Activation of cardiac parasympathetic and sympathetic activity occurs at different skin temperatures during face cooling.

Sufficiently cold-water temperatures (<7°C) are needed to elicit the sympathetic response to the cold pressor test using the hand. However, it is not known if stimulating the trigeminal nerve via face cooling, which increases both sympathetic and cardiac parasympathetic activity, also has a threshold temperature. We tested the hypothesis that peak autonomic activation during a progressive face cooling challenge would be achieved when the stimulus temperature is ≤7°C. Twelve healthy participants (age: 25 ± 3 yr, four women) completed our study. Six pliable bags, each containing water or an ice slurry (34°C, 28°C, 21°C, 14°C, 7°C, and 0°C) were applied sequentially to participants' forehead, eyes, and cheeks for 5 min each. Mean arterial pressure (photoplethysmography; index of sympathetic activity) and heart rhythm (3-lead ECG) were averaged in 1-min increments at the end of baseline and throughout each temperature condition. Heart rate variability in the time [(root mean square of successive differences (RMSSD)] and frequency [high-frequency (HF) power] domains was used to estimate cardiac parasympathetic activity. Data are presented as the increase from baseline ± SD. Mean arterial pressure only increased from baseline in the 7°C (13.1 ± 10.3 mmHg; P = 0.018) and 0°C (25.2 ± 7.8 mmHg; P < 0.001) conditions. Only the 0°C condition increased RMSSD (160.6 ± 208.9 ms; P = 0.009) and HF power (11,450 ± 14,555 ms2; P = 0.014) from baseline. Our data indicate that peak increases in sympathetic activity during face cooling are initiated at a higher forehead skin temperature than peak increases in cardiac parasympathetic activity.

The influence of the CYP1A2-163 C>A polymorphism on the hemostatic response to exercise following caffeine supplementation.

BACKGROUND: Prior work from our group suggests that caffeine increases thrombotic potential after acute exercise. The aim of this study was to determine if hemostatic responses to exercise affected by caffeine are influenced by the CYP1A2-163 C>A polymorphism. METHODS: Forty-two healthy men performed two trials in which a graded maximal exercise test was completed one hour after consuming either 6 mg/kg of caffeine or placebo. Subjects were categorized as possessing the C allele (N.=21) or being homozygous for the A allele (N.=21). RESULTS: Factor VIII increased more (265%) during exercise in the caffeinated condition than the placebo condition (178%) (P<0.05). Tissue plasminogen activator (tPA) activity also increased more following caffeine as compared to placebo (increase of 8.70±4.32 IU/mL vs. 6.77±3.79 IU/mL respectively, P<0.05). There was no treatment × genotype or treatment × time × genotype interactions. CONCLUSIONS: Although caffeine increases factor VIII and tPA responses to maximal exercise, these changes are not influenced by the CYP1A2-163 C>A polymorphism.

Preliminary Evidence of Orthostatic Intolerance and Altered Cerebral Vascular Control Following Sport-Related Concussion.

Concussions have been shown to result in autonomic dysfunction and altered cerebral vascular function. We tested the hypothesis that concussed athletes (CA) would have altered cerebral vascular function during acute decreases and increases in blood pressure compared to healthy controls (HC). Ten CA (age: 20 ± 2 y, 7 females) and 10 HC (age: 21 ± 2 y, 6 females) completed 5 min of lower body negative pressure (LBNP; -40 mmHg) and 5 min of lower body positive pressure (LBPP; 20 mmHg). Protocols were randomized and separated by 10 min. Mean arterial pressure (MAP) and middle cerebral artery blood velocity (MCAv) were continuously recorded. Cerebral vascular resistance (CVR) was calculated as MAP/MCAv. Values are reported as change from baseline to the last minute achieved (LBNP) or 5 min (LBPP). There were no differences in baseline values between groups. During LBNP, there were no differences in the change for MAP (CA: -23 ± 18 vs. HC: -21 ± 17 cm/s; P = 0.80) or MCAv (CA: -13 ± 8 vs. HC: -18 ± 9 cm/s; P = 0.19). The change in CVR was different between groups (CA: -0.08 ± 0.26 vs. HC: 0.18 ± 0.24 mmHg/cm/s; P = 0.04). Total LBNP time was lower for CA (204 ± 92 s) vs. HC (297 ± 64 s; P = 0.04). During LBPP, the change in MAP was not different between groups (CA: 13 ± 6 vs. HC: 10 ± 7 mmHg; P = 0.32). The change in MCAv (CA: 7 ± 6 vs. HC: -4 ± 13 cm/s; P = 0.04) and CVR (CA: -0.06 ± 0.27 vs. HC: 0.38 ± 0.41 mmHg/cm/s; P = 0.03) were different between groups. CA exhibited impaired tolerance to LBNP and had a different cerebral vascular response to LBPP compared to HC.

Hemostatic Adaptations to High Intensity Interval Training in Healthy Adult Men.

Regular exercise is theorized to reduce cardiovascular risk by attenuating coagulation and augmenting fibrinolysis. However, these adaptations have not been consistently observed during traditional exercise programs. The purpose of this study was to examine hemostatic adaptations in healthy men following four (4W) and eight (8W) weeks of high intensity interval training. Twenty-one men (age=25±1 y; body mass index=26.5±6.4 kg/m2) completed eight weeks, three days/week of high intensity interval training on a cycle ergometer. Activated partial thromboplastin time, prothrombin time, and plasma concentrations of thrombin-antithrombin III, fibrinogen, tissue plasminogen activator, and plasminogen activator inhibitor-1 were assessed at baseline (BL), 4W, and 8W. Repeated measures ANOVA were used to determine potential effects of training. There were no significant changes observed for activated partial thromboplastin time (BL=43.3±5.5, 4W=43.2±5.1, 8W=44.2±6.4 s); prothrombin time (BL=13.2±0.9, 4W=13.0±0.6, 8W=13.1±0.8 s); thrombin-antithrombin III (BL=6.0±2.3, 4W=5.8±2.3, 8W=5.6±3.1 ng/mL); tissue plasminogen activator (BL=9.7±3.3, 4W=9.4±3.2, 8W=8.7±2.8 ng/mL); and plasminogen activator inhibitor-1 (BL=19.0±17.5, 4W=19.3±17.0, 8W=18.9±18.9 ng/mL) (all p>0.05). Fibrinogen was significantly lower at 4W (238.6±70.3 mg/dL) compared to BL (285.0±82.1 mg/dL; p<0.05) and 8W (285.3±83.2 mg/dL; p<0.05). These findings indicate that eight weeks of high intensity interval training does not influence coagulation potential and/or stimulate fibrinolysis.

Attenuated Cardiovascular Responses to the Cold Pressor Test in Concussed Collegiate Athletes.

CONTEXT: Cardiovascular responses to the cold pressor test (CPT) provide information regarding sympathetic function. OBJECTIVE: To determine if recently concussed collegiate athletes had blunted cardiovascular responses during the CPT. DESIGN: Cross-sectional study. SETTING: Laboratory. PATIENTS OR OTHER PARTICIPANTS: A total of 10 symptomatic concussed collegiate athletes (5 men, 5 women; age = 20 ± 2 years) who were within 7 days of diagnosis and 10 healthy control individuals (5 men, 5 women; age = 24 ± 4 years). INTERVENTION(S): The participants' right hands were submerged in agitated ice water for 120 seconds (CPT). MAIN OUTCOME MEASURE(S): Heart rate and blood pressure were continuously measured and averaged at baseline and every 30 seconds during the CPT. RESULTS: Baseline heart rate and mean arterial pressure were not different between groups. Heart rate increased throughout 90 seconds of the CPT (peak increase at 60 seconds = 16 ± 13 beats/min; P < .001) in healthy control participants but remained unchanged in concussed athletes (peak increase at 60 seconds = 7 ± 10 beats/min; P = .08). We observed no differences between groups for the heart rate response (P > .28). Mean arterial pressure was elevated throughout the CPT starting at 30 seconds (5 ± 7 mm Hg; P = .048) in healthy control individuals (peak increase at 120 seconds = 26 ± 9 mm Hg; P < .001). Mean arterial pressure increased in concussed athletes at 90 seconds (8 ± 8 mm Hg; P = .003) and 120 seconds (12 ± 8 mm Hg; P < .001). Healthy control participants had a greater increase in mean arterial pressure starting at 60 seconds (P < .001) and throughout the CPT than concussed athletes (peak difference at 90 seconds = 25 ± 10 mm Hg and 8 ± 8 mm Hg, respectively; P < .001). CONCLUSIONS: Recently concussed athletes had blunted cardiovascular responses to the CPT, which indicated sympathetic dysfunction.

Soft drink consumption during and following exercise in the heat elevates biomarkers of acute kidney injury.

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.

Caffeine Augments the Prothrombotic but Not the Fibrinolytic Response to Exercise.

Caffeine, a popular ergogenic supplement, induces neural and vascular changes that may influence coagulation and/or fibrinolysis at rest and during exercise. PURPOSE: The purpose of this study was to assess the effect of a single dose of caffeine on measures of coagulation and fibrinolysis before and after a single bout of high-intensity exercise. METHODS: Forty-eight men (age, 23 ± 3 yr; body mass index, 24 ± 3 kg·m) completed two trials, with 6 mg·kg of caffeine (CAFF) or placebo (PLAC), in random order, followed by a maximal cycle ergometer test. Plasma concentrations of fibrinogen, factor VIII antigen, active tissue plasminogen activator (tPA:c), tissue plasminogen activator antigen (tPA:g), and active plasminogen activator inhibitor-1 (PAI-1:c) were assessed at baseline and immediately after exercise. RESULTS: Exercise led to significant changes in tPA:c (Δ 8.5 ± 4.36 IU·mL for CAFF, 6.6 ± 3.7 for PLAC), tPA:g (Δ 2.4 ± 3.2 ng·mL for CAFF, 1.9 ± 3.1 for PLAC), fibrinogen (Δ 30.6 ± 61.4 mg·dL for CAFF, 28.1 ± 66.4 for PLAC), and PAI-1:c (Δ -3.4 ± 7.9 IU·mL for CAFF, -4.0 ± 12.0 for PLAC) (all P < 0.05), but no effect of condition or time-condition interactions were observed. Main effects of time, condition, and a significant time-condition interaction were observed for factor VIII, which increased from 1.0 ± 0.4 IU·mL to 3.3 ± 1.3 IU·mL with CAFF and 1.0 ± 0.4 IU·mL to 2.4 ± 0.9 IU·mL with PLAC. CONCLUSIONS: Coagulation potential during exercise is augmented after caffeine intake, without a similar increase in fibrinolysis. These results suggest caffeine intake may increase risk of a thrombotic event during exercise.

Thermal Behavior Differs between Males and Females during Exercise and Recovery.

INTRODUCTION: This study tested the hypothesis that females rely on thermal behavior to a greater extent during and after exercise, relative to males. METHODS: 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; F, 129 ± 21 W·m), 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. RESULTS: 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 ± 33.6°C·min vs -64.5°C·min ± 47.8°C·min, P = 0.04), but did not differ during recovery (F, 86.8°C·min ± 37.8°C·min; M, 65.6°C·min ± 35.9°C·min; 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). CONCLUSIONS: 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.

The effect of water immersion and acute hypercapnia on ventilatory sensitivity and cerebrovascular reactivity.

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 .

Face cooling exposes cardiac parasympathetic and sympathetic dysfunction in recently concussed college athletes.

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.

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.

Central chemosensitivity is augmented during 2 h of thermoneutral head-out water immersion in healthy men and women.

NEW FINDINGS: What is the central question of the study? Is central chemosensitivity blunted during thermoneutral head-out water immersion in healthy humans? What is the main finding and its importance? Central chemosensitivity is augmented during thermoneutral head-out water immersion in healthy men and women. Thus, we suggest that the central chemoreceptors do not contribute to CO2 retention during head-out water immersion. ABSTRACT: Carbon dioxide retention occurs during water immersion. Therefore, we tested the hypothesis that central chemosensitivity to hypercapnia is blunted during 2 h of thermoneutral head-out water immersion (HOWI) in healthy young adults. Twenty-six participants (age 22 ± 2 years; body mass index 24 ± 3 kg m-2 ; 14 women) participated in two experimental visits: a HOWI visit (HOWI) and a dry time-control visit (Control). Central chemosensitivity was assessed via a rebreathing test at baseline, 10, 60, 90 and 120 min and after HOWI and Control. End-tidal CO2 tension (P ET ,CO2), minute ventilation, blood pressure and heart rate were recorded continuously. The P ET ,CO2 increased from baseline throughout HOWI (peak increase at 120 min 2 ± 2 mmHg; P < 0.001), and the change in P ET ,CO2 was greater throughout HOWI than Control (P < 0.001). The change in minute and alveolar ventilation was not different throughout time (P ≥ 0.173) or between conditions (P ≥ 0.052). Central chemosensitivity was greater than at baseline throughout HOWI (peak increase 0.74 ± 1.01 l min-1  mmHg-1 at 120 min; P < 0.001), and the change in central chemosensitivity was greater throughout HOWI than Control (P  ≤  0.006). We also divided the cohort into tertiles based on baseline central chemosensitivity (i.e. Low, Intermediate and High) and compared Low versus High during HOWI. Low demonstrated an increase in P ET ,CO2 starting at 10 min (2 ± 3 mmHg; P < 0.001), whereas High did not exhibit an increase in P ET ,CO2 until 60 min (2 ± 2 mmHg; P = 0.018). These data indicate that CO2 retention occurs throughout HOWI despite augmented central chemosensitivity and that having a high baseline central chemosensitivity might delay the onset of CO2 retention.

Thermal behavior remains engaged following exercise despite autonomic thermoeffector withdrawal.

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 ±â€¯1 y) cycled for 60 min (225 ±â€¯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 ±â€¯20 min into recovery (Pre: 33.5 ±â€¯0.2, Post: 33.5 ±â€¯0.2 °C, P = 0.20), at which point, mean skin temperature had recovered (Pre: 29.6 ±â€¯0.4, Post: 29.5 ±â€¯0.5 °C, P = 0.20) and core temperature (Pre: 37.3 ±â€¯0.2, Post: 37.5 ±â€¯0.3 °C, P = 0.01) remained elevated. Post-exercise, skin blood flow (Pre: 59 ±â€¯78, Post: 26 ± 25 PU, P = 0.10) and local sweat rate (Pre: 0.05 ±â€¯0.25, Post: 0.13 ±â€¯0.14 mg/cm2 min-1, P = 0.09) returned to pre-exercise levels, while neck device temperature was depressed (Pre: 27.4 ±â€¯1.1, Post: 21.6 ±â€¯7.4 °C, P = 0.03). These findings suggest that thermal behavior compensates for autonomic thermoeffector withdrawal in the presence of elevated core temperatures post-exercise.

Face cooling reveals a relative inability to increase cardiac parasympathetic activation during passive heat stress.

NEW FINDINGS: What is the central question of this study? Does passive heat stress attenuate the increase in cardiac parasympathetic stimulation, vascular resistance and blood pressure evoked by face cooling? What is the main finding and its importance? Passive heat stress attenuates the capacity to increase cardiac parasympathetic activation and impairs the ability to increase vascular resistance during sympathoexcitation, which ultimately results in a relative inability to increase blood pressure. These findings cast doubt on the efficacy of face cooling at augmenting blood pressure during orthostasis while heat stressed. ABSTRACT: We tested the hypothesis that passive heat stress attenuates the increase in cardiac parasympathetic stimulation, vascular resistance and blood pressure evoked by face cooling. During normothermia and when intestinal temperature was elevated by 1.0 ± 0.2°C, 10 healthy young adults underwent 3 min of face cooling. Face cooling was accomplished by placing a 2.5 litre bag of ice water (0 ± 0°C) over the cheeks, eyes and forehead. Primary variables included forehead skin temperature, mean arterial pressure and systemic, forearm and cutaneous vascular resistances. Indices of heart rate variability in the time domain provided an index of cardiac parasympathetic activity. The magnitude of reduction in forehead skin temperature during face cooling was slightly greater during normothermia (-17.6 ± 1.9 versus -16.3 ± 3.0°C, P = 0.03). Increases in heart rate variability evoked by face cooling were attenuated during heat stress. Changes in systemic, forearm and cutaneous vascular resistances during face cooling were virtually abolished during heat stress (P < 0.01). However, when forearm and vascular data were reported as conductance, differences between normothermia and heat stress were not apparent (P ≥ 0.62). Nevertheless, the increase in mean arterial pressure was attenuated during heat stress with face cooling (at 3 min: 2 ± 7 mmHg) compared with normothermia (at 3 min: 19 ± 7 mmHg, P < 0.01). These data indicate that passive heat stress attenuates face cooling-evoked increases in cardiac parasympathetic activation, vascular resistance and blood pressure. However, they also indicate that changes in indices of vascular resistance do not always reflect equivalent changes in conductance.

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.

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.

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.

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.

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.