Effects of interoceptive accuracy in autonomic responses to external stimuli based on cardiac rhythm

Interoceptive accuracy is an index of the ability to perceive an individual’s internal bodily state, including heartbeat and respiration. Individual differences in interoceptive accuracy influence emotional recognition through autonomic nervous activity. However, the precise mechanism by which interoceptive accuracy affects autonomic reactivity remains unclear. Here, we investigated how cardiac reactivity induced by a non-affective external rhythm differed among individuals, using a heartbeat counting task. Because individuals with poor interoceptive accuracy cannot distinguish an external rhythm from their cardiac cycles, it has been hypothesized that the interoceptive effect on heart rate works differently in individuals with good interoceptive accuracy and those with poor interoceptive accuracy. Study participants observed a visual or auditory stimulus presented at a rhythm similar to the participants’ resting heart rates. The stimulus rhythm was gradually changed from that of their resting heart rate, and we recorded electrocardiographs while participants were exposed to the stimuli. Individuals with good interoceptive accuracy exhibited a deceleration in heart rate when the rhythm of the auditory stimulus changed. In contrast, in the group with poor interoceptive accuracy, the heart rate decreased only when the stimulus became faster. They were unable to distinguish the rhythm of their own heartbeat from that of the external rhythm; therefore, we propose that such individuals recognize the stimuli at the pace of their heart rate. Individuals with good interoceptive accuracy were able to distinguish their heart rates from the external rhythm. A modality difference was not observed in this study, which suggests that both visual and auditory stimuli help mimic heart rate. These results may provide physiological evidence that autonomic reactivity influences the perception of the internal bodily state, and that interoception and the autonomic state interact to some degree.

Blunted Heart Rate Recovery to Spontaneous Nocturnal Arousals in Short Sleeping Adults

Chronic insufficient sleep is a common occurrence around the world, and results in numerous physiological detriments and consequences, including cardiovascular complications. The purpose of the present study was to assess the relationship between habitual total sleep time (TST) measured objectively via at-home actigraphy and heart rate (HR) reactivity to nocturnal cortical arousals. We hypothesized that short habitual TST would be associated with exaggerated cardiac reactivity to nocturnal cortical arousals. Participants included in 35 healthy individuals (20 male, 15 female, age: 24 ± 1, BMI: 27 ± 1 kg/m2), and were split using a median analysis into short (SS; n = 17) and normal sleeping (NS; n = 18) adults based on a minimum of 7 days of at-home actigraphy testing. All participants underwent a full overnight laboratory polysomnography (PSG) testing session, including continuous HR (electrocardiogram, ECG) sampling. HR reactivities to all spontaneous cortical arousals were assessed for 20 cardiac cycles following the onset of the arousal in all participants. Baseline HR was not significantly different between groups (P > .05). Spontaneous nocturnal arousal elicited an augmented HR response in the SS group, specifically during the recovery period [F (4.192, 134.134) = 3.413, p = .01]. There were no significant differences in HR reactivity between sexes [F (4.006, 128.189) = .429, p > .05]. These findings offer evidence of nocturnal cardiovascular dysregulation in habitual short sleepers, independent from any diagnosed sleep disorders.

An investigation of cardiac indices in normal sleepers and those with insomnia disorder

Cardiovascular disease (CVD) is the world’s leading cause of death. Insomnia, a prevalent disorder among Canadian adults, has been identified in some studies as an independent risk factor for CVD. Heart rate variability (HRV), often used as a proxy for autonomic activity in the body, has been demonstrated to be impaired in individuals with insomnia. Scientists have suggested that results implicate exaggerated sympathetic activation in people with insomnia, which can lead to impaired cardiac reactivity and poorer heart health. Much of the research in this field has been with poorly classified clinical groups and potentially confounding comorbid disorders, making the results difficult to interpret. Findings of the present study extend our understanding of the relationship between insomnia and CVD by addressing the weaknesses of prior research and by utilizing contemporary statistical methods. A well-classified clinical group meeting Research Diagnostic Criteria for Insomnia Disorder (ID; N = 26) was compared to normal sleepers (NS; N = 23) on two well-validated indices of cardiovascular health and autonomic activity, cardiac output (CO) and pre-ejection period (PEP). Values of these indices were derived from an acoustic challenge paradigm that allowed the heart to adapt to the environment via autonomic influence. A multi-level modeling (MLM) approach was used to evaluate both the within-person and between-person differences in autonomic activation and cardiac functioning using a group of predictors that are known to be associated with insomnia and/or CVD. Results of the level two MLM analyses revealed that sleep variables are not significantly predictive of cardiac reactivity indices. A post-hoc linear regression analysis using the same predictor variables to predict HRV revealed that insomnia was significantly predictive of HRV. These conflicting results raise important questions about research methodology, validity of chosen indices, and statistical techniques.

An investigation of cardiac indices in normal sleepers and those with insomnia disorder

Cardiovascular disease (CVD) is the world’s leading cause of death. Insomnia, a prevalent disorder among Canadian adults, has been identified in some studies as an independent risk factor for CVD. Heart rate variability (HRV), often used as a proxy for autonomic activity in the body, has been demonstrated to be impaired in individuals with insomnia. Scientists have suggested that results implicate exaggerated sympathetic activation in people with insomnia, which can lead to impaired cardiac reactivity and poorer heart health. Much of the research in this field has been with poorly classified clinical groups and potentially confounding comorbid disorders, making the results difficult to interpret. Findings of the present study extend our understanding of the relationship between insomnia and CVD by addressing the weaknesses of prior research and by utilizing contemporary statistical methods. A well-classified clinical group meeting Research Diagnostic Criteria for Insomnia Disorder (ID; N = 26) was compared to normal sleepers (NS; N = 23) on two well-validated indices of cardiovascular health and autonomic activity, cardiac output (CO) and pre-ejection period (PEP). Values of these indices were derived from an acoustic challenge paradigm that allowed the heart to adapt to the environment via autonomic influence. A multi-level modeling (MLM) approach was used to evaluate both the within-person and between-person differences in autonomic activation and cardiac functioning using a group of predictors that are known to be associated with insomnia and/or CVD. Results of the level two MLM analyses revealed that sleep variables are not significantly predictive of cardiac reactivity indices. A post-hoc linear regression analysis using the same predictor variables to predict HRV revealed that insomnia was significantly predictive of HRV. These conflicting results raise important questions about research methodology, validity of chosen indices, and statistical techniques.

Vagal Tone Biofeedback: Respiratory and Non-respiratory Mediated Modulations of Vagal tone Challenged by Cold Pressor Test

Deficient parasympathetic activity to the heart has been hypothesized to underlie some forms of cardiovascular disease. Consequently, this experiment attempted to induce non- respiratory mediated increases in cardiac parasympathetic activity. Thirty-nine subjects were asked to increase their vagal tone using biofeedback, paced breathing, biofeedback plus paced breathing, or quiet sitting. The cold pressor test was used to examine the relative efficacy of vagal tone increase to mitigate cardiovascular reactivity. Repeated measures ANOVAs and t-tests revealed significant increases in vagal tone for the paced breathing, and biofeedback plus paced breathing groups, relative to controls. However, the quality of these increases could not be tested using the cold pressor test because the test failed to produce homogeneous cardiac reactivity.

4293 Relationship between recent drinking history, subjective response to alcohol, and sex in HRV in non-dependent drinkers

OBJECTIVES/GOALS: Previous research has shown acute and chronic alcohol effects on cardiac function, including elevated heart rate (HR) and lowered heart rate variability (HRV). This study aimed to examine the relationship between cardiac reactivity and subjective response following intravenous (IV) alcohol in non-dependent drinkers. METHODS/STUDY POPULATION: Non-dependent drinkers (N = 46, average age = 25.2) completed a human laboratory IV alcohol self-administration (IV-ASA) session. Subjective response to alcohol was assessed using the Drug Effects Questionnaire (DEQ) and Alcohol Urge Questionnaire (AUQ). Drinking behavior was assessed using the Alcohol Timeline Followback (TLFB) and Alcohol Use Disorders Identification Test (AUDIT). HR was recorded using the Polar Pro Heart Rate monitor throughout the session. HRV measures were calculated using guidelines determined by the Task Force of the European Society of Cardiology and The North American Society of Pacing and Electrophysiology. RESULTS/ANTICIPATED RESULTS: Recent drinking history as measured by the AUDIT and TLFB was not significantly different by sex. Results showed heavier drinking measures (AUDIT and TLFB) were positively associated with HRV measures (all p-values < 0.02). Those who reported a greater increase in alcohol craving (AUQ score) and wanted more alcohol (DEQ) following an alcohol prime, showed a greater change in HRV (p < 0.005). When examining HRV change from baseline throughout the priming session, there was a significant sex interaction for NN50 (p < 0.03) and a trend for PNN50 (p-value < 0.07). DISCUSSION/SIGNIFICANCE OF IMPACT: Acute IV alcohol alters cardiac reactivity measures in non-dependent drinkers. Future directions include examining the role of sex in HRV changes during alcohol consumption during IV-ASA. Understanding the effect of alcohol on cardiac reactivity and physiology may help characterize those at risk for alcohol use disorders.