ORCID Profile
0000-0002-1731-4415
Current Organisation
Indiana University
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Publisher: American Physiological Society
Date: 10-2019
DOI: 10.1152/JAPPLPHYSIOL.00403.2019
Abstract: High environmental temperatures are associated with increased risk of acute kidney injury, which may be related to reductions in renal blood flow. The susceptibility of the kidneys may be increased because of heat stress-induced changes in renal vascular resistance (RVR) to sympathetic activation. We tested the hypotheses that, compared with normothermia, increases in RVR during the cold pressor test (CPT, a sympathoexcitatory maneuver) are attenuated during passive heating and exacerbated after cooling recovery. Twenty-four healthy adults (22 ± 2 yr 12 women, 12 men) completed CPTs at normothermic baseline, after passive heating to a rise in core temperature of ~1.2°C, and after cooling recovery when core temperature returned to ~0.2°C above normothermic baseline. Blood velocity was measured by Doppler ultrasound in the distal segment of the right renal artery (Renal, n = 24 during thermal stress, n = 12 during CPTs) or the middle portion of a segmental artery (Segmental, n = 12). RVR was calculated as mean arterial pressure ided by renal or segmental blood velocity. RVR increased at the end of CPT during normothermic baseline in both arteries (Renal: by 1.0 ± 1.0 mmHg·cm −1 ·s, Segmental: by 2.2 ± 1.2 mmHg·cm −1 ·s, P ≤ 0.03), and these increases were abolished with passive heating ( P ≥ 0.76). At the end of cooling recovery, RVR in both arteries to the CPT was restored to that of normothermic baseline ( P ≤ 0.17). These data show that increases in RVR to sympathetic activation during passive heating are attenuated and return to that of normothermic baseline after cooling recovery. NEW & NOTEWORTHY Our data indicate that increases in renal vascular resistance to the cold pressor test (i.e., sympathetic activation) are attenuated during passive heating, but at the end of cooling recovery this response returns to that of normothermic baseline. Importantly, hemodynamic responses were assessed in arteries going to (renal artery) and within (segmental artery) the kidney, which has not been previously examined in the same study during thermal and/or sympathetic stressors.
Publisher: Elsevier BV
Date: 05-2018
DOI: 10.1016/J.PHYSBEH.2018.02.001
Abstract: We tested the hypothesis that thermal behavior during the exercise recovery compensates for elevated core temperatures despite autonomic thermoeffector withdrawal. In a thermoneutral environment, 6 females and 6 males (22 ± 1 y) cycled for 60 min (225 ± 46 W metabolic heat production), followed by 60 min passive recovery. Mean skin and core temperatures, skin blood flow, and local sweat rate were measured continually. Subjects controlled the temperature of their dorsal neck to perceived thermal comfort using a custom-made neck device. Neck device temperature provided an index of thermal behavior. Mean body temperature, calculated as the average of mean skin and core temperatures, provided an index of the stimulus for thermal behavior. To isolate the independent effect of exercise on thermal behavior during recovery, data were analyzed post-exercise the exact minute mean body temperature recovered to pre-exercise levels within a subject. Mean body temperature returned to pre-exercise levels 28 ± 20 min into recovery (Pre: 33.5 ± 0.2, Post: 33.5 ± 0.2 °C, P = 0.20), at which point, mean skin temperature had recovered (Pre: 29.6 ± 0.4, Post: 29.5 ± 0.5 °C, P = 0.20) and core temperature (Pre: 37.3 ± 0.2, Post: 37.5 ± 0.3 °C, P = 0.01) remained elevated. Post-exercise, skin blood flow (Pre: 59 ± 78, Post: 26 ± 25 PU, P = 0.10) and local sweat rate (Pre: 0.05 ± 0.25, Post: 0.13 ± 0.14 mg/cm
Publisher: American Physiological Society
Date: 04-2020
DOI: 10.1152/AJPRENAL.00374.2019
Abstract: We first tested the hypothesis that consuming a high-fructose corn syrup (HFCS)-sweetened soft drink augments kidney vasoconstriction to sympathetic stimulation compared with water ( study 1). In a second study, we examined the mechanisms underlying these observations ( study 2). In study 1, 13 healthy adults completed a cold pressor test, a sympathoexcitatory maneuver, before (preconsumption) and 30 min after drinking 500 mL of decarbonated HFCS-sweetened soft drink or water (postconsumption). In study 2, venous blood s les were obtained in 12 healthy adults before and 30 min after consumption of 500 mL water or soft drinks matched for caffeine content and taste, which were either artificially sweetened (Diet trial), sucrose-sweetened (Sucrose trial), or sweetened with HFCS (HFCS trial). In both study 1 and study 2, vascular resistance was calculated as mean arterial pressure ided by blood velocity, which was measured via Doppler ultrasound in renal and segmental arteries. In study 1, HFCS consumption increased vascular resistance in the segmental artery at rest (by 0.5 ± 0.6 mmHg·cm −1 ·s −1 , P = 0.01) and during the cold pressor test (average change: 0.5 ± 1.0 mmHg·cm −1 ·s −1 , main effect: P = 0.05). In study 2, segmental artery vascular resistance increased in the HFCS trial (by 0.8 ± 0.7 mmHg·cm −1 ·s −1 , P = 0.02) but not in the other trials. Increases in serum uric acid were greater in the HFCS trial (0.3 ± 0.4 mg/dL, P ≤ 0.04) compared with the Water and Diet trials, and serum copeptin increased in the HFCS trial (by 0.8 ± 1.0 pmol/L, P = 0.06). These findings indicate that HFCS acutely increases vascular resistance in the kidneys, independent of caffeine content and beverage osmolality, which likely occurs via simultaneous elevations in circulating uric acid and vasopressin.
Publisher: American Physiological Society
Date: 11-2018
DOI: 10.1152/AJPREGU.00178.2018
Abstract: We tested the hypothesis that mean skin wettedness contributes to thermal behavior to a greater extent than core and mean skin temperatures. In a 27.0 ± 1.0°C environment, 16 young participants (8 females) cycled for 30 min at 281 ± 51 W·m 2 , followed by 120 min of seated recovery. Mean skin and core temperatures and mean skin wettedness were recorded continuously. Participants maintained a thermally comfortable neck temperature throughout the protocol using a custom-made device. Neck device temperature provided an index of thermal behavior. Linear regression was performed using in idual minute data with mean skin wettedness and core and mean skin temperatures as independent variables and neck device temperature as the dependent variable. Standarized β-coefficients were used to determine relative contributions to thermal behavior. Mean skin temperature differed from preexercise (32.6 ± 0.5°C) to 10 min into exercise (32.3 ± 0.6°C, P 0.01). Core temperature increased from 37.1 ± 0.3°C preexercise to 37.7 ± 0.4°C by end exercise ( P 0.01) and remained elevated through 30 min of recovery (37.2 ± 0.3°C, P 0.01). Mean skin wettedness increased from preexercise [0.14 ± 0.03 arbitrary units (AU)] to 20 min into exercise (0.43 ± 0.09 AU, P 0.01) and remained elevated through 80 min of recovery (0.18 ± 0.06 AU, P ≤ 0.05). Neck device temperature decreased from 26.4 ± 1.6°C preexercise to 18.5 ± 8.7°C 10 min into exercise ( P = 0.03) and remained depressed through 20 min of recovery (14.4 ± 11.2°C, P 0.01). Mean skin wettedness (52 ± 24%) provided a greater contribution to thermal behavior compared with core (22 ± 22%, P = 0.06) and mean skin (26 ± 16%, P = 0.04) temperatures. Skin wettedness is an important contributing factor to thermal behavior during exercise and recovery.
Publisher: Elsevier BV
Date: 04-2021
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 2019
DOI: 10.1249/MSS.0000000000001756
Abstract: This study tested the hypothesis that females rely on thermal behavior to a greater extent during and after exercise, relative to males. In a 24°C ± 1°C (45% ± 10% RH) environment, 10 males (M) and 10 females (F) (22 ± 2 yr) cycled for 60 min (metabolic heat production: M, 117 ± 18 W·m −2 F, 129 ± 21 W·m −2 ), followed by 60-min recovery. Mean skin and core temperatures, skin blood flow and local sweat rates were measured continually. Subjects controlled the temperature of their dorsal neck to perceived thermal comfort using a custom-made device. Neck device temperature provided an index of thermal behavior and mean body temperature provided an index of the stimulus for thermal behavior. Data were analyzed for total area under the curve for exercise and recovery time points. To further isolate the effect of exercise on thermal behavior during recovery, data were also analyzed the minute mean body temperature returned to preexercise levels within a subject. There were no sex differences in metabolic heat production ( P = 0.71) or body temperatures ( P ≥ 0.10) during exercise. Area under the curve for neck device temperature during exercise was greater for F (−98.4°C·min −1 ± 33.6°C·min −1 vs −64.5°C·min −1 ± 47.8°C·min −1 , P = 0.04), but did not differ during recovery (F, 86.8°C·min −1 ± 37.8°C·min −1 M, 65.6°C·min −1 ± 35.9°C·min −1 P = 0.11). In M, mean skin ( P = 0.90), core ( P = 0.70) and neck device ( P = 0.99) temperatures had recovered by the time that mean body temperature had returned to preexercise levels. However, in F, neck device temperature ( P = 0.04) was reduced while core temperature remained elevated ( P 0.01). Females use thermal behavior during exercise to a greater extent than M. During recovery, thermal behavior may compensate for elevated core temperatures in F despite mean body temperatures returning to preexercise levels.
Publisher: Frontiers Media SA
Date: 10-01-2019
Publisher: MDPI AG
Date: 18-12-2019
Abstract: We tested the hypothesis that thermal behavior alleviates thermal discomfort and accelerates core temperature recovery following low intensity exercise. Methods: In a 27 ± 0 °C, 48 ± 6% relative humidity environment, 12 healthy subjects (six females) completed 60 min of exercise followed by 90 min of seated recovery on two occasions. Subjects wore a suit top perfusing 34 ± 0 °C water during exercise. In the control trial, this water continually perfused throughout recovery. In the behavior trial, the upper body was maintained thermally comfortable by pressing a button to receive cool water (3 ± 2 °C) perfusing through the top for 2 min per button press. Results: Physiological variables (core temperature, p ≥ 0.18 mean skin temperature, p = 0.99 skin wettedness, p ≥ 0.09 forearm skin blood flow, p = 0.29 and local axilla sweat rate, p = 0.99) did not differ between trials during exercise. Following exercise, mean skin temperature decreased in the behavior trial in the first 10 min (by −0.5 ± 0.7 °C, p 0.01) and upper body skin temperature was reduced until 70 min into recovery (by 1.8 ± 1.4 °C, p 0.05). Core temperature recovered to pre-exercise levels 17 ± 31 min faster (p = 0.02) in the behavior trial. There were no differences in skin blood flow or local sweat rate between conditions during recovery (p ≥ 0.05). Whole-body thermal discomfort was reduced (by −0.4 ± 0.5 a.u.) in the behavior trial compared to the control trial within the first 20 min of recovery (p ≤ 0.02). Thermal behavior via upper body cooling resulted in augmented cumulative heat loss within the first 30 min of recovery (Behavior: 288 ± 92 kJ Control: 160 ± 44 kJ, p = 0.02). Conclusions: Engaging in thermal behavior that results in large reductions in mean skin temperature following exercise accelerates the recovery of core temperature and alleviates thermal discomfort by promoting heat loss.
Publisher: American Physiological Society
Date: 05-2020
Publisher: American Physiological Society
Date: 10-2019
DOI: 10.1152/JAPPLPHYSIOL.00379.2019
Abstract: We tested the hypothesis that thermal behavior resulting in reductions in mean skin temperature alleviates thermal discomfort and mitigates the rise in core temperature during light-intensity exercise. In a 27 ± 0°C, 48 ± 6% relative humidity environment, 12 healthy subjects (6 men, 6 women) completed 60 min of recumbent cycling. In both trials, subjects wore a water-perfused suit top continually perfusing 34 ± 0°C water. In the behavior trial, subjects maintained their upper body thermally comfortable by pressing a button to perfuse cool water (2.2 ± 0.5°C) through the top for 2 min per button press. Metabolic heat production (control: 404 ± 52 W, behavior: 397 ± 65 W P = 0.44) was similar between trials. Mean skin temperature was reduced in the behavior trial (by −2.1 ± 1.8°C, P 0.01) because of voluntary reductions in water-perfused top temperature ( P 0.01). Whole body ( P = 0.02) and local sweat rates were lower in the behavior trial ( P ≤ 0.05). Absolute core temperature was similar ( P ≥ 0.30) however, the change in core temperature was greater in the behavior trial after 40 min of exercise ( P ≤ 0.03). Partitional calorimetry did not reveal any differences in cumulative heat storage (control: 554 ± 229, behavior: 544 ± 283 kJ P = 0.90). Thermal behavior alleviated whole body thermal discomfort during exercise (by −1.17 ± 0.40 arbitrary units, P 0.01). Despite lower evaporative cooling in the behavior trial, similar heat loss was achieved by voluntarily employing convective cooling. Therefore, thermal behavior resulting in large reductions in skin temperature is effective at alleviating thermal discomfort during exercise without affecting whole body heat loss. NEW & NOTEWORTHY This study aimed to determine the effectiveness of thermal behavior in maintaining thermal comfort during exercise by allowing subjects to voluntarily cool their torso and upper limbs with 2°C water throughout a light-intensity exercise protocol. We show that voluntary cooling of the upper body alleviates thermal discomfort while maintaining heat balance through convective rather than evaporative means of heat loss.
Publisher: American Physiological Society
Date: 04-2020
DOI: 10.1152/JAPPLPHYSIOL.00787.2019
Abstract: Occupational heat stress increases the risk of acute kidney injury (AKI) and kidney disease. This study tested the hypothesis that attenuating the magnitude of hyperthermia (i.e., increase in core temperature) and/or dehydration during prolonged physical work in the heat attenuates increases in AKI biomarkers. Thirteen healthy adults (3 women, 23 ± 2 yr) exercised for 2 h in a 39.7 ± 0.6°C, 32 ± 3% relative-humidity environmental chamber. In four trials, subjects received water to remain euhydrated ( Water), continuous upper-body cooling ( Cooling), a combination of both ( Water + Cooling), or no intervention ( Control). The magnitude of hyperthermia (increased core temperature of 1.9 ± 0.3°C P 0.01) and dehydration (percent loss of body mass of −2.4 ± 0.5% P 0.01) were greatest in the Control group. There were greater increases in the urinary biomarkers of AKI in the Control trial: albumin (increase of 13 ± 11 μg/mL P ≤ 0.05 compared with other trials), neutrophil gelatinase-associated lipocalin (NGAL) (increase of 16 ± 14 ng/dL, P ≤ 0.05 compared with Cooling and Water + Cooling groups), and insulin-like growth factor-binding protein 7 (IGFBP7) (increase of 227 ± 190 ng/mL P ≤ 0.05 compared with other trials). Increases in IGFBP7 in the Control trial persisted after correcting for urine production/concentration. There were no differences in the AKI biomarker tissue inhibitor of metalloproteinase 2 (TIMP-2) between trials ( P ≥ 0.11). Our findings indicate that the risk of AKI is highest with greater magnitudes of hyperthermia and dehydration during physical work in the heat. Additionally, the differential findings between IGFBP7 (preferentially secreted in proximal tubules) and TIMP-2 (distal tubules) suggest the proximal tubules as the location of potential renal injury. NEW & NOTEWORTHY We demonstrate that the risk for acute kidney injury (AKI) is higher in humans with greater magnitudes of hyperthermia and dehydration during physical work in the heat and that alleviating the hyperthermia and/or limiting dehydration equally reduce the risk of AKI. The biomarker panel employed in this study suggests the proximal tubules as the location of potential renal injury.
Publisher: American Physiological Society
Date: 04-2019
DOI: 10.1152/JAPPLPHYSIOL.00992.2018
Abstract: 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 (V̇o 2peak ) or high [78% (SD 6) V̇o 2peak ] 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: R 2 = 0.82, P 0.01 moderate: R 2 = 0.95, P 0.01) and recovery (high: R 2 = 0.97, P 0.01 moderate: R 2 = 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. NEW & NOTEWORTHY This is the first study to determine the effects of exercise intensity on thermal behavior. We show that exercise intensity does not independently modulate thermal behavior during exercise but is dependent on the magnitude of afferent stimuli. In contrast, the withdrawal of thermal behavior after high-intensity exercise is augmented. This may be a consequence of an attenuated perceptual response to afferent stimuli, which may be due to processes underlying postexercise hypoalgesia.
Publisher: Elsevier BV
Date: 10-2018
DOI: 10.1016/J.PHYSBEH.2018.07.009
Abstract: We tested the hypothesis that the motivation to behaviorally thermoregulate in humans is dependent on the magnitude of changes in mean skin temperature. Ten healthy subjects (22 ± 3 y, 5 females) underwent 60 min of seated rest in a 32±1 °C or 42±1 °C environment (20% relative humidity). Trials were completed in a counterbalanced order. The motivation to behaviorally thermoregulate was measured using an operant behavior task on a fixed ratio schedule, in which subjects received thermal reinforcement after clicking a button 100 times. The reinforcer was 30 s of cooling on the dorsal aspect of the neck. The motivation to behave was defined as the cumulative number of button clicks over time and behavioral thermoregulation was defined as the change in neck skin temperature. Mean skin temperature was higher throughout the 42 °C versus the 32 °C trial (at 60 min: 36.3±0.5 °C vs. 34.5±0.5 °C, P < .01) and core temperature became higher in this trial 40 min into heat exposure (at 60 min: 37.2±0.2 °C vs. 37.1±0.1 °C, P ≤ .04), but did not differ from pre- heat exposure (P = .81). Neck skin temperature was lower in the 42 °C compared to the 32 °C trial starting at 30 min (33.7±0.8 °C vs. 35.3±0.5°C, P < .01), which was maintained thereafter (P ≤ .04). Cumulative responding for thermal reinforcement was greater in the 42 °C trial compared to the 32 °C trial at 20 min (180±155 clicks vs. 0±0 clicks, P < .01), which persisted thereafter (P < .01). These data indicate that the motivation to behaviorally thermoregulate during passive heat exposure in humans is dependent on the magnitude of increases in skin temperature.
Publisher: Wiley
Date: 27-05-2020
DOI: 10.1113/JP279537
Location: United States of America
No related grants have been discovered for Blair Johnson.