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

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.

Bridging the gap between military prolonged field care monitoring and exploration spaceflight: the compensatory reserve

“…53 Figure 7 (left panel) presents results from a study in which 12 men were exposed to LBNP in two sessions: (1) normothermia (37 °C core temperature) and (2) hyperthermia (38.2 °C core temperature). 54 Values of CRM over progressive LBNP were significantly different from the start (0 mmHg LBNP) between normothermic (92% CRM) and hyperthermic (43% CRM) conditions. Additionally, hyperthermic subjects exhausted their total reserve to compensate earlier (−60 mmHg) than normothermic subjects (−100 mmHg).…”

“…55 Figure 7 (right panel) shows results from a study in which hydrated and dehydrated conditions were tested in eight men exposed to LBNP following exercise-heat stress. 54 During the hydrated test, subjects exercised for 90 min and fluid loss was fully replaced by orally ingesting warm water to maintain normovolemia and euhydration. During the dehydrated test, subjects did not consume any liquid and exercised until the core body temperature increased to the same level observed during the hydrated condition, creating a sweat-induced dehydration.…”

“…The capacity of the cardiovascular system to sustain blood pressure and cardiac output to maintain adequate DO 2 is a key factor in aerobic performance. 54,56 The greater oxygen uptake needed during progressive-intensity aerobic exercise leads to greater vasodilation in skeletal muscle (i.e., relative hypovolemia). Figure 8 (left panel) details the relationship between progressively increasing power output until reaching maximal oxygen uptake (VO 2max ) and the compensatory reserve.…”

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“…14,18 Many factors can influence the validity of Compensatory Reserve Index, including vasoactive medications and conditions such as dehydration. 36 In the Postural Orthostatic Tachycardia syndrome patient population, dehydration is common, with a decreased blood volume in up to 70% of patients. 36 While dehydration can trigger Postural Orthostatic Tachycardia syndrome symptoms, the specific aetiology for the high rate of dehydration in Postural Orthostatic Tachycardia syndrome patients is poorly understood.…”

Tolerance to Central Hypovolemia Is Greater Following Caffeinated Coffee Consumption in Habituated Users

“…However, it is possible that the findings of this study may be different had we waited for a longer period of time after the ingestion of caffeinated coffee before measuring cardiovascular responses and tolerance to central hypovolemia. Third, the compensatory reserve available to protect arterial blood pressure during central hypovolemia is influenced by blood volume (Stewart et al, 2014;Gagnon et al, 2016). We did not measure an index of circulating blood volume.…”