Why more isn’t necessarily better when it comes to breathing?

Recently, when I was in California I spent an evening practicing holotropic breathwork. I didn’t know much about this beforehand, and you might not either, so I’ll just set the scene. There were about 20 or so of us in a circle, along with a facilitator (whose instructions generally only increased my mystification). After a rambling introduction, he switched on some music, and we divided into pairs. One member of each pair was to be a sitter, whose only job was to observe. The others—the breathers—lay supine on a bed of cushions and blankets. That was me.

Our job as breathers was to breathe as rapidly and deeply as possible, preferably making lots of noise. As a physiology geek, this was an interesting experiment to me, so I was diligent in trying to stay with it. It was much harder than it might sound, though, particularly since we had to keep it up for well over an hour. The longer it went on the more spaced out I became, and the more difficult it became to remember what I was supposed to be doing. Eventually I started to experience muscle spasms; my arms and legs began to jerk about uncontrollably.

In the end, I couldn’t sustain it. Despite the urging of the facilitator, who periodically came around to rally me with loud whooshing breathing sounds, I found myself falling into longer and longer periods of almost involuntary apnea (cessation of breathing). My friend who was observing told me afterward that my reactions were mild compared to others’. “It was like an exorcism,” she said: thrashing limbs, clenching fists, loud crying and sobbing.

My purpose isn’t really to write about holotropic breathwork, which, as I said, I don’t know much about anyway. My point here is that the effects I felt—mental fogginess, involuntary muscle contractions, long spells of apnea—are typical physiological responses to hyperventilation (defined as breathing in excess of physiological needs).
So what does this have to do with yoga? I’ll get to that, but for now I’ll just note that many yoga practitioners and teachers—naively, I think—believe that when it comes to breathing, more is better. As you’ll see, however, that’s not necessarily the case; in fact, over breathing can have very deleterious effects.

You might think the problem is too much oxygen. But in healthy people arterial blood leaving the lungs is already nearly fully saturated with oxygen, even during quiet breathing. In other words, you can’t take in too much oxygen.

Rather, the problem with hyperventilation comes from blowing off too much carbon dioxide. In normal breathing, small amounts of incoming air are mixed with a much larger volume of air remaining within the alveoli (the air sacs in the lungs where gas exchange with the blood takes place). This has the effect of maintaining an internal atmosphere within the lungs that contains a much higher percentage of CO2 than does the air outside (carbon dioxide makes up only a very small percentage of atmospheric air). CO2 levels in the bloodstream closely reflect the composition of this internal atmosphere, so that during hyperventilation, as more carbon dioxide is expelled from the alveoli, CO2 levels in the blood also fall.

We tend to see CO2 as a waste product, something to be disposed of. But in fact we need to keep  CO2 in the blood within a certain range, because it plays an important role in maintaining blood pH. As CO2 levels drop during hyperventilation, the result is a higher, or more alkaline, pH.

Because of this rise in blood pH, hyperventilation has an effect that might at first seem paradoxical—by over breathing, we actually reduce the amount of oxygen getting to the brain, a situation termed cerebral hypoxia.

This became an issue during World War II. Hyperventilating military pilots tended to become confused and disoriented. Researchers studying conscientious objectors in the laboratory were able to confirm that hyperventilation led to a reduction in blood flow to the brain, which had long been suspected. Their supposition was this was due to constriction of cerebral blood vessels. This has subsequently been shown to be the case, and although the exact mechanism is still debated, it’s clear that a rise in blood pH  triggers arterial constriction.

What’s worse is that when blood becomes more alkaline, hemoglobin (the molecule that transports oxygen in the red blood cells) tends to hold on more tightly to oxygen. This makes sense in the context of allocating oxygen to the tissues that need it most: metabolically active tissues that have consumed a lot of oxygen and need to replenish it will have also produced a lot of CO2. This creates a more acidic local environment, which in turn causes hemoglobin to release more oxygen. The reverse is true when conditions are more alkaline; tissues don’t get as much oxygen, because hemoglobin hangs on to it.

Thus, the brain gets hit with a double whammy during hyperventilation—less blood flow, plus less oxygen being released from the blood. No wonder those World War II pilots were so disoriented, or that my brain was so foggy that evening in California.

The muscle contractions I experienced were dramatic. My limbs took on a life of their own, flopping like fish as my hands and feet spasmed (a condition known as tetany), all without conscious volition. There are several hypotheses about why this happens, but the most widely accepted has to do with calcium levels in the bloodstream. As I mentioned earlier, when CO2 levels in the blood drop, pH rises. This alkaline shift causes changes in a blood-borne protein called albumin. Albumin then binds to calcium, reducing the amount of free calcium in circulation. This in turn causes peripheral nerves to become more excitable. These hair trigger nerves then fire repeatedly, sending signals to muscles that cause them to contract involuntarily.

After I quit hyperventilating, I found myself pausing for long periods after my exhalations, in a way that also felt involuntary. To my partner, it looked as if I had stopped breathing altogether. These periods of not breathing have been observed in many people after hyperventilation, but they are not easy to explain.

To understand why, let’s begin with what makes us breathe. Breathing rate is directly controlled by several regions within the brainstem, collectively called the respiratory center. The respiratory center, left to its own devices, generates a regular series of impulses along the phrenic nerve that cause the diaphragm (the main breathing muscle) to rhythmically contract and relax, in turn leading us to breathe in and out. However, the respiratory center doesn’t exist in isolation; it receives inputs from many other parts of the nervous system that alter that rhythm. Some inputs are excitatory, encouraging more frequent breathing; others inhibit breathing.

The primary inputs that stimulate breathing come from sensors known as chemoreceptors, which continuously sample the chemical composition of body fluids. Some chemoreceptors are sensitive to oxygen; when arterial oxygen levels decline, they trigger an inhale. Under normal circumstances, though, oxygen levels don’t drop low enough to stimulate these receptors. They are like a thermostat turned way down; they only click on when oxygen levels are very low, and thus serve more as a last resort than a day in, day out regulator of breathing.

Other chemoreceptors are sensitive to carbon dioxide levels. Those located in the brain stem are the primary regulators of breathing rate. Technically, they don’t sense carbon dioxide; rather they test the pH of the cerebrospinal fluid (the fluid bath the brain and spinal cord float in). However, since the prime determinant of cerebrospinal pH is the carbon dioxide level in the blood, it amounts to the same thing. These sensors are far more sensitive than oxygen sensors; even a small rise in CO2 levels will cause them to fire, sending a signal to the respiratory center to trigger an inhale. Thus, we could say that, by and large, we don’t breathe to take in oxygen, but to get rid of CO2.

There are many other inputs into the respiratory center as well, in particular from the cerebral cortex (the “executive office” of the brain, where conscious decisions are made) and the limbic system (a group of areas of the brain concerned with emotion). It’s not only physiology that determines breathing; emotions and conscious decisions play a role too.

For instance, you could choose not to breathe. Of course, you would soon find that your ability to control your breath in this way is limited. As CO2 levels rise, stimulation from the chemoreceptors will overpower signals from the “higher brain” and you’ll have no choice but to breathe. You can’t kill yourself by holding your breath. (An exception may be divers who hyperventilate before going underwater. Lowering CO2 levels beforehand allows them to hold their breath longer while diving. But if they don’t breathe when they need to, oxygen levels in the brain may drop so low that they lose consciousness and drown.)

This would seem to explain those long periods of suspension after the exhale when I gave up on hyperventilation: CO2 levels in my bloodstream had dropped so low that it took a while for them to build up high enough trigger another inhale. However, there is a problem with this answer. Chemoreceptors respond to increases in CO2; they are indifferent to decreases. In other words, they won’t cause you to stop breathing. This is why people who hyperventilate can continue to do so for long periods of time; there’s nothing to stop them, short of losing consciousness.

There are a lot of discrepancies in the research around this issue. Some studies have found periods of apnea common after hyperventilation; others have found the opposite. Some of this variation is likely due to the length of the period of hyperventilation being studied, with apneas being more common after long sessions than short. (This seems to lend credence to the mechanism I outlined above; the longer the period of hyperventilation, the more CO2 levels would be driven down.) However, even discounting that, there is a great deal of individual variation in how people respond to the aftermath of hyperventilation. Some react as I did, by ceasing breathing. Others don’t. And we still have the problem that there is no clearly explicable physiological reason why low CO2 levels should cause breathing to stop.

Of course, I was not a physiologically naive subject going in. I was aware that hyperventilation lowers CO2 levels, so perhaps at some level I made a conscious decision to stop breathing to bring them back to a normal range to restore blood flow to my fogged up brain. That’s a possibility, but to me, those periods of breath suspension felt involuntary, as if some unconscious part of the brain took over to restore my system to balance. I guess we have to leave it at that, until further research explains what happens.

In any case, not everyone will react to hyperventilation by stopping. Hyperventilation can continue for long periods, because the system of checks and balances that regulate internal conditions within the body don’t work well to restrain it. In fact, it’s possible that hyperventilation could become habitual for some individuals.

In the 1930s, Dr. William Kerr proposed that chronic, low-level hyperventilation could be behind a host of non-specific symptoms in patients suffering from anxiety, where no organic dysfunction could be found. This has sometimes been called the “fat folder syndrome” for the thickness of the patient’s medical file. These patients complained not only of anxiety or panic, but also feelings of air hunger, chest pain, dizziness and faintness, visual disturbances, fatigue, muscle cramps and poor sleep. Many had shuttled from doctor to doctor for years without a definitive diagnosis. Often they were told that the symptoms were all in their head.

To be fair to the doctors, it’s not obvious that a person is a habitual over-breather. Once hyperventilation begins and CO2 levels drop, it only takes an occasional deep breath to maintain that state. However, there are common tell-tale signs. Chronic hyperventilators are typically upper chest breathers. Their breathing tends to be rapid and unsteady, with frequent sighing.
Kerr diagnosed the syndrome by having patients intentionally hyperventilate. If this provocation reproduced their symptoms, he attributed their ailments to chronic hyperventilation, with the presumed mechanism being low levels of blood CO2. In the following years the diagnosis became more common, with the diagnostic test remaining basically the same. Many doctors reported that “fat folder” patients could be helped by restoring healthy breathing patterns.

In the 1980s other doctors began to question the existence of hyperventilation syndrome. Many people who were assumed to be chronic hyperventilators actually had normal CO2 levels, while others who did have low levels of CO2 didn’t have symptoms of the syndrome. Patients who once would have been diagnosed with hyperventilation syndrome were now seen as primarily suffering from anxiety or panic disorders. Hyperventilation was at most a side effect, not the root cause. Researchers also questioned the validity of Kerr’s hyperventilation provocation test; other stressors, such as difficult mental tasks, were found to provoke similar responses. Plus, for patients who improved with breathing retraining, those benefits were found to be as likely to stem from relaxation as from changes in CO2 levels.

Additionally, there were safety concerns. Serious, even life-threatening, conditions such as diabetic ketoacidosis, hypoglycemia or asthma could be masked by the diagnosis of hyperventilation syndrome. (Interestingly, the traditional remedy for hyperventilation, breathing into a paper bag—which in theory involves the hyperventilator re-breathing his own CO2-laden exhaled air until blood CO2 levels normalize—has also been abandoned because of its potential danger for people suffering from hypoxia due to undiagnosed lung disease.)

Since then, the term hyperventilation syndrome has fallen into disuse. Still, there seems to be some association between frequent hyperventilation and the maladies attributed to the syndrome, especially anxiety and panic disorders, even if the causal linkages are not clear. Symptoms of hyperventilation—chest pains, air hunger, dizziness and so forth—could provoke fear, and fear could lead to hyperventilation. It’s just hard to know what’s the chicken and what’s the egg.

You can easily see how chest pains—which could arise from strains to the intercostals and other thoracic muscles from habitual upper chest breathing—might feed into anxiety by triggering fears of a heart attack.

Air hunger is the feeling that it’s difficult to get enough air into the lungs and probably also results from the habit of upper thoracic breathing. The ribcage is elastic; to take a big chest breath you have to overcome that elasticity by forcibly expanding the ribcage. It tends to shrink back to its resting shape and size when you exhale, so to keep it chronically inflated takes a lot of work. You can try this yourself, to get a feeling for what it’s like. Take a big chest breath, keep the chest expanded as you exhale, then try to inhale again. You’ll immediately feel how much effort it is to breathe, and you might feel that you can’t get enough air in. It becomes obvious why those who habitually breathe in this way could feel a need to take deeper and deeper breaths to replenish their lungs.

Of course, if the problem is over-breathing in the first place, trying to breathe more deeply only makes it worse, leading to an upward spiral of increasing breathlessness and anxiety. So, whatever the underlying cause of the ailments of those with fat folder syndrome, we probably can’t discount completely a role for hyperventilation in exacerbating them.

So what does this mean for you? Well, regardless of the existence or non-existence of hyperventilation syndrome as a clinical diagnosis, it’s probably not a good idea to chronically over-breathe, especially if you tend to suffer from anxiety or panic.
How do you tell if you are over-breathing? It’s not obvious. However, because chronic hyperventilation is often coupled with an upper chest breathing pattern, noticing where the movement of your inhale begins is a good first clue. Breathing normally, place one hand on your upper sternum and the other on your abdomen. Where do you feel movement first? While there’s no one right way to breathe, and while under many circumstances it may be advantageous to breathe thoracically, if you habitually move the sternum before the belly, you may tend towards over-breathing.

If so, it will be useful for you to periodically lie on your back and spend a few minutes observing what it’s like to breathe. Particularly notice any feelings of air hunger. Do you feel a need to effort or strain to get air into your lungs? The amount of air that moves in and out of your lungs when you are relaxed is actually quite small, only about a pint per breath. It doesn’t take a lot of effort to move that much air. Just a small increase in the volume of the lungs, and the air will flow into you as a result of the pressure differential. You don’t need to strive to pull the air in.

The muscle that can most efficiently expand the volume of the lungs is the diaphragm. When you reduce extraneous effort enough to let the diaphragm do its job without interference, you’ll feel that the movement of your inhale takes place mostly in the belly and lower ribs, not in the upper chest. The belly rises and the lower ribs widen as the diaphragm contracts on the inhale, and they fall back towards their resting position as the diaphragm relaxes on the exhale. And regardless of the controversy about hyperventilation syndrome, if you re-establish that pattern of relaxed, easy breathing, you will find that it can do wonders for your mental and physical well-being.

Is Kapalabhati Hyperventilation?

You might wonder whether the yogic rapid breathing practice, kapalabhati, which at first glance resembles hyperventilation, would also cause these symptoms. My feeling is that, if done correctly, kapalabhati isn’t actually hyperventilation.
The Sanskrit word kapalabhati means “skull-shining.” It’s one of my favorite practices. I often begin my day with it after using the neti pot. It leaves me feeling both mentally energized and calm—a very different feeling from the agitation that accompanies hyperventilation. And, in fact, despite appearances, kapalabhati isn’t hyperventilation, as long as it’s done properly.

To practice kapalabhati, sit in a comfortable, upright posture such as virasana or a stable cross-legged seat. Contract your abdomen swiftly and vigorously, expelling your breath through your nose while keeping your spine fairly vertical (this means you’ll mainly use the transversus abdominis muscle, whose job is to compress the abdominal contents). Immediately following the contraction, relax your abdominal muscles to let your belly drop, which will allow air to flow back into your lungs. As you get comfortable, you can build up to a fairly rapid pace, but keep the emphasis on the exhalation. Don’t try to inhale actively. Simply allow the inhalations to happen between exhalations.

Experienced practitioners can breathe as rapidly as two breaths per second during kapalabhati. That’s 10 times as fast as a typical quiet breathing rate of 12 breaths per minute. Intuitively, it seems likely that breathing that quickly would blow off significant amounts of CO2, but let’s look at it more closely.

To estimate the volume of air moving through the lungs, we’ll calculate “minute ventilation,” the amount of air you inhale (or exhale) per minute. The “average” person takes in about half a liter (500 ml) of air per breath during normal quiet breathing. This is called “tidal volume.” Multiplying tidal volume by breathing rate gives us his minute ventilation, in this case 6 liters (500 ml x 12 breaths per minute).

(I say “his” deliberately because these “average” figures are based on studies conducted years ago with subjects who were almost always young men. Often they were medical students, since poor students are about the only people willing to endure long experimental procedures for small stipends. Otherwise, they were generally soldiers, who probably had even less choice. Lung capacity depends on size, especially height, as well as age. Since these figures are for a young man of average height and weight for the time, if you’re female or older, or a small male, your actual lung volumes could be smaller. If you’re a big man, they will probably be larger.

At 500 ml per breath and 120 breaths per minute you’d move 60 liters of air in and out every minute practicing kapalabhati. That’s 10 times normal minute ventilation—appropriate if you’re exercising vigorously, but a lot if you’re sitting still. Your abdominal muscles get a workout during kapalabhati, so your ventilation has to increase somewhat, but probably nothing like 60 liters per minute.

Fortunately, your actual tidal volume during kapalabhati is likely a lot less than 500 ml. Measured values range from 130 to 380 ml. (Keep in mind these numbers come from a mere handful of studies, each with very few subjects. There’s probably a large range of individual variability, so treat them as a rough approximation. But, in any case, they match my experience of kapalabhati as a shallow breath.)

Why is tidal volume lower during kapalabhati ?

Normally when you inhale, the diaphragm contracts, pulling down on the bottom of the lungs to stretch them open. As the volume of the lungs increases, their internal pressure drops, and air flows in. Because the lungs are elastic, when the diaphragm stops contracting they recoil to their “resting volume,” driving up the pressure to move air out. (The lungs reach their resting volume when the forces that tend to pull them closed, including their own elasticity, are balanced by the forces that tend to pull them open. Those forces include the downward pull of gravity on the abdomen and the elastic recoil of the ribs, as well as the contraction of inspiratory muscles such as the diaphragm.)

Kapalabhati is different because it’s a non-diaphragmatic breath. When you exhale during kapalabhati, the abdominal muscles contract. They push the abdominal contents upward against the diaphragm, actively compressing the lungs and driving air out. You inhale not by contracting the diaphragm, but by relaxing the abdominal muscles. This causes the abdomen to drop. As gravity pulls the belly down, it also pulls the diaphragm’s central tendon and the base of the lungs down, creating the expansion that brings air in.

Because you’re breathing rapidly, your next exhale begins before your diaphragm has a chance to descend very far. The central tendon probably doesn’t even drop to where it would be at the end of a normal exhale, much less to where it would be after a normal diaphragmatic inhale.

Not only that, to allow the belly to move as freely as possible in kapalabhati, you need to stabilize the base of ribs. You can feel this when you practice kapalabhati by placing your hands on your lower ribs and noting how they don’t widen as they typically do when you breathe diaphragmatically. Because you’re missing the lateral expansion of the lungs that usually accompanies the downward pull on their base during a diaphragmatic inhale, tidal volume is reduced even further.

Another factor also keeps kapalabhati from becoming hyperventilation: only part of that tidal volume is actually involved in gas exchange. To understand why that is, we’ll look at the microscopic anatomy of the lungs.

Gas exchange takes place at the interface between tiny, gossamer-walled air sacs known as alveoli, which make up the bulk of the lung tissue, and the networks of capillaries that surround them. Capillaries are so narrow that red blood cells pass through single file, like customers funneled through a supermarket check-out line, and so thin-walled that oxygen and carbon dioxide can diffuse between the alveoli and the blood.

Since the air that fills the tubing isn’t involved in gas exchange, that volume is called the anatomical dead space. It’s usually estimated at 150 ml. Thus, of the 500 ml taken in during a typical quiet breath, only 350 ml actually reaches the alveoli. At 12 breaths per minute, normal “alveolar ventilation” is 4.2 liters (12 x 350 ml), not the 6 liters that pass through the nostrils.

Before air reaches the alveoli it must pass through an extensive network of tubing, from the nose or mouth through the throat, the trachea, and a series of smaller and smaller branching tubes within the lungs. If the alveolar-capillary interface is the checkout line where the business of breathing is transacted—oxygen for carbon dioxide—the airway is like the network of highways and local streets that conduct goods to and from the market.

Alveolar ventilation rather than total ventilation determines how much CO2 gets expelled, so we’ll need to estimate that for kapalabhati. Arbitrarily splitting the difference between the high and low figures mentioned above for tidal volume during kapalabhati, we get an average of about 250 ml. Subtracting 150 ml of dead space gives us an estimate of 100 ml of alveolar ventilation per breath. 120 breaths per minute would yield 12 liters per minute.

That’s a rough guess, and the actual amounts could be very different for a particular individual, but it fits with laboratory observations. In the small number of studies on the subject, researchers have generally found that expired CO2 levels remain normal even during lengthy bouts of kapalabhati, at least for experienced practitioners. In addition, their cardiovascular parameters don’t reflect what you’d expect to see in hyperventilation. Whatever the increase in alveolar ventilation, it appears to match the body’s increased need for oxygen, and therefore production of CO2. That makes sense in light of the fact that most of the air moving in and out is simply filling and emptying the airway, without reaching the alveoli.

This also yields some insight into why it’s important to practice kapalabhati correctly, and, in particular, to try not to inhale actively. Just let the inhalations happen as you relax the belly between exhalations. Otherwise, you could drive alveolar ventilation too high, turning it into a true hyperventilating breath.

In my experience, this is typically why people feel lightheaded or dizzy during kapalabhati, and why some find it stressful—particularly those who are habitual paradoxical, or reverse, breathers. For them, because it’s difficult to relax the belly while inhaling, kapalabhati turns into a series of rapid forceful thoracic breaths. That’s much more likely to lead to hyperventilation than the series of sharp abdominal exhales that kapalabhati is meant to be.

Of course, it’s not easy to let go of trying to inhale. It requires trust that you will get enough air. But that might just be the most important reason to learn to do kapalabhati safely.


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Image: By National Cancer Institute ([1]) [Public domain], via Wikimedia Commons