Experiments were performed to elucidate the mechanisms contributing to the hyperbaric bradycardia. Ethical approval was obtained and all subjects gave written and informed consent. Heart rate, arterial blood pressure, respiratory activity and carotid sinus baroreceptor reflexes were monitored non-invasively. Four healthy male saturation divers were compressed to 46ATA. Significant reductions in resting heart rate, mean arterial pressure, systolic blood pressure and diastolic blood pressure were observed. Baroreceptor sensitivity was significantly increased at 46ATA. A separate series of investigations determined the effects of breathing an increased gas density and an increased partial pressure of oxygen (<I>P</I>₀₂) on arterial blood pressure, heart rate and baroreceptor sensitivity at 1ATA. Two groups of 6 healthy male subjects participated in the experiments. No significant changes in resting heart rate, arterial blood pressure, respiratory rate, tidal volume or baroreceptor sensitivity were observed breathing an increased gas density up to 5.47gl^-1. Raising the inspired <I>P</I>₀₂ to 0.5bar at 1ATA resulted in a significant reduction in resting heart rate and a significant increase in carotid sinus baroreceptor sensitivity. Respiratory sinus arrhythmia (RSA) was used as a non-invasive estimate of vagal tone to determine whether the hyperbaric bradycardia is associated with changes in vagal autonomic control. No changes in the overall magnitude of RSA were observed over a range of respiratory rates at high pressure compared to controls at 1ATA. These results suggest that increased gas density is not a contributing factor but increased <I>P</I>₀₂ may play a role in the development of hyperbaric bradycardia.

No description available.

In this study I examined the moderating effect of three profiles of respiratory sinus arrhythmia (RSA at baseline, in response to a stressor, and in recovery from a stressor) on the relationship between parental emotion socialization during an emotion-related discussion and parental report of child internalizing symptoms 6 months later. Parents were observed during an emotion discussion task and coded for their use of emotion encouragement and general positive involvement. A total of 65 families with children between the ages of eight and ten years old completed this task while RSA scores were obtained from children during baseline, task, and recovery phases. Regression analyses were conducted to test for main effects of parental emotion socialization and RSA, as well as two-way emotion socialization x RSA interactions, in the development of internalizing symptoms 6 months following the initial interview. Interactions were further examined for the degree they statistically conformed to either a diathesis-stress or biological sensitivity to context framework (BSC). Hypotheses were partially supported: main effects were found for RSA baseline and recovery, whereas RSA reactivity moderated the association between parental emotion encouragement and child internalizing symptoms, such that parents of children exhibiting RSA withdrawal reported greater internalizing symptoms in the context of low emotion encouragement and lesser internalizing symptoms in the context of high emotion encouragement. This study highlights the importance of considering child psychophysiology, particularly reactivity to stress, in the study of the effects of parental emotion socialization on the development of psychopathology during childhood.

Extant literature suggests that experiences of childhood adversity put individuals at increased risk for deleterious emotional-behavioral and metabolic outcomes. However, the precise mechanisms through which early adversity confers risk for such outcomes remains poorly understood. Therefore, this project sought to examine the extent to which Respiratory Sinus Arrhythmia reactivity (RSA-R), a metric of Parasympathetic Nervous System functioning, influences the relationship between adversity exposure and metrics of emotional-behavioral and metabolic health during childhood. Based on prior literature, we hypothesized that RSA-R would significantly moderate the association between exposure to childhood adversity and both emotional-behavioral and metabolic health. This hypothesis was partially supported. Indeed, RSA-R interacted with experiences of childhood adversity to predict internalizing symptoms and metabolic dysfunction. The implications of these findings and directions for future research will be discussed.

Current literature suggests neurological (i.e., insula, amygdala) and autonomic (i.e., respiratory sinus arrhythmia; RSA) markers of language, social, and behavioral challenges in autism spectrum disorders (ASD; Bal et al., 2010; DiMartino, Ross, et al., 2009; Lorenzi, Patriquin, & Scarpa, 2011; Patriquin, Scarpa, Friedman, & Porges, 2011), that hypothetically reflect a defensive neurophysiological circuit (i.e., hyper-arousal within the central and autonomic nervous systems). It is unknown how this neurophysiological state contributes to difficulties in ASD. Therefore, the current study quantified peripheral and central nervous system activity and investigated how this neurophysiological circuit may be related to different social and behavioral patterns that characterize ASD. Participants with (n = 16) and without (n = 30) ASD listened to classical music while brain (via functional magnetic resonance imaging) and autonomic (via pulse oximeter and plethysmogram) data were collected. Results indicated that decreased insula and amygdala activity during physiological hyper-aroused states predicted symptoms associated with ASD, and predicted higher levels of comorbid anxiety, stress, and depression. Contrary to hypotheses, no baseline RSA or amygdala differences were noted between ASD and controls groups, suggesting that adults with ASD may have developed effective coping strategies for reducing physiological threat responses. It will be important for future studies to continue to explore and clarify the neural connections of peripheral nervous system activation in individuals with and without ASD, including extending this research to children. / Ph. D.

In addition to social communication deficits, restricted repetitive behaviors (RRBs) are a key diagnostic feature of autism spectrum disorder (ASD). Two theories regarding the etiology of RRBs in ASD have been proposed: the hyper-arousal theory, and the hypo-arousal theory. Both of these theories posit the autonomic nervous system (ANS) as being dysfunctional in ASD, resulting in the occurrence of RRBs. Many studies investigating ANS activity in ASD have focused solely on its relation to social functioning. The few that have addressed RRBs have had inconclusive findings. Not only do the current theories and studies simplify ANS activity to a measure of baseline arousal levels through vague measures such as heart rate (HR) and skin conductance response (SCR), but the literature has also framed the theories as mutually exclusive. This study used respiratory sinus arrhythmia (RSA) patterns in children with and without an ASD diagnosis as an indicator of ANS functioning to analyze its relationship to the manifestation of RRBs. Baseline RSA and RSA reactivity were found to predict RRB severity and exploratory analyses revealed that these measures were associated with specific subgroups of RRBs. These results are discussed in regards to the current behavioral literature on RRBs and the benefits of finding biomarkers for these behaviors. / Master of Science

No description available.

Although we have several therapeutic interventions for depression, we lack an understanding of the mechanisms that underlie these interventions. To gain a better understanding of the mental health conditions we treat, diagnoses we make, and interventions we use, mechanistic understandings are necessary. There is evidence that exposure to depressive emotion and cognitions can yield therapeutic outcome. The current study examines the physiology associated with an intervention, expressive writing (EW), which other research has shown to produce therapeutic outcomes because it increases exposure to negative feelings. The current study tests the hypothesis that EW increases depressive emotion, cognition, and physiology. Depression has been associated with decreased respiratory sinus arrhythmia (RSA) and increased heart rate (HR). RSA and HR were measured while participants did either EW or a control writing (CW) task. Because measures of RSA can be confounded by respiratory rate (RR), RR was also measured and statistically controlled for. Results revealed that EW does not alter RSA or HR. Interestingly, exploratory regression analyses between HR and RR during EW suggest that EW might trigger exposure to a depressive physiological state. Further investigation into the relationship between HR and RR during EW is warranted. / Thesis / Master of Science (MSc) / The current study examines the emotion, cognition, and physiology associated with an intervention, expressive writing (EW), which is commonly used as a treatment for anxiety and depression. Research has suggested that EW produces therapeutic outcome because it increases exposure to negative feelings. The current study tests the hypothesis that EW increases depressive emotion, cognition, and physiology. Results suggest that EW increases depressive emotion and cognition but does not alter some of the physiological parameters that have been associated with depression in prior research. An unpredicted exploratory result was that EW affected the relationship between heart rate and respiratory rate. Further investigation into the relationship between heart rate and respiratory rate during EW is warranted.

Heart rate variability (HRV) reflects dynamic variation in sympathetic and parasympathetic nervous system (SNS and PNS) activity. The parasympathetic vagus nerve is responsible for HRV between 0.12 and 0.4 Hz, which is thought to index the capacity for effective coping, and is linked to physical and emotional well-being. Yogic breathing to increase vagal activity is often paced below 0.12 Hz (< 7.2 breaths per minute (BrPM)), where its impact HRV can be due to both sympathetic and parasympathetic mechanisms. Five healthy volunteers completed three pharmacological blockade sessions (placebo, sympathetic blockade with Esmolol, and parasympathetic blockade with Glycopyrrolate) about 48 hours apart, and during each session completed 11 Sudarshan Kriya Yogic breathing exercises at 4-9 BrPM. HRV was the lowest under Glycopyrrolate (p < 0.001), and there was no significant difference between placebo and sympathetic blockade with Esmolol. In addition, the spectral power of specific HRV frequencies was greatest at similar frequencies of breathing, a pattern prevented only by Glycopyrrolate. These findings suggest that heart rate is vagally influenced at all breathing rates, and that the SNS is not the mechanism by which slow breathing increases HRV.

Loving-kindness meditation (LKM) has the potential to improve intrapersonal and interpersonal functioning. This unique quality of LKM makes it a desirable candidate for buffering the stress of being social evaluated or socially excluded. Using the Trier Social Stress Test and the Cyberball social exclusion paradigm, the present study investigated the effectiveness of a brief LKM session in buffering against social evaluative and social exclusion stress. Three specific questions were addressed: In what domains can LKM exert positive effects? For whom does it work? And, how does it work? One hundred and thirteen participants (N = 113, 49 men) were randomly assigned to either a 10-minute LKM session or a 10-minute visualization control session. Findings showed that even just 10 minutes of LKM had an immediate relaxing effect as evidenced by increased respiratory sinus arrhythmia (RSA), an index of parasympathetic cardiac control, and decreased respiration rate. In addition, the brief LKM intervention led to greater implicit positivity towards the self relative to the control intervention (p = .052). The brief LKM intervention also protected against some of the negative physiological and psychological effects of social stress. The majority of these effects are moderated by trait social anxiety and pre-meditation mood states (or pre-meditation mood state alone). Contrary to expectation, trait social anxiety alone did not moderate any of the LKM effects. Importantly, receiving a brief session of LKM while not being in a positive mood or being in a negative mood led to iatrogenic physiological and psychological effects. Providing an explanation for one of LKM's effects, findings showed that change in RSA during LKM fully mediated the LKM Intervention x Positive Affect interaction effect on change in post-social-stress RSA. In conclusion, findings of the present study have extended our understanding of LKM and have specific implications for future research and practice.