Simulated Haemorrhagic Challenge Research Articles

Influence of progressive skin heating upon arterial blood pressure and tolerance to a simulated hemorrhage challenge following exercise in a cold environment

Purpose: Our aim was to examine the role of graded skin heating on blood pressure and tolerance to a simulated hemorrhage (lower body negative pressure, LBNP) in individuals who have exercised in a cold environment. We hypothesized that arterial blood pressure and tolerance would be lower during LBNP at higher skin temperatures. Methods: Following completion of a maximal exercise test, 7 participants (181±7 cm, 88.7±14 kg and 25±6 yrs) four exercise cold stress trials, comprising high intensity interval exercise on a cycle ergometer: 5 min at 60% VO2 max (1.9±0.4 L.O2.min) followed by 15 intervals of 60 sec at 88% peak power output (Wmax) (239±51 W) and 60 sec at 10% Wmax (27±6 W) in an environmental chamber (0°C 70% RH, Can-Trol International). Upon completion participants remained in the environmental chamber and underwent LBNP to pre syncope. Rectal (Tcore; °C) and mean skin (8 site average, Tskin; °C) temperatures, arterial blood pressure (Brachial Artery Auscultation, Suntech Tango; MAP; mmHg) and cutaneous vascular conductance (Laser Doppler Flowmetry, Perimed, CVC; AU/mmHg) were measured throughout. After the onset of LBNP, skin temperature was either kept cold (Cold), increased back to baseline (Normothermic), mildly heated (Warm) or severely heated (Hot) using a water perfused suit. LBNP tolerance was calculated via cumulative strain index (CSI). MAP, CVC, Tcore and Tskin were analyzed using a two-way ANOVA with repeated measures. CSI was compared between trials using a one-way ANOVA with repeated measures. Results: After exercise and immediately prior to LBNP, Tcore had increased from baseline 1.0±0.2°C and was not different between trials (P = 0.67), while Tskin was reduced from 33.2±0.5°C to 28.3±1.9°C (P = 0.001). MAP was elevated following exercise and immediately prior to LBNP in all trials relative to baseline, from 82±6 to 89±8mmHg. During LBNP, Tskin remained low in the Cold trial (27.6±1.2 °C) but was increased in all other trials (Normothermic: 32.3±0.8°C, Warm: 34.8±0.5°C and Hot: 36.4±0.7°C, all P < 0.05). MAP was different between trials (Trial Effect P = 0.022). MAP was lowest in the Hot trial whether expressed 3 min after the onset of LBNP or at 60% CSI (81±9mmHg and 78±7 mmHg, respectively) relative to the Cold (89±10 and 84±9 mmHg) Normothermic (86±8 and 82±6 mmHg) and Warm trials (86±7 and 80±6 mmHg), respectively. MAP was reduced at pre syncope in all trials (59±9mmHg). CVC was different between trials (Trial Effect, P < 0.0001). At 60% CSI, CVC was lowest in the Cold trial (0.17±0.11 AU/mmHg) but increased in the Normothermic (0.27±0.08 AU/mmHg) Warm (0.43±0.40 AU/mmHg) and Hot trials (0.60±0.43 AU/mmHg). LBNP tolerance was different between trials (Main Effect: P < 0.01). LBNP tolerance was lowest in the Cold trial (700 ± 346 mmHg*min) and was increased in Normothermic (856±399 mmHg*min) Warm (821±345 mmHg*min) and Hot trials (990±328mmHg*min). Conclusion: These preliminary findings suggest that skin warming >32°C increases tolerance to a simulated hemorrhagic challenge while further heating to ~36°C lowers arterial blood pressure without compromising LBNP tolerance in exercise cold stressed individuals. Supported by a RMACSM Grant. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Facial fanning reduces heart rate but not tolerance to a simulated hemorrhagic challenge following exercise heat stress in young healthy humans.

We investigated whether reducing face skin temperature alters arterial blood pressure control and lower body negative pressure (LBNP) tolerance after exercise heat stress. Eight subjects (1 female; age, 27 ± 9 yr) exercised at ∼63% V̇o2max until core temperature had increased ∼1.5°C before undergoing LBNP to presyncope either with fanning to return face skin temperature to baseline (Δ-5°C, Fan trial) or without (No Fan trial). LBNP tolerance was quantified as cumulative stress index (CSI; mmHg·min). Before LBNP, whole body and face skin temperatures were elevated from baseline in both trials (38.0 ± 0.5°C and 36.3 ± 0.5°C, respectively, both P < 0.001). During LBNP, face skin temperature decreased in the Fan trial (30.9 ± 1.0°C) but was unchanged in the No Fan trial (36.1 ± 0.6°C, between trials P < 0.001). Mean arterial pressure was not different between trials (P = 0.237) and was similarly reduced at presyncope in both trials (from 82 ± 7 to 67 ± 8 mmHg, P < 0.001). During LBNP, heart rate was attenuated in the Fan trial at Mid LBNP (146 ± 16 vs. 158 ± 12 beats/min, P = 0.036) and at peak heart rate (158 ± 15 vs. 170 ± 15 beats/min; P < 0.001). LBNP tolerance was not different between trials (321 ± 248 vs. 328 ± 115 mmHg·min, P = 0.851). In exercise heat-stressed individuals, lowering face skin temperature to normothermic values suppressed heart rate thereby altering cardiovascular control during a simulated hemorrhagic challenge without reducing tolerance.

Modest reductions in face skin temperature do not improve tolerance to a simulated hemorrhagic challenge in exercise heat stressed individuals.

Face cooling is associated with autonomic and cardiovascular alterations that accompany an increased blood pressure. Following an exercise heat stress, even minor increases in heart rate and vascular resistance may permit an improved blood pressure control during a simulated hemorrhagic challenge (Lower Body Negative Pressure, LBNP) and improve tolerance. Our aim was to examine whether modest reductions in face skin temperature would improve LBNP tolerance in exercise heat stressed individuals. Ten healthy subjects (Age: 29 ± 13 yrs; Ht: 177 ± 9 cm; Wt: 72.4 ± 8.0 kg) completed two counterbalanced trials (Trial A and Trial B) cycling at 63 ± 6% of their predetermined VO2Max whilst wearing a warm water perfused suit and face mask until core temperature had increased 1.5°C. Participants then underwent LBNP to pre syncope. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg*min). Face skin temperature represents the average of forehead, cheek and chin skin temperatures. Face skin temperature was maintained at exercise heat stress values throughout LBNP in Trial A but was reduced via facial fanning in Trial B after 1 minute of LBNP. Arterial blood pressure (MAP, Penaz method), heart rate (HR, ECG), stroke volume (SV, Pulse Contour Analysis) were continuously measured and total peripheral resistance (TPR) was calculated. Following exercise heat stress, core (38.6 ± 0.2 °C), mean skin (38.2 ± 0.6 °C) and face skin (36.4 ± 0.5 °C) temperatures were elevated relative to baseline (all P &lt; 0.05) and not different between trials (all P &gt; 0.05). Face skin temperature remained elevated throughout LBNP in Trial A (36.1 ± 0.5 °C) but was reduced in Trial B (31.3 ± 1.6°C, P = 0.0001 between trials). Following exercise and prior to LBNP, HR was increased (63 ± 8 to 121 ±15 BPM) while MAP (86 ± 7 to 70 ± 6 mmHg) and TPR (12.5 ± 2.0 to 7.7 ± 1.6 mmHg/L/min) were similarly lowered relative to baseline in both trials (all P &lt; 0.05). Mean arterial pressure was similarly reduced at pre syncope in both trials (54 ± 11 and 57 ± 5 mmHg; P &lt; 0.0001 relative to prior to LBNP). TPR and HR increased during LBNP in both trials relative to baseline (both P &lt; 0.05) but were not different between trials 2 minutes after the onset of LBNP (TPR: 7.8 ± 1.7 vs. 7.8 ± 1.8 mmHg/L/min and HR: 131 ± 17 vs. 137 ± 22 BPM, main effect of trial both P &gt; 0.05). CSI was not different between trials (Trial A: 332 ± 176 vs. Trial B: 393 ± 261 mmHg*min; P = 0.482). LBNP tolerance was not improved by face skin cooling in exercise heat stressed individuals. These results suggest that modest reductions in face skin temperature are not accompanied by an improved blood pressure control during a simulated hemorrhagic challenge in exercise heat stressed individuals.

High-intensity interval exercise reduces tolerance to a simulated haemorrhagic challenge in heat-stressed individuals.

What is the central question of this study? In heat-stressed individuals, does high-intensity interval exercise reduce tolerance to a simulated haemorrhagic challenge (lower body negative pressure, LBNP) relative to steady state exercise? What is the main finding and its importance? LBNP tolerance was lower in heat-stressed individuals following high-intensity interval exercise relative to steady state exercise. This was likely owing to the greater cardiovascular strain required to maintain arterial blood pressure prior to and early during LBNP following high-intensity interval exercise. These findings are of importance for individuals working in occupations in which combined heat stress and intense intermittent exercise are common and where the risk of haemorrhagic injury is increased. This study investigated whether tolerance to a simulated haemorrhagic challenge (lower body negative pressure, LBNP) was lower in heat-stressed individuals following high-intensity interval exercise relative to steady state exercise. Nine healthy participants completed two trials (Steady State and Interval). Participants cycled continuously at ∼38% (Steady State) or alternating between 10 and ∼88% (Interval) of the maximal power output whilst wearing a hot water perfused suit until core temperatures increased ∼1.4°C. Participants then underwent LBNP to pre-syncope. LBNP tolerance was quantified as cumulative stress index (CSI; mmHgmin). Mean skin and core temperatures were elevated in both trials following exercise prior to LBNP (to 38.1±0.6°C and 38.3±0.2°C, respectively, both P<0.001 relative to baseline) but not different between trials (both P>0.05). In the Interval trial, heart rate was greater (122±12beatsmin-1 ) prior to LBNP, relative to the Steady State trial (107±8beatsmin-1 , P<0.001) while mean arterial pressure was similarly reduced in both trials prior to LBNP (from baseline 89±5 to 77±7mmHg; P=0.001) and at pre-syncope (to 62±9mmHg, P<0.001). CSI was lower in the Interval trial (280±194vs. 550±234mmHgmin; P=0.0085). In heat-stressed individuals, tolerance to a simulated haemorrhagic challenge is reduced following high-intensity interval exercise relative to steady state exercise.

Influence of caffeine upon tolerance to a simulated hemorrhagic challenge in habituated users

Caffeine is an adenosine receptor antagonist and its consumption in caffeine naïve individuals is associated with increased blood pressure. However, the influence of caffeine consumption upon blood pressure in individuals habituated to caffeine is less clear. Approximately 300mg of caffeine is consumed daily by 80% of the United States active duty military yet the influence of caffeine upon tolerance to a simulated hemorrhagic challenge in habituated users is unknown. Our aim was to examine the influence of caffeine consumption upon tolerance to a simulated hemorrhagic challenge (Lower Body Negative Pressure; LBNP) in habitual caffeine consumers. Eight healthy participants (age: 27 ± 6 yrs, Ht: 179 ± 10 cm, Wt: 76.0 ± 14.4 kg) completed three double blinded, counterbalanced trials (Caffeine, Decaffeinated and Water). Following baseline measures of cardiovascular control (including mean arterial pressure, MAP; mmHg and total peripheral resistance, TPR; mmHg/l/min) participants drank (6.25ml/kg body mass) either water (Water; volume control), decaffeinated coffee (Decaffeinated; placebo control) or caffeinated coffee (Caffeine; 4 mg caffeine/kg body mass). Participants were measured again following the ingestion of the drink (pre LBNP) and then underwent a graded LBNP protocol (−20mmHg, −30mmHg, etc.) until pre‐syncope. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg*min). Data are presented at baseline (pre drink), prior to LBNP (pre LBNP and post drink), a common time point during LBNP tolerated by all individuals in all trials (−30mmHg) and at pre syncope. MAP increased from baseline to pre LBNP in all trials (Caffeine: from 84 ± 7 to 98 ± 7 mmHg; Decaffeinated: from 90 ± 10 to 94 ± 7 mmHg and Water: from 89 ± 9 to 97 ± 6 mmHg; P &lt; 0.05 in all trials). MAP was reduced at pre syncope in all trials (Caffeine: 59 ± 4 mmHg; Decaffeinated: 57 ± 4 and Water: 60 ± 7 mmHg; all P &lt; 0.05 relative to pre LBNP). MAP was not different between trials at any time point (P &gt; 0.05). TPR was not different from baseline during LBNP in the Water and Decaffeinated trials (from: 13 ± 2 and 14 ± 2 to −30mmHg: 16 ± 3 and 16 ± 2 mmHg/l/min, respectively both P &gt; 0.05 vs. baseline) but increased during LBNP in the Caffeine trial (from: 13 ± 2 to −30mmHg: 18 ± 3 mmHg/l/min; P = 0.004 vs. baseline). LBNP Tolerance was greater in the Caffeine trial (941 ± 376 mmHg*min, 19.2 ± 4.8 min) relative to the Decaffeinated trial (686 ± 382 mmHg*min, 15.7 ± 5.1 min; CSI: P = 0.021), but was not different relative to the Water trial (Water: 816 ± 383 mmHg*min, 17.5 ± 5.0 min; CSI: P = 0.093). Caffeine consumption alters cardiovascular control during a simulated hemorrhagic challenge and may influence LBNP tolerance in habitual caffeine users, although this affect appears to be small. This may have implications for the treatment of a hemorrhagic insult in individuals who are habitual caffeine users and whom have an elevated risk of hemorrhagic injury (e.g. soldiers).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

High intensity interval exercise reduces tolerance to a simulated hemorrhagic challenge relative to steady state exercise in heat stressed individuals

Individuals who are exposed to an increased risk of experiencing a hemorrhagic insult, such as soldiers and firefighters, are often required to complete intermittent high intensity exercise in the presence of environmental heat stress. In normothermic conditions, increases in heart rate and reductions in vascular resistance can be greater following high intensity interval exercise relative to continuous steady state exercise. These hemodynamic alterations following high intensity interval exercise may reduce the capacity to withstand a hemorrhagic insult. We investigated whether high intensity interval exercise reduces tolerance to a simulated hemorrhagic challenge (lower body negative pressure; LBNP) relative to steady state exercise in heat stressed individuals. Eight healthy participants (Age: 27 ± 5 years; Ht: 179 ± 9 cm; Wt: 78.9 ± 18.7 kg) completed two trials (Steady state and Interval). Participants performed cycling exercise either by alternating between 10 and 88% (Interval) or continuously at 38% (Steady state) of the predetermined maximal aerobic power output whilst wearing a warm water perfused suit until core temperatures increased by 1.40 ± 0.21°C. Participants then underwent progressive LBNP (−20mmHg, −30mmHg, etc.) to pre syncope. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg*min). Following exercise and prior to LBNP, mean skin temperatures were similarly elevated from baseline in both trials (from: 32.35 ± 0.42 to 37.95 ± 0.59°C, P &lt; 0.05). Mean arterial pressure was not different between trials prior to LBNP (Interval: 79 ± 6 vs. Steady state: 77 ± 7 mmHg; P = 0.57) and were similarly reduced in both trials at pre syncope (to 63 ± 6 and 62 ± 6 mmHg respectively, both P &lt; 0.05). CSI was lower in the interval trial relative to the steady state trial (280 ± 204 vs. 518 ± 285 mmHg*min, respectively; P = 0.024). In heat stressed individuals, tolerance to a simulated hemorrhagic challenge was reduced following high intensity interval exercise relative to steady state exercise. These findings have implications for individuals who exercise at intermittent high intensities in hot environments and are at increased risk of experiencing a hemorrhagic injury (e.g. soldiers, firefighters and miners).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Small reductions in skin temperature after onset of a simulated hemorrhagic challenge improve tolerance in exercise heat-stressed individuals.

We investigated whether small reductions in skin temperature 60 s after the onset of a simulated hemorrhagic challenge would improve tolerance to lower body negative pressure (LBNP) after exercise heat stress. Eleven healthy subjects completed two trials (High and Reduced). Subjects cycled at ~55% maximal oxygen uptake wearing a warm water-perfused suit until core temperatures increased by ~1.2°C before lying supine and undergoing LBNP to presyncope. LBNP tolerance was quantified as cumulative stress index (CSI; product of each LBNP level multiplied by time; mmHg·min). Skin temperature was similarly elevated from baseline before LBNP and remained elevated 60 s after the onset of LBNP in both High (37.72 ± 0.52°C) and Reduced (37.95 ± 0.54°C) trials (both P < 0.0001). At 60%CSI skin temperature remained elevated in the High trial (37.51 ± 0.56°C) but was reduced to 34.97 ± 0.72°C by the water-perfused suit in the Reduced trial ( P < 0.0001 between trials). Cutaneous vascular conductance was not different between trials [High: 1.57 ± 0.43 vs. Reduced: 1.39 ± 0.38 arbitrary units (AU)/mmHg; P = 0.367] before LBNP but decreased to 0.67 ± 0.19 AU/mmHg at 60%CSI in the Reduced trial while remaining unchanged in the High trial ( P = 0.002 between trials). CSI was higher in the Reduced (695 ± 386 mmHg·min) relative to the High (441 ± 290 mmHg·min; P = 0.023) trial. Mean arterial pressure was not different between trials at presyncope (High: 62 ± 10 vs. Reduced: 62 ± 9 mmHg; P = 0.958). Small reductions in skin temperature after the onset of a simulated hemorrhagic challenge improve LBNP tolerance after exercise heat stress. This may have important implications regarding treatment of an exercise heat-stressed individual (e.g., soldier) who has experienced a hemorrhagic injury.

Tolerance to a haemorrhagic challenge during heat stress is improved with inspiratory resistance breathing.

What is the central question of this study? Does inspiratory resistance breathing improve tolerance to simulated haemorrhage in individuals with elevated internal temperatures? What is the main finding and its importance? The main finding of this study is that inspiratory resistance breathing modestly improves tolerance to a simulated progressive haemorrhagic challenge during heat stress. These findings demonstrate a scenario in which exploitation of the respiratory pump can ameliorate serious conditions related to systemic hypotension. Heat exposure impairs human blood pressure control and markedly reduces tolerance to a simulated haemorrhagic challenge. Inspiratory resistance breathing enhances blood pressure control and improves tolerance during simulated haemorrhage in normothermic individuals. However, it is unknown whether similar improvements occur with this manoeuvre in heat stress conditions. In this study, we tested the hypothesis that inspiratory resistance breathing improves tolerance to simulated haemorrhage in individuals with elevated internal temperatures. On two separate days, eight subjects performed a simulated haemorrhage challenge [lower-body negative pressure (LBNP)] to presyncope after an increase in internal temperature of 1.3±0.1°C. During one trial, subjects breathed through an inspiratory impedance device set at 0cmH2 O of resistance (Sham), whereas on a subsequent day the device was set at -7cmH2 O of resistance (ITD). Tolerance was quantified as the cumulative stress index. Subjects were more tolerant to the LBNP challenge during the ITD protocol, as indicated by a>30% larger cumulative stress index (Sham, 520±306mmHgmin; ITD, 682±324mmHgmin; P<0.01). These data indicate that inspiratory resistance breathing modestly improves tolerance to a simulated progressive haemorrhagic challenge during heat stress.

Modest Reductions in Skin Temperature After the Onset of a Simulated Hemorrhagic Challenge Improve LBNP Tolerance Following Exercise Heat Stress

Soldiers are often deployed to warm environments where they are exposed to exercise and heat stress whilst wearing body armor, resulting in increased mean skin (Tskin) and core (Tcore) temperatures. Our aim was to investigate whether modestly lowering Tskin 60 seconds after the onset of a simulated hemorrhagic challenge (Lower Body Negative Pressure; LBNP) would improve LBNP tolerance following exercise heat stress. Ten healthy subjects (Age: 26 ± 5 yrs; Ht: 179.3 ± 7.2 cm; Wt: 81.4 ± 18.1 kg) completed two blinded and counterbalanced trials (Trial A and Trial B) where they cycled at 55.7 ± 4.5% of their predetermined VO2Max whilst wearing a warm water perfused suit. Participants then underwent LBNP to pre syncope. The increase in Tcore from the onset of exercise to pre‐LBNP was not different between trials (+1.1 ± 0.2 °C; P &gt; 0.05). In Trial A, Tskin remained elevated throughout LBNP while in Trial B, Tskin was modestly lowered 60 seconds after the onset of LBNP. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg*min). Mean arterial pressure (MAP) was lowered following exercise (pre‐LBNP) relative to baseline in both trials (Trial A from: 90 ± 7 to: 81 ± 9 mmHg and Trial B from: 89 ± 11 to: 79 ± 5 mmHg; both P &lt; 0.05). Tskin was not different between Trial A and Trial B at baseline (32.5 ± 0.3 vs. 32.9 ± 0.7 °C), pre‐LBNP (38.0 ± 0.6 vs. 38.0 ± 0.6 °C), and 60 seconds after the onset of LBNP (37.7 ± 0.5 vs. 37.9 ± 0.6 °C) (all P &gt; 0.05). In Trial A, Tskin remained elevated throughout LBNP (40% CSI: 37.5 ± 0.5 °C and pre syncope: 37.4 ± 0.5 °C). In Trial B, Tskin was lower at 40% CSI and pre syncope (35.1 ± 1.2 and 34.8 ± 0.4 °C, respectively) relative to pre‐LBNP but remained higher relative to baseline (all P &lt; 0.05). In Trial B, Tskin was lower at 40% CSI and pre syncope relative to those respective time points in Trial A (both P &lt; 0.05). CSI was higher in Trial B (760 ± 400 mmHg*min) relative to Trial A (481 ± 272 mmHg*min; P = 0.033). MAP was not different between trials at pre syncope (Trial A: 63 ± 10 vs. Trial B: 64 ± 8 mmHg; P &gt; 0.05). These data indicate that modestly reducing skin temperature shortly after the onset of a simulated hemorrhagic challenge improves LBNP tolerance following an exercise heat stress. Importantly, LBNP tolerance was improved by a slight reduction in Tskin, such that mean skin temperatures were reduced relative to pre‐LBNP yet remained higher than at baseline. This suggests that following an exercise heat stress a modest reduction in skin temperature applied after the onset of a hemorrhagic challenge may improve an individual's tolerance to a hemorrhagic insult. This may have important implications regarding immediate treatment of an exercise and heat stressed individual (e.g. soldier or firefighter) who has experienced a hemorrhagic injury.Support or Funding InformationFunded by UCCS CRCW awardThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Elevated skin and core temperatures both contribute to reductions in tolerance to a simulated haemorrhagic challenge.

What is the central question of this study? Combined increases in skin and core temperatures reduce tolerance to a simulated haemorrhagic challenge. The aim of this study was to examine the separate and combined influences of increased skin and core temperatures upon tolerance to a simulated haemorrhagic challenge. What is the main finding and its importance? Skin and core temperatures increase during many occupational settings, including military procedures, in hot environments. The study findings demonstrate that both increased skin temperature and increased core temperature can impair tolerance to a simulated haemorrhagic challenge; therefore, a soldier's tolerance to haemorrhagic injury is likely to be impaired during any military activity that results in increased skin and/or core temperatures. Tolerance to a simulated haemorrhagic insult, such as lower-body negative pressure (LBNP), is profoundly reduced when accompanied by whole-body heat stress. The aim of this study was to investigate the separate and combined influence of elevated skin (Tskin ) and core temperatures (Tcore ) on LBNP tolerance. We hypothesized that elevations in Tskin as well as Tcore would both contribute to reductions in LBNP tolerance and that the reduction in LBNP tolerance would be greatest when both Tskin and Tcore were elevated. Nine participants underwent progressive LBNP to presyncope on four occasions, as follows: (i)control, with neutral Tskin (34.3±0.5°C) and Tcore (36.8±0.2°C); (ii)primarily skin hyperthermia, with high Tskin (37.6±0.2°C) and neutral Tcore (37.1±0.2°C); (iii)primarily core hyperthermia, with neutral Tskin (35.0±0.5°C) and high Tcore (38.3±0.2°C); and (iv)combined skin and core hyperthermia, with high Tskin (38.8±0.6°C) and high Tcore (38.1±0.2°C). The LBNP tolerance was quantified via the cumulative stress index (in millimetres of mercury×minutes). The LBNP tolerance was reduced during the skin hyperthermia (569±151mmHgmin) and core hyperthermia trials (563±194 mmHgmin) relative to control conditions (1010±246mmHgmin; both P<0.05). However, LBNP tolerance did not differ between skin hyperthermia and core hyperthermia trials (P=0.92). The lowest LBNP tolerance was observed during combined skin and core hyperthermia (257±106mmHgmin; P<0.05 relative to all other trials). These data indicate that elevated skin temperature, as well as elevated core temperature, can both contribute to reductions in LBNP tolerance in heat-stressed individuals. However, heat stress-induced reductions in LBNP tolerance are greatest in conditions when both skin and core temperatures are elevated.

Beneficial effects of elevating cardiac preload on left-ventricular diastolic function and volume during heat stress: implications toward tolerance during a hemorrhagic insult.

Volume loading normalizes tolerance to a simulated hemorrhagic challenge in heat-stressed individuals, relative to when these individuals are thermoneutral. The mechanism(s) by which this occurs is unknown. This project tested two unique hypotheses; that is, the elevation of central blood volume via volume loading while heat stressed would 1) increase indices of left ventricular diastolic function, and 2) preserve left ventricular end-diastolic volume (LVEDV) during a subsequent simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Indices of left ventricular diastolic function were evaluated in nine subjects during the following conditions: thermoneutral, heat stress, and heat stress after acute volume loading sufficient to return ventricular filling pressures toward thermoneutral levels. LVEDV was also measured in these subjects during the aforementioned conditions prior to and during a simulated hemorrhagic challenge. Heat stress did not change indices of diastolic function. Subsequent volume infusion elevated indices of diastolic function, specifically early diastolic mitral annular tissue velocity (E') and early diastolic propagation velocity (E) relative to both thermoneutral and heat stress conditions (P < 0.05 for both). Heat stress reduced LVEDV (P < 0.05), while volume infusion returned LVEDV to thermoneutral levels. The reduction in LVEDV to LBNP was similar between thermoneutral and heat stress conditions, whereas the reduction after volume infusion was attenuated relative to both conditions (P < 0.05). Absolute LVEDV during LBNP after volume loading was appreciably greater relative to the same level of LBNP during heat stress alone. Thus, rapid volume infusion during heat stress increased indices of left ventricular diastolic function and attenuated the reduction in LVEDV during LBNP, both of which may serve as mechanisms by which volume loading improves tolerance to a combined hyperthermic and hemorrhagic challenge.

Active and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge.

Passive heat stress increases core and skin temperatures and reduces tolerance to simulated hemorrhage (lower body negative pressure; LBNP). We tested whether exercise-induced heat stress reduces LBNP tolerance to a greater extent relative to passive heat stress, when skin and core temperatures are similar. Eight participants (6 males, 32 ± 7 yr, 176 ± 8 cm, 77.0 ± 9.8 kg) underwent LBNP to presyncope on three separate and randomized occasions: 1) passive heat stress, 2) exercise in a hot environment (40°C) where skin temperature was moderate (36°C, active 36), and 3) exercise in a hot environment (40°C) where skin temperature was matched relative to that achieved during passive heat stress (∼38°C, active 38). LBNP tolerance was quantified using the cumulative stress index (CSI). Before LBNP, increases in core temperature from baseline were not different between trials (1.18 ± 0.20°C; P > 0.05). Also before LBNP, mean skin temperature was similar between passive heat stress (38.2 ± 0.5°C) and active 38 (38.2 ± 0.8°C; P = 0.90) trials, whereas it was reduced in the active 36 trial (36.6 ± 0.5°C; P ≤ 0.05 compared with passive heat stress and active 38). LBNP tolerance was not different between passive heat stress and active 38 trials (383 ± 223 and 322 ± 178 CSI, respectively; P = 0.12), but both were similarly reduced relative to active 36 (516 ± 147 CSI, both P ≤ 0.05). LBNP tolerance is not different between heat stresses induced either passively or by exercise in a hot environment when skin temperatures are similarly elevated. However, LBNP tolerance is influenced by the magnitude of the elevation in skin temperature following exercise induced heat stress.

Active and passive heat stress similarly compromises tolerance to a simulated hemorrhagic challenge (1104.22)

Passive heat stress increases core and skin temperatures and reduces tolerance to simulated hemorrhage, as assessed via lower body negative pressure (LBNP). It is unknown whether exercise induced heat stress reduces LBNP tolerance to a similar extent relative to passive heat stress. Eight males (32 ± 7 yrs, 176 ± 8 cm, 77.0 ± 9.8 kg) underwent LBNP to pre‐syncope on three separate and randomized occasions: passive heat stress and two occasions of exercise induced heat stress where skin temperature was moderate (~36°C, Active 36) or warm (~38°C, Active 38). LBNP tolerance was quantified using the cumulative stress index (CSI). Prior to LBNP, increases in core temperature were similar in all trials (1.18 ± 0.20°C; P &lt; 0.05), and while mean skin temperature was similar between passive heat stress (38.2 ± 0.5°C) and Active 38 (38.2 ± 0.8°C; P = 0.90) both trials were greater compared to Active 36 (36.6 ± 0.5°C; P &lt; 0.05). LBNP tolerance was not different between passive heat stress and Active 38 (383 ± 223 and 322 ± 178 CSI; P = 0.12) but both were similarly reduced relative to the Active 36 (516 ± 147 CSI, both P &lt; 0.05). At pre‐syncope mean arterial pressure and heart rate were not different between trials. These data suggest that tolerance to a simulated hemorrhagic challenge is similar following passive and exercise induced heat stress when skin temperatures are similarly elevated.Grant Funding Source: DOD: W81XWH‐09‐2‐0194 and NIH: HL61388

Heat stress does not augment ventilatory responses to presyncopal limited lower body negative pressure

Simulated haemorrhage, e.g. lower body negative pressure (LBNP), reduces central blood volume and mean arterial pressure, while ventilation increases. Passive whole-body heat stress likewise increases ventilation. The objective of this project was to test the hypothesis that ventilatory responses to reductions in central blood volume and arterial pressure during simulated haemorrhage are enhanced when individuals are heat stressed rather than normothermic. Eight healthy men (34 ± 9 years old, 176 ± 6 cm tall and 80.2 ± 4.2 kg body weight) underwent a simulated haemorrhagic challenge via LBNP until presyncope on two separate occasions, namely normothermic control and whole-body heat-stress trials. Baseline ventilation and core and mean skin temperatures were not different between trials (all P > 0.05). Prior to LBNP, heat stress increased core (from 36.8 ± 0.2 to 38.2 ± 0.2°C, P < 0.05) and mean skin temperatures (from 33.9 ± 0.5 to 38.1 ± 0.6°C, P < 0.05), as well as minute ventilation (from 8.01 ± 2.63 to 13.68 ± 6.68 l min(-1), P < 0.01). At presyncope, mean arterial pressure and middle cerebral artery blood velocity decreased in both trials (P < 0.05). At presyncope, ventilation increased to 23.22 ± 6.78 (P < 0.01) and 25.88 ± 10.16 l min(-1) (P < 0.01) in the normothermic and hyperthermic trials, respectively; however, neither the increase in ventilation from the pre-LBNP period nor the absolute ventilation was different between normothermic and hyperthermic trials (P > 0.05). These data suggest that the increase in ventilation during simulated haemorrhage induced via LBNP is not altered in heat-stressed humans.

Acute volume expansion attenuates hyperthermia-induced reductions in cerebral perfusion during simulated hemorrhage

Hyperthermia reduces the capacity to withstand a simulated hemorrhagic challenge, but volume loading preserves this capacity. This study tested the hypotheses that acute volume expansion during hyperthermia increases cerebral perfusion and attenuates reductions in cerebral perfusion during a simulated hemorrhagic challenge induced by lower-body negative pressure (LBNP). Eight healthy young male subjects underwent a supine baseline period (pre-LBNP), followed by 15- and 30-mmHg LBNP while normothermic, hyperthermic (increased pulmonary artery blood temperature ~1.1°C), and following acute volume infusion while hyperthermic. Primary dependent variables were mean middle cerebral artery blood velocity (MCAvmean), serving as an index of cerebral perfusion; mean arterial pressure (MAP); and cardiac output (thermodilution). During baseline, hyperthermia reduced MCAvmean (P = 0.001) by 12 ± 9% relative to normothermia. Volume infusion while hyperthermic increased cardiac output by 2.8 ± 1.4 l/min (P < 0.001), but did not alter MCAvmean (P = 0.99) or MAP (P = 0.39) compared with hyperthermia alone. Relative to hyperthermia, at 30-mmHg LBNP acute volume infusion attenuated reductions (P < 0.001) in cardiac output (by 2.5 ± 0.9 l/min; P < 0.001), MAP (by 5 ± 6 mmHg; P = 0.004), and MCAvmean (by 12 ± 13%; P = 0.002). These data indicate that acute volume expansion does not reverse hyperthermia-induced reductions in cerebral perfusion pre-LBNP, but that it does attenuate reductions in cerebral perfusion during simulated hemorrhage in hyperthermic humans.

Elevated local skin temperature impairs cutaneous vasoconstrictor responses to a simulated haemorrhagic challenge while heat stressed

During a simulated haemorrhagic challenge, syncopal symptoms develop sooner when individuals are hyperthermic relative to normothermic. This is due, in part, to a large displacement of blood to the cutaneous circulation during hyperthermia, coupled with inadequate cutaneous vasoconstriction during the hypotensive challenge. The influence of local skin temperature on these cutaneous vasoconstrictor responses is unclear. This project tested the hypothesis that local skin temperature modulates cutaneous vasoconstriction during simulated haemorrhage in hyperthermic humans. Eight healthy participants (four men and four women; 32 ± 7 years old; 75.2 ± 10.8 kg) underwent lower-body negative pressure to presyncope while heat stressed via a water-perfused suit sufficiently to increase core temperature by 1.2 ± 0.2 °C. At forearm skin sites distal to the water-perfused suit, local skin temperature was either 35.2 ± 0.6 (mild heating) or 38.2 ± 0.2 °C (moderate heating) throughout heat stress and lower-body negative pressure, and remained at these temperatures until presyncope. The reduction in cutaneous vascular conductance during the final 90 s of lower-body negative pressure, relative to heat-stress baseline, was greatest at the mildly heated site (-10 ± 15% reduction) relative to the moderately heated site (-2 ± 12%; P = 0.05 for the magnitude of the reduction in cutaneous vascular conductance between sites), because vasoconstriction at the moderately heated site was either absent or negligible. In hyperthermic individuals, the extent of cutaneous vasoconstriction during a simulated haemorrhage can be modulated by local skin temperature. In situations where skin temperature is at least 38 °C, as is the case in soldiers operating in warm climatic conditions, a haemorrhagic insult is unlikely to be accompanied by cutaneous vasoconstriction.

Local skin temperature alters cutaneous vasoconstrictor responses to a simulated hemorrhagic challenge while heat stressed

Tolerance to simulated hemorrhage is reduced with hyperthermia, due in part to inadequate cutaneous vasoconstriction. It is unclear how elevated skin temperatures, as experienced by soldiers on active duty, influence cutaneous vasoconstriction during simulated hemorrhage. 8 healthy males (34 ± 9 yr, 80.2 ± 4.2 kg) underwent a simulated hemorrhagic challenge via lower body negative pressure (LBNP) to pre‐syncope while heat stressed sufficient to increase core (Tcore Δ1.2 ± 0.2°C) and mean skin temperatures (Tsk mean 38.2 ± 0.7°C). Local skin temperatures at three forearm sites were held at 35.2±0.6°C, 38.2±0.2°C and 41.3± 0.7°C throughout heat stress and LBNP. At pre‐syncope mean arterial pressure declined (74±6 to 53 ± 8 mmHg P &lt; 0.0001) while mean Tsk (38.2±0.7°C; P = 0.92) and local Tsk (35.1±0.8; 38.3±0.3 and 41.5±0.6°C; P &gt; 0.05) were unchanged relative to heat stress baseline (i.e., pre‐LBNP). The magnitude of reduction in cutaneous vascular conductance during the final 90 seconds of LBNP from heat stress baseline was influenced by local Tsk (8% at ~35°C; 3% at ~38°C and 2% at ~42°C; P &lt; 0.0001). In hyperthermic individuals the extent of cutaneous vasoconstriction during a simulated hemorrhage is dependent on skin temperature. In situations where a soldier's skin temperature exceeds 38°C, cutaneous vasoconstriction to a hemorrhagic challenge is likely negligible.NIH HL61388 and HL84072

Tolerance to a hemorrhagic challenge during heat stress is improved with inspiratory resistance breathing

The mechanism(s) by which heat stress alters blood pressure control and tolerance to a simulated hemorrhagic challenge is multifaceted; however, heat‐induced reductions in central blood volume play a key role. Inspiratory resistance breathing improves blood pressure control and tolerance during simulated hemorrhage in normothermic individuals. It is unknown if similar improvements occur with this maneuver in heat stress conditions. This study tested the hypothesis that inspiratory resistance breathing improves tolerance to simulated hemorrhage in individuals with elevated internal temperatures. On 2 separate days, 8 subjects performed a simulated hemorrhage challenge (lower body negative pressure, LBNP) to pre‐syncope following an increase in internal temperature of 1.5 °C. During one trial subjects breathed through an inspiratory impedance device set at 0 cmH20 of resistance (Sham) while on the other day the device was set at −7 cmH20 of resistance (Experimental). Tolerance was quantified as cumulative stress index (CSI). Subjects were more tolerant to the LBNP challenge during the Experimental protocol as indexed by a larger CSI (Sham: 520±306 mmHg × min; Experimental: 682±324 mmHg × min, P&lt;0.01). These data indicate that inspiratory resistance breathing modestly improves tolerance to a simulated hemorrhagic challenge during heat stress.Support NIH‐HL61388 &amp; HL84072

When filling the glass only leaves it half empty!– Insight into the cardiovascular physiology of haemorrhage under heat stress

When filling the glass only leaves it half empty!– Insight into the cardiovascular physiology of haemorrhage under heat stress

Colloid volume loading does not mitigate decreases in central blood volume during simulated haemorrhage while heat stressed

Heat stress results in profound reductions in the capacity to withstand a simulated haemorrhagic challenge; however, this capacity is normalized if the individual is volume loaded prior to the challenge. The present study tested the hypothesis that volume loading during passive heat stress attenuates the reduction in regional blood volumes during a simulated haemorrhagic challenge imposed via lower-body negative pressure (LBNP). Seven subjects underwent 30 mmHg LBNP while normothermic, during passive heat stress (increased internal temperature ∼1◦C), and while continuing to be heated after intravenous colloid volume loading (11 ml kg⁻¹). Relative changes in torso and regional blood volumes were determined by gamma camera imaging with technetium-99m labelled erythrocytes. Heat stress reduced blood volume in all regions (ranging from 7 to 16%), while subsequent volume loading returned those values to normothermic levels. While normothermic,LBNP reduced blood volume in all regions (torso: 22 ± 8%; heart: 18 ± 6%; spleen: 15 ± 8%). During LBNP while heat stressed, the reductions in blood volume in each region were markedly greater when compared to LBNP while normothermic (torso: 73 ± 2%; heart: 72 ± 3%; spleen: 72 ± 5%, all P<0.001 relative to normothermia). Volume loading during heat stress did not alter the extent of the reduction in these blood volumes to LBNP relative to heat stress alone (torso: 73 ± 1%; heart: 72 ± 2%; spleen: 74 ± 3%, all P>0.05 relative to heat stress alone). These data suggest that blood volume loading during passive heat stress (via 11 ml kg⁻¹ of a colloid solution) normalizes regional blood volumes in the torso, but does not mitigate the reduction in central blood volume during a simulated haemorrhagic challenge combined with heat stress.