Oxytocin helps synchronize heartbeat and breathing, newly uncovered neural pathway suggests

When humans and other animals are in a calm state, they tend to breathe slower, and their heartbeat also slows down. Contrarily, when they are exercising or under psychological stress, both their breath and heartbeat tend to speed up.

The innate variation in time between heartbeats that are synchronized with the breath is described by the term respiratory heart rate variability (RespHRV). The synchronization between the heart and breath is known to be an indicator of heart health and of the correct functioning of the autonomic nervous system.

In contrast, some medical conditions, such as chronic heart failure or hypertension, have been linked to a poor synchronization between the heart and breath (i.e., a diminished RespHRV). While the health implications of RespHRV are well-documented, the neural mechanisms that link the rate of breathing with the heart’s rhythm have not yet been clearly elucidated.

New research uncovers neural pathway in mice

Researchers at Aix-Marseille University recently carried out a study involving mice aimed at further elucidating the neural underpinnings of RespHRV. Their findings, published in Nature Neuroscience, suggest that the neurotransmitter oxytocin (OT) modulates the synchronization of the breath and heartbeat, via a newly uncovered neural pathway that links the hypothalamus, brainstem and heart.

“Relaxation and positive socio-emotional states can amplify RespHRV, yet the underlying mechanism remains largely unknown,” wrote Julie Buron, Ambre Linossier and their colleagues in their paper. “We identify a hypothalamus–brainstem neuronal pathway in rodents through which OT amplifies RespHRV during calming behavior. OT neurons from the caudal paraventricular nucleus in the hypothalamus regulate the activity of a subgroup of inhibitory neurons in the pre-Bötzinger complex, the brainstem nucleus that generates the inspiratory rhythm.”

How oxytocin influences heart and breath synchronization

To investigate the neurobiological underpinnings of RespHRV, Buron, Linossier and their colleagues carried out a series of experiments involving mice. Employing a series of advanced imaging and experimental methods, they looked at how the release of OT influenced the synchronization between the animal’s heart and breathing, while also tracking how oxytocin-producing neurons influenced other brain cells.

This ultimately allowed them to uncover a previously unknown pathway involving neurons in the hypothalamus, a neuron population in the brain stem (i.e., the pre-Bötzinger complex) and the heart. The collective activity of these neurons and the release of OT was found to modulate the synchronization between the mice’s heartbeat and breathing.

Potential for new therapies targeting stress and anxiety

“Specifically, OT enhances the glycinergic input from OT-receptor-expressing neurons in the pre-Bötzinger complex to cardiac-innervating parasympathetic neurons in the nucleus ambiguus during inspiration,” wrote the authors. “This leads to amplified respiratory modulation of parasympathetic activity to the heart, thereby enhancing RespHRV. We show that OT neurons participate in the restoration of RespHRV amplitude during recovery from stress in mice, indicating that OT acts centrally to regulate cardiac activity during a calming behavior.”

The results of this recent study highlight the key role of OT in the synchronization between breathing and the heart’s rhythm, while also pin-pointing the neural mechanisms via which this neurotransmitter might boost relaxation and RespHRV. After the team’s findings are explored further and validated in other studies, they could inform the development of new therapeutic interventions that could aid stress recovery or ease some of the symptoms of anxiety disorders.

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