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.

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.

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.

Blunted Cardiac Parasympathetic Activation in Student Athletes With a Remote History of Concussion: A Pilot Study.

Introduction: Blunted cardiac autonomic nervous system (ANS) responses, quantified using heart rate variability (HRV), have been reported after sport-related concussion (SRC). Research suggests this persists beyond clinical recovery. This study compared cardiac parasympathetic responses in student athletes with a remote history of SRC (> 1-year ago, Concussion History: CH) with those who reported no lifetime history of SRC (Concussion Naïve: CN). Design: Retrospective nested case-control. Setting: University laboratory. Patients or Other Participants: CH (n = 9, 18.3 ± 2 years, 44% male, median 2 years since injury) were student athletes with a remote history of concussion(s) from more than 1 year ago. CN (n = 21, 16.7 ± 3 years, 67% male) were student athletes with no lifetime history of concussion. Exclusion criteria included taking medications that could affect ANS function, history of concussion within the past year, persistent concussion symptoms, lifetime history of moderate to severe brain injury, and lifetime history of more than 3 concussions. Material and Methods: Participants performed the Face Cooling (FC) test for 3-min after 10-min of supine rest while wearing a 3-lead electrocardiogram in a controlled environment. Outcome Measures: Heart rate (HR), R-R interval (RRI), root mean square of the successive differences (RMSSD) of RRI, high frequency (HF) and low frequency to HF (LF:HF) ratios. Results: At baseline, CH had a lower resting HR than CN (62.3 ± 11 bpm vs. 72.9 ± 12, p = 0.034). CH had a different HR response to FC than CN (+8.9% change from baseline in CH vs. -7.5% in CN, p = 0.010). CH also had a smaller RMSSD increase to FC than CN (+31.8% change from baseline in CH vs. +121.8% in CN, p = 0.048). There were no significant group differences over time in RRI (p = 0.106), HF (p = 0.550) or LF:HF ratio (p = 0.053). Conclusion: Asymptomatic student athletes with a remote history of concussion had a blunted cardiac parasympathetic response to FC when compared with athletes with no lifetime history of concussion. These data suggest that an impaired autonomic response to a physiological stressor persists after clinical recovery from SRC for longer than previously reported.

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.