Browsing by Author "Crandall, C. G."

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Active and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge
(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2014-10-01) Pearson, J.; Lucas, R. A. I.; Schlader, Z. J.; Zhao, J.; Gagnon, D.; Crandall, C. G.
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.
Acute volume expansion attenuates hyperthermia-induced reductions in cerebral perfusion during simulated hemorrhage
(Journal of Applied Physiology, 2013-06-15) Schlader, Z. J.; Seifert, T.; Wilson, T. E.; Bundgaard-Nielsen, M.; Secher, N. H.; Crandall, C. G.
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.
Aerobic fitness is disproportionately low in adult burn survivors years after injury
(Journal of Burn Care and Research, 2015-07-01) Ganio, M. S.; Pearson, J.; Schlader, Z. J.; Brothers, R. M.; Lucas, R. A. I.; Rivas, E.; Kowalske, K. J.; Crandall, C. G.
Objective A maximal aerobic capacity below the 20th percentile is associated with an increased risk of all-cause mortality.1 Adult burn survivors have a lower aerobic capacity compared to non-burned adults when evaluated 38±23 days post-injury.2 However, it is unknown if burn survivors with well-healed skin grafts (i.e., multiple years post injury), also have low aerobic capacity. This project tested the hypothesis that aerobic fitness, as measured by maximal aerobic capacity (VO2max), is reduced in well-healed adult burn survivors when compared to normative values from non-burned individuals. Methods Twenty-five burn survivors (36 ± 12 years old; 13 females) with well-healed split thickness grafts (median: 16 years post-injury, range: 1 to 51 years) covering at least 17% of their body surface area (mean: 40±16%; range: 17 to 75%) performed a graded cycle ergometry exercise test to volitional fatigue. Expired gases and minute ventilation were measured via a metabolic cart for the determination of VO2max. Each subject’s VO2max was compared with sex- and age-matched normative values from population data published by the American College of Sports Medicine (ACSM), the American Heart Association (AHA), and recent epidemiological data.3 Results Subjects had a VO2max of 29.4 ± 10.1 ml O2/kg body mass/min (median: 27.5; range: 15.9 to 53.3). Using ACSM normative values, mean VO2max of the subjects was in the lower 24th percentile (median: 10th percentile). 88% of the subjects had a VO2max below AHA age-adjusted normative values. Similarly 20 of the 25 subjects had a VO2max in the lower 25% percentile of recent epidemiological data. Conclusions Relative to non-grafted subjects, 80–88% of the evaluated skin graft subjects had a very low aerobic capacity. Based upon these findings, adult burn survivors are disproportionally unfit relative to the general U.S. population, and this puts them at an increased risk of all-cause mortality.
Age-related changes to cardiac systolic and diastolic function during whole-body passive hyperthermia
(Experimental Physiology, 2015-01-15) Lucas, R. A. I.; Sarma, S.; Schlader, Z. J.; Pearson, J.; Crandall, C. G.
The effect of ageing on hyperthermia-induced changes in cardiac function is unknown. This study tested the hypothesis that hyperthermia-induced changes in left ventricular systolic and diastolic function are attenuated in older adults when compared with young adults. Eight older (71 ± 5 years old) and eight young adults (29 ± 5 years old), matched for sex, physical activity and body mass index, underwent whole-body passive hyperthermia. Mean arterial pressure (Finometer Pro), heart rate, forearm vascular conductance (venous occlusion plethysmography) and echocardiographic indices of diastolic and systolic function were measured during a normothermic supine period and again after an increase in internal temperature of ~1.0 °C. Hyperthermia decreased mean arterial pressure and left ventricular end-diastolic volumes and increased heart rate to a similar extent in both groups (P > 0.05). Ageing did not alter the magnitude of hyperthermia-induced changes in indices of systolic (lateral mitral annular S′ velocity) or diastolic function (lateral mitral annular E′ velocity, peak early diastolic filling and isovolumic relaxation time; P > 0.05). However, with hyperthermia the global longitudinal systolic strain increased in the older group, but was unchanged in the young group (P = 0.03). Also, older adults were unable to augment late diastolic ventricular filling [i.e. E/A ratio and A/(A + E) ratio] during hyperthermia, unlike the young (P <0.05). These findings indicate that older adults depend on a greater systolic contribution (global longitudinal systolic strain) to meet hyperthermic demand and that the atrial contribution to diastolic filling was not further augmented in older adults when compared with young adults.
Baroreceptor unloading does not limit forearm sweat rate during severe passive heat stress
(Journal of Applied Physiology, 2015-02-15) Schlader, Z. J.; Gagnon, D.; Lucas, R. A. I.; Pearson, J.; Crandall, C. G.
This study tested the hypothesis that sweat rate during passive heat stress is limited by baroreceptor unloading associated with heat stress. Two protocols were performed in which healthy subjects underwent passive heat stress that elicited an increase in intestinal temperature of ∼1.8°C. Upon attaining this level of hyperthermia, in protocol 1 (n = 10, 3 females) a bolus (19 ml/kg) of warm (∼38°C) isotonic saline was rapidly (5–10 min) infused intravenously to elevate central venous pressure (CVP), while in protocol 2 (n = 11, 5 females) phenylephrine was infused intravenously (60–120 μg/min) to return mean arterial pressure (MAP) to normothermic levels. In protocol 1, heat stress reduced CVP from 3.9 ± 1.9 mmHg (normothermia) to −0.6 ± 1.4 mmHg (P < 0.001), while saline infusion returned CVP to normothermic levels (5.1 ± 1.7 mmHg; P > 0.999). Sweat rate was elevated by heat stress (1.21 ± 0.44 mg·cm−2·min−1) but remained unchanged during rapid saline infusion (1.26 ± 0.47 mg·cm−2·min−1, P = 0.5), whereas cutaneous vascular conductance increased from 77 ± 10 to 101 ± 20% of local heating max (P = 0.029). In protocol 2, MAP was reduced with heat stress from 85 ± 7 mmHg to 76 ± 8 mmHg (P = 0.048). Although phenylephrine infusion returned MAP to normothermic levels (88 ± 7 mmHg; P > 0.999), sweat rate remained unchanged during phenylephrine infusion (1.39 ± 0.22 vs. 1.41 ± 0.24 mg·cm−2·min−1; P > 0.999). These data indicate that both cardiopulmonary and arterial baroreceptor unloading do not limit increases in sweat rate during passive heat stress.
Cardiopulmonary and arterial baroreceptor unloading during passive hyperthermia does not contribute to hyperthermic-induced hyperventilation
(Experimental Physiology, 2015-08-24) Lucas, R. A. I.; Pearson, J.; Schlader, Z. J.; Crandall, C. G.
This study tested the hypothesis that baroreceptor unloading during passive hyperthermia contributes to increases in ventilation and decreases in end-tidal partial pressure of carbon dioxide (PET,CO2) during that exposure. Two protocols were performed, in which healthy subjects underwent passive hyperthermia (increasing intestinal temperature by ~1.8°C) to cause a sustained increase in ventilation and reduction in PET,CO2. Upon attaining hyperthermic hyperventilation, in protocol 1 (n = 10; three females) a bolus (19 ± 2 ml kg−1) of warm (~38°C) isotonic saline was rapidly (5–10 min) infused intravenously to restore reductions in central venous pressure, whereas in protocol 2 (n = 11; five females) phenylephrine was infused intravenously (60–120 μg min−1) to return mean arterial pressure to normothermic levels. In protocol 1, hyperthermia increased ventilation (by 2.2 ± 1.7 l min−1, P < 0.01), while reducing PET,CO2 (by 4 ± 3 mmHg, P = 0.04) and central venous pressure (by 5 ± 1 mmHg, P <0.01). Saline infusion increased central venous pressure by 5 ± 1 mmHg (P < 0.01), restoring it to normothermic values, but did not change ventilation or PET,CO2 (P > 0.05). In protocol 2, hyperthermia increased ventilation (by 5.0 ± 2.7l min−1, P <0.01) and reduced PET ,CO2 (by 5 ± 2 mmHg, P < 0.01) and mean arterial pressure (by 9 ± 7 mmHg, P <0.01). Phenylephrine infusion increased mean arterial pressure by 12 ± 3 mmHg (P < 0.01), restoring it to normothermic values, but did not change ventilation or PET,CO2 (P > 0.05). The absence of a reduction in ventilation upon reloading the cardiopulmonary and arterial baroreceptors to pre-hyperthermic levels indicates that baroreceptor unloading with hyperthermia is unlikely to contribute to hyperthermic hyperventilation in humans.
Cognitive and perceptual responses during passive heat stress in younger and older adults
(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2015-05-15) Schlader, Z. J.; Gagnon, D.; Adams, A.; Rivas, E.; Cullum, C. M.; Crandall, C. G.
We tested the hypothesis that attention, memory, and executive function are impaired to a greater extent in passively heat-stressed older adults than in passively heat-stressed younger adults. In a randomized, crossover design, 15 older (age: 69 ± 5 yr) and 14 younger (age: 30 ± 4 yr) healthy subjects underwent passive heat stress and time control trials. Cognitive tests (outcomes: accuracy and reaction time) from the CANTAB battery evaluated attention [rapid visual processing (RVP), choice reaction time (CRT)], memory [spatial span (SSP), pattern recognition memory (PRM)], and executive function [one touch stockings of Cambridge (OTS)]. Testing was undertaken on two occasions during each trial, at baseline and after internal temperature had increased by 1.0 ± 0.2°C or after a time control period. For tests that measured attention, reaction time during RVP and CRT was slower (P ≤ 0.01) in the older group. During heat stress, RVP reaction time improved (P < 0.01) in both groups. Heat stress had no effect (P ≥ 0.09) on RVP or CRT accuracy in either group. For tests that measured memory, accuracy on SSP and PRM was lower (P < 0.01) in the older group, but there was no effect of heat stress (P ≥ 0.14). For tests that measured executive function, overall, accuracy on OTS was lower, and reaction time was slower in the older group (P ≤ 0.05). Reaction time generally improved during heat stress, but there was no effect of heat stress on accuracy in either group. These data indicate that moderate increases in body temperature during passive heat stress do not differentially compromise cognitive function in younger and older adults.
The effect of passive heat stress and exercise-induced dehydration on the compensatory reserve during simulate hemorrhage
(Shock, 2016-09) Gagnon, D.; Schlader, Z. J.; Adams, A.; Rivas, E.; Mulligan, J.; Grudic, G. Z.; Convertino, V. A.; Howard, J.; Crandall, C. G.
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.
Elevated skin and core temperatures both contribute to reductions in tolerance to a simulated hemorrhagic challenge
(Experimental Physiology, 2017-02-01) Pearson, J.; Lucas, R. A. I.; Schlader, Z. J.; Gagnon, D.; Crandall, C. G.
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 ± 151 mmHg min) and core hyperthermia trials (563 ± 194 mmHg min) relative to control conditions (1010 ± 246 mmHg min; 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.
Fluid restriction during exercise in the heat reduces tolerance to progressive central hypovolemia
(Experimental Physiology, 2015-08-06) Schlader, Z. J.; Gagnon, D.; Rivas, E.; Convertino, V. A.; Crandall, C. G.
This study tested the hypothesis that dehydration induced via exercise in the heat impairs tolerance to central hypovolaemia. Eleven male subjects (32 ± 7 years old, 81.5 ± 11.1 kg) walked (O2 uptake 1.7 ± 0.4 l min−1) in a 40°C, 30% relative humidity environment on three occasions, as follows: (i) subjects walked for 90 min, drinking water to offset sweat loss (Hydrated, n =11); (ii) water intake was restricted, and exercise was terminated when intestinal temperature increased to the same level as in the Hydrated trial (Isothermic Dehydrated, n = 11); and (iii) water intake was restricted, and exercise duration was 90 min (Time Match Dehydrated, n = 9). For each trial, tolerance to central hypovolaemia was determined following exercise via progressive lower body negative pressure and quantified as time to presyncope. Increases in intestinal temperature prior to lower body negative pressure were not different (P = 0.91) between Hydrated (1.1 ± 0.4°C) and Isothermic Dehydrated trials (1.1 ± 0.4°C), but both were lower than in the Time Match Dehydrated trial (1.7 ± 0.5°C, P < 0.01). Prior to lower body negative pressure, body weight was unchanged in the Hydrated trial (−0.1 ± 0.2%), but was reduced in Isothermic Dehydrated (−0.9 ± 0.4%) and further so in Time Match Dehydrated trial (−1.9 ± 0.6%, all P < 0.01). Time to presyncope was greater in Hydrated (14.7 ± 3.2 min) compared with Isothermic Dehydrated (11.9 ± 3.3 min, P < 0.01) and Time Match Dehydrated trials (10.2 ± 1.6 min, P = 0.03), which were not different (P = 0.19). These data indicate that inadequate fluid intake during exercise in the heat reduces tolerance to central hypovolaemia independent of increases in body temperature.
Hypercapnia-induced increases in cerebral blood flow do not improve lower body negative pressure tolerance during hyperthermia
(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2013-09-15) Lucas, R. A. I.; Pearson, J.; Schlader, Z. J.; Crandall, C. G.
Heat-related decreases in cerebral perfusion are partly the result of ventilatory-related reductions in arterial CO2 tension. Cerebral perfusion likely contributes to an individual's tolerance to a challenge like lower body negative pressure (LBNP). Thus increasing cerebral perfusion may prolong LBNP tolerance. This study tested the hypothesis that a hypercapnia-induced increase in cerebral perfusion improves LBNP tolerance in hyperthermic individuals. Eleven individuals (31 ± 7 yr; 75 ± 12 kg) underwent passive heat stress (increased intestinal temperature ∼1.3°C) followed by a progressive LBNP challenge to tolerance on two separate days (randomized). From 30 mmHg LBNP, subjects inhaled either (blinded) a hypercapnic gas mixture (5% CO2, 21% oxygen, balanced nitrogen) or room air (SHAM). LBNP tolerance was quantified via the cumulative stress index (CSI). Mean middle cerebral artery blood velocity (MCAvmean,) and end-tidal CO2 (PetCO2) were also measured. CO2 inhalation of 5% increased PetCO2 at ∼40 mmHg LBNP (by 16 ± 4 mmHg) and at LBNP tolerance (by 18 ± 5 mmHg) compared with SHAM (P < 0.01). Subsequently, MCAvmean was higher in the 5% CO2 trial during ∼40 mmHg LBNP (by 21 ± 12 cm/s, ∼31%) and at LBNP tolerance (by 18 ± 10 cm/s, ∼25%) relative to the SHAM (P < 0.01). However, hypercapnia-induced increases in MCAvmean did not alter LBNP tolerance (5% CO2 CSI: 339 ± 155 mmHg × min; SHAM CSI: 273 ± 158 mmHg × min; P = 0.26). These data indicate that inhaling a hypercapnic gas mixture increases cerebral perfusion during LBNP but does not improve LBNP tolerance when hyperthermic.
Hyperthermia does not alter the capacity to increase cerebral perfusion during a cognitive task
(Experimental Physiology, 2013-07-17) Schlader, Z. J.; Lucas, R. A. I.; Pearson, J.; Crandall, C. G.
This study tested the hypothesis that hyperthermia attenuates the increase in cerebral perfusion during cognitive activation. Mean middle cerebral artery blood velocity (MCAVmean) served as an index of cerebral perfusion, while the nBack test (a test of working memory) was the cognitive task. Hyperthermia was characterized by elevations (P < 0.001) in skin (by 5.0 ± 0.8°C) and intestinal temperatures (by 1.3 ± 0.1°C) and reductions (P < 0.020) in mean arterial pressure (by 11 ± 10 mmHg), end‐tidal CO2 tension (by 3 ± 6 mmHg) and MCAVmean (by 10 ± 9 cm s−1). Hyperthermia had no influence on nBack test performance (mean difference from normothermia to hyperthermia, −1 ± 11%; P= 0.276) or, counter to the hypothesis, the increase in MCAVmean during nBack testing (mean difference from normothermia to hyperthermia: 0 ± 16 cm s−1; P= 0.608). These findings indicate that the capacity to increase cerebral perfusion during cognitive activation is unaffected by hyperthermia.
Mechanisms of orthostatic intolerance during heat stress
(Autonomic Neuroscience, 2016-04-01) Schlader, Z. J.; Wilson, T. E.; Crandall, C. G.
Heat stress profoundly and unanimously reduces orthostatic tolerance. This review aims to provide an overview of the numerous and multifactorial mechanisms by which this occurs in humans. Potential causal factors include changes in arterial and venous vascular resistance and blood distribution, and the modulation of cardiac output, all of which contribute to the inability to maintain cerebral perfusion during heat and orthostatic stress. A number of countermeasures have been established to improve orthostatic tolerance during heat stress, which alleviate heat stress induced central hypovolemia (e.g., volume expansion) and/or increase peripheral vascular resistance (e.g., skin cooling). Unfortunately, these countermeasures can often be cumbersome to use with populations prone to syncopal episodes. Identifying the mechanisms of inter-individual differences in orthostatic intolerance during heat stress has proven elusive, but could provide greater insights into the development of novel and personalized countermeasures for maintaining or improving orthostatic tolerance during heat stress. This development will be especially impactful in occuational settings and clinical situations that present with orthostatic intolerance and/or central hypovolemia. Such investigations should be considered of vital importance given the impending increased incidence of heat events, and associated cardiovascular challenges that are predicted to occur with the ensuing changes in climate.
Non-grafted skin surface area best predicts exercise core temperature responses in burned individuals.
(Medicine and Science in Sports and Exercise, 2015-10-01) Ganio, M. S.; Schlader, Z. J.; Pearson, J.; Lucas, R. A. I.; Rivas, E.; Kowalske, K. J.; Crandall, C. G.
Abstract Grafted skin impairs heat dissipation, but it is unknown to what extent this impacts body temperature during exercise in the heat. PURPOSE We examined core body temperature responses during exercise in the heat in a group of individuals with a large range of grafts covering their body surface area (BSA; 0-75%). METHODS Forty-three individuals (19 females) were stratified into groups based upon BSA grafted: Control (0% grafted, n=9), 17-40% (n=19), and >40% (n=15). Subjects exercised at a fixed rate of metabolic heat production (339 ± 70 W; 4.3 ± 0.8 W/kg) in an environmental chamber set at 40°C, 30% RH for 90 min or until exhaustion (n=8). Whole-body sweat rate and core temperatures were measured. RESULTS Whole body sweat rates were similar between groups (Control: 14.7±3.4 ml/min, 17-40%: 12.6±4.0 ml/min, and >40%: 11.7±4.4 ml/min, P>0.05), but the increase in core temperature at the end of exercise in the >40% BSA grafted group (1.6±0.5°C) was greater than the 17-40% (1.2±0.3°C) and Control (0.9±0.2°C) groups (P<0.05). Absolute BSA of non-grafted skin (expressed in m2) was the strongest independent predictor of the core temperature increase (r2=0.41). When re-grouping all subjects, individuals with the lowest BSA of non-grafted skin (<1.0 m2) had greater increases in core temperature (1.6±0.5°C) than those with >1.5 m2 non-grafted skin (1.0±0.3°C, P<0.05). CONCLUSIONS These data imply that individuals with grafted skin have greater increases in core temperature when exercising in the heat and that the magnitude of this increase is best explained by the amount of non-grafted skin available for heat dissipation.
Normothermic central hypovolemia tolerance reflects hyperthermic tolerance
(Clinical Autonomic Research, 2014-04-04) Schlader, Z. J.; Crandall, C. G.
Purpose To test the hypothesis that those who are highly tolerant to lower body negative pressure (LBNP) while normothermic are also highly tolerant to this challenge while hyperthermic. Methods Sixty pairs of normothermic and hyperthermic LBNP tests to pre-syncope were evaluated. LBNP tolerance was quantified via the cumulative stress index (CSI), which is calculated as the sum of the product of the LBNP level and the duration of each level until test termination (i.e., 20 mmHg × 3 min + 30 mmHg × 3 min, etc.). CSI was compared between normothermic and hyperthermic trials. Internal and skin temperatures, heart rate, and arterial pressure were measured throughout. Results Hyperthermia reduced (P<0.001) CSI from 997 ± 437 to 303 ± 213 mmHg min. There was a positive correlation between normothermic and hyperthermic LBNP tolerance (R2 = 0.38; P<0.001). As a secondary analysis, the 20 trials with the highest LBNP tolerance while normothermic were identified (indicated as the HIGH group; CSI 1,467 ± 356 mmHg min), as were the 20 trials with the lowest normothermic tolerance (indicated as the LOW group; CSI 565 ± 166 mmHg min; P<0.001 between groups). While hyperthermia unanimously reduced CSI in both HIGH and LOW groups, in this hyperthermic condition CSI was ~threefold higher in the HIGH group (474 ± 226 mmHg min) relative to the LOW group (160 ± 115 mmHg min; P<0.001). Conclusions LBNP tolerance while hyperthermic is related to normothermic tolerance and, associated with this finding, those who have a high LBNP tolerance while normothermic remain relatively tolerant when hyperthermic.
One of these things is not like the other: the heterogeneity of the cerebral circulation
(The Journal of Physiology, 2013-01-14) Schlader, Z. J.; Lucas, R. A. I.; Pearson, J.; Crandall, C. G.
The human cerebral vasculature is highly sensitive to changes in arterial blood gases (i.e. arterial carbon dioxide and oxygen tensions), such that hypercapnia/hypoxia and hypocapnia/hyperoxia cause global increases and decreases in cerebral blood flow. It is generally accepted that all cerebral arter‐ioles – traditionally considered to be the regulators of brain blood flow – are equally sensitive to changes in arterial blood gases. However, this classic dogma may not be the case.
Post-junctional sudomotor and cutaneous vascular responses in non-injured skin following heat acclimation in burn survivors
(Journal of Burn Care and Research, 2017-01-01) Pearson, J.; Ganio, M. S.; Schlader, Z. J.; Lucas, R. A. I.; Rivas, E.; Davis, S. L.; Kowalske, K. J.; Crandall, C. G.
Thermal tolerance is improved in burn survivors following 7 days of exercise heat acclimation. It is unknown whether post junctional sudomotor and/or cutaneous vascular adaptations in noninjured skin contribute to this improvement. Thirty-three burn survivors were stratified into moderately (17–40% BSA grafted, n = 19) and highly (>40% BSA grafted, n = 14) skin-grafted groups. Nine nonburned subjects served as controls. All subjects underwent a 7-day heat acclimation protocol, which improved thermal tolerance in all groups. Before and after this heat acclimation protocol, post junctional cutaneous vascular responses were assessed by administering increasing doses of sodium nitroprusside (SNP) and methacholine (MCh) using intradermal microdialysis in noninjured skin. MCh infusion was also used to assess post junctional responses in sudomotor function in noninjured skin. Cutaneous vascular responses to SNP and MCh were not different between pre- and post heat acclimation in either group of burn survivors (both P > .05). The maximal sweating rate to MCh increased post acclimation in the control group (0.41 ± 0.20 to 0.54 ± 0.21 mg·min−1·cm−1; P = .016) but was unchanged in both groups of burn survivors (both P > .05). The number of sweat glands activated during the highest dose of MCh was elevated in the >40% BSA-grafted group (49 ± 16 to 56 ± 18 glands·cm2; P = .005) but was unchanged in control subjects and the <40% BSA-grafted group (both P > .05). Given that post junctional administration of MCh and SNP did not alter sweating or skin blood flow from noninjured skin of burn survivors, improved thermal tolerance in these individuals following heat acclimation is more likely a result of either an increased sweating efficiency or an increased neural drive for sweating.
Sympathetic activity during passive heat stress in healthy aged humans
(The Journal of Physiology, 2015-03-05) Gagnon, D.; Schlader, Z. J.; Crandall, C. G.
Cardiovascular adjustments during heat stress are generally attenuated in healthy aged humans, which could be due to lower increases in sympathetic activity compared to the young. We compared muscle sympathetic nerve activity (MSNA) between 11 young (Y: 28 ± 4 years) and 10 aged (A: 70 ± 5 years) subjects prior to and during passive heating. Furthermore, MSNA responses were compared when a cold pressor test (CPT) and lower body negative pressure (LBNP) were superimposed upon heating. Baseline MSNA burst frequency (Y: 15 ± 4 vs. A: 31 ± 3 bursts min−1, P ≤ 0.01) and burst incidence (Y: 26 ± 8 vs. A: 50 ± 7 bursts (100 cardiac cycles (CC))−1, P ≤ 0.01) were greater in the aged. Heat stress increased core temperature to a similar extent in both groups (Y: +1.2 ± 0.1 vs. A: +1.2 ± 0.0°C, P = 0.99). Absolute levels of MSNA remained greater in the aged during heat stress (burst frequency: Y: 47 ± 6 vs. A: 63 ± 11 bursts min−1, P ≤ 0.01; burst incidence: Y: 48 ± 8 vs. A: 67 ± 9 bursts (100 CC)−1, P ≤ 0.01); however, the increase in both variables was similar between groups (both P ≥ 0.1). The CPT and LBNP further increased MSNA burst frequency and burst incidence, although the magnitude of increase was similar between groups (both P ≥ 0.07). These results suggest that increases in sympathetic activity during heat stress are not attenuated in healthy aged humans.
Tissue oxygen saturation during hyperthermic progressive central hypovolemia
(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2014-09-15) Schlader, Z. J.; Rivas, E.; Soller, B. R.; Convertino, V. A.; Crandall, C. G.
During normothermia, a reduction in near-infrared spectroscopy (NIRS)-derived tissue oxygen saturation (So2) is an indicator of central hypovolemia. Hyperthermia increases skin blood flow and reduces tolerance to central hypovolemia, both of which may alter the interpretation of tissue So2 during central hypovolemia. This study tested the hypothesis that maximal reductions in tissue So2 would be similar throughout normothermic and hyperthermic central hypovolemia to presyncope. Ten healthy males (means ± SD; 32 ± 5 yr) underwent central hypovolemia via progressive lower-body negative pressure (LBNP) to presyncope during normothermia (skin temperature ≈34°C) and hyperthermia (+1.2 ± 0.1°C increase in internal temperature via a water-perfused suit, skin temperature ≈39°C). NIRS-derived forearm (flexor digitorum profundus) tissue So2 was measured throughout and analyzed as the absolute change from pre-LBNP. Hyperthermia reduced (P < 0.001) LBNP tolerance by 49 ± 33% (from 16.7 ± 7.9 to 7.2 ± 3.9 min). Pre-LBNP, tissue So2 was similar (P = 0.654) between normothermia (74 ± 5%) and hyperthermia (73 ± 7%). Tissue So2 decreased (P < 0.001) throughout LBNP, but the reduction from pre-LBNP to presyncope was greater during normothermia (−10 ± 6%) than during hyperthermia (−6 ± 5%; P = 0.041). Contrary to our hypothesis, these findings indicate that hyperthermia is associated with a smaller maximal reduction in tissue So2 during central hypovolemia to presyncope.