Autonomic Conflict Research Articles

Unlocking the depths: multiple factors contribute to risk for hypoxic blackout during deep freediving

PurposeTo examine the effect of freediving depth on risk for hypoxic blackout by recording arterial oxygen saturation (SpO2) and heart rate (HR) during deep and shallow dives in the sea.MethodsFourteen competitive freedivers conducted open-water training dives wearing a water-/pressure proof pulse oximeter continuously recording HR and SpO2. Dives were divided into deep (> 35 m) and shallow (10–25 m) post-hoc and data from one deep and one shallow dive from 10 divers were compared.ResultsMean ± SD depth was 53 ± 14 m for deep and 17 ± 4 m for shallow dives. Respective dive durations (120 ± 18 s and 116 ± 43 s) did not differ. Deep dives resulted in lower minimum SpO2 (58 ± 17%) compared with shallow dives (74 ± 17%; P = 0.029). Overall diving HR was 7 bpm higher in deep dives (P = 0.002) although minimum HR was similar in both types of dives (39 bpm). Three divers desaturated early at depth, of which two exhibited severe hypoxia (SpO2 ≤ 65%) upon resurfacing. Additionally, four divers developed severe hypoxia after dives.ConclusionsDespite similar dive durations, oxygen desaturation was greater during deep dives, confirming increased risk of hypoxic blackout with increased depth. In addition to the rapid drop in alveolar pressure and oxygen uptake during ascent, several other risk factors associated with deep freediving were identified, including higher swimming effort and oxygen consumption, a compromised diving response, an autonomic conflict possibly causing arrhythmias, and compromised oxygen uptake at depth by lung compression possibly leading to atelectasis or pulmonary edema in some individuals. Individuals with elevated risk could likely be identified using wearable technology.

The influence of training status and parasympathetic blockade on the cardiac rate, rhythm and functional response to autonomic stress.

Apnea (breath-holding) elicits co-activation of sympathetic and parasympathetic nervous systems, affecting cardiac control. In situations of autonomic co-activation (e.g., cold water immersion), cardiac arrhythmias are observed during apnea. Chronic endurance training reduces resting heart rate in part via elevation in parasympathetic tone, and has been identified as a risk factor for development of arrhythmias. However, few studies have investigated autonomic control of the heart in trained athletes during stress. Therefore, we determined whether heightened vagal tone resulting from endurance training promotes a higher incidence of arrhythmia during apnea. We assessed the heart rate, rhythm (ECG lead II), and cardiac inotropic (speckle-tracking echocardiography) response to apnea in 10 endurance trained and 7 untrained participants. Participants performed an apnea at rest and following sympathetic activation using post-exercise circulatory occlusion (PECO). All apneas were performed prior to (CON) and following vagal block using glycopyrrolate (GLY). Trained participants had lower heart rates at rest (p=0.03) and during apneas (p=0.009) under CON. At rest, 3 trained participants exhibited instances of junctional rhythm and 4 trained participants developed ectopy during CON apneas, whereas 3 untrained participants developed ectopic beats only with concurrent sympathetic activation (PECO). Following GLY, no arrhythmias were noted in either group. Vagal block also revealed increased cardiac chronotropy (heart rate) and inotropy (strain rate) during apnea, demonstrating a greater sympathetic influence in the absence of parasympathetic drive. Our results highlight that endurance athletes may be more susceptible to ectopy via elevated vagal tone, whereas untrained participants may only develop ectopy through autonomic conflict. .

A DIVER WITH SWIMMING-INDUCED PULMONARY EDEMA AND CARDIAC ARREST

TOPIC: Occupational and Environmental Lung Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: Swimming-induced pulmonary edema (SIPE) is classically considered to be a self-resolving, non-fatal condition that occurs in high exertion surface swimmers and divers. We report an unusual case of a scuba diver who had both SIPE and presumed cardiac arrest. CASE PRESENTATION: A 71-year old man with atrial fibrillation on apixaban, diabetes mellitus, and hypertension developed shortness of breath during a scuba dive at 50 feet of seawater. The maximum dive depth was 70 feet with an average water temperature of 67° Fahrenheit. He ascended per protocol. After being pulled onto the boat, the patient syncopized. Chest compressions and rescue breaths were initiated, and he regained consciousness 2-3 minutes later. Upon EMS arrival, the patient had oxygen saturation by pulse oximetry in the mid-70s. He was placed on 15 L/min of supplemental oxygen and transported to the hospital by helicopter. EKG and telemetry showed atrial fibrillation with a normal rate. Chest radiograph showed pulmonary edema, and CTA chest showed pulmonary edema with no pulmonary embolism. Transthoracic echocardiogram showed an ejection fraction of 55-60%, mild valvular disease, and no evidence of hypertrophy or shunting. Coronary angiogram showed mild non-obstructive coronary artery disease. The patient's hypoxia resolved within 24 hours of presentation, with resolution of the pulmonary edema on repeat chest radiograph. DISCUSSION: Swimming-induced pulmonary edema is primarily thought to be self-resolving and non-fatal. However, this case prompts the question of an association between SIPE and cardiac arrest that has not been described to our knowledge. The patient was presumed to have cardiac arrest, as opposed to non-cardiogenic syncope, given continued loss of consciousness during chest compressions. Coronary angiogram was pursued because the arrest was indistinguishable between sudden cardiac arrest (SCA) and provoked cardiac arrest, for example from hypoxia. SIPE is hypothesized to be a hydrostatic pulmonary edema that occurs due to elevated pulmonary artery pressures from increased peripheral vascular resistance and central redistribution of blood flow. Meanwhile, SCA is typically due to coronary disease, structural disease, or congenital arrhythmias. The absence of these pathologies in this patient suggest that SIPE may have played a distinct role in his SCA. Water immersion has been proposed to cause SCA through "autonomic conflict," whereby simultaneous sympathetic activation from exertion and parasympathetic activation from immersion increases likelihood of arrhythmia. However, the precise impact of SIPE on cardiac activity is not clear. CONCLUSIONS: Swimming induced pulmonary edema may have contributed to this patient's cardiac arrest. The possibility for life-threatening secondary complications of SIPE such as cardiac arrest warrants further investigation. REFERENCE #1: Spencer S, Dickinson J, Forbes L. Occurrence, Risk Factors, Prognosis and Prevention of Swimming-Induced Pulmonary Oedema: a Systematic Review [Internet]. Sport. Med. - Open. 2018 [cited 2021 Apr 28];4(1):43. REFERENCE #2: Moon RE, Martina SD, Peacher DF, et al. Swimming-induced pulmonary edema - Pathophysiology and Risk Reduction with Sildanefil. Circulation [Internet] 2016 [cited 2021 Apr 28];133(10):988–996. REFERENCE #3: Shattock MJ, Tipton MJ. 'Autonomic conflict': a different way to die during cold water immersion? J Physiol [Internet] 2012 [cited 2021 Apr 28];590(14):3219–3230. DISCLOSURES: No relevant relationships by Christopher Androski, source=Web Response Advisory Committee Member relationship with Actelion Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee Consultant relationship with Actelion Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee Advisory Committee Member relationship with Arena Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee Advisory Committee Member relationship with Bayer Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee Advisory Committee Member relationship with United Therapeutics Please note: $5001 - $20000 by Richard Channick, source=Web Response, value=Consulting fee No relevant relationships by Estebes Hernandez, source=Web Response No relevant relationships by Laura Santoso, source=Web Response No relevant relationships by Michael Tripp, source=Web Response

Duration at High Altitude Influences the Onset of Arrhythmogenesis During Apnea

Excitation of both sympathetic and parasympathetic systems occur concurrently at high-altitude (chronic hypoxia), via the carotid chemoreflex. We have demonstrated this autonomic conflict manifests as cardiac arrhythmias during voluntary apnea. We sought to determine the duration of hypoxic exposure at high-altitude necessary to unmask cardiac arrhythmias during instances of voluntary apnea. We hypothesized that the occurrence of cardiac arrhythmias during apnea would be increased following 24 hours of high-altitude exposure. Measurements of oxygen saturation (SpO2; pulse oximetry) and continuous electrocardiogram (ECG; lead II) were collected in 22 participants (8 females) at low altitude (1045m) and over 8 consecutive days at high-altitude (3800m). Following a 2 minute baseline participants performed an end-expiratory apnea to volitional breakpoint. ECG rate and rhythm were evaluated at baseline and during apnea. The nadir heart rate was used to quantify bradycardia and abnormal ECG rhythm was classified based on origin (e.g., sinus node) and type (e.g., sinus arrest). Differences in resting ventilation, SpO2, and the heart rate response to apnea on each day at high-altitude (Day 1-8) were compared to that at low altitude (Day 0) using a repeated-measures ANOVA design, with a Holm-Sidak post-hoc analysis where main effect of time was significant. Baseline SpO2 was lower for all days at high-altitude (average of all days, 89±3) compared to low altitude (98 ± 2) (p<0.01). At high-altitude (all days), baseline heart rate was higher compared to low altitude (p<0.01). A main effect of time (p<0.01) was identified for the delta change in heart rate during apnea. At low altitude, the average apnea induced decrease in heart rate was -9±15bpm, whereas the average decrease in heart rate at high altitude (all days) was -24±16bpm. Bradycardia became more pronounced with acclimatization, with the greatest drop in heart rate (-31±16bpm) occurring on Day 5. At low altitude 14% (3/22) of participants developed arrhythmias during apnea. At high-altitude, cardiac arrhythmias during apnea became most prevalent (>50%) following Day 5. Changes in saturation during apnea and apnea duration were not associated with the magnitude of bradycardia during apnea (saturation, r= -0.007 p=0.92; apnea duration, r=0.005 p=0.94). Interestingly, the magnitude of bradycardia was correlated with the incidence (percentage) of arrhythmia per day (r=0.8; p=0.004), suggesting a similar underlying mechanism. Our data indicate chronic hypoxia is associated with a progressive increase in vagal tone, as indicated by augmented bradycardia during apnea and progressively increased incidence of arrhythmia at high-altitude. Additionally, the increased incidence of arrhythmia with acclimatization suggests that chemoreflex sensitization may play a role in this phenomenon. This study provides insight into cardiac electrophysiology at high-altitude and has implications as a future functional model for exploring the effects of heightened chemoreflex stress on autonomic control of heart.

Indices of Heart Rate Variability and Performance During a Response-Conflict Task Are Differently Associated With ADHD and Autism

We investigated autonomic arousal, attention and response conflict, in ADHD and autism. Heart rate variability (HRV), and behavioral/electrophysiological indices of performance, were recorded during a task with low and high levels of response conflict in 78 children/adolescents (7–15 years old) with ADHD, autism, comorbid ADHD+autism, or neurotypical. ANOVA models were used to investigate effects of ADHD and autism, while a mediation model was tested to clarify the relationship between ADHD and slower performance. Slower and less accurate performance characterized ADHD and autism; however, atypical electrophysiological indices differently characterized these conditions. The relationship between ADHD and slower task performance was mediated by reduced HRV in response to the cue stimulus. Autonomic hypo-arousal and difficulties in mobilizing energetic resources in response to sensory information (associated with ADHD), and atypical electrophysiological indices of information processing (associated with autism), might negatively affect cognitive performance in those with ADHD+autism.

Cardiac Conduction Disease in Huntington's Disease Mouse Model (BACHD)

ObjectiveHuntington's disease (HD) is a progressive neurodegenerative disease caused by a CAG repeat expansion in the gene encoding the huntingtin protein. In addition to the central nervous system, recent evidence indicates cardiac involvement in HD patients. ECG screening in HD patients suggested an increased prevalence of conduction abnormalities and compromised sinoatrial node (SAN) function. Here we tested if the huntingtin gene defect would cause increased arrhythmia susceptibility.MethodsWe used a conditional human huntingtin (HTT) Bacterial Artificial Chromosome (BACHD) transgenic mouse model at 8 months (motor dysfunction present) and 18+ months of age (advanced disease). Fibrosis level was assessed histologically. Surface ECG was measured in mice anesthetized with isoflurane and arrhythmia susceptibility was tested in response to sympathetic and parasympathetic agonists and their combination (autonomic conflict).ResultsIn 18+ month‐old mice overall cardiac structure was unremarkable. BACHD hearts were slightly larger, but HW/BW ratio was normal. Baseline ECG recordings showed prolonged QRS duration in BACHD mice. Stimulation with carbachol (parasympathetic agonist) resulted in increased premature atrial contractions (PACs), SAN exit block, tachy‐brady syndrome in BACHD mice. Stimulation with combined sympathetic and parasympathetic agonists (norepinephrine, epinephrine and carbachol) resulted in increased premature ventricular contractions, PACs, bigeminy and couplets in BACHD mice. Some of these events occurred also in younger BACHD mice, but to a lesser extent.Conclusions/Broader ImpactsThe BACHD mice showed signs of cardiac conduction system abnormalities and SA node dysfunction. This was observed in the absence of gross histological changes and during isoflurance anesthesia which dampened the influence of the autonomic nervous system. Stimulation with parasympathetic and sympathetic agonists uncovered increased atrial and ventricular arrhythmia susceptibility. Our study indicates that the huntingtin gene defect may cause progressive cardiac conduction system pathology that might increase the susceptibility to sudden cardiac death.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Autonomic conflict exacerbates long QT associated ventricular arrhythmias

This study tested the hypothesis that concomitant sympathetic and parasympathetic stimulation (“autonomic conflict”) may act as a trigger for arrhythmias in long QT syndrome (LQTS). Studies were performed in isolated innervated rabbit hearts treated with clofilium (100 nmol/L); a potassium channel blocker. The influence of vagus nerve stimulation (VNS) on spontaneous ventricular arrhythmias was assessed in the absence/presence of sustained noradrenaline perfusion (100 nmol/L) and with sudden adrenergic stress (injections of noradrenaline into the perfusion line). Hearts were instrumented for a pseudo-electrocardiogram and monophasic action potential recordings. VNS, which slows heart rate, was associated with a stimulation frequency-dependent incidence of spontaneous early after-depolarisations (EADs) and ventricular tachycardia (VT), best predicted by the duration of the electrocardiographic T-wave and by triangulation of the ventricular action potential. In the presence of sustained (steady-state) noradrenaline perfusion, the incidence of EADs and VT with VNS was decreased from 73/55% to 45/27%, respectively. However, sudden adrenergic stress, imposed during periods of sustained VNS, was associated with a transient increase in the incidence of severity of observed arrhythmias, as indicated by an increase in the average arrhythmias score (1.6 ± 0.4 vs. 2.1 ± 0.7, p = .01). Analysis of electrophysiological parameters suggests that sudden adrenergic stress is associated with a transient prolongation, and increased triangulation, of the ventricular action potential, which may predispose to triggered activity. This study demonstrates that autonomic conflict is a pro-arrhythmic stimulus in LQTS. However, combined adrenergic and parasympathetic stimulation has a complex relationship with arrhythmogenicity, with differences in the effects of steady-state adrenergic activation vs. sudden adrenergic stress.

Heart rate regulation in diving sea lions: the vagus nerve rules.

Recent publications have emphasized the potential generation of morbid cardiac arrhythmias secondary to autonomic conflict in diving marine mammals. Such conflict, as typified by cardiovascular responses to cold water immersion in humans, has been proposed to result from exercise-related activation of cardiac sympathetic fibers to increase heart rate, combined with depth-related changes in parasympathetic tone to decrease heart rate. After reviewing the marine mammal literature and evaluating heart rate profiles of diving California sea lions (Zalophus californianus), we present an alternative interpretation of heart rate regulation that de-emphasizes the concept of autonomic conflict and the risk of morbid arrhythmias in marine mammals. We hypothesize that: (1) both the sympathetic cardiac accelerator fibers and the peripheral sympathetic vasomotor fibers are activated during dives even without exercise, and their activities are elevated at the lowest heart rates in a dive when vasoconstriction is maximal, (2) in diving animals, parasympathetic cardiac tone via the vagus nerve dominates over sympathetic cardiac tone during all phases of the dive, thus producing the bradycardia, (3) adjustment in vagal activity, which may be affected by many inputs, including exercise, is the primary regulator of heart rate and heart rate fluctuations during diving, and (4) heart beat fluctuations (benign arrhythmias) are common in marine mammals. Consistent with the literature and with these hypotheses, we believe that the generation of morbid arrhythmias because of exercise or stress during dives is unlikely in marine mammals.

Physiology Of Drowning: A Review.

Drowning physiology relates to two different events: immersion (upper airway above water) and submersion (upper airway under water). Immersion involves integrated cardiorespiratory responses to skin and deep body temperature, including cold shock, physical incapacitation, and hypovolemia, as precursors of collapse and submersion. The physiology of submersion includes fear of drowning, diving response, autonomic conflict, upper airway reflexes, water aspiration and swallowing, emesis, and electrolyte disorders. Submersion outcome is determined by cardiac, pulmonary, and neurological injury. Knowledge of drowning physiology is scarce. Better understanding may identify methods to improve survival, particularly related to hot-water immersion, cold shock, cold-induced physical incapacitation, and fear of drowning.

Drug-induced long QT syndrome increases the risk of drowning

There is strong evidence linking inherited long QT syndromes with an increased risk of drowning due to fatal arrhythmias in the water. Drug-induced long QT syndrome (DILQTS) is hypothesized to increase the risk of drowning by similar mechanisms. It is suggested that QT prolongation caused by a drug or drugs, when combined with the autonomic conflict associated with the mammalian dive reflex and/or the cold shock reflex, sets up conditions that may result in a sudden fatal arrhythmia while in water – thus an increased risk of drowning related to a drug-induced prolongation of the QT interval. Many widely used drugs prolong the QT interval thus raising a drug safety issue that needs confirmation or refutation.

Concomitant vagal and adrenergic stimulation does not precipitate ventricular arrhythmias in a healthy rabbit heart model of autonomic conflict

Experimental studies indicate that cold-water immersion is associated with incidence of supraventricular and ventricular arrhythmia in young, seemingly, healthy subjects [1]. We recently hypothesised that the sudden and simultaneous sympathetic and parasympathetic activity, termed autonomic conflict (AC), may be a cause of arrhythmias associated with cold-water immersion and, when combined with other risk factors, may explain immersion-related sudden death. The aim of the present study was to investigate the arrhythmic consequences of AC in normal healthy rabbit hearts.

Cardiorespiratory responses and reduced apneic time to cold-water face immersion after high intensity exercise

Apnea after exercise may evoke a neurally mediated conflict that may affect apneic time and create a cardiovascular strain. The physiological responses, induced by apnea with face immersion in cold water (10°C), after a 3-min exercise bout, at 85% of VO2max,were examined in 10 swimmers. A pre-selected 40-s apnea, completed after rest (AAR), could not be met after exercise (AAE), and was terminated with an agonal gasp reflex, and a reduction of apneic time, by 75%. Bradycardia was evident with immersion after both, 40-s of AAR and after AAE (P<0.05). The dramatic elevation of, systolic pressure and pulse pressure, after AAE, were indicative of cardiovascular stress. Blood pressure after exercise without apnea was not equally elevated. The activation of neurally opposing functions as those elicited by the diving reflex after high intensity exercise may create an autonomic conflict possibly related to oxygen-conserving reflexes stimulated by the trigeminal nerve, and those elicited by exercise.

Hypoxic Blackout: Diagnosis, Risks, and Prevention

Hypoxic blackout, also called underwater blackout syndrome, is a distinct and preventable cause of drowning. The sudden and unexpected death of a young, fit swimmer or diver, almost always male, necessitates the consideration of a differential diagnosis which includes four syndromes-preexistent cardiac disease, electrical conduction abnormalities, epilepsy, and hypoxic blackout. The pathophysiology of hypoxic blackout (overriding the carbon dioxide sensor by presubmersion hyperventilation) may be induced by autonomic conflict between cold shock diving reflexes in certain predisposed individuals. Death occurs in both public and private swimming pools and in the sea, and case series include those training for underwater hockey, synchronized swimming, free diving, and playful submersion endurance challenges. The sole preventive stratagem is advocacy for awareness of risks, suitably targeted to at risk groups.

Hypoxic Blackout: Diagnosis, Risks, and Prevention

Hypoxic blackout, also called underwater blackout syndrome, is a distinct and preventable cause of drowning. The sudden and unexpected death of a young, fit swimmer or diver, almost always male, necessitates the consideration of a differential diagnosis which includes four syndromes—preexistent cardiac dis- ease, electrical conduction abnormalities, epilepsy, and hypoxic blackout. The pathophysiology of hypoxic blackout (overriding the carbon dioxide sensor by presubmersion hyperventilation) may be induced by autonomic conflict between cold shock diving reflexes in certain predisposed individuals. Death occurs in both public and private swimming pools and in the sea, and case series include those training for underwater hockey, synchronized swimming, free diving, and playful submersion endurance challenges. The sole preventive stratagem is advocacy for awareness of risks, suitably targeted to “at risk” groups.

Pre hospital care 2012

Pre hospital care 2012

‘Autonomic conflict’: a different way to die during cold water immersion?

Cold water submersion can induce a high incidence of cardiac arrhythmias in healthy volunteers. Submersion and the release of breath holding can activate two powerful and antagonistic responses: the 'cold shock response' and the 'diving response'. The former involves the activation of a sympathetically driven tachycardia while the latter promotes a parasympathetically mediated bradycardia. We propose that the strong and simultaneous activation of the two limbs of the autonomic nervous system ('autonomic conflict') may account for these arrhythmias and may, in some vulnerable individuals, be responsible for deaths that have previously wrongly been ascribed to drowning or hypothermia. In this review, we consider the evidence supporting this claim and also hypothesise that other environmental triggers may induce autonomic conflict and this may be more widely responsible for sudden death in individuals with other predisposing conditions.

Feeling we’re biased: Autonomic arousal and reasoning conflict

Human reasoning is often biased by intuitive beliefs. A key question is whether the bias results from a failure to detect that the intuitions conflict with logical considerations or from a failure to discard these tempting intuitions. The present study addressed this unresolved debate by focusing on conflict-related autonomic nervous system modulation during biased reasoning. Participants' skin conductance responses (SCRs) were monitored while they solved classic syllogisms in which a cued intuitive response could be inconsistent or consistent with the logical correct response. Results indicated that all reasoners showed increased SCRs when solving the inconsistent conflict problems. Experiment 2 validated that this autonomic arousal boost was absent when people were not engaged in an active reasoning task. The presence of a clear autonomic conflict response during reasoning lends credence to the idea that reasoners have a "gut" feeling that signals that their intuitive response is not logically warranted. Supplemental materials for this article may be downloaded from http://cabn.psychonomic-journals.org/content/supplemental.

ECG During Helicopter Underwater Escape Training

Coincidental stimulation of the sympathetic and parasympathetic nervous system can cause "autonomic conflict" and consequent cardiac arrhythmias. The present study tested the hypotheses that: 1) cardiac arrhythmias would be seen in those undertaking helicopter underwater escape training (HUET); 2) the occurrence of arrhythmias in individuals could be predicted; and 3) the heart rate response to HUET would habituate with repeated runs. There were 26 male volunteers who each undertook 5 HUET submersions into water at 29.5 degrees C, with each run separated by 10 min. Each submersion included a 3-min, 40-s pre-submersion period, a 10-s submersion, and 40-s post-submersion period. Participants wore a three-lead telemetric ECG system beneath an immersion suit and underclothing. Skin temperature was measured in one participant. Each participant undertook tests to establish their autonomic function, including heart rate variability, face immersion, cold pressor test, and aerobic capacity assessment. The heart rate response to HUET was reduced by the fourth run when compared to the first run. Across all runs, 32 cardiac arrhythmias were identified (25%) in 22 different participants; all but 6 of the arrhythmias occurred just after submersion. Only aerobic fitness appeared inversely associated with the occurrence of arrhythmias. The heart rate response to HUET habituates. HUET produces cardiac arrhythmias; these are asymptomatic and probably of little clinical significance in young, fit individuals. It remains to be seen if this is the case with either an older, less fit cohort of people or in those undertaking longer breath holds in colder water.

Autonomic arousal and conflict avoidance in anorexia nervosa: a pilot study

This study examined the nature and relevance of autonomic arousal during conflict negotiation between anorexic patients and their mothers. Twenty anorexia nervosa patients and 14 psychiatric control patients, and their mothers were monitored for heart rate and skin conductance levels during low- and high-conflict discussion tasks, and self-reports of family functioning. Anorexic patients showed significantly greater arousal during high-conflict discussions than their mothers and psychiatric controls. Mothers of anorexics showed a slowing of heart rate during the high-conflict task compared to their daughters. Heightened arousal in anorexic patients during high-conflict discussions was strongly associated with self-reported difficulties in family problem solving. These results suggest that a relationship exists between autonomic arousal and conflict avoidance in anorexia nervosa which warrants further investigation. Copyright © 2000 John Wiley & Sons, Ltd and Eating Disorders Association.

Diving reflex after physical training.

ArticleDiving reflex after physical training.A A Bove, P R Lynch, J V Connell Jr, and J M HardingA A Bove, P R Lynch, J V Connell Jr, and J M HardingPublished Online:01 Jul 1968https://doi.org/10.1152/jappl.1968.25.1.70MoreSectionsPDF (561 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByHistory of Strength Training Research in Man: An Inventory and Quantitative Overview of Studies Published in English Between 1894 and 197924 February 2021 | Journal of Strength and Conditioning Research, Vol. 35, No. 5Cold Water Immersion Syndrome and Whitewater Recreation FatalitiesWilderness & Environmental Medicine, Vol. 30, No. 3Diurnal variation in the diving bradycardia response in young men21 January 2016 | Clinical Autonomic Research, Vol. 26, No. 2Cardiovascular Concerns in Water SportsClinics in Sports Medicine, Vol. 34, No. 3‘Autonomic conflict’: a different way to die during cold water immersion?14 June 2012 | The Journal of Physiology, Vol. 590, No. 14Cold face test in persons with spinal cord injury: age versus inactivity6 May 2009 | Clinical Autonomic Research, Vol. 19, No. 4Effects of head and body cooling on hemodynamics during immersed prone exercise at 1 ATAT. E. Wester, A. D. Cherry, N. W. Pollock, J. J. Freiberger, M. J. Natoli, E. A. Schinazi, P. O. Doar, A. E. Boso, E. L. Alford, A. J. Walker, D. M. Uguccioni, D. Kernagis, and R. E. Moon1 February 2009 | Journal of Applied Physiology, Vol. 106, No. 2Arrhythmias in Special SituationsCardiovascular responses to facial cooling are age and fitness dependentMedicine & Science in Sports & Exercise, Vol. 31, No. 8Bradycardic responses to vagally mediated bedside maneuvers in healthy volunteersThe American Journal of Medicine, Vol. 90, No. 6Bradycardic responses to vagally mediated bedside maneuvers in healthy volunteersThe American Journal of Medicine, Vol. 90, No. 1Effects of Apnea and Face Immersion in Water on the Time Components of the Cardiac Cycle17 March 2013 | Research Quarterly. American Alliance for Health, Physical Education and Recreation, Vol. 47, No. 4Underwater bradycardia23 April 2016 | The Journal of Sports Medicine, Vol. 2, No. 3Schwimmen und Tauchen bei 3?10 j�hrigen KindernZeitschrift f�r Kinderheilkunde, Vol. 118, No. 1The Bradycardia Reflex in Competitive Swimmers17 March 2013 | Research Quarterly. American Association for Health, Physical Education and Recreation, Vol. 42, No. 3 More from this issue > Volume 25Issue 1July 1968Pages 70-2 https://doi.org/10.1152/jappl.1968.25.1.70PubMed5661157History Published online 1 July 1968 Published in print 1 July 1968 Metrics