“What really happens when we breathe deeply?”
Maggi Mars Brisbin - RYT-200
Pranayama is defined by the meanings of the two Sanskrit roots that make up the word: prana and ayama; prana means respiration, breath, life-force, or animating energy and ayama means to lengthen, stretch, or extend. Taking the definitions of these two words together, pranayama means to lengthen, stretch, and extend the breath or life-force (Dharmashakti, F-18). In Patanjali’s Yoga Sutras, the primary text of yoga, pranayama is only mentioned in sutras 2.49-2.53. In these sutras, Patanjali states that pranayama is the control of the movement of the inhalations and exhalations, that “modifications of the life-breath are external, internal, or stationary” and are “regulated by space, time, and number and are either long or short.” Patanjali advises that if pranayama is practiced and mastered, the “veil over the inner light is destroyed, and the mind becomes fit for concentration (Carrer, 369-370).” Despite the limited amount of information provided by Patanjali, there has been a large repertoire of pranayama practices created to provide an array of physical, mental, and emotional benefits to the practitioner. Several common pranayama practices include Deergha Swasam, Nadi Suddhi, and Kapalabhati and their many declared benefits include, but are not limited to, oxygenation and purification of the blood, improved resistance to infections, calming of the central nervous system, stimulation of the parasympathetic nervous system, relaxation of skeletal muscles, drawing of the mind inward, preparation to enter a meditative state, and improved vitality (Dharmashakti, F-18). Many of these effects are challenging to measure and quantify and it can be difficult for a skeptical practitioner to accept them without scientific experimentation and explanation. As it turns out, some of the purported benefits of pranayama have been medically investigated and validated, while others lack scientific evidence.
In order to understand how the benefits of pranayama, particularly the oxygenation and purification of blood, may or may not occur in the body, it is necessary to examine the physiology of breathing. The respiratory system includes the respiratory airways leading into and out of the lungs and the lungs. Air entering the nasal cavities proceeds to the pharynx, trachea, primary bronchi, secondary bronchi, tertiary bronchi, bronchioles, and then the alveoli of the lungs, which are the site of gas exchange. Gas exchange, the primary function of the respiratory system, is executed through the process of diffusion and therefore relies completely on concentration gradients. At sea level, air pressure is 1atm or 760mm Hg. The air is composed of a mix of gases, mostly oxygen, nitrogen, and carbon dioxide, and the total air pressure is therefore composed of the partial pressures of these individual gas components. In the ambient air, the partial pressure of oxygen (PO2) is about 160 mm Hg or 21% of the total pressure. Inside the alveoli of a normal, resting human being, the partial pressure of oxygen is about 104mm Hg and the partial pressure of CO2 (PCO2) is 40mmHg. Blood returning to the lungs from the body has a PO2 of 40mmHg and a PCO2 of 45mmHg, so there is a large concentration difference between the blood and the air inside the alveoli. Subsequently, oxygen diffuses into the blood and carbon dioxide diffuses out of the blood (http://people.eku.edu/ritchisong/301notes6.htm).
The PO2 gradient described is significant because it necessitates that the blood entering the alveolar capillaries will leave with 100% oxygen saturation (PO2 100mmHg and PCO2 40mmHg). The blood is then pumped through the heart (no gas exchange) and into systemic circulation. Body cells are low in oxygen and high in carbon dioxide from the energy producing process of cellular respiration. Following the concentration gradient, oxygen diffuses into body cells and carbon dioxide diffuses into the blood, where it binds with hemoglobin or is transported as bicarbonate ions. When the blood returns to the alveolar capillaries, it again has a PO2 40mmHg and PCO2 45mmHg, allowing for gas exchange between the alveoli and alveolar capillaries once more. In order for gas exchange to continue, the concentration gradient must be maintained; this is accomplished by breathing and continuously bringing fresh air into the alveoli (http://people.eku.edu/ritchisong/301notes6.htm).
To aid in understanding the effects of PO2 on the oxygen saturation of hemoglobin, the oxygen-hemoglobin dissociation (saturation) curve visually describes the oxygen saturation of hemoglobin along varying partial pressures of oxygen and different conditions. Under normal resting conditions within the body, hemoglobin is near oxygen saturation (75-80%) at a relatively low partial pressure of oxygen (40mmHg). Keeping resting conditions in the body, the saturation of hemoglobin will increase with increasing PO2 until it reaches 100% saturation; hemoglobin is 97% saturated at PO2 of 60mmHg and 100% saturated at PO2 of about 100mmHg. Remember that the PO2 in the alveoli of the lungs is 104mmHg, so as blood leaves the lungs, the hemoglobin is 100% saturated with oxygen.
Body cells generally have low levels of oxygen (PO2 40mmHg), meaning about 20-25% of hemoglobin molecules passing by will give up their bound oxygen to them. This is extremely adaptive as it allows more oxygen to be released where it is needed if a person becomes more active. Active tissue may have a PO2 much lower than 40mmHg and blood will quickly offload oxygen to active tissue. In addition to a more dramatic PO2 concentration gradient, active cells with increased cellular respiration produce heat along with metabolic waste products such as carbon dioxide. Carbon dioxide undergoes a reaction in the blood that produces free hydrogen ions and lowers the pH. Increased temperature and lowered pH both decrease the affinity of hemoglobin towards oxygen, allowing more oxygen to be released from the hemoglobin molecules. Finally, active cells will produce a substance called 2,3-diphosphoglycerate, which changes the shape of the hemoglobin molecule causing oxygen to be released more readily. Active cells therefore change their immediate environment – increase temperature, increase carbon dioxide levels, decrease pH, and increase 2,3-diphosphogylcerate – to assure that oxygen is delivered exactly it is most needed in the body (http://people.eku.edu/ritchisong/301notes6.htm).
Pranayama practices that involve long, deep breathing are said to deliver more oxygen to the body and to detoxify the blood. With an understanding of hemoglobin saturation in the body, it is clear that breathing more deeply cannot increase the amount of oxygen in the blood nor would it remove carbon dioxide more quickly. These claims surrounding deep breathing are most likely based on an understanding of respiratory volumes and capacities. Tidal volume (TV) refers to the volume of air moving in and out of the lungs during normal, resting breath and is generally 0.5L in adults. Inspiratory reserve volume (IRV) is the volume of air that can be inhaled after a normal breath and is approximately 2.3-3.2L in adults. Expiratory reserve volume (ERV) is the volume of air that is able to be forcefully expelled after a normal exhalation and is about 1.0-2.0L in adults. The residual volume (RV) is the volume of air that remains in the respiratory system after the ERV has been expelled. The RV, generally 1.2L, is the air that cannot be purged from the respiratory system. The inspiratory capacity (IC) is the TV+IRV or the maximum amount of air that can be inhaled. The functional residual capacity (FRC) is all of the air that is not expelled during normal breathing (ERV+RV). The vital capacity (VC) is the total volume of air that an individual is capable of moving in and out of the lungs (TV+IRV+ERV). In adults, there is also about 150mL of dead space or dead air, which is air that is moved in and out during breathing but does not reach a gas exchange surface and does not participate in gas exchange. While we are breathing normally at rest, we are moving only the tidal volume in and out of the respiratory system. Because of the reserve volume, residual volume, and dead space, there is mixing of inhaled and exhaled air. This is the reason that the partial pressure of oxygen in the alveoli during normal, resting breathing is only 104mmHg instead of equaling the partial pressure of oxygen in the surrounding air, which is 160mmHg. If a person is utilizing the full vital capacity of the lungs while breathing deep slow breaths, they may be able to increase the partial pressure of oxygen in the alveoli by more completely expelling air from the lungs and therefore inhaling a larger amount of fresh air with less mixing. This, however, will not actually provide more oxygen to the body, since hemoglobin is already 100% saturated when the partial pressure of oxygen in the alveoli is only 60mmHg (http://people.eku.edu/ritchisong/301notes6.htm).
In an experiment illustrating the noneffect of deep breathing on blood oxygenation, Pratap et al. (1978) drew arterial blood from ten volunteers proficient in pranayama breathing techniques before and immediately following pranayama practices. The levels of carbon dioxide and oxygen in the blood were measured and compared; no significant changes in arterial blood gases were found after pranayama breathing practices. Pratap et al. concluded that a neural, rather than chemical, mechanism must be responsible for the reported benefits of pranayama (Pratap et al. 1978).
The action of breathing consciously and unconsciously is controlled by skeletal muscles regulated by the phrenic nerves, several control centers in the brain, and chemoreceptors and mechanoreceptors in the body. The physical movements of breathing are performed by skeletal muscles. During a normal inhalation, the external intercostals and the diaphragm contact. Contraction of the external intercostals elevates the ribs and sternum and increases the front to back dimension of the thoracic cavity. Contraction of the diaphragm pulls the diaphragm downwards, which increases the vertical dimensions of the thoracic cavity. The contraction of these muscles increases the volume of the lungs by about 0.5L and decreases the pulmonary pressure by 1mmHg, which causes air to enter the lungs. During exhalation, the external intercostals and diaphragm are relaxed and the volume of the thoracic cavity returns to the pre-inspiratory volume, which increases pressure in the lungs and forces air out. The external intercostals and the diaphragm are innervated by the phrenic nerves that originate mostly from the 4th cervical nerve, but also from the 3rd and 5th cervical nerves. The phrenic nerves, with sole motor control of the diaphragm, contain motor, sensory, and sympathetic nerve fibers and are influenced by the respiratory center in the medulla (http://people.eku.edu/ritchisong/301notes6.htm).
The medulla’s respiratory center is divided into the ventral and dorsal group; the dorsal group or inspiratory center is composed of “I neurons” that stimulate the phrenic nerves that bring about contraction of the external intercostals and diaphragm. The dorsal group also contains “E neurons” which inhibit the “I neurons” and allow the external intercostals and diaphragm to relax and therefore allows for exhalation. The ventral group, or the expiratory center, stimulates phrenic nerves and then intercostal nerves that innervate the internal intercostals and abdominals. The expiratory center produces a “forced exhalation.” There are also two respiratory centers in the Pons: the pneumotaxic center and the apneustic center. The pneumotaxic center slightly inhibits the medulla and causes shorter, shallower, quicker breaths, while the apneustic center stimulates the medulla and causes longer, deeper, slower breaths. These four centers control normal breathing, but respiratory centers in the hypothalamus can impact breathing based on emotional responses, pain, and sexual arousal and respiratory centers in the cerebral cortex exhibit voluntary control over breathing and can override the medulla during talking, singing, and exercise (http://people.eku.edu/ritchisong/301notes6.htm).
During exercise, there is often an increase in breathing rate and depth. When breathing in this manner, the scalene muscles, the sternocleidomastoid, and the pectorals are recruited to aid the external intercostals and the diaphragm in increasing the volume of the thoracic cavity. These muscles are voluntary and the increased rate and depth of breathing during exercise is due to a conscious awareness of exercise. The cerebral cortex responds to the awareness of increased activity by stimulating the accessory muscles of external respiration and the respiratory center in the medulla. There is a steady state increase in rate and depth, which is gradually altered to match gas exchange needs (http://people.eku.edu/ritchisong/301notes6.htm). In purposeful deep breathing practices, the cortex is used to override natural resting breath and the muscles recruited for deep breathing during exercise are consciously engaged.
Chemoreceptors in the body respond to chemical changes in the blood and convey signals to the respiratory centers of the brain, which induce changes in breathing rates and depths. The peripheral chemoreceptors in the carotid arteries and the central chemoreceptors in the medulla are very sensitive to the amount of carbon dioxide dissolved in the blood. An increase in carbon dioxide and/or the resulting decrease in pH stimulates the inspiratory center and results in increased ventilation. A severe decrease in oxygen levels in the blood will stimulate increased ventilation, but a moderate decrease in oxygen levels in the blood will not have this effect (http://people.eku.edu/ritchisong/301notes6.htm). Many people are surprised to learn that the desperate urge to breathe that is experienced during prolonged breath holds is a response to increased carbon dioxide rather than lack of oxygen.
The importance of mechanoreceptors to breathing is seen in the Hering-Breuer Reflex. The Hering-Breuer reflex prevents the over-inflation of the lungs by sending nerve impulses along the vagus nerve to the brain in response to the stimulation of pulmonary stretch receptors in the smooth muscles of the airways. The inspiratory region of the medulla is directly inhibited and the apneustic area of the pons is inhibited, which stops it from stimulating the medulla’s inspiratory area, resulting in exhalation. This neural circuit involves several regions of the central nervous system and utilizes motor and sensory components of the vagus nerve. The lung afferent neurons also send inhibitory projections to the cardiac vagal motor neurons, which send motor fibers to the heart by way of the vagus nerve and cause tonic inhibitory control of heart rate. Therefore, an increase in the Hering-Breuer reflex causes an inhibition of the cardiac vagal motor neurons and an elevation of heart rate. (http://en.wikipedia.org/wiki/Hering%E2%80%93Breuer_reflex). This is part of the system that causes an increase in heart rate during inhalation and a decrease in heart rate during exhalation. This normal varying of heart rate is referred to as sinus arrhythmia (Pal et al. 2004). Slow, deep breathing stimulates pulmonary stretch receptors and by initiating the neural loop described by the Hering-Breuer reflex, it is believed that slow, deep breathing tones the vagal nerve, improves autonomic nervous system functions, and shifts the system towards parasympathetic control (Pal et al. 2004, Jerath et al. 2006).
Pal et al. (2004) investigated the effects of pranayama on the autonomic nervous system using several common tests of autonomic function - basal heart rate, heart rate response to standing, the difference in heart rate during inhale and exhale while deep breathing, and the heart rate response to a prolonged Valsalva maneuver – before and after the experiment. In the experiment, 60 volunteers were divided into the slow breathing (n=30) and fast breathing (n=30) groups and the groups were further divided into test and control groups. In the slow breathing test group, volunteers were instructed to inhale through one nostril for 6 seconds, hold the breath for 6 seconds, and then exhale out the other nostril for 6 seconds. This practice was done twice a day (am and pm) for 30 minutes over the course of 3 months. The fast breathing test group was instructed to take deep and fast inspirations and expirations for one minute and then rest for 3 minutes and to repeat this exercise 8-10 times over a 30 minute period twice a day for 3 months. The results showed that the in the slow-breathing group, basal heart rate was significantly decreased, the heart rate response to standing was significantly altered, the difference between heart-rate during a deep inhale and a deep exhale significantly increased, and there was no difference in heart rate during a prolonged Valsalva maneuver. Interestingly, there were no significant changes in the fast breathing group. The study demonstrated that slow deep breathing lowered basal heart rate, which is a function of the parasympathetic nervous system. The study suggests that decreased heart rate and blood pressure is accomplished by improving the tone of the vagal nerve and decreasing sympathetic discharge (Pal et al. 2004).
In another study, Pramanik et al. (2009) investigated the effects of deep slow breathing with and without the administration of hyoscine-N-butylbromide, a parasympathetic blocker drug. Volunteers (n=39) breathed at a rate of 6 breaths/ minute for 5 minutes with a 4 second inhale and a 6 second exhale while sitting in a comfortable seated position. The blood pressure and heart rate of each volunteer were measured before and after the breathing exercise. Another group (n=10) took the parasympathetic blocker drug and performed the same breathing exercise with the same parameters measured before and after the exercise. In the group that did not take the drug, systolic and diastolic blood pressure decreased significantly and the heart rate fell slightly. In the group that was administered hyocine-N-butylbromide, no significant change in heart rate or blood pressure was measured. This study shows a clear connection between slow deep breathing and the parasympathetic nervous system. Benefits from deep, slow, purposeful breath are the result of activation of pulmonary stretch receptors leading to the activation of the parasympathetic system and the inhibition of sympathetic activities. Over time, the activation of the parasympathetic system leads to improved functioning of the autonomic nervous system (Pramanik et al. 2009).
Improved function of the autonomic nervous system and a shift towards parasympathetic control can account for many of the reported benefits of slow, deep breathing, including decreased oxygen consumption, decreased heart rate, decreased blood pressure, improved immune function, and reduced stress levels (Jerath et al. 2006). The increased ability to meditate and the turning inward of the mind may be explained by another result of the activation of pulmonary stretch receptors. Hyperpolarization of neural and non-neural tissue has been observed in response to the stimulation of pulmonary stretch receptor. Hyperpolarization of nueral and non-neural tissue means that a larger stimulus is necessary to trigger an action potential in the tissue. This may mean that small physical disturbances and distractions are less disruptive because they are unable to trigger action potentials (Jeranth et al. 2009).
There is quite a bit of ongoing discussion and research regarding the effects of slow, deep breathing and other pranayama practices. Much of the interest surrounds how reported benefits can be explained in terms of human physiology and the root cause of many benefits have not yet be illuminated. While many will be better understood in the future, it is possible that some reported experiences surrounding pranayama may be a result of the placebo effect. Regardless of the science behind the practice, pranayama has brought physical, emotional, and mental benefits to humans for thousands of years and is a practice worthy of the interest it attracts.
Carrere, Jaganath. “Inside the Yoga Sutras. ” Integral Yoga Publications, Buckingham, Virginia; 2006.
Dharmashakti Yogin “Intensive Study Program and Yoga Intensive & Teacher Certification Program Training Manual.” Nob Hill Yoga, Albuquerque, NM; 2012.
Jerath, Ravinder, Edry, John W., Barnes, Vernon A., Jerath, Vanda (2006) “Physiology of long pranayamic breathing: neural respiratory elements may provide a mechanism that explains how slow deep breathing shifts the sutonomic nervous system.” Medical Hypothesis.
Pal, G.K., Velkumary, S., Madanmohan (2004) “Effect of short-term practice of breathing exercises on autonomic functions in normal human volunteers.” Indian J Med Res. 120: 115-121.
Pramanik, T., Sharma, H.O., Mishra, S., Mishra, A., Prjapati, R., Singh, S. (2009) “Immediate effect of slow pace Bhatrika Pranayama on blood pressure and heart rate.” The Journal of Alternative and Complementary Medicine. 15(3): 293-295.
Pratap, V., Berrettini, W.H., Smith, C. (1978) “ Arterial Blood Gases in Prana Yama Practice” Perceptual and Motor Skills. 46: 171-174.