, Rivas E, Mulligan J, Grudic GZ, Convertino VA, Howard JT, Crandall CG
Shock (Augusta, Ga.) · 17 citations
How it was studied
- Design
- Controlled clinical trial (classified by our AI screen)
- Studied in
- People
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
- Government
- National Institute of General Medical Sciences
- Government
- NIGMS NIH HHS
- Grants
- National Institute of General Medical Sciences (R01GM068865)
Based on 2 listed funder(s).
Publication
- Published
- 2016-05-13 · Shock · vol. 46 · issue 3S · pp. 74–82
- Publisher
- Lippincott Williams & Wilkins
- Cited
- 21 citations · more than 82% of similar papers · 1.5× the field average
- References
- 39 works
- Access
- Open access (repository copy)
- Research areas
- Thermoregulation and physiological responses · Climate Change and Health Impacts · Hemodynamic Monitoring and Therapy
- Keywords
- Dehydration, Decompensation, Core temperature, Hyperthermia, Thermoregulation, Chemistry, Heart rate, Blood volume, Internal medicine, Cardiac output, Medicine, Hemodynamics, Heat stress, Core (optical fiber), Blood pressure, Anesthesia, Cardiology, Endocrinology, Animal science, Biochemistry
- MeSH
- humans, dehydration, hemorrhage, lower body negative pressure, exercise, blood volume, blood pressure, algorithms, adult, male, hot temperature, young adult
9 authors
From US
- Daniel GagnonFlashback Technologies (United States); Institute for Exercise and Environmental Medicine
- Zachary J. SchladerFlashback Technologies (United States)
- Amy N. AdamsFlashback Technologies (United States)
- Eric RivasFlashback Technologies (United States)
- Jane MulliganFlashback Technologies (United States)
- Gregory Z. GrudićFlashback Technologies (United States)
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.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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