Fear Bradycardia Research Articles

Threat of suffocation and defensive reflex activation.

The current study examined emotional reflex reactions of participants threatened with respiratory distress caused by imposing a resistive load at inspiration. Cues signaling threat (breathing MAY be difficult) and safe periods were intermixed while startle reflexes, heart rate, skin conductance, and facial EMG activity were measured. Compared to safe cues, threat cues elicited significant startle potentiation, enhanced skin conductance, heightened corrugator EMG changes, and pronounced "fear bradycardia" consistent with defensive activation in the context of threatened respiratory dysfunction. These data indicate that anticipating respiratory resistance activates defensive responding, which may mediate symptomatology in patients with panic and other anxiety disorders.

Effects of affective picture viewing on postural control

BackgroundEmotion theory holds that unpleasant events prime withdrawal actions, whereas pleasant events prime approach actions. Recent studies have suggested that passive viewing of emotion eliciting images results in postural adjustments, which become manifest as changes in body center of pressure (COP) trajectories. From those studies it appears that posture is modulated most when viewing pictures with negative valence. The present experiment was conducted to test the hypothesis that pictures with negative valence have a greater impact on postural control than neutral or positive ones. Thirty-four healthy subjects passively viewed a series of emotion eliciting images, while standing either in a bipedal or unipedal stance on a force plate. The images were adopted from the International Affective Picture System (IAPS). We analysed mean and variability of the COP and the length of the associated sway path as a function of emotion.ResultsThe mean position of the COP was unaffected by emotion, but unipedal stance resulted in overall greater body sway than bipedal stance. We found a modest effect of emotion on COP: viewing pictures of mutilation resulted in a smaller sway path, but only in unipedal stance. We obtained valence and arousal ratings of the images with an independent sample of viewers. These subjects rated the unpleasant images as significantly less pleasant than neutral images, and the pleasant images as significantly more pleasant than neutral images. However, the subjects rated the images as overall less pleasant and less arousing than viewers in a closely comparable American study, pointing to unknown differences in viewer characteristics.ConclusionOverall, viewing emotion eliciting images had little effect on body sway. Our finding of a reduction in sway path length when viewing pictures of mutilation was indicative of a freezing strategy, i.e. fear bradycardia. The results are consistent with current knowledge about the neuroanatomical organization of the emotion system and the neural control of behavior.

A freezing‐like posture to pictures of mutilation

Postural sway and heart rate were recorded in young men viewing emotionally engaging pictures. It was hypothesized that they would show a human analog of "freezing" behavior (i.e., immobility and heart rate deceleration) when confronted with a sustained block of unpleasant (mutilation) images, relative to their response to pleasant/arousing (sport action) or neutral (objects) pictures. Volunteers stood on a stabilometric platform during picture viewing. Significantly reduced body sway was recorded during the unpleasant pictures, along with increased mean power frequency (indexing muscle stiffness). Heart rate during unpleasant pictures also showed the expected greater deceleration. This pattern resembles the "freezing" and "fear bradycardia" seen in many species when confronted with threatening stimuli, mediated by neural circuits that promote defensive survival.

Metabolic fright responses of different-sized largemouth bass (Micropterus salmoides) to two avian predators show variations in nonlethal energetic costs

Recently, researchers have identified that nonlethal costs of predation may arise not only from lost energy intake but also potentially from increased energetic expenditure. During periods of heightened stress following unsuccessful predation attempts, organisms may remain in an altered physiological state with elevated metabolism for some time. Few studies have quantified these nonlethal energetic costs of predation. We monitored the cardiac response (cardiac output (Q), heart rate (fH), and stroke volume (SVH)) of largemouth bass, Micropterus salmoides, ranging in size from 200 to 425 mm, to simulated avian predation attempts by great blue heron, Ardea herodias, and osprey, Pandion haliaetus. Fear bradycardia during a 30-s predation attempt varied depending upon the size of the fish and the type of predator. The magnitude of the bradycardia decreased with increasing size of the fish; however, the disturbances were more extreme in response to osprey than to blue heron models. Maximal cardiac disturbance following simulated predation attempts by osprey were consistent among size classes of bass. However, the magnitude of the disturbance following heron predation attempts reduced as the size of the fish increased. Size-specific trends were even more extreme for cardiac-recovery durations. Largemouth bass of all sizes exposed to osprey predation attempts required ~40 min for Q and fH and ~30 min for SVH to return to predisturbance levels. Although small bass exposed to heron predation attempts required recovery times similar to fish exposed to osprey predation attempts, as the size of largemouth bass exposed to the heron model increased above ~300 mm, the recovery time decreased significantly. We conclude that the size-specific response of largemouth bass to different predators is reflective of their ability to assess the risk posed by different predators. In addition, the nonlethal costs of predation can be substantial and should be considered in future bioenergetics models.

Fear bradycardia in the eastern fox squirrel, Sciurus niger, and eastern grey squirrel, S. carolinesis

1. 1. Biotelemetry transmitters were surgically implanted in the abdominal cavity of two eastern grey squirrels, Sciurus carolinesis and one eastern fox squirrel, S. niger. Heart rate response to fear was investigated by recording heart rate before, during and after a frightening stimulus. Squirrels were tested in the laboratory and free ranging under natural conditions. 2. 2. Laboratory results showed a mean bradycardia of −25%., in grey squirrels (when they had a box to retreat into) and fear tachycardia (+160%) for the fox squirrel. 3. 3. Field results clearly showed a marked fear bradycardia for both species if suitable cover was available for hiding. Over-stimulation, or lack of cover, resulted in fleeing and tachycardia.

Control of fear bradycardia in the swamp rabbit, Sylvilagus aquaticus

1. 1. Biotelemetry transmitters were surgically implanted into the abdominal cavity of each of 9 mature swamp rabbits, Sylvilagus aquaticus, and the heart rate response to threatening stimuli investigated. 2. 2. Each rabbit tested in the field and under laboratory conditions exhibited a marked bradycardia in response to different threatening stimuli. Onset of this fear bradycardia was rapid and recovery required several minutes. No recovery tachycardia was observed. Mean heart rate values for 40 experiments during pre-stimulus (10 min), stimulus (5 min), and recovery (10 min) periods were 200 ± 6.4, 129 ± 5.6 and 190 ± 4.7 ( X ± SE) bpm , respectively, in untreated swamp rabbits. Mean bradycardia was 35.5% and the rate of onset was −63 (bpm)/sec (obtained from the slope of line of a least-squares fit of instantaneous heart during the transition from prestimulus to stimulus). 3. 3. Atropine (8.5 mg/kg) was injected 20 min prior to each experiment to block vagal influence of the heart. Fear bradycardia was present in each of 17 experiments, but was reduced to 18.2%. Mean values were 248 ± 13.7, 203 ± 11.6 and 252 ± 13.0 bpm, respectively. The rate of onset of bradycardia was reduced to −5.0 (bpm)/sec. 4. 4. Propranolol (6.3 mg/kg) was given orally 20 min before each experiment. This resulted in 31.7% fear bradycardia with values of 186 ± 11.1, 127 ± 10.4 and 174 ± 9.6 bpm, respectively. Onset was −70.0 (bpm)/sec. Treatment with both propranolol and atropine abolished fear bradycardia (mean values of 229 ± 9.4, 219 ± 10.5 and 228 ± 8.4 bpm). 5. 5. Together these data suggest removal of sympathetic tone in conjunction with increased parasympathetic activity is responsible for fear bradycardia in swamp rabbits, with parasympathetic activity contributing to the rapid onset of the response.

Fear bradycardia in captive eastern chipmunk, Tamias striatus

1. 1. Biotelemetry transmitters were surgically implanted in the abdominal cavity of three eastern chipmunks, Tamias striatus, and the heart rate response to fear was investigated. 2. 2. Each chipmunk showed fear bradycardia. Mean heart rate values during prestimulus, stimulus and poststimulus were 259 ± 10, 184 ± 13, and 246 ± 18 (X̄ ± SE) beats/min respectively. 3. 3. Respiratory sinus arrhythmia (RSA) occurred throughout the experiments, but increased during stimulus. Percent RSA were 10.0, 33.9 and 12.0 respectively. 4. 4. Atropine treatment increased heart rate and abolished respiratory sinus arrhythmia and fear bradycardia. 5. 5. Frightened chipmunk retreating to a safe refugium respond with a marked fear bradycardia. Respiratory sinus arrhythmia increased during fright. Harassment within the refugium resulted in subsequent fear tachycardia.

Effect of atropine on the onset of fear bradycardia in eastern cottontail rabbits Sylvilagus floridanus

1. Biotelemetry transmitters were surgically implanted in the abdominal cavity of six mature eastern cottontail rabbits, Sylvilagus floridanus, and the effect of atropine on the rate of onset of fear bradycardia investigated. 2. Electrocardiogram records were obtained from demodulation of magnetically recorded data on a physiograph. Instantaneous heart rate was obtained and averaged for each second. Ten seconds of pre-stimulus data was obtained, followed by thirty seconds of data obtained while frightening the rabbit. 3. A marked fear bradycardia was present in all untreated and atropine-treated animals. 4. Mean heart rate values for untreated rabbits were 195 ± 2.9 and 125 ± 2.1 ( x ± SE) bpm during pre-stimulus and stimulus respectively. 5. Mean values for atropine-treated animals were 241 ± 1.1 and 162 ± 5.0 bpm during prestimulus and stimulus respectively. 6. Atropine reduced fear bradycardia from 36.1% to 33.8%, but reduced the rate of onset from −9.25 to −3.14 bpm/sec. 7. Fear bradycardia can occur without parasympathetic activity, but parasympathetic activity is necessary for the normal rapid onset of fear bradycardia.