Browsing by Author "Schlader, Z. J."

Now showing 1 - 20 of 42

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.
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.
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.
Defining the determinants of endurance running performance in the heat
(Temperature, 2017-08-04) James, C. A.; Hayes, M.; Willmott, A. G. B.; Gibson, O. R.; Flouris, A. D.; Schlader, Z. J.; Maxwell, N. S.
In cool conditions, physiologic markers accurately predict endurance performance, but it is unclear whether thermal strain and perceived thermal strain modify the strength of these relationships. This study examined the relationships between traditional determinants of endurance performance and time to complete a 5-km time trial in the heat. Seventeen club runners completed graded exercise tests (GXT) in hot (GXTHOT; 32°C, 60% RH, 27.2°C WBGT) and cool conditions (GXTCOOL; 13°C, 50% RH, 9.3°C WBGT) to determine maximal oxygen uptake (V̇O2max), running economy (RE), velocity at V̇O2max (vV̇O2max), and running speeds corresponding to the lactate threshold (LT, 2 mmol.l−1) and lactate turnpoint (LTP, 4 mmol.l−1). Simultaneous multiple linear regression was used to predict 5 km time, using these determinants, indicating neither GXTHOT (R2 = 0.72) nor GXTCOOL (R2 = 0.86) predicted performance in the heat as strongly has previously been reported in cool conditions. vV̇O2max was the strongest individual predictor of performance, both when assessed in GXTHOT (r = −0.83) and GXTCOOL (r = −0.90). The GXTs revealed the following correlations for individual predictors in GXTHOT; V̇O2max r = −0.7, RE r = 0.36, LT r = −0.77, LTP r = −0.78 and in GXTCOOL; V̇O2max r = −0.67, RE r = 0.62, LT r = −0.79, LTP r = −0.8. These data indicate (i) GXTHOT does not predict 5 km running performance in the heat as strongly as a GXTCOOL, (ii) as in cool conditions, vV̇O2max may best predict running performance in the heat.
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.
The effect of water immersion and acute hypercapnia on ventilatory sensitivity and cerebrovascular reactivity
(Physiological Reports, 2018-10-20) Sackett, J. R.; Cruz, C.; Schlader, Z. J.; Johnson, B. D.
The partial pressure of end tidal carbon dioxide (PETCO2), ventilatory sensitivity to CO2, and cerebral perfusion are augmented during thermoneutral head out water immersion (HOWI). We tested the hypotheses that HOWI and acute hypercapnia augments minute ventilation, ventilatory sensitivity to CO2, cerebral perfusion, and cerebrovascular reactivity to CO2. Twelve subjects (age: 24 ± 3 years, BMI: 25.3 ± 2.9 kg/m2, 6 women) participated in two experimental visits: a HOWI visit (HOWI) and a matched hypercapnia visit (Dry + CO2). A rebreathing test was conducted at baseline, 10, 30, 60 min, and post HOWI and Dry + CO2. PETCO2, minute ventilation, expired gases, blood pressure, heart rate, and middle cerebral artery blood velocity were recorded continuously. PETCO2 increased throughout HOWI (baseline: 42 ± 2 mmHg; maximum at 10 min: 44 ± 2 mmHg, P ≤ 0.013) and Dry + CO2 (baseline: 42 ± 2 mmHg; maximum at 10 min: 44 ± 2 mmHg, P ≤ 0.013) and was matched between conditions (condition main effect: P = 0.494). Minute ventilation was lower during HOWI versus Dry + CO2 (maximum difference at 60 min: 13.2 ± 1.9 vs. 16.2 ± 2.7 L/min, P < 0.001). Ventilatory sensitivity to CO2 and middle cerebral artery blood velocity were greater during HOWI versus Dry + CO2 (maximum difference at 10 min: 2.60 ± 1.09 vs. 2.20 ± 1.05 L/min/mmHg, P < 0.001, and 63 ± 18 vs. 53 ± 14 cm/sec, P < 0.001 respectively). Cerebrovascular reactivity to CO2 decreased throughout HOWI and Dry + CO2 and was not different between conditions (condition main effect: P = 0.777). These data indicate that acute hypercapnia, matched to what occurs during HOWI, augments minute ventilation but not ventilatory sensitivity to CO2 or middle cerebral artery blood velocity despite an attenuated cerebrovascular reactivity to CO2.
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.
Exercise in personal protective equipment in a hot, humid environment does not affect risk propensity
(Temperature, 2016-04-08) Schlader, Z. J.; Temple, J. L.; Hostler, D.
We tested the hypothesis that heat stress created by light exertion in encapsulating personal protective equipment (PPE) in a hot, humid environment increases risk propensity. Ten healthy subjects (29 ± 7 y) completed 2 trials presented in a counter-balanced manner. Subjects donned encapsulating PPE, and in one trial they wore a tube-lined shirt underneath that was perfused with 5°C water. Subjects completed 2 15 min bouts of walking exercise on a treadmill at ˜50% maximal heart rate in a 32°C, 81% RH environment. Subjects completed the Balloon Analog Risk Task (BART), an objective measure of risk-taking, before, between the 2 exercise bouts, and following the final exercise bout. Personal cooling lowered (P < 0.01) mean skin temperature by 8.0 ± 1.6°C. Intestinal temperature rose (P < 0.01) in both trials, but was lower (P < 0.01) at the end of exercise in the cooling trial (38.0 ± 0.3°C vs. 37.6 ± 0.3°C). BART derived indices of risk propensity were not affected by trial or time (trial × time interaction: P ≥ 0.33). These data indicate that 60 min of exposure to mild heat stress created by light exertion in encapsulating PPE does not affect risk-taking behavior.
Exercise intensity independently modulates thermal behavior during exercise recovery, but not during exercise
(Journal of Applied Physiology, 2019-01-17) Vargas, N. T.; Chapman, C. L.; Johnson, B. D.; Gathercole, R.; Schlader, Z. J.
We tested the hypothesis that thermal behavior is greater during and after high- compared with moderate-intensity exercise. In a 27°C, 20% relative humidity environment, 20 participants (10 women, 10 men) cycled for 30 min at moderate [53% (SD 6) peak oxygen uptake (V̇o2peak) or high [78% (SD 6) V̇o2peak] intensity, followed by 120 min of recovery. Mean skin and core temperatures and mean skin wettedness were recorded continuously. Participants maintained thermally comfortable neck temperatures with a custom-made neck device. Neck device temperature provided an index of thermal behavior. The weighted average of mean skin and core temperatures and mean skin wettedness provided an indication of the afferent stimulus to thermally behave. Mean skin and core temperatures were greater at end-exercise in high intensity (P < 0.01). Core temperature remained elevated in high intensity until 70 min of recovery (P = 0.03). Mean skin wettedness and the afferent stimulus were greater at 10–20 min of exercise in high intensity (P ≤ 0.03) and remained elevated until 60 min of recovery (P < 0.01). Neck device temperature was lower during exercise in high versus moderate intensity (P ≤ 0.02). There was a strong relation between the afferent stimulus and neck device temperature during exercise (high: R2 = 0.82, P < 0.01; moderate: R2 = 0.95, P < 0.01) and recovery (high: R2 = 0.97, P < 0.01; moderate: R2 = 0.93, P < 0.01). During exercise, slope (P = 0.49) and y-intercept (P = 0.91) did not differ between intensities. In contrast, slope was steeper (P < 0.01) and y-intercept was higher (P < 0.01) during recovery from high-intensity exercise. Thermal behavior is greater during high-intensity exercise because of the greater stimulus to behave. The withdrawal of thermal behavior is augmented after high-intensity exercise.
Face cooling exposes cardiac parasympathetic and sympathetic dysfunction in recently concussed college athletes
(Physiological Reports, 2018-05-09) Johnson, B. D.; O'Leary, M. C.; McBryde, M.; Sackett, J. R.; Schlader, Z. J.; Leddy, J. J.
We tested the hypothesis that concussed college athletes (CA) have attenuated parasympathetic and sympathetic responses to face cooling (FC). Eleven symptomatic CA (age: 20 ± 2 years, 5 women) who were within 10 days of concussion diagnosis and 10 healthy controls (HC; age: 24 ± 4 years, 5 women) participated. During FC, a plastic bag filled with ice water (~0°C) was placed on the forehead, eyes, and cheeks for 3 min. Heart rate (ECG) and blood pressure (photoplethysmography) were averaged at baseline and every 60 sec during FC. High‐frequency (HF) power was obtained from spectral analysis of the R‐R interval. Data are presented as a change from baseline. Baseline heart rate (HC: 61 ± 12, CA: 57 ± 12 bpm; P = 0.69), mean arterial pressure (MAP) (HC: 94 ± 10, CA: 96 ± 13 mmHg; P = 0.74), and HF (HC: 2294 ± 2314, CA: 2459 ± 2058 msec2; P = 0.86) were not different between groups. Heart rate in HC decreased at 2 min (−7 ± 11 bpm; P = 0.02) but did not change in CA (P > 0.43). MAP increased at 1 min (HC: 12 ± 6, CA: 6 ± 6 mmHg), 2 min (HC: 21 ± 7, CA: 11 ± 7 mmHg), and 3 min (HC: 20 ± 6, CA: 13 ± 7 mmHg) in both groups (P < 0.01 for all) but the increase was greater at each interval in HC (P < 0.02). HF increased at 1 min (12354 ± 11489 msec2; P < 0.01) and 2 min (5832 ± 8002 msec2; P = 0.02) in HC but did not change in CA (P > 0.58). The increase in HF at 1 min was greater in HC versus CA (P < 0.01). These data indicate that symptomatic concussed patients have impaired cardiac parasympathetic and sympathetic activation.
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.
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.
Head temperature modulates thermal behavior in the cold in humans
(Temperature, 2016-04-08) Mündel, T.; Raman, A.; Schlader, Z. J.
We tested the hypothesis that skin temperature, specifically of the head, is capable of modulating thermal behavior during exercise in the cold. Following familiarization 8 young, healthy, recreationally active males completed 3 trials, each consisting of 30 minutes of self-paced cycle ergometry in 6°C. Participants were instructed to control their exercise work rate to achieve and maintain thermal comfort. On one occasion participants wore only shorts and shoes (Control) and on the 2 other occasions their head was either warmed (Warming) or cooled (Cooling). Work rate, rate of metabolic heat production, thermal perceptions, rectal, mean weighted skin and head temperatures were measured. Exercise work rate was reduced during Warming and augmented during Cooling after the first and second minutes of exercise, respectively (P ≤ 0.04), with the rate of metabolic heat production mirroring work rate. At this early stage of exercise (≤5 min) the changes over time for rectal temperature were negligible and similar (0.1 ± 0.1°C, P = 0.51), while the decrease in mean skin temperature was not different between all trials (1.7 ± 0.6°C, P = 0.13). Mean head temperature was either decreased (Control: 1.5 ± 1.1°C, Cooling: 2.9 ± 0.8°C, both P < 0.01) or increased (Warming: 1.7 ± 0.9°C, P < 0.01). Head thermal perception was warmer and more comfortable in Warming and cooler and less comfortable in Cooling (P < 0.01). Participants achieved thermal comfort similarly in all trials (P > 0.09) after 10 ± 7 min and this was maintained until the end of exercise. These results indicate that peripheral temperatures modulate thermal behavior in the cold.
Heat acclimation improves heat exercise tolerance and heat dissipation in individuals with extensive skin grafts
(Journal of Applied Physiology, 2015-07-01) Schlader, Z. J.; Ganio, M. S.; Pearson, J.; Lucas, R. A. I.; Rivas, E.
Burn survivors with extensive skin grafts have impaired heat dissipation and thus heat tolerance. This study tested the hypothesis that heat acclimation (HA) improves these factors in this population. Thirty-four burn survivors were stratified into highly [>40% body surface area (BSA) grafted, n = 15] and moderately (17-40% BSA grafted, n = 19) grafted groups. Nine healthy nonburned subjects served as controls. Subjects underwent 7 days of HA involving 90 min of exercise at ∼50% peak oxygen uptake in 40°C, 30% relative humidity. On days 1 and 7, subjects exercised in the heat at a fixed rate of metabolic heat production. Pre-HA, all controls and 18/19 subjects in the 17–40% group completed 90 min of exercise. Conversely, heat exercise tolerance was lower (P < 0.01) in the >40% group, with 7/15 subjects not completing 90 min of exercise. Post-HA, heat exercise tolerance was similar between groups (P = 0.39) as all subjects, except one, completed 90 min of exercise. Pre-HA, the magnitude of the increase in internal temperature during exercise occurred sequentially (P ≤ 0.03) according to BSA grafted (>40%: 1.6 ± 0.5°C; 17–40%: 1.2 ± 0.3°C; control: 0.9 ± 0.2°C). HA attenuated (P < 0.01) increases in internal temperature in the control (by 0.2 ± 0.3°C), 17–40% (by 0.3 ± 0.3°C), and >40% (by 0.3 ± 0.4°C) groups, the magnitude of which was similar between groups (P = 0.42). These data indicate that HA improves heat tolerance and dissipation in burn survivors with grafted skin, and the magnitude of these improvements are not influenced by the extent of skin grafting.
Hemodynamic responses upon the initiation of thermoregulatory behavior in young healthy humans
(Temperature, 2016-04-13) Schlader, Z. J.; Sarker, S.; Mündel, T.; Coleman, G.; Chapman, C. L.; Sackett, J. R.; Johnson, B. D.
We tested the hypotheses that thermoregulatory behavior is initiated before changes in blood pressure and that skin blood flow upon the initiation of behavior is reflex mediated. Ten healthy young subjects moved between 40°C and 17°C rooms when they felt ‘too warm’ (W→C) or ‘too cool’ (C→W). Blood pressure, cardiac output, skin and rectal temperatures were measured. Changes in skin blood flow between locations were not different at 2 forearm locations. One was clamped at 34°C ensuring responses were reflex controlled. The temperature of the other was not clamped ensuring responses were potentially local and/or reflex controlled. Relative to pre-test Baseline, skin temperature was not different at C→W (33.5 ± 0.7°C, P = 0.24), but was higher at W→C (36.1 ± 0.5°C, P < 0.01). Rectal temperature was different from Baseline at C→W (−0.2 ± 0.1°C, P < 0.01) and W→C (−0.2 ± 0.1°C, P < 0.01). Blood pressure was different from Baseline at C→W (+7 ± 4 mmHg, P < 0.01) and W→C (−5 ± 5 mmHg, P < 0.01). Cardiac output was not different from Baseline at C→W (−0.1 ± 0.4 L/min, P = 0.56), but higher at W→C (0.4 ± 0.4 L/min, P < 0.01). Skin blood flow between locations was not different from Baseline at C→W (clamped: −6 ± 15 PU, not clamped: −3 ± 6 PU, P = 0.46) or W→C (clamped: +21 ± 23 PU, not clamped: +29 ± 15 PU, P = 0.26). These data indicate that the initiation of thermoregulatory behavior is preceded by moderate changes in blood pressure and that skin blood flow upon the initiation of this behavior is under reflex control.