Orderly recruitment of thermoeffectors in resting humans.

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.

Face cooling increases blood pressure during central hypovolemia.

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.

Sustained increases in blood pressure elicited by prolonged face cooling in humans.

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.

Activation of autonomic thermoeffectors preceding the decision to behaviourally thermoregulate in resting humans.

What is the central question of this study? Do increases in metabolic heat production and sweat rate precede the initiation of thermoregulatory behaviour in resting humans exposed to cool and warm environments? What is the main finding and its importance? Thermoregulatory behaviour at rest in cool and warm environments is preceded by changes in vasomotor tone in glabrous and non-glabrous skin, but not by acute increases in metabolic heat production or sweat rate. These findings suggest that sweating and shivering are not obligatory for thermal behaviour to be initiated in humans. We tested the hypothesis that acute increases in metabolic heat production and sweating precede the initiation of thermoregulatory behaviour in resting humans exposed to cool and warm environments. Twelve healthy young subjects passively moved between 17 and 40°C rooms when they felt 'too cool' (C→W) or 'too warm' (W→C). Skin and internal (intestinal) temperatures, metabolic heat production, local sweat rate (forearm and chest) and cutaneous vascular conductance (CVC; forearm and fingertip) were measured continually. Compared with pretest baseline (31.8 ± 0.3°C), skin temperature was higher at C→W (32.0 ± 0.7°C; P = 0.01) and W→C (34.5 ± 0.5°C; P < 0.01). Internal temperature did not differ (P = 0.12) between baseline (37.2 ± 0.3°C), C→W (37.2 ± 0.3°C) and W→C (37.0 ± 0.3°C). Metabolic heat production was not different from baseline (40 ± 9 W m-2 ) at C→W (39 ± 7 W m-2 ; P = 0.50). Forearm (0.06 ± 0.01 mg cm-2  min-1 ) and chest (0.04 ± 0.02 mg cm-2  min-1 ) sweat rate at W→C did not differ from baseline (forearm, 0.05 ± 0.02 mg cm-2  min-1 and chest, 0.04 ± 0.02 mg cm-2  min-1 ; P ≥ 0.23). Forearm CVC was not different from baseline (0.30 ± 0.21 perfusion units (PU) mmHg-1 ) at C→W (0.24 ± 0.11 PU mmHg-1 ; P = 0.17), but was higher at W→C (0.65 ± 0.33 PU mmHg-1 ; P < 0.01). Fingertip CVC was different from baseline (2.6 ± 2.0 PU mmHg-1 ) at C→W (0.70 ± 0.42 PU mmHg-1 ; P < 0.01) and W→C (4.49 ± 1.66 PU mmHg-1 ; P < 0.01). Thermoregulatory behaviour at rest in cool and warm environments is preceded by changes in vasomotor tone in glabrous and non-glabrous skin, but not by acute increases in metabolic heat production or sweat rate.

Behavioral thermoregulation in older adults with cardiovascular co-morbidities.

We tested the hypotheses that older adults with cardiovascular co-morbidities will demonstrate greater changes in body temperature and exaggerated changes in blood pressure before initiating thermal behavior. We studied twelve healthy younger adults (Younger, 25 ± 4 y) and six older adults ('At Risk', 67 ± 4 y) taking prescription medications for at least two of the following conditions: hypertension, type II diabetes, hypercholesterolemia. Subjects underwent a 90-min test in which they voluntarily moved between cool (18.1 ± 1.8°C, RH: 29 ± 5%) and warm (40.2 ± 0.3°C, RH: 20 ± 0%) rooms when they felt 'too cool' (C→W) or 'too warm' (W→C). Mean skin and intestinal temperatures and blood pressure were measured. Data were analyzed as a change from pretest baseline. Changes in mean skin temperature were not different between groups at C→W (Younger: +0.2 ± 0.8°C, 'At Risk': +0.7 ± 1.8°C, P = 0.51) or W→C (Younger: +2.7 ± 0.6°C, 'At Risk': +2.9 ± 1.9°C, P = 0.53). Changes in intestinal temperature were not different at C→W (Younger: 0.0 ± 0.1°C, 'At Risk': +0.1 ± 0.2, P = 0.11), but differed at W→C (-0.1 ± 0.2°C vs. +0.1 ± 0.3°C, P = 0.02). Systolic pressure at C→W increased (Younger: +10 ± 9 mmHg, 'At Risk': +24 ± 17 mmHg) and at W→C decreased (Younger: -4 ± 13 mmHg, 'At Risk': -23 ± 19 mmHg) to a greater extent in 'At Risk' (P ≤ 0.05). Differences were also apparent for diastolic pressure at C→W (Younger: -2 ± 4 mmHg, 'At Risk': +17 ± 23 mmHg, P < 0.01), but not at W→C (Younger Y: +4 ± 13 mmHg, 'At Risk': -1 ± 6 mmHg, P = 0.29). Despite little evidence for differential control of thermal behavior, the initiation of behavior in 'at risk' older adults is preceded by exaggerated blood pressure responses.

Peripheral chemosensitivity is not blunted during 2 h of thermoneutral head out water immersion in healthy men and women.

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.

Firefighter Work Duration Influences the Extent of Acute Kidney Injury.

PURPOSE: We tested the hypothesis that elevations in biomarkers of acute kidney injury are influenced by the magnitude of hyperthermia and dehydration elicited by two common firefighter work durations. METHODS: Twenty-nine healthy adults (10 females) wearing firefighter protective clothing completed two randomized trials where they walked at 4.8 km·h, 5% grade in a 38°C, 50% RH environment. In the short trial, subjects completed two 20-min exercise bouts. In the long trial (LONG), subjects completed three 20-min exercise bouts. Each exercise bout was separated by 10 min of standing rest in an ~20°C environment. Venous blood samples were obtained before and immediately after exercise, and after 1 h recovery. Dependent variables included changes in core temperature, body weight, plasma volume, serum creatinine, and plasma neutrophil gelatinase-associated lipocalin, a marker of renal tubule injury. RESULTS: Changes in core temperature (+2.0°C ± 0.7°C vs +1.1°C ± 0.4°C, P < 0.01), body weight (-0.9% ± 0.6% vs -0.5% ± 0.5%, P < 0.01), and plasma volume (-11% ± 5% vs -8% ± 6%, P < 0.01) during exercise were greater in LONG. Increases in creatinine were higher in LONG postexercise (0.18 ± 0.15 vs 0.08 ± 0.07 mg·dL, P < 0.01) and after recovery (0.21 ± 0.16 vs 0.14 ± 0.10 mg·dL, P < 0.01). Increases in neutrophil gelatinase-associated lipocalin were greater in LONG postexercise (27.0 ± 20.5 vs 12.7 ± 18.0 ng·mL, P = 0.01) and after recovery (16.9 ± 15.6 vs 1.5 ± 15.1 ng·mL, P = 0.02). CONCLUSIONS: Biomarkers of acute kidney injury are influenced by the magnitude of hyperthermia and hypovolemia elicited by exercise in the heat.

Hemodynamic responses upon the initiation of thermoregulatory behavior in young healthy adults.

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.