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Breathing & Bracing pt. 1

Updated: Jan 5, 2021

By Michael Edgar

Through my experiences in health and fitness, I started to run into terms such as, ‘diaphragmatic breathing’ and ‘core bracing.’ These terms intrigued me, as human nature tends to have us looking for some form of secret or ‘holy grail’ so-to-speak in our respective fields. On my never-ending journey to figure out all things in musculoskeletal rehabilitation, I clasped on to these ideas without truly giving them their due diligence and critically appraising their utility. You’re welcome to join me on this journey down the rabbit hole, as we delve deep into the topics of breathing and bracing in a two-part research review.

Topics discussed in part one will involve breathing physiology and mechanics, the mechanism of action and efficacy behind breathing techniques, mouth versus nose breathing, and sleep apnea. Part two will then focus on the musculature involved in breathing under load as it relates to bracing and the pelvic floor musculature. Finally, we will discuss its apparent importance in relation to diastasis recti of the abdominal musculature (DRAM), various measurement techniques of DRAM, and the current beliefs surrounding DRAM symptomatology.

So, let’s start from the beginning…

The Fundamentals of Breathing (You Can Skip Past This Section If You’d Like)

Although this may be a refresher for some, I think it’s important for us to discuss the underlying mechanisms of breathing before lifting off into the nebulous realm of nuance. Breathing can be thought to have two distinct phases, expiration and inspiration (1-2). During inspiration, the rib cage volume increases as the external intercostal muscles pull the ribs upward. This occurs with simultaneous contraction of the diaphragm, which moves downward (1-2). Consequentially, the volume of the rib cage expands and the pressure within the lungs decreases. Air flows from regions of high pressure to areas of lower pressure which in turn, inflates the lungs (1-2). The second phase, typically quiet expiration, involves the relaxation of these primary muscles, whereas active expiration involves the utility of additional accessory muscles to force air out of the lungs, such as during strenuous activity (1-2). We need to quickly differentiate between breathing, the act of bringing air into the lungs, and respiration, the act of gas diffusion between the alveoli of the lung tissues and blood vessels surrounding it (1-2).

Regulation of breathing is a slightly more complex phenomenon as we inherently understand that it can be controlled both unconsciously and consciously, lending us the ability to voluntarily control its rate and rhythm at times (1-2). In our brain stem, the medulla maintains stable breathing while the pons allows for smooth respiration patterns (1-2). These functions are considered automatic, involuntary, and continuous. Rate and depth of breathing are tightly regulated by the levels of carbon dioxide, oxygen, and acidosis in the arterial blood with blood oxygen levels fluctuating between 95-100% saturation (1-3). This is generally considered metabolic control of breathing (3).

Voluntary Versus Involuntary Control of Breathing

Whereas involuntary control of breathing can be thought of as a primitive mechanism regulated at the level of the brain stem (some call it the reptile brain), voluntary breathing is regulated at the level of the cortex, the area of our brain considered pertinent for higher order thinking (4). It is typically a self-initiated, short-lived change in breathing exemplified by rate and depth changes which occur before some events such as, vigorous activity, speaking or singing.

This ability of ours to control our breathing voluntarily has popularized the development of such phenomenon like, mind-body fitness. This is considered a combination of muscular activity and an internally directed “mindful” focus on awareness of the self through one’s breath. It was derived from Eastern traditions and includes disciplines such as tai-chi, qigong, and yoga (5). To elaborate on this, yoga defines several breathing types, in which I will list a few (5-6). Firstly, the complete yoga breath involves consciously attempting to breath into the lower, middle, and upper portions of the lungs (5-6). Secondly, interval breathing involves altering the duration of inhalation and exhalation cycles, such as fast, shallow, and rhythmic breathing (5-6). Two others which are used involve alternate nostril breathing and belly breathing, which tend to be self-explanatory (5-6). From a physiological standpoint, the issue with these practices such as belly breathing relates to the idea that anatomically speaking, we have no sensory nerve endings in the diaphragm, meaning we cannot feel it and in turn, cannot appropriately use biofeedback to change its contraction pattern. Potentially though, we may have secondary sensation from the torso with expansion of the rib cage due to air volume.

Types of Breathers – “You Need To Use Your Diaphragm! Don’t Chest Breathe!”

Before elaborating on how one can modify one’s breathing, it’s important to understand that there are several breathing type classifications in the literature (7-8). These classifications relate to the muscles that contract in every breath during quiet breathing and are considered ‘obligatory’ muscles of respiration (7-8). Some of these muscles include, the diaphragm, scalenes (yes, you read this right), parasternals, and external intercostal muscles (7-8). Additional, ‘accessory’ muscles have been shown to contract when demand on the respiratory system changes, such as during deep breathing (7-8). These muscles are typically believed to include the latissimus dorsi, sternocleidomastoid, and trapezius muscles (7-8).

From this information, the classifications involve firstly, the costo-diaphragmatic breathing type, which is considered optimal for maximal lung expansion (7-8). Secondly, there is the upper costal breathing type, which is thought to produce smaller rib cage expansion (7-8). Lastly, there is the mixed breathing type, which has no clear predominance (7-8). Research into this area has found some interesting results though. One study involved healthy subjects performing normal quiet breathing, speaking the word ‘Mississippi,’ swallowing saliva or performing a forced deep breath. On all tasks, sternocleidomastoid and latissimus dorsi EMG activity was not significantly different between breathing types in all activities (7). More so, the diaphragm and external intercostal activity was significantly higher in the upper costal than in the costo-diaphragmatic breathing type in all activities (7). If we are constantly purporting the benefits of increased breathing using the diaphragm, why does the breathing type considered ‘sub-optimal’ produce more activity in the diaphragmatic muscle? I don’t know the answer, but I thought this was an interesting disconnect between research and clinical knowledge translation.

You may have remembered me stating that the scalenes (a muscle in the neck region) were a necessary muscle group for inspiration, but what exactly is this based on if most people consider muscle activation in the neck during breathing to be ‘pathological?’ Well, an EMG study done on healthy subjects looking at activity in this muscle and several others found that the scalenes and parasternal intercostals were invariably active during quiet natural inspiration in normal humans (8). More so, they found a clear cut phasic inspiratory and post-inspiratory activity for the scalenes and parasternal muscles which was unchanged when individuals were coached to breathe through the mouth instead of the nose (8).

Where did this idea that the scalenes were inactive during quiet inspiration come from? Well, the authors of this study explained that the initial breathing EMG data done in preliminary studies used skin surface electrodes, a technique that is generally unable to recognize low levels of EMG activity (8). This led to the erroneous beliefs that the scalenes and sternocleidomastoid (SCM) were accessory muscles only activated upon more vigorous breathing (8-9). Although contradictory to this initial study, it highlights how our knowledge of basic physiology has adapted over time.

To build on this information, the authors tried to further manipulate subjects by having them perform a breathing maneuver with the rib cage alone or diaphragm alone (8). This was done in order to avoid using the scalenes and parasternal muscles. They ended up finding that during rib cage type breathing, subjects ended up having their abdomen paradoxically displaced inward, while the inspiratory EMG activity in both the scalenes and the parasternal intercostals markedly increased (8). We can relate this to the analogy of, “don’t think of a big, purple elephant.” Sadly, you end up thinking about a big, purple elephant.

More so, during ‘diaphragm alone’ breathing, they noticed marked abdominal diameter and decreased rib cage diameter with a decreased scalene inspiratory activity and marked increased in abdominal and lower rib cage musculature activity (8). Both forms tended to lead to aberrant rib cage and abdominal mechanics devoid of position (supine or upright). They concluded that such cueing tends to cause ‘pathological’ breathing. To me, this highlights that breathing mechanics are complicated and although we may feel that we can control specific muscular activity, it may simply be a wasted effort to demonize specific muscles used.

Mindfulness and Breathing

We spoke briefly to the idea of mind-body fitness derived from Eastern traditions. This can be synonymously thought of in some regards to mindfulness practice (10). The Eastern meditation practice is aimed at facilitating an attentional stance of detached observation (10). One aims to refocus the mind on the present and increase their awareness of their external surroundings and inner sensations (10). In a rehabilitative setting, this is purposed to be non-elaborative, non-judgmental moment-to moment awareness, a means to accept and trust in one’s own experience (10). A systematic review looking at the efficacy of mindfulness found small improvements in pain perception after 12 weeks compared to control groups. However, substantial heterogeneity among studies and possible publication bias was noted (10). Although they found efficacy for the utility of mindfulness on pain, they did not differ by type of intervention, such as breathing versus yoga, which lends itself to the question, is breathing therapy intrinsically any better than other forms of mindfulness?

Further building on the utility of mindfulness is its utility toward combating musculoskeletal conditions such as low back pain (11). Low back pain is currently one of the largest burdens of disease on individuals and health care systems (11). It is also the most common condition for which complementary therapies such as mindfulness are used (11). A systematic review aimed to investigate mindfulness-based stress reduction (MBSR) utility for the treatment of low back pain (11). They found a low number of studies and inconclusive evidence for the effectiveness of MBSR in improving pain intensity or disability in chronic low back pain patients (11). Although, they did seem to note that there is limited evidence that MBSR can improve pain acceptance, an interesting and less talked about experience (11).

Now that we better understand the utility of mindfulness as a broad category of interventions, we can better focus in on whether breathing, in itself, offers any unique benefits. Several studies have looked at this. One performed attention to breathing tasks, either attentive breathing, guided by an external respiratory feedback task with a fixed cadence, or relaxed breathing, in which one picked a self-chosen pace (12). They also included a control group which did not focus on anything and made sure each group had a similar breathing frequency (12). They found that both attention-to-breath groups showed decreased amygdala activation and increased prefrontal integration of the amygdala during aversive emotions (12-13). Although this is the case, only decreased pain pressure thresholds were noted in the relaxed breathing group (12). They concluded that the benefits were not inherent to breath control but more so keeping one’s focus of attention on something considered ‘relaxing (12).’ This is emphasized further by the fact that breathing frequency did not explain a significant amount of variance (12).

Breathing and the Vagus Nerve

A second study aimed to further manipulate the breathing cycle with slow deep breathing causing greater fluctuations in intrathoracic pressure, cardiac filling, and blood pressure along the respiratory cycle due to greater respiratory sinus arrhythmia (RSA) (13). RSA occurs due to the breathing cycle’s physiological effect on one’s heart rate and is commonly used as a means to highlight the ‘power of the vagus nerve (13).’ The popular theory regarding augmentation of cardiac vagal activity and the baroreflex relates to vagal outflow facilitation to the heart during expiration and inhibition during inspiration (13). As a consequence of this, heart rate decreases during expiration and increases during inspiration (13). In this study, they grouped healthy individuals into an unpaced breathing group, breathing set at a fixed cadence group, slow deep breathing with a high inspiration:expiration ratio (6000 ms:500ms) group, and a slow deep breathing with a low inspiration:expiration ratio (500 ms:6000ms) group (13).

They found that despite cardiovascular effects of slow deep breathing, these cardiovascular changes did not mediate the effects of breathing patterns on pain (13). Pain ratings were lower during each of the three instructed breathing patterns, highlighting that pain appears to be modulated by attentional re-allocation caused by other non-respiratory types of stimuli and is not purely a vagal nerve phenomenon (13). The latter appears to be too reductionist, although you may sound smart to individuals who don't know better. Based on these findings and the other studies noted, it appears that the less glamorous benefits of breathing techniques are primarily mediated by distraction, emotion modulation, and expectations induced by voluntary, top-down mechanisms (10-14).

Breathing and Hyperventilation – The Paper Bag Approach

Up to this point, we have specifically talked about breathing techniques and therapy in relation to healthy populations… but what about populations that have noted, pathological breathing? A study looking at individuals with anxiety aimed to understand the importance of breathing therapy for this population (15). It was initially thought that physical symptoms of anxiety were due to hyperventilation. From a physiological standpoint, a decrease in alveolar and arterial carbon dioxide pressure (PCO2) and an increase of pH (less acidity) in the blood and cerebrospinal fluid led to constriction of the arteries in the brain and in the hands, increased neural excitability, increased production of lactic acid, and lowering of phosphate level in arterial blood (15). Through this convoluted mechanism, it was believed this was the cause of breathlessness, tightness in the chest, pounding of the heart, tachycardia (increased heart rate), dizziness, tingling, sweating, nausea, fatigue, nervousness, and anxiety (15). All of this due to abnormal breathing during hyperventilation (15).

From this model, treatment procedures were developed with the overall goal of alleviating symptoms of hyperventilation syndrome (HVS) to increase alveolar and arterial PCO, to normal levels (15). Through this therapy, people would be focused on respiratory rate reduction and cognitive reattribution of physical symptoms, instead of catastrophic causes further perpetuating the issue (15).

The authors of this study questioned the specificity of these techniques for HVS, as both breathing retraining and standard cognitive reattribution helped alleviate anxiety in patients with HVS or related disorders (15). In addition, they found several studies in which individuals with panic attacks had physical symptoms, yet only half had signs of hyperventilation noted by decreases in PCO2 (15). To elaborate, no differences were observed in the symptoms between panic attacks with or without hyperventilation (15). This does not support the idea that hyperventilation is an important causal mechanism in producing panic attack symptoms (15). In addition, a study using controlled versus uncontrolled CO2 inhalation to provoke panic when one was given actual control over symptoms, real or illusory, generally inhibited anxiety or panic (15).

To further add insult to injury, breathing retraining has been shown to work with anxious patients who show no signs of hyperventilating (15). It appears that the reductionist perspective does not hold up once again (15). The authors of the article used the term “rational placebo” to characterize breathing therapy (15). A rational placebo is described as a treatment that appear logical, but on closer inspection does not work as supposed (15). I’d argue that many therapies we continue to perform in a musculoskeletal rehabilitation setting would fall under this category. In summary, it appears that breathing therapy is mediated by more so, non-specific effects, but can be used as a means to distract individuals from feelings of anxiety and promote self-reliance (15).

It’s a long article, I know…Take a deep breath.

Mouth Versus Nose Breathing - Make Sure to Breathe Through Your Face

Going from here, I think it’s important to speak to a highly debated topic regarding mouth versus nose breathing. There tends to be a camp of individuals who swear by nose breathing, similar to diaphragmatic breathing advocates, believing that it is the holy grail to longevity. What do we actually know about it though? Well, the nose is an inherently more efficient filter than the mouth for particles. There’s also a common belief that nose breathing is better for overall lung capacity than mouth breathing.

Many cite an initial study that looked at the effects of oronasal obstruction on lung volumes and arterial oxygenation (16). The study had two types of nasal obstruction. The first group of subjects had partial, chronic nasal obstruction with surgical relief, measured before surgery and 6-8 weeks later (16). The second group had a complete overnight nasal blockage using Vaseline and gauze overnight (16). Participants in the second group were hospital staff and measures were taken with the nose clear and once with the nose packed at least one week apart (16). They also included a third group in which mouth breathing was blocked through wiring the teeth together (16). The individuals in this group had elective mandibular osteotomy and subsequent interdental wiring for 6-8 weeks (16). Measures were taken before the interdental wiring, 6-8 weeks after the teeth were wired together, and 2-3 weeks after the wires had been removed (16).

The results ended up showing that lung volume decreased after surgical intervention in the chronic nasal obstruction group and in the overnight nasal packing groups (16). This is in contrast to the interdental wiring group which saw increased lung volumes during mouth wiring fixation, although this increase was also maintained after fixation removed (16). Although this may show some promise, there are some glaring issues with this study, such as non-uniform, small group sizes as groups ranged from 7 to 27 individuals with differing timelines for measures between groups (16). In addition, no blinding or randomization was done as they specifically noted hospital staff were used solely in one group (16). They also had groups with previously pathological conditions, surgical interventions, and artificial airway obstruction which cannot be generalized to healthy individuals (16). Overall, I would not hang my hat on this study or use it to come to any conclusions, whatsoever.

When we move into less artificial conditions with healthy individuals, there seems to be differences in mouth and nose breathing… but how much of this can we actually control (17)? For example, it has been shown that males tend to mouth breathe more in proportion than females (17). In addition, on average, individuals typically inhale 90% of their air through the nose during quiet reading or inspiration (17). Yet when one speaks, this number drops to 10-30% as the mouth becomes the predominant airway (17). From a pragmatic standpoint, it appears to be something inherent in our daily lives. Therefore, is it something we need to really worry about? Should we instead have our patients or clients simply text us instead?

If we want to complicate things even more, we can look into the conversion of airway use during exercise. Research has shown that there are typically three forms of breathers: normal augmenter, nose, and mouth. A 'normal augmenter’ breathes through the nose at rest and switch to oronasal breathing with increasing respiratory needs (18-20), whereas, nose and mouth breathers respire only nasally or orally both at rest and during strenuous submaximal exercise (18-20). In regard to normal augmenters, the switching point ranges widely from one person to another with no differences based on sex (18-20). Instead, the transition appears to be driven by rating of perceived exertion of breathing as exercise intensity increases and to a smaller extent, nasal work of breathing (18-20). This is predominantly due to a greater volume of air being able to be transported through the oral passageway, which may be required as exercise intensity goes up and oxygen demands increase (18-20). We can also note to our refresher on breathing mechanics at the beginning regarding CO2 as a trigger for increased ventilation, which then may lead some to mouth breathe to accommodate this.

Based on the literature it appears that a male’s switching point occurs at approximately 66.2 L/min and 44.9 L/min in females (18-20). Using artificial means of airway control, such as athletic tape over the mouth or a nose clip, it appears oxygen consumption is about 8-10% lower at all exercise intensities for nose breathing (18-20). In addition, VO2 max was also lower at each intensity level for nose breathing (18-20). Based on the findings, it appears that nose breathing is sufficient for work output at lower intensities but hinders at higher intensities (18-20). I do want to make note that sufficient and optimal are very different things when it comes to performance and work output.

Sleep Apnea – “You Take My Breath Away”

The final area I want to touch on in part one of this two-part series is the topic of sleep apnea. Sleep apnea is a disturbed breathing pattern and can occur hundreds of times a night causing broken up sleep (21-23). Due to this, brain oxygenation decreases which in turn activates both the sympathetic, adrenomedullary, and the hypothalamic-pituitary-adrenal (HPA) axis limbs of the stress system (21-23). The two major forms of sleep apnea are firstly, obstructive sleep apnea (OSA), which involves blockage of the airway due to soft tissue in the back of the throat collapsing during sleep (21-23). The second form is central sleep apnea (CSA), in which the brain fails to signal muscles of respiration during sleep due to instability in the respiratory control center. We spoke about some of these areas of the brain in the initial part of this article (21-23). Sleep apnea, in general, has many chronic, negative health effects, such as increased diastolic and mean blood pressure, decreased mental acuity, increased chance of stroke and heart failure, increased insulin resistance and diabetes, depression, and headaches (21-23).

For the purpose of clinical relevance, we will focus on OSA due to its prevalence in society compared to CSA (21-23). A quick clinical guide to the potential diagnosis of OSA is the STOPBANG criteria, in which three or more positive signs put one at risk for the condition. STOPBANG stands for snoring, tiredness upon waking, observed apnea event, in which one stops breathing briefly, elevated blood pressure, body mass index (BMI) greater than 35, age over 50, neck circumference over 40 cm, and male gender (21-23). Although many may construe this condition to only be in individuals holding excessive fat, it can affect anyone with above average body weight. For example, rates of sleep apnea have been found to be 4 to 5 times higher in NFL players than males of similar ages (23). You may be thinking to yourself that you may have some of these symptoms or know of someone with them. Not surprisingly, the condition is extremely common, although highly under-diagnosed (24).

When one typically suspects sleep apnea, they will be sent for a sleep study using polysomnogram (say that ten times, fast) (25-26). This device electronically transmits and records specific physical activities during sleep through surface electrodes on the face and scalp (25-26). In addition, belts around the chest and abdomen are used to measure breathing while a bandage-like oximeter probe on one’s finger is used to measure the amount of oxygen in the blood (25-26). It’s not exactly a restful sleep but it is a necessary test for appropriate diagnosis. In regard to diagnosis, an apnea hypopnea index (AHI) is given, which is the number of apneas and hypopneas per hour (25-26). An AHI of less than 10 indicates no sleep apnea, an AHI of 10-19 indicated mild sleep apnea, and an AHI above 20 indicates severe sleep apnea (25-26).

The treatment of OSA can be done through several methods such as decreasing one’s body weight, avoiding alcohol and sleep medication, avoiding sleeping supine, smoking cessation, mouth guard or a continuous pulmonary airway pressure (CPAP) device (25-26). The most common intervention is the use of a CPAP device (25-26). The mask of this device is worn over nose and mouth and delivers a continuous flow of air into the nose to keep the airways open. Based on the literature, it appears that the use of a CPAP can reduce the cumulative risk of all-cause mortality for individuals suffering from OSA back to baseline levels of healthy individuals, as demonstrated by the graph (26). It seems this may be the holy grail, at least for people with OSA.

If you’ve made it this far, I give you credit and hopefully there were at least a few pieces of information that make you question previously held beliefs.

Take Home Points

1. Breathing is a fundamental part of life.

2. We may think we have more control over our breathing mechanics than we actually do.

3. Short term voluntary changes in breathing mechanics may not matter.

4. Using our diaphragm more does not mean we are breathing ‘better’ – more on this in part two.

5. Breathing does not seem to have any unique benefits compared to general mindfulness.

6. Breathing therapy tends to work through distraction and re-attentional focus.

7. Vagus nerve modulation does not seem to matter, at least not in the sense or extent we thought it did.

8. Breathing techniques for hyperventilation appear to be rational placebos.

9. Breathing through your mouth is not bad. It’s pragmatically not likely to reduce it unless you want to stop talking.

10. Mouth breathing has an adaptive response as exercise intensity increases.

11. Sleep apnea has a lot of chronic health effects, so be aware of the signs and symptoms, and how to help treat it.



1. Gilbert C. Biochemical aspects of breathing. Recognizing and Treating Breathing Disorders E-Book. 2014 Jan 1;61.

2. Bouhuys A. The physiology of breathing: a textbook for medical students. Saunders; 1977.

3. Willmore H, Costill L. Physiological of Sport and Exercise.

4. Gallego J, Nsegbe E, Durand E. Learning in respiratory control. Behavior modification. 2001 Sep;25(4):495-512.

5. Collins C. Yoga: Intuition, preventive medicine, and treatment. Journal of Obstetric, Gynecologic, & Neonatal Nursing. 1998 Sep;27(5):563-8.

6. Miles WR. Oxygen consumption during three yoga-type breathing patterns. Journal of Applied Physiology. 1964 Jan 1;19(1):75-82.

7. Celhay I, Cordova R, Miralles R, Meza F, Erices P, Barrientos C, Valenzuela S. Effect of upper costal and costo-diaphragmatic breathing types on electromyographic activity of respiratory muscles. CRANIO®. 2015 Apr 1;33(2):100-6.

8. Cordova R, Miralles R, Bull R, Gamboa NA, Santander H, Valenzuela S. Respiratory EMG Activity between Subjects with Costo-diaphragmatic, Upper Costal or Mixed Breathing Type. J Sleep Disord Ther. 2019;8(306):2167-0277.

9. Participation of the sternocleidomastoid muscle on deep inspiration in man. An electromyographic study.

10. Hilton L, Hempel S, Ewing BA, Apaydin E, Xenakis L, Newberry S, Colaiaco B, Maher AR, Shanman RM, Sorbero ME, Maglione MA. Mindfulness meditation for chronic pain: systematic review and meta-analysis. Annals of Behavioral Medicine. 2017 Apr 1;51(2):199-213.

11. Cramer H, Haller H, Lauche R, Dobos G. Mindfulness-based stress reduction for low back pain. A systematic review. BMC complementary and alternative medicine. 2012 Dec;12(1):162.

12. Busch V, Magerl W, Kern U, Haas J, Hajak G, Eichhammer P. The effect of deep and slow breathing on pain perception, autonomic activity, and mood processing—an experimental study. Pain Medicine. 2012 Feb 1;13(2):215-28.

13. Doll A, Hölzel BK, Bratec SM, Boucard CC, Xie X, Wohlschläger AM, Sorg C. Mindful attention to breath regulates emotions via increased amygdala–prefrontal cortex connectivity. Neuroimage. 2016 Jul 1;134:305-13.

14. Jafari H, Gholamrezaei A, Franssen M, Van Oudenhove L, Aziz Q, Van den Bergh O, Vlaeyen JW, Van Diest I. Can slow deep breathing reduce pain? An experimental study exploring mechanisms. The Journal of Pain. 2020 Jan 22.

15. Garssen B, De Ruiter C, Van Dyck R. Breathing retraining: a rational placebo?. Clinical Psychology Review. 1992 Jan 1;12(2):141-53.

16. Swift AC, Campbell IT, Mckown T. Oronasal obstruction, lung volumes, and arterial oxygenation. The Lancet. 1988 Jan 16;331(8577):73-5.

17. Camner P, Bakke B. Nose or mouth breathing?. Environmental research. 1980 Apr 1;21(2):394-8.

18. Niinimaa VP, Cole P, Mintz S, Shephard RJ. The switching point from nasal to oronasal breathing. Respiration physiology. 1980 Oct 1;42(1):61-71.

19. LaComb CO, Tandy RD, Lee SP, Young JC, Navalta JW. Oral versus nasal breathing during moderate to high intensity submaximal aerobic exercise. International Journal of Kinesiology and Sports Science. 2017 Jan 31;5(1):8-16.

20. Morton AR, King K, Papalia S, Goodman C, Turley KR, Wilmore JH. Comparison of maximal oxygen consumption with oral and nasal breathing. Australian journal of science and medicine in sport. 1995 Sep;27(3):51-5.

21. Eisensehr I, Ehrenberg BL, Noachtar S, Korbett K, Byrne A, McAuley A, Palabrica T. Platelet activation, epinephrine, and blood pressure in obstructive sleep apnea syndrome. Neurology. 1998 Jul 1;51(1):188-95.

22. Garcia-Rio F, Racionero MA, Pino JM, Martinez I, Ortuno F, Villasante C, Villamor J. Sleep apnea and hypertension. Chest. 2000 May 1;117(5):1417-25.

23. George CF, Kab V, Levy AM. Increased prevalence of sleep-disordered breathing among professional football players. New England journal of medicine. 2003 Jan 23;348(4):367-8.

24. Kapur V, Strohl KP, Redline S, Iber C, O’connor G, Nieto J. Underdiagnosis of sleep apnea syndrome in US communities. Sleep and Breathing. 2002 Apr;6(2):49-54.

25. Mcardle N, Devereux G, Heidarnejad H, Engleman HM, Mackay TW, Douglas NJ. Long-term use of CPAP therapy for sleep apnea/hypopnea syndrome. American journal of respiratory and critical care medicine. 1999 Apr 1;159(4):1108-14.

26. Martínez-García MÁ, Soler-Cataluña JJ, Ejarque-Martinez L, Soriano Y, Román-Sánchez P, Illa FB, Canal JM, Duran-Cantolla J. Continuous positive airway pressure treatment reduces mortality in patients with ischemic stroke and obstructive sleep apnea: a 5-year follow-up study. American journal of respiratory and critical care medicine. 2009 Jul 1;180(1):36-41.

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