Relation of heart rate control to heartbeat perception

The relation of heartbeat perception to voluntary control of heart rate (HR) and to learning of enhanced HR control during feedback was studied in three experiments. In Experiment I heartbeat perception was unrelated to voluntary control of HR but was negatively correlated with HR learning. Experiments II and III showed that heartbeat perception was unrelated to either initial voluntary control or learning and suggested that sampling error accounted for the negative correlation in Experiment I. Experiment I also demonstrated that learned increases in HR are retained for at least 10 weeks following feedback training. Autonomic Perception Questionnaire scores were not predictive of voluntary HR control or learning.     

Instructed heart rate control

Forty subjects participated in an experiment designed to test the effects of different feedback displays on instructed heart rate speeding and slowing. One group of subjects received information about interpulse interval length every beat. This display included specific information about when systole occurred, in addition to information about performance relative to a criterion. Two other groups received similar information about performance, but their displays were not triggered by systole; rather, information about average interpulse interval was presented either every second or every 6 seconds. A fourth group of subjects participated in a perceptual motor task in which no instructions were given to control heart rate.Results indicated that the instructed subjects generated significantly greater heart rate speeding than slowing. Groups receiving feedback produced greater changes when compared to the control group only during the speeding seassions. No differences among feedback groups were present in the slowing task. During speeding, the 1-second group's performance deteriorated dramatically in the second session. The results suggested that, in the context of a feedback task, it is information about the occurrence of systole that facilitates heart rate speeding. Real-time displays are less facilitating of heart rate change and may disrupt speeding performance when information is presented at certain critical frequencies. Slowing performance was again shown to be unrelated to information frequency or reinforcement rate.     

Skinfold thickness is related to cardiovascular autonomic control as assessed by heart rate variability and heart rate recovery

The purpose of this study was to determine if heart rate recovery (HRR) and heart rate variability (HRV) are related to maximal aerobic fitness and selected body composition measurements. Fifty men (age = 21.9 ± 3.0 years, height = 180.8 ± 7.2 cm, weight = 80.4 ± 9.1 kg, volunteered to participate in this study. For each subject, body mass index (BMI), waist circumference (WC), and the sum of skinfolds across the chest, abdomen, and thigh regions (SUMSF) were recorded. Heart rate variability (HRV) was assessed during a 5-minute period while the subjects rested in a supine position. The following frequency domain parameters of HRV were recorded: normalized high-frequency power (HFnu), and low-frequency to high-frequency power ratio (LF:HF). To determine maximal aerobic fitness (i.e., VO2max), each subject performed a maximal graded exercise test on a treadmill. Heart rate recovery was recorded 1 (HRR1) and 2 (HRR2) minutes during a cool-down period. Mean VO2max and BMI for all the subjects were 49.5 ± 7.5 ml·kg(-1)·min(-1) and 24.7 ± 2.2 kg·m(-2), respectively. Although VO2max, WC, and SUMSF was each significantly correlated to HRR and HRV, only SUMSF had a significant independent correlation to HRR1, HRR2, HFnu, LF:HF (p < 0.01). The results of the regression procedure showed that SUMSF accounted for the greatest variance in HRR1, HRR2, HFnu, and LF:HF (p < 0.01). The results of this study suggest that cardiovascular autonomic modulation is significantly related to maximal aerobic fitness and body composition. However, SUMSF appears to have the strongest independent relationship with HRR and HRV, compared to other body composition parameters and VO2max.     

Estimation of the involvement of subconsciousness in heartbeat perception in healthy volunteers

The results of analysis of heartbeat parameters and characteristics of its self-monitoring by 25 healthy volunteers have been used as the basis for original estimation of the involvement of subconsciousness in heartbeat perception. The first objective index for such estimation is proposed. It is calculated as the individual fragmentation coefficient of heartbeat perception. The discreteness of heartbeat perception is related to changes in the degree (weight) of involvement of subconsciousness in the perception of cardiac signals. A conclusion is drawn on the relationship between the efficiency of perception of one’s own heartbeat and the degree of involvement of subconsciousness in this process. The practical implication of the study is the possibility of using a similar approach to estimating the weight of unconscious processes in perception of stimuli of different types, including those used in psychodiagnostic studies.     

Neuronal control of heartbeat in the medicinal leech

Summary The leech heartbeat consists of a constriction-dilation rhythm of two lateral heart tubes extending over the length of the body. The beats of the segmental sections of these two tubes are coordinated in such a manner that the heart tube of one body side produces a frontward peristaltic wave while the heart tube on the other body side produces nearly concerted constrictions. This rhythm is metastable, in that left and right heart tubes alternate between peristaltic and concerted constriction modes, with a given mode lasting for tens or hundreds of beat cycles.The constriction-dilation cycles of the segmental heart tube sections are controlled by a set of rhythmically active motor neurons, the heart excitors, or HE cells. A bilateral pair of HE cells is located in all but the two frontmost and the two rearmost segmental ganglia of the ventral nerve cord. Each HE cell innervates via excitatory synapses the circular muscle fibers in the wall of the ipsilateral heart tube section. The activity cycle of the HE cells consists of an active phase, during which they are depolarized and produce a burst of impulses, and an inactive phase during which they are repolarized by a burst of inhibitory synaptic potentials. The intersegmentally coordinated activity cycles of the HE cell set are maintained in an isolated ventral nerve cord. Hence the generation of the heart excitor rhythm does not require sensory feedback.We are indepted to Amy Kelly and King-Wai Yau for advice on the use of the intracellular staining technique and to John Kretz for calling to our attention the existence of an afferent impulse burst rhythm emanating from denervated heart tube preparations. We thank Georgia Harper for excellent technical assistance. This research was supported by Grant GB 31933X from the National Science Foundation and NIH research grants GM17866 and Training Grant GM 01389 from the Institute of General Medical Sciences.     

Autonomic control of heart rate during exercise studied by heart rate variability spectral analysis.

Spectral analysis of heart rate variability (HRV) might provide an index of relative sympathetic (SNS) and parasympathetic nervous system (PNS) activity during exercise. Eight subjects completed six 17-min submaximal exercise tests and one resting measurement in the upright sitting position. During submaximal tests, work rate (WR) was increased for the initial 3 min in a ramp fashion until it reached constant WRs of 20 W, or 30, 60, 90, 100, and 110% of the predetermined ventilatory threshold (Tvent). Ventilatory profile and alveolar gas exchange were monitored breath by breath, and beat-to-beat HRV was measured as R-R intervals of an electrocardiogram. Spectral analysis was applied to the HRV from 7 to 17 min. Low-frequency (0-0.15 Hz) and high-frequency (0.15-1.0 Hz) areas under power spectra (LO and HI, respectively) were calculated. The indicator of PNS activity (HI) decreased dramatically (P less than 0.05) when the subjects exercised compared with rest and continued to decrease until the intensity reached 60% Tvent. The indicator of SNS activity (LO/HI) remained unchanged up to 100% Tvent, whereas it increased abruptly (P less than 0.05) at 110% Tvent. The results suggested that (cardiac) PNS activity decreased progressively from rest to a WR equivalent to 60% Tvent, and SNS activity increased only when exercise intensity exceeded Tvent.     

Chronic intermittent hypoxia impairs baroreflex control of heart rate but enhances heart rate responses to vagal efferent stimulation in anesthetized mice

Chronic intermittent hypoxia (CIH) leads to increased sympathetic nerve activity and arterial hypertension. In this study, we tested the hypothesis that CIH impairs baroreflex (BR) control of heart rate (HR) in mice, and that decreased cardiac chronotropic responsiveness to vagal efferent activity contributes to such impairment. C57BL/6J mice were exposed to either room air (RA) or CIH (6-min alternations of 21% O(2) and 5.7% O(2), 12 h/day) for 90 days. After the treatment period, mice were anesthetized (Avertin) and arterial blood pressure (ABP) was measured from the femoral artery. Mean ABP (MABP) was significantly increased in mice exposed to CIH (98.7 +/- 2.5 vs. RA: 78.9 +/- 1.4 mmHg, P < 0.001). CIH increased HR significantly (584.7 +/- 8.9 beats/min; RA: 518.2 +/- 17.9 beats/min, P < 0.05). Sustained infusion of phenylephrine (PE) at different doses (0.1-0.4 microg/min) significantly increased MABP in both CIH and RA mice, but the ABP-mediated decreases in HR were significantly attenuated in mice exposed to CIH (P < 0.001). In contrast, decreases in HR in response to electrical stimulation of the left vagus nerve (30 microA, 2-ms pulses) were significantly enhanced in mice exposed to CIH compared with RA mice at low frequencies. We conclude that CIH elicits a sustained impairment of baroreflex control of HR in mice. The blunted BR-mediated bradycardia occurs despite enhanced cardiac chronotropic responsiveness to vagal efferent stimulation. This suggests that an afferent and/or a central defect is responsible for the baroreflex impairment following CIH.     

Autonomic heart rate control and regional vascular reactions

Rheovasographic parameters (the thigh region) were recorded in groups of subjects with high and low heart rate variability (HRV). Correlation between the rheovasographic parameters and the sympathetic-parasympathetic balance value (LF/HF) was found. It was established that vagosympathetic balance in the first group was interrelated with the parameters of the ascending portion of the rheological wave; in the second group, with the parameters characterizing the blood flow in the microcirculatory bed. Thus, predominance of the autonomic loop of regulation mainly ensures an optimal regional arterial blood flow; the predominance of the central loop of regulation of cardiac activity, an optimal blood flow in microvessels.     

Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate

Systemic corticosterone (Cort) modulates arterial baroreflex control of both heart rate and renal sympathetic nerve activity. Because baroreceptor afferents terminate in the dorsal hindbrain (DHB), an area with dense corticosteroid receptor expression, we tested the hypothesis that prolonged activation of DHB Cort receptors increases the midpoint and reduces the gain of arterial baroreflex control of heart rate in conscious rats. Small (3-4 mg) pellets of Cort (DHB Cort) or Silastic (DHB Sham) were placed on the surface of the DHB, or Cort was administered systemically by placing a Cort pellet on the surface of the dura (Dura Cort). Baroreflex control of heart rate was determined in conscious male Sprague Dawley rats on each of 4 days after initiation of treatment. Plots of arterial pressure vs. heart rate were analyzed using a four-parameter logistic function. After 3 days of treatment, the arterial pressure midpoint for baroreflex control of heart rate was increased in DHB Cort rats (123 +/- 2 mmHg) relative to both DHB Sham (108 +/- 3 mmHg) and Dura Cort rats (109 +/- 2 mmHg, P < 0.05). On day 4, baseline arterial pressure was greater in DHB Cort (112 +/- 2 mmHg) compared with DHB Sham (105 +/- 2 mmHg) and Dura Cort animals (106 +/- 2 mmHg, P < 0.05), and the arterial pressure midpoint was significantly greater than mean arterial pressure in the DHB Cort group only. Also on day 4, maximum baroreflex gain was reduced in DHB Cort (2.72 +/- 0.12 beats x min(-1) x mmHg(-1)) relative to DHB Sham and Dura Cort rats (3.51 +/- 0.28 and 3.37 +/- 0.27 beats x min(-1) x mmHg(-1), P < 0.05). We conclude that Cort acts in the DHB to increase the midpoint and reduce the gain of the heart rate baroreflex function.     

Neuronal control of heart rate in isolated mouse atria

A novel mouse isolated atrial preparation with intact postganglionic autonomic innervation was used to investigate the neuronal control of heart rate. To establish whether autonomic activation was likely to alter heart rate by modulating the hyperpolarization-activated current (If), the L-type Ca2+ current (ICa,L), or the ACh-activated K+ current (IK,ACh), the effects of nerve stimulation (right stellate ganglion or right vagus, 1-30 Hz) and autonomic agonists (0.1 microM norepinephrine or 0.3 microM carbachol) on heart rate were investigated in the presence of inhibitors of these currents, cesium chloride (Cs+, 1 mM), nifedipine (200 nM), and barium chloride (Ba2+, 0.1 mM), respectively. The positive chronotropic response to stellate ganglion stimulation was reduced by approximately 20% with Cs+ and nifedipine (P < 0.05), whereas the heart rate response to norepinephrine was only reduced with Cs+ (P < 0.05). Ba2+ attenuated the decrease in heart rate with vagal stimulation and carbachol by approximately 60% (P < 0.05). These results are consistent with the idea that sympathetic nerve stimulation modulates If to increase heart rate in the mouse. Activation of ICa,L also appears to contribute to the sympathetic heart rate response. However, the decrease in heart rate with vagal stimulation or carbachol is likely to result primarily from the activation of IK,ACh.     

Sympathetic control of heart rate in nNOS knockout mice

Inhibition of neuronal nitric oxide synthase (nNOS) in cardiac postganglionic sympathetic neurons leads to enhanced cardiac sympathetic responsiveness in normal animals, as well as in animal models of cardiovascular diseases. We used isolated atria from mice with selective genetic disruption of nNOS (nNOS(-/-)) and their wild-type littermates (WT) to investigate whether sympathetic heart rate (HR) responses were dependent on nNOS. Immunohistochemistry was initially used to determine the presence of nNOS in sympathetic [tyrosine hydroxylase (TH) immunoreactive] nerve terminals in the mouse sinoatrial node (SAN). After this, the effects of postganglionic sympathetic nerve stimulation (1-10 Hz) and bath-applied norepinephrine (NE; 10(-8)-10(-4) mol/l) on HR were examined in atria from nNOS(-/-) and WT mice. In the SAN region of WT mice, TH and nNOS immunoreactivity was virtually never colocalized in nerve fibers. nNOS(-/-) atria showed significantly reduced HR responses to sympathetic nerve activation and NE (P < 0.05). Similarly, the positive chronotropic response to the adenylate cyclase activator forskolin (10(-7)-10(-5) mol/l) was attenuated in nNOS(-/-) atria (P < 0.05). Constitutive NOS inhibition with L-nitroarginine (0.1 mmol/l) did not affect the sympathetic HR responses in nNOS(-/-) and WT atria. The paucity of nNOS in the sympathetic innervation of the mouse SAN, in addition to the attenuated HR responses to neuronal and applied NE, indicates that presynaptic sympathetic neuronal NO does not modulate neuronal NE release and SAN pacemaking in this species. It appears that genetic deletion of nNOS results in the inhibition of adrenergic-adenylate cyclase signaling within SAN myocytes.