“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.
Works Cited
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.
Websites Consulted
http://people.eku.edu/ritchisong/301notes6.htm
http://en.wikipedia.org/wiki/Hering%E2%80%93Breuer_reflex
Namaste
