Researchers at Stanford University may have uncovered link between how you breathe and how your brain functions.
It has long been known that slow, deep breathing induces relaxation and a sense of calm. Despite the benefits of controlled breathing, research has yet to fully elucidate the mechanisms through which alterations in breath reduce stress and anxiety. In a new study, researchers at Stanford University may have solved this mystery, at least in mice.
Breathing is an autonomic function that is largely unconscious. Similar to heart rhythm, inhalation and exhalation are dynamic, constant, and highly responsive to environmental demands. Unlike the heart, the speed and depth of respiration can be altered at will via higher-order brain functions. This is why you can hold your breath while jumping into water, gasp suddenly, and even yawn.
Although breathing is essential to survival, we know remarkably little about the specific brain sites and mechanisms responsible for its regulation. In the 1990s, researchers at UCLA uncovered what they referred to as the “breathing pacemaker,” a small network of roughly 3,000 neurons in the brainstems of animals and people believed to control most aspects of respiration. These neurons, part of the Pre-Botzinger Complex in the ventrolateral medulla, are believed to generate respiratory rhythm.
In recent years, scientists at Stanford and UCLA have used sophisticated genetic techniques to disentangle how the individual neurons within this pacemaker work. By isolating different proteins produced by the genes in each cell, they identified distinct subtypes of cells thought to regulate specific breathing functions.
Within these subtypes, a cluster of approximately 175 neurons was identified as a potential pathway linking the “breathing pacemaker” to regions in the brain associated with higher-order brain functions such as attention, arousal and panic. By manipulating pacemaker neurons, scientists could test whether breath patterns influence cognitive and emotional experience.
One strategy for understanding how neurons work is to disable them. For this study, a sample of mice had the receptors in these 175 neurons genetically engineered to be sensitive to a specific toxin. The toxin was then administered, functionally disabling these neurons while leaving the remainder of the breathing pacemaker intact.
Mice were then placed in a pressurized chamber that measured the size and frequency of their breath. Contrary to expectation, disabling these neurons did not alter the mice’s breathing. It did, however, change their behavior. Instead of engaging in typical exploratory activities, mice spent a preponderance of time sitting, grooming, and in states of calm. Although illuminating the chamber increased their levels of arousal and anxiety, these effects were only temporary.
Based on these data, the study’s authors concluded that signals coming from the respiratory center of the brain “communicate directly with and control higher-order brain structures associated with behavioral arousal”. In other words, breathing patterns are synchronous with arousal.
Mice are relaxed when respiration is slow and regular, and aroused when breathing is rapid or irregular. Indeed, human research shows a similar relationship between breath cycles and behavior, with alertness, anxiety and panic being linked to accelerated or erratic breathing, and relaxation and calm being associated with slow, controlled respiration.
Although this study did not demonstrate that mouse and human breathing pacemaker systems are functionally equivalent, it does suggest that similar to humans, the mouse breathing center exerts a powerful influence on higher-order brain function and behavior. This provides further evidence that interventions that emphasize controlled breathing, and practices like yoga and meditation, may be important therapeutic targets for decreasing arousal and reducing symptoms of chronic stress, anxiety and panic.
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