Zachary Schlader Research Collection
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Item 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.Item The relative overlooking of human behavioral temperature regulation – A paradox worth resolving(Temperature, 2014-03-22) Schlader, Z. J.It has long been appreciated that behavior is the most powerful and diverse thermoregulatory mechanism. In animal-based studies a behavioral assay is typically the first assessment when investigating the effect of a perturbation on thermoregulation, highlighting its importance. Oddly however, such an approach has been largely ignored in human research.Item The human thermoneutral and thermal comfort zones: Thermal comfort in your own skin blood flow(Temperature, 2014-11-07) Schlader, Z. J.Human thermoregulation is achieved via autonomic and behavioral responses. Autonomic responses involve 2 synchronous ‘components’. One counteracts large thermal perturbations, eliciting robust heat loss or gain (i.e., sweating or shivering). The other fends off smaller insults, relying solely on changes in sensible heat exchange (i.e., skin blood flow). This sensible component occurs within the thermoneutral zone [i.e., the ambient temperature range in which temperature regulation is achieved only by sensible heat transfer, without regulatory increases in metabolic heat production (e.g., shivering) or evaporative heat loss (e.g., sweating)].1 The combination of behavior and sensible heat exchange permits a range of conditions that are deemed thermally comfortable, which is defined as the thermal comfort zone.1 Notably, we spend the majority of our lives within the thermoneutral and thermal comfort zones. It is only when we are unable to stay within these zones that deleterious health and safety outcomes can occur (i.e., hypo- or hyperthermia). Oddly, although the thermoneutral zone and thermal preference (a concept similar to the thermal comfort zone) has been extensively studied in non-human animals, our understanding of human thermoregulation within the thermoneutral and thermal comfort zones remains rather crude.Item 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.Item Practical Hydration Solutions for Sports(Nutrients, 2019-07-09) Bevel, L.; Hosokawa, Y.; Casa, D.; Adams, W.; Armstrong, L.; Baker, L.; Burke, L.; Cheuvront, S.; Chiampas, G.; Gonzalez-Alonso, J.; Huggins, R.; Kavouras, S.; Lee, E.; McDermott, B.; Miller, K.; Schlader, Z. J.; Sims, S.; Stearns, R.; Troyanos, C.; Wingo, J.Personalized hydration strategies play a key role in optimizing the performance and safety of athletes during sporting activities. Clinicians should be aware of the many physiological, behavioral, logistical and psychological issues that determine both the athlete’s fluid needs during sport and his/her opportunity to address them; these are often specific to the environment, the event and the individual athlete. In this paper we address the major considerations for assessing hydration status in athletes and practical solutions to overcome obstacles of a given sport. Based on these solutions, practitioners can better advise athletes to develop practices that optimize hydration for their sports.Item The potential for renal injury elicited by physical work in the heat(Nutrients, 2019-09-04) Schlader, Z. J.; Hostler, D.; Parker, M. D.; Pryor, R.; Lohr, J. W.; Johnson, B. D.; Chapman, C. L.An epidemic of chronic kidney disease (CKD) is occurring in laborers who undertake physical work in hot conditions. Rodent data indicate that heat exposure causes kidney injury, and when this injury is regularly repeated it can elicit CKD. Studies in humans demonstrate that a single bout of exercise in the heat increases biomarkers of acute kidney injury (AKI). Elevations in AKI biomarkers in this context likely reflect an increased susceptibility of the kidneys to AKI. Data largely derived from animal models indicate that the mechanism(s) by which exercise in the heat may increase the risk of AKI is multifactorial. For instance, heat-related reductions in renal blood flow may provoke heterogenous intrarenal blood flow. This can promote localized ischemia, hypoxemia and ATP depletion in renal tubular cells, which could be exacerbated by increased sodium reabsorption. Heightened fructokinase pathway activity likely exacerbates ATP depletion occurring secondary to intrarenal fructose production and hyperuricemia. Collectively, these responses can promote inflammation and oxidative stress, thereby increasing the risk of AKI. Equivalent mechanistic evidence in humans is lacking. Such an understanding could inform the development of countermeasures to safeguard the renal health of laborers who regularly engage in physical work in hot environments.Item Cardiac autonomic control in elite juvenile cyclists(Medicina Sportiva, 2011-03-02) Brown, S. J.; Raman, A.; Schlader, Z. J.; Stannard, S. R.Introduction: Frequency domain analysis of heart rate variability (HRV) may potentially identify the dominance exhibited by different branches of the autonomic nervous system. Autonomic contribution to cardio-deceleration following exercise has been studied in adults; however, no data are available for endurance trained juvenile athletes. Aim: The aim of this study was to evaluate the association between the increase in heart rate following exercise and any change in HRV frequency components in trained juveniles. Methods: A 6 min resting ECG (lead 2) was recorded from trained juvenile cyclists (23 male, 7 female, mean age 14.7 years), before (Pre) and after (Post) incremental exercise to volitional exhaustion on a stationary cycle ergometer. Each subject performed a progressive ramp protocol where power increased by 20W min-1, with initial power set at 60 W for females and 100 W for males. Oxygen uptake (VO2) was measured using breath-by-breath techniques. ECG was analysed in both time and frequency domains using commercially available software. Results: Mean VO2 max was 75.5 ml Kg-1 min-1, and mean power at VO2 max was 440 W. The R-R interval SD was lower following exercise (Pre: 86ms vs. Post: 36ms, P<0.01). Normalised high frequency HRV was lower (Pre: 36.5 vs. Post: 18.7, P<0.01) and normalised low frequency HRV was higher (Pre: 58.5 vs. Post: 75.0, P<0.01) following exercise. Conclusions: In elite juvenile athletes there were no associations between exercise-induced changes in high frequency variability and heart rate (R2=0.073). This suggests that in elite juveniles, the heart may be less sensitive to vagal influences- a suggestion further supported by the relatively high pre-exercise resting heart rates with normal high frequency variability.Item 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.Item 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.Item 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.Item 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.Item 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.Item 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.Item 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.Item 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.Item 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.Item 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.Item Sustained increases in blood pressure elicited by prolonged face cooling in humans(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2016-10-01) Schlader, Z. J.; Coleman, G. L.; Sackett, J. R.; Sarker, S.; Johnson, B. D.We tested the hypothesis that increases in blood pressure are sustained throughout 15 min of face cooling. Two independent trials were carried out. In the Face-Cooling Trial, 10 healthy adults underwent 15 min of face cooling where a 2.5-liter bag of ice water (0 ± 0°C) was placed over their cheeks, eyes, and forehead. The Sham Trial was identical except that the temperature of the water was 34 ± 1°C. Primary dependent variables were forehead temperature, mean arterial pressure, and forearm vascular resistance. The square root of the mean of successive differences in R-R interval (RMSSD) provided an index of cardiac parasympathetic activity. In the Face Cooling Trial, forehead temperature fell from 34.1 ± 0.9°C at baseline to 12.9 ± 3.3°C at the end of face cooling (P < 0.01). Mean arterial pressure increased from 83 ± 9 mmHg at baseline to 106 ± 13 mmHg at the end of face cooling (P < 0.01). RMSSD increased from 61 ± 40 ms at baseline to 165 ± 97 ms during the first 2 min of face cooling (P ≤ 0.05), but returned to baseline levels thereafter (65 ± 49 ms, P ≥ 0.46). Forearm vascular resistance increased from 18.3 ± 4.4 mmHg·ml−1·100 g tissue−1·min at baseline to 26.6 ± 4.0 mmHg·ml−1·100 g tissue−1·min at the end of face cooling (P < 0.01). There were no changes in the Sham Trial. These data indicate that increases in blood pressure are sustained throughout 15 min of face cooling, and face cooling elicits differential time-dependent parasympathetic and likely sympathetic activation.Item Face cooling increases blood pressure during central hypovolemia(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2017-11-09) Johnson, B. D.; Sackett, J. R.; Sarker, S.; Schlader, Z. J.A reduction in central blood volume can lead to cardiovascular decompensation (i.e., failure to maintain blood pressure). Cooling the forehead and cheeks using ice water raises blood pressure. Therefore, face cooling (FC) could be used to mitigate decreases in blood pressure during central hypovolemia. We tested the hypothesis that FC during central hypovolemia induced by lower-body negative pressure (LBNP) would increase blood pressure. Ten healthy participants (22 ± 2 yr, three women, seven men) completed two randomized LBNP trials on separate days. Trials began with 30 mmHg of LBNP for 6 min. Then, a 2.5-liter plastic bag of ice water (0 ± 0°C) (LBNP+FC) or thermoneutral water (34 ± 1°C) (LBNP+Sham) was placed on the forehead, eyes, and cheeks during 15 min of LBNP at 30 mmHg. Forehead temperature was lower during LBNP+FC than LBNP+Sham, with the greatest difference at 21 min of LBNP (11.1 ± 1.6 vs. 33.9 ± 1.4°C, P < 0.001). Mean arterial pressure was greater during LBNP+FC than LBNP+Sham, with the greatest difference at 8 min of LBNP (98 ± 15 vs. 80 ± 8 mmHg, P < 0.001). Cardiac output was higher during LBNP+FC than LBNP+Sham with the greatest difference at 18 min of LBNP (5.9 ± 1.4 vs. 4.9 ± 1.0 liter/min, P = 0.005). Forearm cutaneous vascular resistance was greater during LBNP+FC than LBNP+Sham, with the greatest difference at 15 min of LBNP (7.2 ± 3.4 vs. 4.9 ± 2.7 mmHg/perfusion units (PU), P < 0.001). Face cooling during LBNP increases blood pressure through increases in cardiac output and vascular resistance.Item Orderly recruitment of thermoeffectors in resting humans(American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 2018-02-01) Schlader, Z. J.; Sackett, J. R.; Sarker, S.; Johnson, B. D.The recruitment of thermoeffectors, including thermoregulatory behavior, relative to changes in body temperature has not been quantified in humans. We tested the hypothesis that changes in skin blood flow, behavior, and sweating or metabolic rate are initiated with increasing changes in mean skin temperature (Tskin) in resting humans. While wearing a water-perfused suit, 12 healthy young adults underwent heat (Heat) and cold stress (Cold) that induced gradual changes in Tskin. Subjects controlled the temperature of their dorsal neck to their perceived thermal comfort. Thus neck skin temperature provided an index of thermoregulatory behavior. Neck skin temperature (Tskin), core temperature (Tcore), metabolic rate, sweat rate, and nonglabrous skin blood flow were measured continually. Data were analyzed using segmental regression analysis, providing an index of thermoeffector activation relative to changes in Tskin. In Heat, increases in skin blood flow were observed with the smallest elevations in Tskin (P < 0.01). Thermal behavior was initiated with an increase in Tskin of 2.4 ± 1.3°C (mean ± SD, P = 0.04), while sweating was observed with further elevations in Tskin (3.4 ± 0.5°C, P = 0.04), which coincided with increases in Tcore (P = 0.98). In Cold, reductions in skin blood flow occurred with the smallest decrease in Tskin (P < 0.01). Thermal behavior was initiated with a Tskin decrease of 1.5 ± 1.3°C, while metabolic rate (P = 0.10) and Tcore (P = 0.76) did not change throughout. These data indicate that autonomic and behavioral thermoeffectors are recruited in coordination with one another and likely in an orderly manner relative to the comparative physiological cost.
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