How Breath Training Alleviates Sleep Apnea – The Science
How Breath Training Alleviates Sleep Apnea – The Science
There is evidence that breath training helps with snoring and other symptoms of sleep apnea. However, until now, such simple low-cost methods are not commonplace. The reason? No scientific theory explaining the link has been produced. We have reviewed hundreds of published documents and find that there is, in fact, sound scientific research explaining how this link is possible. Simply put, special breath training exercises are designed to mimic sleep apnea events and teach your brain how to control them. Then, while you are asleep your brain quickly detects a sleep interruption, and immediately breaks the 'stopped breathing followed by gasping' cycle, characteristic of chronic sleep apnea.
Special breath training exercises are designed to mimic sleep apnea events and teach your brain how to control them
This blog will help you understand how the breathesimple app helps to improve disturbed sleep using these techniques.
Is there a theory explaining how breath training alleviates sleep apnea and snoring?
Academic research shows that:
Apnea is often a result, not only of collapsed upper airways, but poor breathing control. Poor control when awake highly correlates with poor control in sleep and the occurrence of sleep apnea.
Poor breathing habits and control can be improved using breathing exercises while awake providing long term benefits in alleviating asthma, panic attacks, anxiety and improving recovery in cardiovascular and other diseases, and now sleep apnea.
Neuro-plastic changes in the brain occur as a result of focused attention to breathing combined with breathing changes. These changes occur both in the short-term and, with extended exercises, in the much longer term. Permanent neuro-plastic changes require repetition of exercises typically daily for a few weeks. Learn more about Neuroplasticity.
Mild intermittent reduction of blood oxygen levels (hypoxia) shows benefits in apnea alleviation and can be applied using voluntary breath holding exercises.
These results support a scientific explanation for how breath training alleviates sleep apnea. Specifically, poor breathing control can be improved while awake using breathing exercises which combine mild self-imposed hypoxic sequences with interspersed relaxed breathing. Repetition of these exercises result in permanent neuro-plastic changes within the automatic breathing control center in the brain. These changes permanently enhance breathing stability while improving stimulation of the muscles that keep the upper airway clear. The result: reduction of sleep disturbed breathing episodes such as sleep apnea and snoring.
The result: reduction of sleep disturbed breathing episodes such as sleep apnea and snoring.
How does breath training help reduce chronic diseases?
There are many studies reporting the benefit of breath training for many chronic conditions associated with poor breathing habits. These conditions include asthma, Chronic Obstructive Pulmonary Disease (COPD), cardiac disturbance, chronic anxiety and panic disorder.
In humans with dysfunctional breathing, automatic breathing control mechanisms that keep the body’s functions in balance, breathing volume, rhythm and carbon dioxide levels can become chronically disordered. This occurs in part from an increased sensitivity of our built-in bio-sensors which monitor:
an increase in need to breath for patients with heart disease
respiratory threats from asthma and COPD
poor regulation in the brain stem and central nervous system
These breathing control disturbances are widespread and occur during wakefulness and sleep.
Breath training has been found to be effective in such patients helping to restore normal breathing behavior. Benefits are:
reduction in medication needs
reduction in panic attacks
improved general health
..and in the case of heart disease decreasing the number of cardiac events by 30%
Conditions successfully treated by breathing therapies include those that commonly occur with SDB, e.g. asthma and chronic airway obstruction, nasal obstruction and mouth breathing, heart disease and hypertension, and autonomic nervous system dysfunction. It has been reported that individuals who undertake breathing exercises for asthma, chronic rhinitis, anxiety or other conditions experience reduction of SDB symptoms. It has also been proposed that some common mechanisms link these conditions.
Signs of disordered automatic breathing control with a tendency to breathing instability and hyperventilation have also been observed in individuals with CSA and OSA during a normal waking state. Increased tendency to hyperventilate as evidenced by heightened central chemo-sensitivity is a common finding in CSA and also in OSA where the extent of this increased chemo-sensitivity is positively related to the severity of OSA.
Automatic breathing is controlled by complex processes involving the integration of neural signals by respiratory control centers in the pons and medulla located at the brain stem. These normally exert tight control over respiratory rate, volume and breathing pattern. However the motor cortex, at the top of the brain can override these involuntary mechanisms while we are conscious. This ability is unique to humans and is believed to have evolved with the development of complex language skills . There is experimental evidence that voluntary breathing modulation provides a mechanism for humans to re-program autonomous breathing cycles through neuro-plastic modification. This suggests that disordered and dysfunctional breathing patterns such as exist in SDB may be amenable to breathing retraining.
Do breath holding exercises help in controlling apnea?
Mild intermittent hypoxia, (MIH) is a series of lowered blood oxygen levels (hypoxic events) that are below the level at which potential pathological impacts may arise. Of course, sleep apnea is known to give rise to a number of dangerous outcomes but typically sleep apneic events are well beyond the level and duration imposed with MIH. There is now considerable evidence that the application of MIH in a controlled way can be highly beneficial to a range of chronic diseases including various forms of SDB, asthma, cardio-vascular and even neuro-physiological pathologies. . It is important to ensure that the level of hypoxic stress is maintained at a level below which it could have a detrimental effect. This implies periodic rather than continuous imposition for a limited time daily , . In a research environment, intermittent hypoxia is usually applied externally by, for example, modifying the gas mixture concentrations provided to the subject, but can be self-applied more safely and less intensively by the subject themselves through techniques such as breath holding and voluntary hypoventilation. A recent meta-study undertaken for the National Institute of Health in the United States, after reviewing extensive clinical evidence concludes that types of breathing techniques are both safe and effective in the treatment of asthma.
Are Asthma and apnea related?
There are at least 22 acceptably rigorous clinical trials that show that breath training using breathing control methods including slow breathing and hypoventilation combined with breath holding can alleviate the symptoms of asthma while reducing the use of reliever inhalers by two or more uses per day. Further, practitioners in breath training using hypoventilation combined with breath holding methods have observed that such protocols can relieve the symptoms of sleep apnea. There is a significant volume of such cases providing a substantial body of evidence indicating that imposition of periods of hypercapnia and hypoxia for a short time daily, may reduce apnea symptoms. In all the case reports and trials using breath training for apnea, benefits were equally observed for both OSA and CSA. Asthma attacks are much more likely to occur during early morning sleeping hours and those attacks are more likely to be dangerous or even fatal . There is a statistically significant co-morbidity between apnea and asthma. High OSA risk is associated with poorly controlled asthma independent of known asthma aggravators. It is recommended that patients who have difficulty achieving adequate asthma control should be screened for OSA.
What role does neuro-plasticity play in breath training?
According to the principles of neuro-plasticity, the brain is constantly changing in response to external stimuli. Many different specialized parts of the brain have been shown to exhibit neuro-plastic changes in response to the manipulation of stimuli or particular behaviors, sometimes with remarkable results . Neuro-plastic interventions are now accepted into a wide range of clinical practices such as rehabilitation from stroke, trauma and spinal cord injuries, the treatment of psychiatric, pediatric and developmental disorders, and as help in dealing with aging and other neuro-degenerative symptoms.
With the increasing capability of brain scans it is possible to map the brain in considerable detail showing rather precisely where, and to what extent, physical changes in the brain take place during different “training” stimulations, such as navigation, music, second language, and intense studying.
In particular, in a recent study on mindfulness meditation centered on breath training, 16 participants took part in an eight-week mindfulness-based stress reduction program. Brain images showed increased gray-matter density in the hippocampus, important for learning and memory, and in structures associated with self-awareness, compassion, and introspection. Reductions in stress correlated with decreased gray-matter density in the amygdala, known to play an important role in anxiety and stress.
There is evidence that the two breathing control centers in the brain, volitional and automatic, can interact. For example, prompting small gradual changes in breathing rate are retained even when the prompts are removed demonstrating that volitional modifications altered subsequent autonomous control.
Brain neuro-plasticity in breathing control is also evident in so-called respiratory Long-Term Facilitation (rLTF) whereby, after a series of hypoxic events such as those that occur during obstructive sleep apnea, there is a long-term (> one hour) enhancement of upper airway muscle tone and general respiratory muscle activity. This serves to reduce the possible pathological effects of repeated depletion of oxygen. In a further study, it has been shown that the beneficial effects of rLTF are reduced when sleep patterns are disturbed. That is, if OSA advances to a stage where there is significant sleep deprivation, the mitigating effect of rLTF is reduced thereby increasing the possible pathological impact.
The beneficial effects of intermittent hypoxia induced rLTF of upper airway and respiratory muscles function and therefore breathing stability, are not realized in cases where chemo-reflex sensitivity is excessive. Mitchell and co-workers conjecture on the possible therapeutic benefits of using neuro-plasticity for the alleviation of OSA symptoms. To quote from their publications:
“OSA is associated with inadequate neuro-modulation and hyper-excitable brainstem respiratory motor neurons. Inadequate motor output from these neurons predisposes to upper airway collapse and repetitive apneas during sleep. By harnessing respiratory plasticity it may be possible to restore synaptic inputs thereby increasing respiratory motor output to upper airway muscles and protecting upper airway patency during sleep.”
“Since repetitive intermittent hypoxia elicits respiratory motor neuron plasticity and meta-plasticity, it may be a viable means of restoring respiratory function in ventilatory control disorders. The critical issue is to develop a protocol of intermittent hypoxia that elicits the intended plasticity without unintended consequences associated with more chronic severe hypoxia.”
In other words, imposing carefully designed hypoxia sequences that maintain normal carbon dioxide levels may invoke neuro-plastic changes in the breathing control centers in the brain that can mitigate the periodic apneas that occur in OSA.
A clinical study showed that daily exposure to twelve four-minute periodic episodes of hypoxia and sustained hypercapnia during waking for 10 days, reduced apnea events noticeably. The results were remained well beyond the time that the exposures took place.
Summarizing this section, there is evidence that the breathing control centers in the brain have memory which can be altered via neuro-plasticity. rLTF is one example of this. The breathing control centers may act to alleviate the symptoms of OSA via rLTF responding to the periodic reduction in oxygen saturation. However, this feedback mechanism may be compromised in OSA sufferers. Reprogramming the control centers by imposing regulated hypoxic sequences has been shown to alleviate OSA symptoms, the results lasting beyond the period of imposition. References
Meuret A. and Ritz T. Hyperventilation in panic disorder and asthma: Empirical evidence and clinical strategies. Intl J of Psychophysio. 2010; 78(1): 68-79.
Hagman C, Janson C, Emtner M. A comparison between patients with dysfunctional breathing and patients with asthma. Clin Respir J. 2008; 2(2):86-91
Law N, Ruane L E, Low K, Hamza K, Bardin P G. Dysfunctional breathing is more frequent in chronic obstructive pulmonary disease than in asthma and in health. Resp Physiol Neurobiol. 2018; 247:20-23.
Wilhelm, F H, Gertivz R, Roth W. Respiratory dysregulation in anxiety, functional, cardiac, and pain disorders: assessment, phenomenology, and treatment. Behav Mod. 2001; 25: 513-545.
Thomas M, McKinley R K, Freeman E, Foy C. Prevalence of dysfunctional breathing in patients treated for asthma in primary care: cross sectional survey. BMJ. 2001; 322:1098-1100.
Gardner W, Meah, M.S, Bass C. Controlled study of respiratory responses during prolonged measurement in patients with chronic hyperventilation. Lancet. 1986;2:826-830.
Jack S, Rossiter H B, Warburton C J, Whipp B J. Behavioral influences and physiological indices of ventilatory control in subjects with idiopathic hyperventilation. Behav Modif. 2003;27(5): 637-652.
Wilhelm F H, Gevirtz R, Roth W T. Respiratory dysregulation in anxiety, functional, cardiac, and pain disorders: Assessment, phenomenology, and treatment. Behav Mod. 2001;25:513-545.
Grossman P. Respiration, stress and cardiovascular function. Psychophysiol. 1983;20(3): 284-300.
Gardner W. The pathophysiology of hyperventilation disorders. Chest 1995;109: 516-333.
Thomas M, McKinley R K, Freeman E, Foy C. Prevalence of dysfunctional breathing in patients treated for asthma in primary care. BMJ. 2001:322.
Perna G, Caldirola D, Bellodi L. Panic disorder: from respiration to the homeostatic brain. Acta Neuropsychiatr. 2004;16:57-67.
Caldirola D, Bellodi L, Caumo A, Migliarese G, Perna G. Approximate entropy of respiratory patterns. Am J Psychiatry. 2004;161(79-87):79-87.
Jack S, Rossiter H B, Pearson M G, Ward S A, Warburton C J, Whipp B J. Ventilatory responses to inhaled carbon dioxide, hypoxia, and exercise in idiopathic hyperventilation. Am J Resp Crit Care Med. 2004;170:118-1125.
Folgering H, Colla P. Some anomalies in the control of PACO2 in patients with a hyperventilation syndrome. Bull. Eur Physiopathol Respir. 1978;14:503-512.
Cowie R L, Conley D P, Underwood M F, Reader P G. A randomised controlled trial of the Buteyko technique as an adjunct to conventional management of asthma. Resp Med. 2008;102(5): 726-732.
Meuret A, Ritz T. Hyperventilation in panic disorder and asthma: Empirical evidence and clinical strategies. Intl J Psychophysiol. 2010;78(1):68-79.
Katsamanis M, Lehrer P M, Escobar J I, Gara M A, Kotay A, Liu R. Psychophysiological treatment for patients with medically unexplained symptoms: a randomized controlled trial. Psychosomatics. 2011;52(3):218-229.
Courtney R, van Dixhoorn J, Greenwood K M, Anthonissen E L. Medically unexplained dyspnea: partly moderated by dysfunctional (thoracic dominant) breathing pattern. J Asthma. 2011;48(3):259-265.
van Dixhoorn J, Duivenvooden H. Effects of relaxation therapy on cardiac events after mycardial infarction: a 5-year follow-up study. J Cardiopulm Rehabil. 1999;19(3): 178-185.
Kwon J S, Wolfe L F, Lu B S, Kalhan R. Hyperinflation is associated with lower sleep efficiency in COPD with co-existent obstructive sleep apnea. COPD. 2009;Vol. 6, No. 6:441-445.
Teodorescu M, Consens F B, Bria W F, et al. Predictors of habitual snoring and obstructive sleep apnea risk in patients with asthma. Chest. 2009;vol.135:5;1125-1132.
Kim H Y, Min J Y, Cho D Y, Chung S K, et al. Influence of upper airway narrowing on the effective continuous positive airway pressure level. Laryngoscope. 2007;Vol.117, 1, 82–85.
Pack A T, Gislason T. Obstructive sleep apnea and cardiovascular disease: A perspective and future directions. Prog Cardiovasc Dis. 2009; Vol. 51:5,434-451.
Budhiraja R, Budhiraja P, Quan S F. Sleep disordered breathing and cardiovascular disorders. Respir Care. 2010:55(10): 1322–1332.
Narkiewicz K, Somers V K. The sympathetic nervous system and obstructive sleep apnea: implications for hypertension. J Hypertens. 1997;Vol. 15:12:1613-1619.
Ito R, Hamada H, Yokoyama A. Successful treatment of obstructive sleep apnea syndrome improves autonomic nervous system dysfunction, Clin Exp Hypertens. 2005;Vol. 27, No. 2-3:259-267.
McKeown P. “Sleep with Buteyko”. Loughwell, Moycullen, Co Galway, Ireland, Buteyko Books. 2010.
Alkhalil M, Schulman E, Getsy J. Obstructive sleep apnea syndrome and asthma: what are the links? J Clin Sleep Med. 2009; 5(1):71–78.
Wang D, Grunstein R R, Teichtahl H. Association between ventilatory response to hypercapnia and obstructive sleepapnea-hypopnea index in asymptomatic subjects. Sleep Breath. 2007;11(2):103-108.
Younes M, Ostrowski M, Atkar R, Laprairie J, Siemens A, Hanly P. Mechanisms of breathing instability in patients with obstructive sleep apnea. J Appl Physiol. 2007;103(6): 1929-1241.
Maclarnon A, Hewitt G. Increased breathing control: Another factor in the evolution of human language, Evol Anthrop, 2004;Vol. 13, 5;181-197.
Haouzi P, Bell H J. Control of breathing and volitional respiratory rhythm in humans. J Appl Physiol. 2009;Vol. 106:3 904-910.
Lei Xi and Tatiana Serebrovskaya Eds. Intermittent Hypoxia and Human Diseases, Springer Press, 2012.
Mitchell G S, Baker T L, Nanda S A, et al. Invited Review: Intermittent hypoxia and respiratory plasticity. J Appl Physiol. 2001; Vol. 90:6:2466-2475.
Mateika J H, Syed Z. Intermittent hypoxia, respiratory plasticity and sleep apnea in humans: present knowledge and future investigations. Respir Physiol Neurobiol. 2013;Vol. 188: 3:289–300.
O’Connor E, Patnode C D, Burda B U, Buckley D I, Whitlock E P. Breathing Exercises and/or Retraining Techniques in the Treatment of Asthma: Comparative Effectiveness. Comparative Effectiveness Review No. 71. (Prepared by the Oregon Evidence-based Practice Center under Contract No. 290-2007-10057-I.) AHRQ Publication No. 12-EHC092-EF. Rockville, MD: Agency for Healthcare Research and Quality. 2012.
Yokhana S S, Gerst D G 3rd, Lee D S, Badr M S, Qureshi T, Mateika J H. Impact of repeated daily exposure to intermittent hypoxia and mild sustained hypercapnia on apnea severity. J Appl Physiol. 2012;112:367–377.
Kowal K, Du Buske L. The mechanisms of nocturnal asthma. Allergy Frontiers.Springer; 2009; Vol 3,227-46.
Teodorescu M, Polomis D A, Hall S V, et al. Association of obstructive sleep apnea risk with asthma control in adults. Chest. 2010;138(3):543-550.
Doidge N. “The Brain that Changes Itself” 2007, Penguin Books.
Cramer S C, Sur M, Dobkin B H, et al. Harnessing neuro-plasticity for clinical applications– a review article. Brain. 2011:134; 1591–1609.
Ashburner J, Friston K J. Voxel-based morphometry—the methods. Neuroimage. 2000;11:805–821.
Maguire E A, Gadian D G, Johnsrude I S, et al. Navigation-related structural change in the hippocampi of taxi-drivers. PNAS. 2000; 97:8:4403
Maguire E A, Woollett K, Spiers H J. London taxi drivers and bus drivers: a structural MRI and neuropsychological analysis. Hippocampus. 2006;Vol.16:12:1091–1101.
Gaser C, Schlaug G. Brain structures differ between musicians and non-musicians. J Neuroscience. 2003; 23(27):9240 –9245.
Angrea Mechelli A, Crinion J T, Noppeney U, et al. Neurolinguistics: structural plasticity in the bilingual brain. Nature. 2003: 431:757:14.
Draganski B, Gaser C, Kempermann G, Kuhn H G, Winkler J, Büchel C, May A. Temporal and spatial dynamics of brain structure changes during extensive learning. J Neuroscience. 2006; 26(23):6314–6317.
Hölzel B K, Carmody J, Vangel M, Congleton C, Yerramsetti S M, Gard T, Lazar S W. Mindfulness practice leads to increases in regional brain gray matter density. Psychiatry. Res: Neuroimaging. 2011;Vol.191;1:36–43.
Mitchell G S, Johnson S M. Neuro-plasticity in respiratory motor control – an invited review. J Appl Physiol. 2003;94:358-374.
Morris K F, Baekey D M, Nuding S C, Dick T E, Shannon R, Lindsey B G. Invited review: neural network plasticity in respiratory control. J Appl Physiol. 2003; 94:1242-1252.
Tadjalli A, Peever J. Sleep loss reduces respiratory motor plasticity. Adv Exp Med Biol. 2010;289f.
Mitchell G S. Respiratory Plasticity Following Intermittent Hypoxia: a Guide for Novel Therapeutic Approaches to Ventilatory Control Disorders? Genetic Basis for Respiratory Control Disorders Ed, Gaultier, C., Springer Press, 2008, 291-311.
Mahamed S, Mitchell G S. Is there a link between intermittent hypoxia-induced respiratory plasticity and obstructive sleep apnoea? Exp Physio. 2007;92.1:27–37.
Follow us on Linkedin to learn more: