Yoga physiology, anatomy and movement science
Category Archives: Breathing/pranayama
To refresh your memory, Santaella and his colleagues studied the effects of bhastrika practice in elderly individuals (1). They tested several measures of respiratory function at the beginning of the study and again after four months of training. Those measures included forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and maximum expiratory and inspiratory pressures (PEmax, or MEP, and PImax, or MIP). Don’t worry about the abbreviations. Scientific research tends to read like acronym soup, but in general I’ll stick to the full names.
Breathe in as much as you can, then exhale out as much as possible. The amount of air you exhaled is your forced vital capacity. You’ll never empty all the air out of your lungs, so vital capacity doesn’t represent your lungs’ total capacity, but it’s a good measure of their useable capacity.
The air that’s left in the lungs after a complete exhalation is called the residual volume. Residual air is important. It helps to maintain a moist, carbon dioxide-rich atmosphere in the lungs and allows for continual gas exchange even after you’ve exhaled.
Vital capacity is a function of the size of your lungs, which is correlated with the size of your body, particularly your height. It’s also a function of your age. As you grow older, your lungs lose elasticity and your chest becomes stiffer. This leaves more air trapped in the lungs, increasing the residual volume, which leads to a gradual decline in vital capacity.
Now do the same exercise, breathing in and out as much as possible, but try to exhale as quickly as you can. The amount of air you exhale within the first second is called forced expiratory volume in one second, or FEV1. You may have done this test in your doctor’s office. FEV1 is an important measure of the health of your lungs. If you’re healthy, you should be able to empty out 80% or more of your vital capacity in the first second. If you can’t, because there’s some obstruction to the air flow, it could be a sign of asthma, chronic bronchitis or emphysema.
Maximum inspiratory and expiratory pressures are self-explanatory. They are measures of the maximum pressure you can generate while inhaling and exhaling through a mouthpiece. Both of them are indirect measures of the strength of your respiratory muscles.
The elderly lose both muscle mass and strength as they age, a process called sarcopenia. Exercise does a lot to mitigate sarcopenia, but some loss seems to be inevitable. Not surprisingly, as the strength of the respiratory musculature declines, maximum inspiratory and expiratory pressures also decline. That can be a serious problem for the elderly when conditions such as pneumonia place an extra load on the respiratory muscles. Since vital capacity and respiratory pressures decline with age, anything that improves them would be good news for the elderly.
So, did bhastrika practice help? The results were mixed. Maximum inspiratory and expiratory pressures improved significantly in the bhastrika group. Forced vital capacity and FEV1 increased slightly in the bhastrika group, but the difference was not statistically significant. The control group remained essentially unchanged, despite the fact that they were also practicing yoga (but without the bhastrika practice).
Research has generally shown that you can’t improve vital capacity with exercise. (On land at least. Swimming does increase vital capacity, probably because of the greater resistance to breathing that water provides.)
Some research suggests that yoga practice can improve vital capacity, but there are enough weaknesses in those studies that I’m not convinced. Most of the evidence comes from uncontrolled studies on students who were teenagers or young adults (2, 3). Women don’t reach full vital capacity until around age 20. For men, it’s around age 25. Without a control group, it’s hard to know whether those young people’s vital capacity would have increased regardless of yoga training. One large uncontrolled study (3) of college students did find increases across the board, regardless of age and gender. That’s suggestive of a training effect, but aside from the lack of a control group, there was also enough room for error in the testing procedures that those results aren’t as compelling as they could be.
I’ve only found one controlled study (4) showing a link between improved vital capacity and yoga. Unfortunately, there were major differences in the composition of the experimental and control groups in that study, and no details about the selection process, so again, I’m cautious about the results.
Other studies have found no correlation between yoga practice and vital capacity. It would be nice if there were better-designed studies to answer the question, especially for mature adults, but for the time being I’m not convinced that yoga does much to increase vital capacity. If it does, my guess is that the effect is small, unless you’re young. In that respect Santaella’s results weren’t surprising.
On the other hand, maximum inspiratory and expiratory pressures are a function of muscle strength. You can strengthen muscles, so you’d expect those measures to improve with training, and, in fact they did in this study. Overall, there hasn’t been much research on this topic. What little there is suggests that yoga practice can increase inspiratory and expiratory pressures (5), although in one of those studies (6) the difference was not statistically significant.
The bhastrika practice in this current study consisted of rounds of kapalabhati followed by breath retentions incorporating bandhas. I’ve written about kapalabhati before. It’s a strengthening exercise for the expiratory musculature, specifically the transversus abdominis as well as other abdominal muscles.
Inhalation retentions, particularly using jalandhara bandha, strengthen the muscles of inspiration. Jalandhara bandha is the “net-holding lock,” sometimes called chin lock. It requires you to hold the ribcage in a lifted position while bringing your chin towards your sternum. At some point, I’ll write about the physiological rationale for jalandhara bandha, but for now I’ll just point out that maintaining the position of the ribcage necessitates a strong contraction of the external intercostals along with the scalenes and the diaphragm, all of which are muscles of inspiration.
So, for the elderly individuals in this study, bhastrika practice seems to have strengthened their respiratory muscles. I should point out one caveat, though. The researchers in this study tested their subjects first to make sure they were healthy, and did not include any with evidence of cardiovascular disease in the study. Both kapalabhati and breath retentions can affect blood pressure. Because high blood pressure is common in the elderly, I wouldn’t recommend that senior citizens practice them unless they have a physician’s approval.
In the next post in this series, I’ll discuss the findings relating to heart rate variability.
1. Santaella DF, Devesa CRS, Rojo MR, et al. Yoga respiratory training improves respiratory function and cardiac sympathovagal balance in elderly subjects:
a randomised controlled trial. BMJ Open 2011;1:e000085. doi:10.1136/ bmjopen-2011-000085
5. Madanmohan, et al. Effect of six weeks yoga training on weight loss following step test, respiratory pressures, handgrip strength and handgrip endurance in young healthy subjects. Indian J Physiol Pharmacol. 2008;52(2):164-70.
Image from Wikipedia Commons
Narisara’s question in response to my kapalabhati post inspired me to write about this recent study: Yoga respiratory training improves respiratory function and cardiac sympathovagal balance in elderly subjects: a randomised controlled trial. I thought it would serve both as an opportunity to explore some interesting aspects of physiology and as a primer on scientific research in general.
You don’t need to know anything about science to practice yoga. The ancient yogis didn’t. Their method was introspection. They discovered the effects of yogic practices through sustained attention to their own internal physical and mental states. Given how much variation there is between individuals, that’s probably still the best way for you to determine the effects of your own practice.
However, yoga and meditation also teach us how untrustworthy our interpretation of things can be. We see what we want to see. Patanjali describes it in the Yoga Sutras as viparyaya—misconception.
One of the fundamental ways we are primed by evolution to mis-conceive is to see causality where none exists. “I practiced headstand, and my headache went away, so headstand much have cured it.” Not necessarily. Just because two events are correlated doesn’t mean one caused the other. And even if it did, that doesn’t mean it would work for anyone else.
A lot of scientific studies simply find correlations. That’s particularly true in epidemiological research, where scientists look at large populations to discover things like “people who drink coffee have higher rates of depression.” (I’m just making that up. I don’t know if there’s any such study.) The media often report those studies with headlines like “Coffee causes depression.” Well does it? Maybe. But maybe not. We can’t tell, because it’s simply an association. Correlation doesn’t prove causality. At most, it can generate hypotheses, which then have to be tested.
From a scientific point of view, the only way to demonstrate causality is in a randomized controlled trial. Take two groups of randomized individuals, who—in theory—don’t differ in any significant way. Test each group at the beginning of the experiment, then give one group some sort of experimental treatment with the other group acting as a control. Re-test everybody at the end. Assuming that the only difference between the groups was the treatment you gave—which is a very big assumption—any change in the experimental group had to have come from the treatment. However, this process can go wrong in all sorts of ways, which is why one trial doesn’t prove much of anything. In fact, to be accurate, no amount of trials can prove anything. All a scientific trial can really do is disprove a hypothesis. There’s always the possibility that another, unidentified factor caused the results we see, and not the experimental treatment.
Hopefully, that wasn’t too basic an introduction to the scientific method, but, since I plan to periodically review yoga research here, I wanted to cover the background first. The main point is that scientific studies vary in quality. Unfortunately, much of the yoga-related scientific literature is not very compelling. Many studies are poorly designed, or else so poorly reported that it’s hard to interpret their results—which amounts to the same thing from a scientific point of view.
This study, however, was well designed and reported, so I’m hoping it can serve as an example of what to look for in scientific research. Plus, you don’t have to rely on the abstract. You can read the full text here. It’s free, unlike many studies that require you either to be a subscriber to the journal or to pay an exorbitant fee to read the full text.
Anyway, on to the study. Investigators in Brazil hypothesized that practicing “bhastrika” would improve respiratory and autonomic nervous system function in healthy senior citizens. I put “bhastrika” in quotes because, while the term comes up a lot in pranayama research, it seems every researcher uses it to mean something different—probably because different schools of yoga define it differently. In this case, they mean kapalabhati with surya bhedana: 45 kapalabhati breaths, followed by an inhalation through the right nostril, a retention with bandhas, and a long, slow exhalation. (There’s a video here.)
This was a randomized controlled trial, which is generally the highest quality study design you’ll find in yoga research. (You’ll almost never see “blind” or “double blind” randomized controlled trials, which are the scientific gold standard, because it’s pretty obvious whether you’re doing yoga or not. Some studies have had control groups do “sham” yoga as a way of blinding participants as to which group they’re in, but that’s generally unconvincing.)
The groups were small, with 15 participants in the experimental group and 14 in the control. Those are pretty typical numbers for exercise training studies, because it’s expensive and difficult to recruit larger groups.
On the other hand, if the groups are too small, a few random outliers could mask an effect that’s actually there, so researchers need enough participants to ensure what’s called statistical power. It’s a good sign in a study when the authors include an analysis of statistical power, as they do here.
The authors provide a flow chart that gives some insight into the difficulties of recruiting subjects for these kinds of studies. They began with a pool of 150 participants in a yoga program for the elderly. Only 76 people volunteered for the experiment. Of those, 46 were excluded for health reasons such as cardiovascular disease, or because they were taking medications which could affect the results. That left 30 people, or two groups of 15. (One person in the control group didn’t attend the required classes and was dropped from the experiment.)
The authors also list demographic and biochemical statistics for the two groups to show that there weren’t obvious significant differences between them. If there were big differences, say one group were significantly older or had more men or women, those could affect the results. Randomization is supposed to eliminate such differences, but it doesn’t always, so it’s a good sign when researchers check. Of course, there could be other important differences they overlooked, but nevertheless, it’s a good sign.
Everyone in the study participated in an hour-long yoga asana class twice a week for four months. The experimental group followed that up with an extra half-hour of training in bhastrika, while the control group did 30 more minutes of asana. The experimental group also practiced bhastrika twice a day on their own for 10 minutes at a time, recording the sessions in a diary to verify compliance.
Most yoga studies have focused on the effect of a comprehensive practice that often includes asana, pranayama and meditation, and even lifestyle and dietary changes. That’s useful because it tells us something about the overall benefits of a yoga practice, but it doesn’t say anything about what specific exercises do. Was it the asana or the meditation that made a difference? We don’t know.
To me, the most interesting aspect of this study is that the authors chose not to do that, instead opting to test the effects of one specific practice. Everyone, both the control and the experimental subjects, did essentially the same yoga practice. The difference was that the experimental group added bhastrika. Therefore, we can expect that any differences in the results we see between groups will—probably—be due to bhastrika.
Participants were tested at the beginning of the study and again at the end. Those tests included measures of respiratory function, autonomic nervous system balance, and quality of life. I’ll wait to describe those in more detail over the next couple of posts because I also want to explore some of the underlying physiology along the way.
Part two of this series will look at how the bhastrika practice affected participants’ respiratory function.
Santaella DF, Devesa CRS, Rojo MR, et al. Yoga respiratory training improves respiratory function and cardiac sympathovagal balance in elderly subjects:
a randomised controlled trial. BMJ Open 2011;1:e000085. doi:10.1136/ bmjopen-2011-000085
This series on hyperventilation, or over-breathing, concludes with a look at kapalabhati, a yoga breathing technique that at first glance resembles 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.
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.
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.
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.
Frostell C, et al. Effects of high-frequency breathing on pulmonary ventilation and gas exchange. J Appl Physiol: Respirat Environ Exercise Physiol. 55(6):1854-1861,1983
Karambelkar PV, et al. Some respiratory studies in respect of kapalabhati and voluntary hyperventilation. Yoga-Mimamsa. 21(1-2):54-58,1982
Miles WR. Oxygen consumption during three yoga-type breathing patterns. J Appl Physiol. 19(1):75-82, 1964
Wenger MA & Bagchi BK. Studies of autonomic functions of practitioners of yoga in India. Behav Sci. 6:312-23, 1961
Image: By National Cancer Institute () [Public domain], via Wikimedia Commons
In the previous two parts of this series I covered the physiology of hyperventilation—what happens when we breathe more than we need to. This installment will look at what happens when people chronically hyperventilate.
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.
Bass C. Hyperventilation syndrome: a chimera? J Psychosom Res. 42(5):421-6, 1997
Gardner WN. The Pathophysiology of Hyperventilation Disorders. Chest. 109:516-534, 1996
Kerr WJ, et al. Physical Phenomena Associated with Anxiety States: The Hyperventilation Syndrome. Cal West Med. 48(1):12-6, 1938
Lum LC. Hyperventilation and anxiety state. J R Soc Med. 74(1):1-4, 1981
Lum LC. Hyperventilation syndromes in medicine and psychiatry: a review. J R Soc Med. 80(4):229-31, 1987
Lum LC. Hyperventilation: the tip and the iceberg. J Psychosom Res. 19(5-6):375-83, 1975
This is part two of a series of posts devoted to the physiology of hyperventilation.
In part one of this series, I covered what might seem like a paradoxical outcome of hyperventilation—that breathing more than necessary actually reduces the amount of oxygen to the brain. In this installment, I’ll explore two more effects of over-breathing: involuntary muscle spasms while hyperventilating and long periods of apnea (not breathing) afterwards.
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 next installment, I will look at what happens in that case.
Gardner WN. The Pathophysiology of Hyperventilation Disorders. Chest. 109:516-534, 1996
Meah MS & Gardner WN. Post-hyperventilation apnoea in conscious humans. J Physiol. 477(Pt 3):527-38, 1994
Tawadrous FD & Eldridge FL. Posthyperventilation breathing patterns after active hyperventilation in man. J Appl Physiol. 37(3):353-6, 1974
This is part one of a series of posts I plan to write on the physiology of hyperventilation.
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.
In the next installment of this series, I’ll discuss more physiological effects of hyperventilation.
Kety SS & Schmidt CF. The effects of active and passive hyperventilation on cerebral blood flow, cerebral oxygen consumption, cardiac output, and blood pressure of normal young men. J Clin Invest. 25:107-19, 1946
Raichle ME & Plum F. Hyperventilation and Cerebral Blood Flow. Stroke. 3:566-575, 1972
Tomashefski JF, et al. Carbon dioxide and acid-base transients during hyperventilation. J Appl Physiol. 17(2): 228-232, 1962