Browsing by Author "Johnson, B. D."

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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.
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.
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.
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.
Peripheral chemosensitivity is not blunted during two hours of head out water immersion in healthy men and women
(Physiological Reports, 2017-10-19) Sackett, J. R.; Schlader, Z. J.; Sarker, S.; Chapman, C. L.; Johnson, B. D.
Carbon dioxide (CO2) retention occurs during water immersion, but it is not known if peripheral chemosensitivity is altered during water immersion, which could contribute to CO2 retention. We tested the hypothesis that peripheral chemosensitivity to hypercapnia and hypoxia is blunted during 2 h of thermoneutral head out water immersion (HOWI) in healthy young adults. Peripheral chemosensitivity was assessed by the ventilatory, heart rate, and blood pressure responses to hypercapnia and hypoxia at baseline, 10, 60, 120 min, and post HOWI and a time‐control visit (control). Subjects inhaled 1 breath of 13% CO2, 21% O2, and 66% N2 to test peripheral chemosensitivity to hypercapnia and 2–6 breaths of 100% N2 to test peripheral chemosensitivity to hypoxia. Each gas was administered four separate times at each time point. Partial pressure of end‐tidal CO2 (PETCO2), arterial oxygen saturation (SpO2), ventilation, heart rate, and blood pressure were recorded continuously. Ventilation was higher during HOWI versus control at post (P = 0.037). PETCO2 was higher during HOWI versus control at 10 min (46 ± 2 vs. 44 ± 2 mmHg), 60 min (46 ± 2 vs. 44 ± 2 mmHg), and 120 min (46 ± 3 vs. 43 ± 3 mmHg) (all P < 0.001). Ventilatory (P = 0.898), heart rate (P = 0.760), and blood pressure (P = 0.092) responses to hypercapnia were not different during HOWI versus control at any time point. Ventilatory (P = 0.714), heart rate (P = 0.258), and blood pressure (P = 0.051) responses to hypoxia were not different during HOWI versus control at any time point. These data indicate that CO2 retention occurs during thermoneutral HOWI despite no changes in peripheral chemosensitivity.
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.
Renal and segmental artery hemodynamics during whole-body passive heating and cooling recovery
(Journal of Applied Physiology, 2019-08-15) Chapman, C. L.; Benati, J. M.; Johnson, B. D.; Vargas, N. T.; Lema, P. C.; Schlader, Z. J.
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 divided 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.
Renal hemodynamics during sympathetic activation following aerobic and anaerobic exercise
(Frontiers in Physiology, 2019-01-10) Schlader, Z. J.; Chapman, C. L.; Benati, J. M.; Gideon, E. A.; Vargas, N. T.; Lema, P. C.; Johnson, B. D.
We tested the hypotheses that prior aerobic (Study 1) or anaerobic (Study 2) exercise attenuates the increase in renal vascular resistance (RVR) during sympathetic stimulation. Ten healthy young adults (5 females) participated in both Study 1 (aerobic exercise) and Study 2 (anaerobic exercise). In Study 1, subjects completed three minutes of face cooling pre- and post- 30 min of moderate intensity aerobic exercise (68 ± 1% estimate maximal heart rate). In Study 2, subjects completed two minutes of the cold pressor test pre- and post- the completion of a 30 s maximal effort cycling test (Wingate Anaerobic Test). Both face cooling and the cold pressor test stimulate the sympathetic nervous system and elevate RVR. The primary dependent variable in both Studies was renal blood velocity, which was measured at baseline and every minute during sympathetic stimulation. Renal blood velocity was measured via the coronal approach at the distal segment of the right renal artery with pulsed wave Doppler ultrasound. RVR was calculated from the quotient of mean arterial pressure and renal blood velocity. In Study 1, renal blood velocity and RVR did not differ between pre- and post- aerobic exercise (P ≥ 0.24). Face cooling decreased renal blood velocity (P < 0.01) and the magnitude of this decrease did not differ between pre- and post- aerobic exercise (P = 0.52). RVR increased with face cooling (P < 0.01) and the extent of these increases did not differ between pre- and post- aerobic exercise (P = 0.74). In Study 2, renal blood velocity was 2 ± 2 cm/s lower post- anaerobic exercise (P = 0.02), but RVR did not differ (P = 0.08). The cold pressor test decreased renal blood velocity (P < 0.01) and the magnitude of this decrease did not differ between pre- and post- anaerobic exercise (P = 0.26). RVR increased with the cold pressor test (P < 0.01) and the extent of these increases did not differ between pre- and post- anaerobic exercise (P = 0.12). These data indicate that 30 min of moderate intensity aerobic exercise or 30 s of maximal effort anaerobic exercise does not affect the capacity to increase RVR during sympathetic stimulation following exercise.
Skin wettedness is an important contributor to thermal behavior during exercise and recovery
(American Journal of Physiology, 2018-08-22) Vargas, N. T.; Chapman, C. L.; Johnson, B. D.; Gathercole, R.; Schlader, Z. J.
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·m2, 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 individual 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.
Soft drink consumption during and following exercise in the heat elevates biomarkers of acute kidney injury
(American Journal of Physiology, 2019-02-21) Chapman, C. L.; Johnson, B. D.; Sackett, J. R.; Parker, M. D.; Schlader, Z. J.
The purpose of this study was to test the hypothesis that consuming a soft drink (i.e., a high-fructose, caffeinated beverage) during and following exercise in the heat elevates biomarkers of acute kidney injury (AKI) in humans. Twelve healthy adults drank 2 liters of an assigned beverage during 4 h of exercise in the heat [35.1 (0.1)°C, 61 (5)% relative humidity] in counterbalanced soft drink and water trials, and ≥1 liter of the same beverage after leaving the laboratory. Stage 1 AKI (i.e., increased serum creatinine ≥0.30 mg/dl) was detected at postexercise in 75% of participants in the Soft Drink trial compared with 8% in Water trial (P = 0.02). Furthermore, urinary neutrophil gelatinase-associated lipocalin (NGAL), a biomarker of AKI, was higher during an overnight collection period after the Soft Drink trial compared with Water in both absolute concentration [6 (4) ng/dl vs. 5 (4) ng/dl, P < 0.04] and after correcting for urine flow rate [6 (7) (ng/dl)/(ml/min) vs. 4 (4) (ng/dl)/(ml/min), P = 0.03]. Changes in serum uric acid from preexercise were greater in the Soft Drink trial than the Water trial at postexercise (P < 0.01) and 24 h (P = 0.05). There were greater increases from preexercise in serum copeptin, a stable marker of vasopressin, at postexercise in the Soft Drink trial (P < 0.02) than the Water trial. These findings indicate that consuming a soft drink during and following exercise in the heat induces AKI, likely via vasopressin-mediated mechanisms.
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.
Thermal behavior alleviates thermal discomfort during steady-state exercise without affecting whole-body heat loss
(Journal of Applied Physiology, 2019-10-11) Vargas, N. T.; Chapman, C. L.; Johnson, B. D.; Gathercole, R.; Cramer, M. N.; Schlader, Z. J.
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.