Sighs are as involuntary as breathing, and they may serve an equally important purpose in sustaining life and lung function, according to a new study conducted by researchers at UCLA and Stanford. The researchers also found that certain neurons located in the brain stem transform regular breaths into sighs, providing new insights into the ways that the brain controls our behavior.

We often associate sighing with emotion — we sigh more frequently when we’re feeling down, tired, or depressed; but we can also sigh with relief, or sometimes for no apparent reason. A sigh is different from a regular breath because it’s deeper and fills your lungs with more oxygen — and usually feels fulfilling to have your lungs fill up to the brim with air.

“A sigh is a deep breath, but not a voluntary deep breath,” Mark Krasnow, a professor of biochemistry at the Stanford University School of Medicine and an author of the study, said in the press release. “It starts out as a normal breath, but before you exhale, you take a second breath on top of it.”

During a sigh, the lungs’ alveoli, or air sacs, expand, providing us with a sense of relief. While sighs may seem like an expression of emotion, it turns out that they serve a specific function — to inflate these air sacs when some of them have collapsed. This process helps keep the lungs functioning long-term.

“When alveoli collapse, they compromise the ability of the lung to exchange oxygen and carbon dioxide,” Jack Feldman, a professor of neurobiology at the David Geffen School of Medicine at UCLA and an author of the study, said in the press release. “The only way to pop them open again is to sigh, which brings in twice the volume of a normal breath. If you don’t sigh, your lungs will fail over time.”

In fact, “if you don’t sigh every five minutes or so, the alveoli will slowly collapse, causing lung failure,” Feldman continued. “That’s why patients in early iron lungs had such problems, because they never sighed.”

In the study, the researchers examined over 19,000 gene-expression patterns in the brain cells of mice. They found some 200 neurons in the brain stem that produce two particular neuropeptides, which have previously been linked to sighing. These neuropeptides in turn triggered another 200 neurons to activate the mice’s breathing muscles in sighing 40 times an hour. Blocking one of the peptides resulted in reducing the amount of sighs in mice in half; blocking both of them turned off the sighing function completely.

Why would learning about the neuronal mechanisms behind sighing matter? The researchers believe that for a subset of people who can’t breathe deeply on their own, finding a way to “turn on” the sighing function could be a new therapy for them.

It’s particularly acute for patients who may have anxiety disorders or other mental health issues where breathing properly is a problem for them. Breathing is closely linked to emotional state; when you’re anxious, you’re more likely to hyperventilate and take short, shallow breaths. Anxious people are also more likely to be hyper-aware of their breathing, attempt to sigh too many times to get that satisfying “full breath” of air to no avail — something referred to casually as “air hunger.”

"These molecular pathways are critical regulators of sighing, and define the core of a sigh-control circuit," Krasnow said in the press release. "It may now be possible to find drugs that target these pathways to control sighing."

Source: Feldman J, Krasnow M, et al. Nature, 2016.