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.

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.

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.