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Control of respiration provides a powerful voluntary portal to entrain and modulate central autonomic networks. Slowing and deepening breathing as a relaxation technique has shown promise in a variety of cardiorespiratory and stress-related disorders, but few studies have investigated the physiological mechanisms conferring its benefits. Recent evidence suggests that breathing at a frequency near 0.1 Hz (6 breaths per minute) promotes behavioral relaxation and baroreflex resonance effects that maximize heart rate variability. Breathing around this frequency appears to elicit resonant and coherent features in neuro-mechanical interactions that optimize physiological function. Here we explore the neurophysiology of slow, deep breathing and propose that coincident features of respiratory and baroreceptor afferent activity cycling at 0.1 Hz entrain central autonomic networks. An important role is assigned to the preferential recruitment of slowly-adapting pulmonary afferents (SARs) during prolonged inhalations. These afferents project to discrete areas in the brainstem within the nucleus of the solitary tract (NTS) and initiate inhibitory actions on downstream targets. Conversely, deep exhalations terminate SAR activity and activate arterial baroreceptors via increases in blood pressure to stimulate, through NTS projections, parasympathetic outflow to the heart. Reciprocal SAR and baroreceptor afferent-evoked actions combine to enhance sympathetic activity during inhalation and parasympathetic activity during exhalation, respectively. This leads to pronounced heart rate variability in phase with the respiratory cycle (respiratory sinus arrhythmia) and improved ventilation-perfusion matching. NTS relay neurons project extensively to areas of the central autonomic network to encode important features of the breathing pattern that may modulate anxiety, arousal, and attention. In our model, pronounced respiratory rhythms during slow, deep breathing also support expression of slow cortical rhythms to induce a functional state of alert relaxation, and, via nasal respiration-based actions on olfactory signaling, recruit hippocampal pathways to boost memory consolidation. Collectively, we assert that the neurophysiological processes recruited during slow, deep breathing enhance the cognitive and behavioral therapeutic outcomes obtained through various mind-body practices. Future studies are required to better understand the physio-behavioral processes involved, including in animal models that control for confounding factors such as expectancy biases.

In humans, exercises involving slowed respiratory rate (SRR) counter autonomic sympathetic bias and reduce responses to stressors, including in individuals with various degrees of autonomic dysfunction. In the rat, we examined whether operant conditioning could lead to reductions in respiratory rate (RR) and performed preliminary studies to assess whether conditioned SRR was sufficient to decrease physiological and behavioral responsiveness to stressors. RR was continuously monitored during 20 2-h sessions using whole body plethysmography. SRR conditioned, but not yoked control rats, were able to turn off aversive visual stimulation (intermittent bright light) by slowing their breathing below a preset target of 80 breaths/min. SRR conditioned rats greatly increased the incidence of breaths below the target RR over training, with average resting RR decreasing from 92 to 81 breaths/min. These effects were significant as a group and vs. yoked controls. Preliminary studies in a subset of conditioned rats revealed behavioral changes suggestive of reduced reactivity to stressful and nociceptive stimuli. In these same rats, intermittent sessions without visual reinforcement and a post-training priming stressor (acute restraint) demonstrated that conditioned rats retained reduced RR vs. controls in the absence of conditioning. In conclusion, we present the first successful attempt to operantly condition reduced RR in an animal model. Although further studies are needed to clarify the physio-behavioral concomitants of slowed breathing, the developed model may aid subsequent neurophysiological inquiries on the role of slow breathing in stress reduction.