liveonearth (liveonearth) wrote,

Breathing Innervation Question

I've been told by meditation & yoga instructors and naturopathic doctors that inhalation is controlled by sympathetic innervation, and exhalation is parasympathetic. Based in this, we are taught to change our meditation breathing based on whether we desire to emphasize activation or calming. The idea is that by extending the inhale and shortening the exhale, you increase your sympathetic activity. More often the idea of extending the exhale to double or more the length of the inhale is used, to help us release the stresses of modern life.

My question is this: It seems reasonable to me and I do believe that the autonomic innervation of breathing is as they say. My issue comes with the fact that by intentionally altering our breathing pattern, we are no longer breathing autonomically, or automatically. We have shifted over to another pathway for governing breathing, that starts at the frontal cortex with our will, instead of in the medullary (brainstem) breathing center. Are these new pathways also sympa/parasympathetic? Or not?

Based on my own experience (I breathe a lot) I would say that exhalation is only parasympathetic when you release and let the body do it autonomically. When I intentionally extend my exhale it no longer feels as relaxing to me. Anybody have more knowledge or experience with this???

EDIT 7/18/09:
I cross posted this and received many replies mostly from the Buddhists, who hastened to remind me that Buddhist meditation involves observing the breath but not controlling it. I come from a broader base, and so I consider breath control and mantras both to be meditative tools. The purpose in my view is to stabilize the mind, to stop it from flitting about like a hummingbird from thought to thought. Practices that involve focussing on something train the mind, so that it is possible to remain conscious for longer periods of time. This, as far as I can tell, is the purpose of nearly all practices that call themselves meditation.

But back to my original question, I learned a little more:


these centers located in the reticular formation:

governs inspiration rate and rhythm
usu 12-16 breaths/minute in humans
input from CN 9 & 10, glossopharyngeal and vagal
chemoreceptor in medulla stimulated by acidic pH and increased pCO2
chemoreceptor in carotid bodies (CN 9) stimulated by same
chemoreceptor in aortic bodies (CN 10) stimulated by decreased pO2 !!!
output via phrenic nerve to diaphragm (wikipedia says external intercostals too)
(accessory breathing muscles not involved)
unconscious breathing incl diaphragmatic exertion for inhale only (exhale is relaxation)
composed of cells in the solitary tract nucleus
found in many types of fish and mammals

governs active expiration
contains both inspiratory and expiratory neurons
responsible for motor control of inspiratory and expiratory muscles during exercise
2nd in line for initiation of inspiratory activity, after DRG
nucleus para-ambiguus is active during inspiration
nucleus retrofacialis and the nucleus retroambiguus are active during exhalation


lower pons
stimulates inspiration, gasping, apneusis
prolongs inspiration
controls intensity of breathing
signals dorsal respiratory ctr (medulla)
signal: delay 'off' signal for inspiratory ramp from pneumotaxic centre of pons
inhibited by pulmonary strech receptors

aka pontine respiratory group (PRG)
upper pons
inhibits inspiration: 'off' signal
regulates rate and volume
antagonises the apneustic center, cyclically inhibiting inspiration
limits the burst of action potentials in the phrenic nerve
decreases tidal volume
absence of PRG results in an increase in depth of respiration and a decrease in respiratory rate

periodic breathing, abnormal pattern
oscillation of ventilation between apnea and tachypnea
crescendo-decrescendo pattern in the depth of respirations
caused by damage to respiratory centers (which ones??? late response to changing pCO2???)
characteristic of newborns with immature respiratory systems
ETIO: heart failure, stroke, brain injury dt trauma or tumor, altitude, CO2 poisoning, morphine
may occur during sleep

consistent very deep resp at normal or increased rate
deep and labored
ETIO: severe metabolic acidosis (DKA), renal failure
during acidosis, breathing is first rapid and shallow-->deep, slow, labored and gasping

hyper/hypo ventilation
hyper = any breathing pattern that reduces plasma CO2 dt incr rate/depth of resp

Question remains: what recruits the accessory muscles of inspiration? the VRG??
* External intercostal muscles
* Scalene muscles
* Sternocleidomastoid muscle
* Trapezius muscle
Tags: meditation, nervous system, respiratory, stress, yoga

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