Humans make a wide variety of decisions every day - from which route to take to the store to which job offer to accept. It has recently been proposed that two different systems, one affective and intuitive (System 1), the other logical and deliberative (System 2) interact to guide decision making. Neuroimaging research has supported this hypothesis, but other physiological indices of emotion regulation have been largely unexplored in the context of decision making. Respiratory Sinus Arrhythmia (RSA) is an index of cardiac vagal control, and has been shown to mediate emotion regulation, and vary under stress. Both impaired sleep and the phase of the sleep/wake circadian schedule also influence the expression and regulation of emotion. Sleep deprivation has been shown to lead to poor decision-making, but the relationship between sleep/wake circadian rhythms and decision making has been largely unexplored. Physiological indicators of emotion regulation (such as RSA) are likely to interact with sleep/wake circadian rhythms to influence the strategies used in decision making. The present study found that while time of day did not have an independent influence on decision making or risk taking, these functions appear to fluctuate with body temperature, a physiological index of circadian phase, with optimal performance occurring at higher body temperatures. Furthermore, while RSA appears to be unrelated to decision making and risk taking, circadian phase may influence physiological responses to stress (as measured by RSA) at different times of the day. In particular, morning-types may be more reactive to stress in the evening than during the day. Further research is needed to validate and clarify these findings.

Slow and deep breathing (SDB) has long been regarded as a nonpharmacological method for dealing with several physiological and emotional imbalances, and widely used for relaxation purposes. There is, however, limited understanding of the putative mechanisms by which SDB acutely impacts the cardiovascular and autonomic systems to elicit chronic adaptations. The present thesis explored how the manipulation of breathing pattern and intrathoracic pressure during SDB could further the understanding of the regulatory mechanisms that underpin the acute cardiovascular response to SDB. This thesis makes an original contribution to the existing knowledge by reporting a previously undescribed inversion of normal within-breath (inspiration vs. expiration) left ventricular stroke volume (LVSV) pattern for breathing frequencies < 8 breaths∙min-1. This finding might reflect the influence of a lag between enhanced right atrial filling and right ventricular stroke volume during inspiration, and its expression in left ventricular stroke volume; this lag results from the time required for blood to transit the pulmonary circulation. Furthermore, blood pressure variability (BPV) was reduced significantly at the lowest breathing frequencies, likely due to the involvement of baroreflex mediated responses. The pattern of responses was consistent with the buffering of respiratory-driven fluctuations in left ventricular cardiac output (Q̇) and arterial blood pressure (ABP) by within breath fluctuations in heart rate (fc), i.e., respiratory sinus arrhythmia (RSA) (Chapter 4). Chapter 5 demonstrated that magnifying negative intrathoracic pressure with inspiratory loading during SDB increased inspiratory pressure-driven fluctuations in LVSV and fc, and enhanced Q̇, independently of changes in VT and fR. The data support an important contribution to the amplification of RSA, during SDB, of previously underappreciated reflex, and/or 'myogenic', cardiac response mechanisms. The findings in Chapter 6 confirmed that inspiratory loading during SDB amplified the effects observed with un-loaded SDB (reported in chapter 5). In contrast, expiratory loading increased ABP and attenuated RSA, LVSV and Q̇ during SDB. A lower RSA for higher ABP, supports the presence of a formerly underappreciated contribution of sinoatrial node stretch to RSA, and throws into question the clinical benefits of expiratory resisted SDB, particularly in hypertensive populations. In conclusion, the findings of the present thesis provide novel information regarding the mechanisms contributing to acute cardiovascular response to SDB. These new insights may contribute to the development of more effective SDB interventions, geared towards maximising the perturbation to the cardiovascular control systems.

Heart rate variability (HRV) is a naturally occurring cardiovascular phenomenon referring to the changing timing between consecutive heartbeats. The connection between HRV and overall cardiovascular health and autonomic nervous system function has been well established through prior research and well documented in existing literature. The existing studies, however, included shorter HRV subject recording session, using traditional HRV monitoring methods that do not typically combine electrocardiogram (ECG), seismocardiogram (SCG) and galvanic skin response (GSR) respiration monitoring. The inclusion of longer HRV subject recording may allow for further insight on the possible effects of given observable biological phenomenon on HRV. The current technology for the collection and storage of analog voltage HRV signals exists as separate ECG, SCG and GSR data collection units; all of which are required to make meaningful conclusions about HRV. These individual units work independently from one another, are not portable, must be connected to a power grid at all times, require attachments to the subject at specific body surface locations to ensure data accuracy and require technical expertise to operate efficiently and interpret the obtained data. The study proposes a long-term simultaneous recording device capable of tracking these signals which will allow more detailed inter-signal analysis that can provide more insight into cardiac activity in the presence of changing observable biological phenomena over time.