Heart-rate reactivity to cold pressor stress following biofeedback training

Three previous studies have shown that biofeedback training is useful in modifying heart-rate and pain ratings during ice water stimulation (cold pressor test). Subjects were given an initial cold pressor followed by heart-rate biofeedback training and a final cold pressor test in which they were instructed to control their heart rate in accordance with the prior training. It was assumed that a heart-rate control skill had been learned. In the present study, two groups of subjects (N = 9 each) were given either increase or decrease heart-rate biofeedback training following the same procedures as previously, but subjects were not instructed to control their heart rate during the final cold pressor test. Heart rate, skin conductance, electromyographic activity, and respiration were measured. The biofeedback training effects replicate the previous results. However, no heart-rate or pain rating differences were found between the two groups during the final cold pressor test. Thus, previous findings cannot be accounted for simply by a shift in heart rate and/or pain reactivity following training itself. The findings suggest that a biofeedback strategy may be useful in modifying physiological and subjective responses to painful stimuli but only if it can be used as an active coping skill.     

Learned control of heart rate during exercise in patients with borderline hypertension

Twelve patients with borderline hypertension [less than or equal to 21 X 33/12.6, greater than or equal to 18 X 6/12.0 kPa (less than or equal to 160/95; greater than or equal to 140/90 mm Hg)] participated in an experiment aimed at testing whether they could learn to attenuate heart rate while exercising on a cycle ergometer. Six experimental (E) subjects received beat-to-beat heart-rate feedback and were asked to slow heart rate while exercising; six control (C) subjects received no feedback. Averaged over 5 days (25 training trials) the exercise heart-rate of the E group was 97.8 bt min-1, whereas the C group averaged 107 bt min-1 (P = 0.03). Systolic blood pressure was unaffected by feedback training. Generally, changes in rate-pressure product reflected changes in heart-rate. Oxygen consumption was lower in the E than in the C group late in training. We conclude that neurally mediated changes associated with exercise in patients with borderline hypertension can be brought under behavioral control through feedback training.     

Individual differences in motor skills ability affect the self-regulation of heart rate

Twenty males who scored relatively high on the rotor-pursuit motor skills task (High performance group) were given seven 2-minute trials to increase heart rate and seven 2-minute trials to decrease heart rate, as were 20 males who scored relatively low on the rotor-pursuit task (Low performance group). Visual analogue feedback was not provided during the first and last acceleration and deceleration trials but was presented during all other trials. Both groups of subjects were able to decrease heart rate significantly with and without feedback. Subjects in the High performance group were able to increase heart rate significantly with feedback and could generalize this increase to a no-feedback trial following feedback trials. Subjects in the Low performance group could not increase heart rate with or without feedback. Changes in respiration rate paralleled those noted for heart rate, but changes in chin electromyographic activity generally did not parallel the heart rate results. The heart rate data are discussed in terms of motor skills theories of self-regulation of heart rate.     

Individual differences in motor skills ability affect the self-regulation of heart rate

Twenty males who scored relatively high on the rotor-pursuit motor skills task (High performance group) were given seven 2-minute trials to increase heart rate and seven 2-minute trials to decrease heart rate, as were 20 males who scored relatively low on the rotor-pursuit task (Low performance group). Visual analogue feedback was not provided during the first and last acceleration and deceleration trials but was presented during all other trials. Both groups of subjects were able to decrease heart rate significantly with and without feedback. Subjects in the High performance group were able to increase heart rate significantly with feedback and could generalize this increase to a no-feedback trial following feedback trials. Subjects in the Low performance group could not increase heart rate with or without feedback. Changes in respiration rate paralleled those noted for heart rate, but changes in chin electromyographic activity generally did not parallel the heart rate results. The heart rate data are discussed in terms of motor skills theories of self-regulation of heart rate.Some of the results reported in this article are based on a doctoral dissertation submitted to the Graduate School of Northern Illinois University by the second author. The heart rate data were presented at the Convention of the American Psychological Association, Anaheim, 1983.     

The effects of the distribution of training on learning feedback-assisted cardiac acceleration

In order to test a hypothesis derived from a motor skills learning model of cardiac acceleration control, groups of subjects were given biofeedback training for four sessions to learn cardiac acceleration under four different training schedules: (1) all sessions in one day, (2) daily sessions, (3) sessions every other day, and (4) weekly sessions. Ability to accelerate heart rate both with and without feedback was determined at each session. Also ability to accelerate heart rate without feedback was determined 1 week after the last training session as a measure of retention. Although there was highly significant (p less than.0001) evidence of heart rate control both with and without feedback, there were no differences in degree of control attributable to distribution of training sessions. There was, however, a trend (p less than .10) for subjects trained under the most distributed training schedule (weekly) to show more retention than subjects trained under a less distributed schedule (daily).     

The use of feedback training and a stimulus control procedure to obtain large magnitude increases in heart rate outside of the laboratory

A series of eight single-subject experiments were performed to test the feasibility of using a stimulus control procedure to teach subjects to control heart rate in the absence of feedback and outside of the laboratory. Four of the six subjects who completed the experiments were able to demonstrate increases in heart rate of from 15 to 35 beats per minute without the assistance of feedback and outside of the laboratory. These increases were consistently produced over six daily sessions. Through the use of a systematic replication series of experiments, it was possible tentatively to rule out age, sex, and basal heart rate of subject, as well as type of previous feedback training and number of prior training sessions, as accounting for the differential success.     

A comparison of the heart rate at different ambient temperatures during long-term hibernation in the garden dormouse, Eliomys quercinus L.

Heart rate in hibernating garden dormice, Eliomys quercinus, was studied by means of permanently implanted electrodes; ambient temperatures (TA's) were maintained at 0, 4, 6.5, and 9 degrees C during the 6-month test period in each winter study. The animals were kept under constant conditions in darkness and without food or water. Heart rate remained at a low level during deep hibernation at all TA's studied. There were no differences in midwinter values between the TA's of 6.5 and 9 degrees C: the means were 9-12 beats/min during apnea. Heart rate thus differs from other hibernation parameters studied simultaneously, which were strongly TA dependent. However, the optimal TA of 4 degrees C could be distinguished and heart rate was significantly lower, 8-10 beats/min. At 0 degree C the values were slightly higher: 12-13 beats/min. The TA of 0 degree C was exceptional for all parameters studied. At the beginning of the hibernation season was a transition period with elevated heart rate values. Respiratory-related heart-rate changes appeared during periodic respiration, heart rate being significantly higher during respiratory periods at all TA's. At 0, 6.5, and 9 degrees C tachycardia occurred also during apnea, very close to the respiratory period. There are responses that are comparable to hypoxic environmental conditions during hibernation, diving, and pregnancy and under high-altitude conditions. Parallel adaptations appear in heart rate and respiration, i.e., bradycardia and periodic respiration. In conclusion, heart-rate values were low during deep hibernation, and compared with other parameters measured at different TA's heart rate is maintained inside narrow limits during deep hibernation.     

Physiological mechanism of digital vasoconstriction training

Recent work in our laboratory has shown that vasodilation produced during temperature biofeedback training is mediated through a nonneural, beta-adrenergic mechanism. Here we sought to determine if the effects of feedback training for vasoconstriction are produced through a neural or nonneural pathway and whether other measures of physiological activity are correlated with these changes. Nine normal subjects received temperature feedback vasoconstriction training in which feedback was delivered only during periods of successful performance. In a subsequent session, the nerves to one finger were blocked with a local anesthetic while finger blood flow was recorded from this and other fingers. Vasoconstriction occurred during feedback in the intact fingers but not in the nerve-blocked finger and was accompanied by increased skin conductance and heart rate. These data demonstrate that temperature feedback vasoconstriction training is mediated through an efferent, sympathetic nervous pathway. In contrast, temperature feedback vasodilation training is mediated through a nonneural, beta-adrenergic mechanism.     

The role of behavioral conditioning in the cardiovascular adjustment to exercise

The purpose of this study was to determine if normal subjects could be trained to attenuate their cardiovascular responses while exercising on a bicycle ergometer. Ten young, untrained subjects exercised on a bicycle ergometer for five sessions. Half of the group was asked to slow their heart rate while exercising with heart rate feedback during exercise. Their average heart rate increase was 20% less than that of the control subjects, who exercised without feedback. The control subjects subsequently also received feedback during exercise and they were able to attenuate their heart rate responses comparably. Systolic blood pressure was not affected by feedback training. Changes in rate-pressure product paralleled changes in heart rate. These data show that autonomically mediated adjustments to exercise can be brought under experimental control through the use of appropriate behavioral techniques.     

Physiological mechanism of digital vasoconstriction training

Recent work in our laboratory has shown that vasodilation produced during temperature biofeedback training is mediated through a nonneural, beta-adrenergic mechanism. Here we sought to determine if the effects of feedback training for vasoconstriction are produced through a neural or nonneural pathway and whether other measures of physiological activity are correlated with these changes. Nine normal subjects received temperature feedback vasoconstriction training in which feedback was delivered only during periods of successful performance. In a subsequent session, the nerves to one finger were blocked with a local anesthetic while finger blood flow was recorded from this and other fingers. Vasoconstriction occurred during feedback in the intact fingers but not in the nerve-blocked finger and was accompanied by increased skin conductance and heart rate. These data demonstrate that temperature feedback vasoconstriction training is mediated through an efferent, sympathetic nervous pathway. In contrast, temperature feedback vasodilation training is mediated through a nonneural, beta-adrenergic mechanism.This work was supported by research grant HL-30604 from the National Heart, Lung, and Blood Institute.     

Prostaglandins are important in thermoregulation of a reptile (Pogona vitticeps)

The effectiveness of behavioural thermoregulation in reptiles is amplified by cardiovascular responses, particularly by differential rates of heart beat in response to heating and cooling (heart-rate hysteresis). Heart-rate hysteresis is ecologically important in most lineages of ectothermic reptile, and we demonstrate that heart-rate hysteresis in the lizard Pogona vitticeps is mediated by prostaglandins. In a control treatment (administration of saline), heart rates during heating were significantly faster than during cooling at any given body temperature. When cyclooxygenase 1 and 2 enzymes were inhibited, heart rates during heating were not significantly different from those during cooling. Administration of agonists showed that thromboxane B(2) did not have a significant effect on heart rate, but prostacyclin and prostaglandin F(2alpha) caused a significant increase (3.5 and 13.6 beats min(-1), respectively) in heart rate compared with control treatments. We speculate that heart-rate hysteresis evolved as a thermoregulatory mechanism that may ultimately be controlled by neurally induced stimulation of nitric oxide production, or maybe via photolytically induced production of vitamin D.     

Time-Dependent Effects of Training on Cardiovascular Control in Spontaneously Hypertensive Rats: Role for Brain Oxidative Stress and Inflammation and Baroreflex Sensitivity

Baroreflex dysfunction, oxidative stress and inflammation, important hallmarks of hypertension, are attenuated by exercise training. In this study, we investigated the relationships and time-course changes of cardiovascular parameters, pro-inflammatory cytokines and pro-oxidant profiles within the hypothalamic paraventricular nucleus of the spontaneously hypertensive rats (SHR). Basal values and variability of arterial pressure and heart rate and baroreflex sensitivity were measured in trained (T, low-intensity treadmill training) and sedentary (S) SHR at weeks 0, 1, 2, 4 and 8. Paraventricular nucleus was used to determine reactive oxygen species (dihydroethidium oxidation products, HPLC), NADPH oxidase subunits and pro-inflammatory cytokines expression (Real time PCR), p38 MAPK and ERK1/2 expression (Western blotting), NF-κB content (electrophoretic mobility shift assay) and cytokines immunofluorescence. SHR-S vs. WKY-S (Wistar Kyoto rats as time control) showed increased mean arterial pressure (172±3 mmHg), pressure variability and heart rate (358±7 b/min), decreased baroreflex sensitivity and heart rate variability, increased p47^phox and reactive oxygen species production, elevated NF-κB activity and increased TNF-α and IL-6 expression within the paraventricular nucleus of hypothalamus. Two weeks of training reversed all hypothalamic changes, reduced ERK1/2 phosphorylation and normalized baroreflex sensitivity (4.04±0.31 vs. 2.31±0.19 b/min/mmHg in SHR-S). These responses were followed by increased vagal component of heart rate variability (1.9-fold) and resting bradycardia (−13%) at the 4th week, and, by reduced vasomotor component of pressure variability (−28%) and decreased mean arterial pressure (−7%) only at the 8th week of training. Our findings indicate that independent of the high pressure levels in SHR, training promptly restores baroreflex function by disrupting the positive feedback between high oxidative stress and increased pro-inflammatory cytokines secretion within the hypothalamic paraventricular nucleus. These early adaptive responses precede the occurrence of training-induced resting bradycardia and blood pressure fall.     

Autonomic Substrates of the Response to Pups in Male Prairie Voles

Caregiving by nonparents (alloparenting) and fathers is a defining aspect of human social behavior, yet this phenomenon is rare among mammals. Male prairie voles (Microtus ochrogaster) spontaneously exhibit high levels of alloparental care, even in the absence of reproductive experience. In previous studies, exposure to a pup was selectively associated with increased activity in oxytocin and vasopressin neurons along with decreased plasma corticosterone. In the present study, physiological, pharmacological and neuroanatomical methods were used to explore the autonomic and behavioral consequences of exposing male prairie voles to a pup. Reproductively naïve, adult male prairie voles were implanted with radiotransmitters used for recording ECG, temperature and activity. Males responded with a sustained increase in heart-rate during pup exposure. This prolonged increase in heart rate was not explained by novelty, locomotion or thermoregulation. Although heart rate was elevated during pup exposure, respiratory sinus arrhythmia (RSA) did not differ between these males and males exposed to control stimuli indicating that vagal inhibition of the heart was maintained. Blockade of beta-adrenergic receptors with atenolol abolished the pup-induced heart rate increase, implicating sympathetic activity in the pup-induced increase in heart rate. Blockade of vagal input to the heart delayed the males’ approach to the pup. Increased activity in brainstem autonomic regulatory nuclei was also observed in males exposed to pups. Together, these findings suggest that exposure to a pup activates both vagal and sympathetic systems. This unique physiological state (i.e. increased sympathetic excitation of the heart, while maintaining some vagal cardiac tone) associated with male caregiving behavior may allow males to both nurture and protect infants.     

The role of EMG awareness in EMG biofeedback learning

Underlying most research on biofeedback learning is a theoretical model of the processes involved. The current study tested a prediction from the Awareness Model: High initial EMG awareness should facilitate response control during EMG biofeedback training. Seventy-two undergraduates were assessed for forehead EMG awareness by asking them to produce target responses from 1.0 to 5.0 µV every 15 s for 16 trials. Based on this assessment, two groups (high and low awareness) were trained for 64 trials to produce these target levels with either EMG biofeedback, practice (no feedback), or noncontingent EMG feedback. A transfer task was identical to the initial assessment. During training, the biofeedback group deviated less from target than the practice and noncontingent groups. The biofeedback group was the only group to improve from initial EMG awareness activity. During transfer, only the low awareness biofeedback group remained below initial EMG awareness level. These findings can be interpreted in terms of the Two-Process Model.     

Abrupt rate accelerations or premature beats cause life-threatening arrhythmias in mice with long-QT3 syndrome

Deletion of amino-acid residues 1505-1507 (KPQ) in the cardiac SCN5A Na(+) channel causes autosomal dominant prolongation of the electrocardiographic QT interval (long-QT syndrome type 3 or LQT3). Excessive prolongation of the action potential at low heart rates predisposes individuals with LQT3 to fatal arrhythmias, typically at rest or during sleep. Here we report that mice heterozygous for a knock-in KPQ-deletion (SCN5A(Delta/+)) show the essential LQT3 features and spontaneously develop life-threatening polymorphous ventricular arrhythmias. Unexpectedly, sudden accelerations in heart rate or premature beats caused lengthening of the action potential with early afterdepolarization and triggered arrhythmias in Scn5a(Delta/+) mice. Adrenergic agonists normalized the response to rate acceleration in vitro and suppressed arrhythmias upon premature stimulation in vivo. These results show the possible risk of sudden heart-rate accelerations. The Scn5a(Delta/+) mouse with its predisposition for pacing-induced arrhythmia might be useful for the development of new treatments for the LQT3 syndrome.     

Effect of needle-EMG on blood-pressure and heart-rate.

Though immediate pain is reported by nearly all patients undergoing needle-EMG, little is known about its cardiovascular risk from changes in blood-pressure or heart-rate. This study was thus conducted to investigate if, and to which degree, blood-pressure and heart-rate are influenced by needle-EMG. In 50 patients, 24 women, 26 men, aged 26-78 years, conventional needle-EMGs from 54 muscles were recorded. Pain was assessed on a verbal analogue pain-scale (1-10) and blood-pressure and heart-rate were measured before, during and after EMG. Mean pain-ratings before, during and after EMG were 0.8, 4.1 and 1.0, respectively. Mean systolic/diastolic blood-pressure was 144/87 mmHg before, 145/86 mmHg during and 144/87 mmHg after EMG. Mean heart-rate before, during and after EMG was 77, 77 and 78 beats/min, respectively. Systolic/diastolic blood-pressure increased above 145/85 mmHg in only 2/6 patients during EMG. The weak affection of blood-pressure and heart-rate by pain from needle-EMG was found in patients with and without hypertension. Mean blood-pressure, heart-rate and pain-ratings before, during and after EMG were independent of age, sex and muscle. The correlation between pain-ratings and blood-pressure and heart-rate was not significant. This study shows that needle-EMG moderately hurts but does not increase blood-pressure or heart-rate, irrespective of known arterial hypertension. Based upon these findings, the cardiovascular risk of needle-EMG from changes in blood-pressure or heart-rate is regarded negligibly low.     

Autonomic mechanisms of training bradycardia: beta-adrenergic receptors in humans

To address the autonomic mechanisms underlying the bradycardia of physical training in human subjects, we performed a cross-sectional study comparing the heart-rate responses to graded doses of isoproterenol in 7 elite marathon runners and 7 age-matched controls, and a longitudinal study in 12 normal volunteers of the effects of 6 wk of intense physical training on lymphocyte beta-adrenergic receptors identified by l-[3H]dihydroalprenolol. We observed no significant differences between marathoners and controls in the dose of isoproterenol that produced a 25-beat/min increment in heart rate, either in the absence (1.9 +/- 0.6 vs. 2.5 +/- 0.6 microgram; P, 0.509) or in the presence of cholinergic blockade (4.4 +/- 1.3 vs. 3.1 +/- 0.4 microgram: P, 0.320). Likewise, we observed no effects of physical training on lymphocyte beta-adrenergic receptors in terms of receptors number (53 +/- 11 vs. 56 +/- 10 fmol/mg protein) or receptor affinity (Kd 4.0 +/- 0.7 vs. 3.6 +/- 0.7 nM) (P, 0.9178). Although our data cannot exclude reduced chronotropic sensitivity to catecholamines as contributing to lowered heart rate in some highly conditioned individuals, these results are consistent with the hypothesis that altered neuronal input to the sinus node is usually a more important mechanism of training bradycardia.     

Noninvasive determination of baroreflex sensitivity in man by means of spectral analysis.

The spectral analysis technique was applied for noninvasive assessment of heart-rate baroreflex sensitivity (BRS). The coherence between fluctuation of blood pressure and heart rate at 0.1 Hz and at respiratory frequency is high. This fact enables the assessment of BRS by means of calculating the modulus (or gain) of the transfer function between variations in blood pressure and heart rate. The noninvasive continuous blood pressure registration according to Penáz was used. During voluntarily controlled breathing intervals, the amplitude of 0.1 Hz and respiratory peaks in the spectra of heart rate and blood pressure changed markedly. Nevertheless, the average sensitivity of the baroreflex (modulus) changed insignificantly. This result indicated that the stability of BRS can be advantageous for the use of BRS in clinical practice. The difference between the modulus at 0.1 Hz and at the breathing rate indicates that baroreflex is only one of the factors causing respiratory arrhythmia. We also compared the determination of BRS by spectral analysis with the following alternative method: both lower extremities were occluded for 5 minutes. The release of pressure in the occluding cuffs decreased blood pressure which was followed by a baroreceptor-mediated increase of heart rate. Both methods correlated, but more detailed analysis revealed the role of the low pressure receptors in BRS determined by spectral analysis.     

Transfer of Heart Rate Feedback Training to Reduce Heart Rate Response to Laboratory Tasks

To examine whether transfer of heart rate (HR) feedback training to tasks not used during training could be improved by using multiple tasks during training, a modified multiple baseline across tasks, single subject design study was conducted using six high HR-reactive young adults. Participants received HR feedback training during the presentation of a videogame, and transfer of training was assessed to a mental arithmetic challenge and handgrip task. Transfer of training was next assessed following training with the mental arithmetic challenge and handgrip task. HR responses to each training task with no HR feedback were assessed during a pre-treatment session, an immediate post-training period following training on each task, a short delay (1–2 days) post-training session, and a long delay (1–2 weeks) post-training session. HR response to a novel speech task was assessed at pre-treatment and during short delay and long delay post-training sessions. Results revealed that participants reduced HR during training and generally maintained this reduction in HR during the immediate post-training assessment when HR feedback was not present. Participants were not able to reduce HR responses to tasks during short delay and long delay post-training sessions, and they were unable to transfer HR reduction skills to the speech task. Transfer of HR feedback training to new tasks was limited in nature and efforts to train across multiple stressors did not appear to improve transfer of training.     

Effects of various taste stimuli on heart rate in humans

Relationships between taste stimuli and heart rate were evaluated in 29 healthy university students. The test solutions were sucrose, NaCl, citric acid, quinine-HCl and monosodium glutamate (MSG). Heart rate increased by 7.1-13.6% for all the taste stimuli after use as compared with pre-stimuli values. The maximum increases in heart rate came approximately 25 s after the taste stimuli. After the increases, heart rate returned to pre-stimuli levels after between 80 and 100 s. Heart rate reached its maximum with citric acid. Recovery from the heart-rate increase was more delayed for quinine-HCl and MSG than for the other stimuli. Except for sucrose, increases in heart rate and the hedonic scale values of the taste solutions showed significant negative correlation. These findings show that the taste stimuli solutions increased the heart rate and that the increase differed with the concentration and taste solution used.