Respiratory sinus arrhythmia (RSA) is being used increasingly in psychophysiological studies as an index of vagal control of the heart and may be among the most selective noninvasive indices of parasympathetic control of cardiac functions. A comprehensive understanding of RSA, however, requires an appreciation of its multiple autonomic and physiological origins. We review the physiological bases of RSA and show that RSA arises from multiple tonic and phasic processes of both central and peripheral origin. These underlying mechanisms are at least partially differentiated, have distinct dynamics and consequences, and may be differentially sensitive to behavioral and cognitive events. These multiple mechanisms are relevant for psychophysiological studies of RSA, and a thorough understanding of RSA can only be achieved through an appreciation of the dynamics of its underlying origins. There is a distinction between the psychophysiological and neurophysiological domains, and conceptual and empirical bridges between these domains are needed.

Contemporary findings reveal that the multiple modes of autonomic control do not lie along a single continuum extending from parasympathetic to sympathetic dominance but rather distribute within a 2-dimensional space. The physiological origins and empirical documentation for the multiple modes of autonomic control are considered. Then a formal 2-dimensional conception of autonomic space is proposed, and a quantitative model for its translation into a functional output surface is derived. It is shown that this model (a) accounts for much of the error variance that has traditionally plagued psychophysiological studies, (b) subsumes psychophysiological principles such as the law of initial values, (c) gives rise to formal laws of autonomic constraint, and (d) has fundamental implications for the direction and interpretation of a wide array of psychophysiological studies.

In this paper, we integrate recent theoretical and empirical developments in predictive coding and active inference accounts of interoception (including the Embodied Predictive Interoception Coding model) with working hypotheses from the theory of constructed emotion to propose a biologically plausible unified theory of the mind that places metabolism and energy regulation (i.e. allostasis), as well as the sensory consequences of that regulation (i.e. interoception), at its core. We then consider the implications of this approach for understanding depression. We speculate that depression is a disorder of allostasis, whose myriad symptoms result from a ‘locked in’ brain that is relatively insensitive to its sensory context. We conclude with a brief discussion of the ways our approach might reveal new insights for the treatment of depression. This article is part of the themed issue ‘Interoception beyond homeostasis: affect, cognition and mental health’.

The classical view of emotion hypothesizes that certain emotion categories have a specific autonomic nervous system (ANS) "fingerprint" that is distinct from other categories. Substantial ANS variation within a category is presumed to be epiphenomenal. The theory of constructed emotion hypothesizes that an emotion category is a population of context-specific, highly variable instances that need not share an ANS fingerprint. Instead, ANS variation within a category is a meaningful part of the nature of emotion. We present a meta-analysis of 202 studies measuring ANS reactivity during lab-based inductions of emotion in nonclinical samples of adults, using a random effects, multilevel meta-analysis and multivariate pattern classification analysis to test our hypotheses. We found increases in mean effect size for 59.4% of ANS variables across emotion categories, but the pattern of effect sizes did not clearly distinguish 1 emotion category from another. We also observed significant variation within emotion categories; heterogeneity accounted for a moderate to substantial percentage (i.e., I2 ≥ 30%) of variability in 54% of these effect sizes. Experimental moderators epiphenomenal to emotion, such as induction type (e.g., films vs. imagery), did not explain a large portion of the variability. Correction for publication bias reduced estimated effect sizes even further, increasing heterogeneity of effect sizes for certain emotion categories. These findings, when considered in the broader empirical literature, are more consistent with population thinking and other principles from evolutionary biology found within the theory of constructed emotion, and offer insights for developing new hypotheses to understand the nature of emotion. (PsycINFO Database Record

Heart period, systolic time intervals, low and high frequency heart period variability, blood pressure, and respiration were measured in female subjects under three drug conditions (saline, atropine sulfate, metoprolol) while sitting and standing on three consecutive days. Following preinfusion baseline recordings, saline, metoprolol (14 mg), or atropine sulfate (2 mg) was infused for 15 min (by using a double-blind procedure). Recordings were taken during a postinfusion baseline and in response to an orthostatic stressor (standing versus sitting postures). At the end of the metoprolol session, atropine sulfate was infused and responses were monitored during the postinfusion (i.e., double blockade) baseline and during orthostatic stressor. Analyses of the blockade data revealed that the preejection period (PEP) reflected sympathetic but not vagal influences on the heart, and high frequency (HF, 0.12-0.40 Hz) heart rate variability (respiratory sinus arrhythmia) reflected vagal but not sympathetic influences on the heart. No other measure provided a specific index of the tonic sympathetic or vagal activation of the heart. Postinfusion PEP under saline predicted individual differences in postinfusion cardiac sympathetic activation, whereas postinfusion heart period (but not HF variability) under saline predicted individual differences in postinfusion cardiac vagal activation.