The Science of Breathing Well

Original Editor - Tania Clifton-Smith Top Contributors - Jess Bell

Introduction

Breathing affects all body systems; these systems in turn influence breathing. Optimal breathing patterns help to maintain homeostasis, but when breathing is disrupted, significant issues can arise.

Physiotherapists are well placed to assess and treat breathing pattern disorders. It is, however, important to understand the science behind optimal breathing in order to recognise and manage the symptoms that occur with dysfunctional breathing. The science of breathing can essentially be broken down into three subcategories:

  • The mechanics of breathing well (ie biomechanics)
  • The physiology of breathing well (ie biochemistry)
  • The psychophysiology of breathing well (or psychology)

The Mechanics of Breathing Well

Brief Anatomy Review

For more information on the anatomy of breathing, click here, but in brief the respiratory conduction zone consists of the:[1]

  • Nasal cavity
  • Pharynx
  • Larynx
  • Trachea
  • Bronchi and bronchioles

The nose plays an important role in nitric oxide production, which impacts latency and dilation of blood vessels. It is also involved in sterilisation of air in the airways.[2][3] The larynx transports air down to the lungs.

The respiratory muscles are:[4]

  • Diaphragm, which acts as a vital pump
  • Rib cage muscles
  • Abdominal muscles

The thoracic and abdominal cavities essentially form a canister with the larynx and vocal cords on top, diaphragm in the middle and the pelvic floor at the base. All work together to ensure optimal respiration, as well as to maintain / modulate intra-thoracic and intra-abdominal pressure.[3]

How Do the Biomechanics of Breathing Influence Other Systems and Organs?

Heart

Other organs and systems are influenced by the biomechanics of breath, including the heart. The heart is encased in, and moves with, the diaphragm, which influences heart tone.[3] Similarly, when the diaphragm descends and ascends, the heart is, in essence, “micro-massaged”, which affects its baroreceptors.[3][5] Baroreceptors are a type of mechanoreceptor which enable information about blood pressure to be sent to the autonomic nervous system.[6]

Heart rate variability (HRV) is also influenced by breathing.[7] HRV refers to the variation in time intervals between heart beats.[7] HRV is an important indicator of health, as well as mood and our ability to adapt. A number of physiological systems influence heart rhythm. Higher HRV is generally a marker of good physiological functioning whereas lower HRV predicts morbidity and mortality. Low HRV is also more common in individuals who have depression, anxiety and chronic stress.[7]

Intra-abdominal and Intra-thoracic Pressure

The diaphragm works with the anterior abdominal wall muscles to increase intra-abdominal pressure, enhancing processes such as gut motility, defecation, micturition (urination) and parturition (giving birth).[8]

As mentioned above, the diaphragm acts as a vital pump.[3] On inhalation, its descent decreases intra-thoracic pressure and increases intra-abdominal pressure. This pressure helps the inferior vena cava to push deoxygenated blood into the right atrium. It also compresses the abdominal lymph vessels, which aids lymphatic movement.[8] Similarly, cerebrospinal fluid is pumped into the brain on inhalation and pumped back down on exhalation.[9]

Continence and Voice Quality

Continence and vocal quality are also affected as they make up the base and top of the canister.[3]

Contraction of the pelvic floor muscles and diaphragmatic motion correlate with breathing. Moreover, breathing is more effective when the pelvic floor contracts.[10]

The relationship to the diaphragm and vocal quality has been studied most extensively in singing, but it has been found that co-activation of the diaphragm during phonation may impact voice quality.[11][12]

Musculoskeletal System

Breathing mechanics affect posture and spinal stabilisation. Breathing pattern disorders contribute to pain and motor control deficits and can result in muscular imbalance and physiological adaptations.[13] For instance, a significant correlation between low back pain and breathing pattern disorders has been demonstrated.[3] Moreover, a clear link has been found between the diaphragm and various musculoskeletal disorders. For instance, a recent study by Finta and colleagues found that diaphragm strengthening combined with other training may be beneficial in the management of chronic nonspecific low back pain.[14] Similarly. a link between chronic ankle instability and altered diaphragm contractility has been established.[15]

The Physiology of Breathing Well

The main purpose of breathing is to maintain homeostasis, which is achieved by the inspiration of oxygen and the exhalation of carbon dioxide (CO2). This process stabilises pH. The normal range of pH in the human body is 7.35-7.45, with an average of 7.4.[16] Every organ system in the body depends on this pH balance. pH is modulated by both the respiratory and renal systems.[16]

When breathing does not match the level required by the body, homeostasis is disrupted. As it is essential that pH remains stable, the level of CO2 in the bloodstream (PaCO2) will increase or decrease based on requirements.[3]

  • NB When assessing breathing patterns, it is important to first assess a patient at rest and then move on to dynamic breathing and movement as there will often be greater mismatch during breathing at rest [3]
  • Often patients will report feelings of air hunger (i.e. a sense that they cannot get enough air). Using pulse oximetry can be useful as patients with breathing pattern disorders will often have readings above normal levels of 96-98% saturation. This result will help to demonstrate that they are over-breathing at rest and not in need of more oxygen. If saturation readings are low (less than 94%) then other causes must be considered with respect to lung function[3]

PaCO2 level plays a key role in our breathing. Normal resting levels of PaCO2 is 40 milligrams of mercury (mmHg). PaCO2 is the main driver of the rate and depth of breathing.[3]

Typically, large changes in PaCO2 and the resultant changes in pH are controlled by the hydrogen ion buffering system. Without this system, even brief periods of apnea would cause death due to hypercapnia.[17] However, the respiratory centre is more sensitive to CO2 levels than oxygen levels. If pH becomes more acidic (i.e. PaCO2 decreases), the central and peripheral chemoreceptors will stimulate respiratory drive through bronchodilation and hypoxic vasoconstriction. This will increase CO2 clearance and improve ventilation / perfusion matching.[17]

There is a close relationship between increases in PaCO2 and alveolar ventilation. While there are individual variations, there is roughly a 1 to 4 L/min increase in minute ventilation for each 1 mmHg increase in PaCO2.[17] However, during times of hyperoxia, CO2 sensitivity will decrease. Conversely, during periods of hypoxia, it will increase. Thus, when we over-breathe (hyperoxia) the body is less sensitive to hypercapnia and only the central chemoreceptors will respond to increase ventilation.[17]

When hypocapnia is mild, it does not tend to have a significant impact on healthy people, but common signs / symptoms of hypocapnia include:[18]

  • paresthesias
  • palpitations
  • myalgic cramps
  • seizures

However, hypocapnia does have the potential to cause various pathological processes:[3][18]

  • The cerebral artery constricts, resulting in signs and symptoms such as dizziness, detachment and reduced clarity of thought.[19] For every 1mmHg reduction in PaCO2, there is a two percent decrease in cerebral blood flow.[3][20] A decrease of 5mmHG will result in a ten percent reduction of blood flow, which can have a significant impact.[3] Initially blood flow reduces to the cerebral cortex, which is responsible for planning, logic and thinking. Later, areas that trigger primitive reflexes will be affected, including the amygdala, which plays a key role in fear response and the fight or flight response.[21][3]
  • Uptake of oxygen by haemoglobin is altered. During optimal breathing, oxygen and haemoglobin attach and release readily (known as the Bohr Effect. See video below). However, during periods of over-breathing when CO2 levels decrease, oxygen and haemoglobin attach, but will not readily detach.[22] This accounts for readings of 100% saturation shown on pulse oximetry in patients with breathing pattern dysfunctions.
  • This increased affinity of oxygen to haemoglobin results in impaired oxygen release to peripheral tissues (brain, heart, liver, kidney).[22] It will also cause decreased blood flow in the periphery (i.e. hands, feet and mouth) and increased activity of the nervous tissue and nerve synapses.[3]
[23]
  • A reduction in PaCO2, will result in an imbalance of calcium and magnesium, which will increase the likelihood of spasm and fatigue.[3]
  • Similarly, low levels of CO2 in the bloodstream affects lactic acid buffering. This is often present in individuals who have myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), chronic fatigue or post-viral fatigue. Lactic acid is the byproduct of exercise and, usually, it is easily removed due to the bicarbonate buffering system. However, in patients with chronic hyperventilation syndrome, the bicarbonate buffer becomes depleted. Thus, they quickly develop a build up of lactic acid, resulting in muscle aches and pains. Patients who have chronic fatigue or post-viral fatigue should, therefore, be assessed for breathing pattern dysfunction with the aim to restore a good breathing pattern at rest.[3]

All of these symptoms of hypocapnia can be worrisome for patients, resulting in further stress.

The effects of chronic over-breathing with the associated chronic depletion of CO2, include:[3]

  • Breathlessness disproportionate to actual fitness
  • A state of fight or flight with catecholamines released
  • Lactic acid build up due to the depletion of the bicarbonate buffer

The Psychophysiology of Breathing Well

The Autonomic Nervous System

The autonomic nervous system (ANS) consists of three branches: the sympathetic nervous system (SNS), the parasympathetic nervous system (PNS) and the enteric nervous system (ENS).[24][25] In general, SNS activation will cause a state of increased activity and attention (i.e. the fight or flight response). Blood pressure and heart rate increase and gastrointestinal peristalsis stops.[24] In contrast, the PNS is the rest and digest system. It lowers heart rate and blood pressure and restarts peristalsis and digestion. Unlike the SNS, which innervates most tissues in the body, including the musculoskeletal system, the PNS only innervates the head, viscera and external genitalia.[24]

A good breathing pattern at rest (i.e. nose breathing, low and slow pattern) will activate the PNS.[3] If this resting breathing pattern is disrupted (i.e. breathing at higher volumes, increased respiratory rate and dysregulation), the SNS will dominate.

Both PNS and SNS play a key role in homeostasis throughout the day, but remaining in a prolonged state of SNS due to over-breathing will have a negative effect, resulting in depletion, exhaustion with adrenal burnout.[3]

Amygdala

The amygdala is associated with the primitive fight or flight reflex.[3] It is part of the limbic system, which controls emotions and behaviours, as well as memory formation.[26] The amygdala helps to regulate anxiety, aggression, fear conditioning, emotional memory and social cognition. It also has a modulatory effect on acquiring / consolidating memories that result in an emotional response.[26]

[27]

When individuals do not breathe effectively, their amygdala is activated and they become reactive. It is important to remember that when we breathe optimally, the brain will be fully oxygenated, with appropriate blood flow through the frontal cortex. However, if this pattern is disrupted and we over-breathe, this system is disrupted and the amygdala will be triggered, resulting in further over-breathing, and a cycle of panic, anxiety and fear.[3]

Consciously reducing respiratory rate can counteract this effect, deactivating the amygdala and improving rational and logical thought. Thus, when retraining breathing, it is important to focus on extending the pause at the end of the breath. Widening the gap between a reaction and a response can sometimes be sufficient to slow the system down. This enables the frontal cortex to re-engage and prevent an over-reaction. This breathing technique is, therefore, an important tool to aid self-regulation, as well as to combat stress, anxiety and to enhance rational decision making.[3]

Pain and Breathing

Altered pain perception has been associated with respiration[28] and ineffective breathing may result in a decreased pain threshold.[3] Chronic pain and chronic hyperventilation often co-exist.[29] This may be related to both the neuro-chemistry and the biomechanics of pain.[3] Pain can cause an increase in respiratory rates generally. Moreover, patients with abdominal or pelvic pain often splint their abdominal muscles, which results in upper chest breathing[29] and they will often experience muscle tension / tightness. However, individuals who breathe well, tend to present with greater flexibility.[3]

Normal Breathing Patterns

A normal breathing pattern at rest will be nose / abdominal. Normal resting respiratory rate changes throughout life:[3]

  • Babies breathe 35 - 58 times per minute
  • Toddlers 15-22 times per minute
  • Adolescents 12-16 times per minute
  • Once lungs stop growing at around 22 years of age, adults adopt a respiratory rate of 10-14 breaths per minute

When assessing a breathing pattern, it is also important to assess for regular movement. Exhalation should be slightly longer than inhalation and there should be a slight pause at the end of exhalation. This pattern is vital to maintain homeostasis and pH.  If this ratio changes, the SNS will be triggered.[3]

What Causes this Pattern to Change?

There are many reasons that dysfunctional breathing patterns may develop.

Mouth breathing

Mouth breathing is common in patients with breathing pattern disorders. It is known to cause a variety of symptoms, including: daytime sleepiness, headaches, agitation and nocturnal enuresis, fatigue, poor appetite, bruxism, problems at school, learning deficits and behavioral problems[30], like ADHD, as well as sleep disorders.[31]

If you note that a patient is a mouth breather, consider whether or not their nose is obstructed (e.g. is it broken? Do they have chronic rhinitis?) Or is it a habitual pattern?

If a young child is mouth breathing, the cause must be determined (e.g. tonsils / adenoids causing obstruction).[3] This pattern can have a significant impact on a young child’s oral-fascial structures.[32][3]

Environmental Factors

Consider the environment and biochemical triggers. Spending time in a hot, humid room for prolonged periods is known to alter breathing.[3] Similarly, hyperventilation of hot, humid air has been shown to cause transient bronchoconstriction in patients who have asthma[33] and cough responses and throat irritation in patients with allergic rhinitis.[34]

Hormonal Factors

The respiratory rates of women change throughout their hormone cycle. Progesterone is a respiratory stimulant and it peaks in the post-ovulation phase. This can result in reduced PaCO2 levels. These levels further decrease during pregnancy.[29]

Fever / Viral Infections

Hyperthermia in humans causes various thermoregulatory responses, including sweating, and cutaneous vasodilation, as well as an increase in ventilation. This reduces arterial PaCO2 pressure.[35]

Altitude

Altitude can also cause imbalances, resulting in over-breathing. It has been found that the level of impairment or symptoms most closely correlates to the degree of hypocapnia rather than the degree of hypoxia.[18] If an individual already has a breathing pattern disorder, they often experience more symptoms at altitude.[3]

Caffeine / Drugs

Excessive use of recreational drugs or caffeine affects breathing. These substances are stimulants, as well as panicogens, which cause panic attacks and anxiety. Key panicogens in the body are CO2 and lactic acid. Thus, even in the absence of stress, a reduction in CO2 can trigger a panic attack.[3]

Laughter / Talking

Laughter can also trigger signs and symptoms if an individual is CO2 intolerant, as can talking a lot.[3]

Stress, Anxiety and Fatigue

Stress, anxiety and fatigue can all exacerbate and be exacerbated by breathing pattern disorders through autonomic pathways. Similarly, boredom, depression, learnt responses, misattribution, pain, history of abuse and trauma can have a significant impact, so these are important issues to consider in a subjective history.[3]

Pre-existing Conditions

Organic disease can also contribute to the development of breathing pattern disorders, including post nasal drips, rhinitis, asthma, COPD and interstitial lung disease, as well as metabolic disorders.[36][29] Thus, these conditions can exist with breathing pattern disorders. Moreover, if a breathing pattern is improved, patients may experience improvements in quality of life and a reduction in some of the symptoms of their original condition.[3]

Email Apnea

It is interesting to note that there is a current trend of “email apnea” or “screen apnea”. This occurs when people breath-hold while reading emails or using laptops / computers / tablets. This causes a reduction in CO2 levels with time, but over the course of a day, oxygen levels can also reduce, resulting in an apneic episode.[3]

In all these situations, it only takes 24 hours for an altered breathing pattern to become habitual. Thus, an individual may recover from a virus, move to a different environment etc, but the breathing pattern dysfunction remains.[3]

Key Management Approaches for Physiotherapists

In order to retrain breathing, it is essential to educate patients about the effects of over-breathing. The physiotherapist must help the patient to break the cycle of dysfunctional breathing by retraining the patient's breathing pattern (i.e. nose, low and slow in an effortless pattern).

Carbon Dioxide Resilience

One aspect of breathing retraining focuses on improving CO2 resilience, so that PaCO2 levels are able to increase / decrease slightly more without triggering symptoms[3]. For example, if an individual with a breathing pattern disorder is exposed to a combination of triggers mentioned above (e.g. hot, humid room, altitude, required to talk a lot, consumed caffeine), she / he will likely experience symptoms associated with decreased CO2 levels (breathlessness, decreased blood flow to the brain, pins and needles, numbness, muscle tension etc). However, if this individual has a good buffer or a resilient carbon dioxide receptor in the brain, it will take more for him / her to become symptomatic.[3]

It is key to educate your patient about these triggers, as well as triggers associated with over-thinking and emotional factors, so that they are better equipped to note what may be causing symptoms.[3]

Summary

Breathing well affects all our body systems. The science of breathing can be broken down into three main areas:

  • The mechanics of breathing well (ie biomechanics)
  • The physiology of breathing well (ie biochemistry)
  • The psychophysiology of breathing well (or psychology)

All areas are interconnected and if a good breathing pattern is restored, there will be many positive improvements including:[3]

  • Enhanced cellular action, metabolism and mitochondria function
  • Enhanced digestion, posture, stability and vocal quality
  • Regulation of the the ANS and pain processing
  • An ability to relax / calm anxious minds
  • Greater self-regulation

References

  1. Cedar SH. Every breath you take: the process of breathing explained. Nursing Times [online]. 2018; 114(1): 47-50.
  2. Lundberg JO, Settergren G, Gelinder S, Lundberg JM, Alving K, Weitzberg E. Inhalation of nasally derived nitric oxide modulates pulmonary function in humans. Acta Physiol Scand. 1996;158(4): 343-347.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 3.23 3.24 3.25 3.26 3.27 3.28 3.29 3.30 3.31 3.32 3.33 3.34 3.35 3.36 3.37 3.38 3.39 3.40 3.41 3.42 Clifton-Smith T. The Science of Breathing Well Course. Physioplus. 2020.
  4. Aliverti A. The respiratory muscles during exercise. Breathe (Sheff). 2016; 12(2):165-168.
  5. Baekey DM, Molkov YI, Paton JF, Rybak IA, Dick TE. Effect of baroreceptor stimulation on the respiratory pattern: insights into respiratory-sympathetic interactions. Respir Physiol Neurobiol. 2010;174(1-2):135-145.
  6. Armstrong M, Kerndt CC, Moore RA. Physiology, Baroreceptors. [Updated 2020 Apr 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538172/
  7. 7.0 7.1 7.2 Steffen PR, Austin T, DeBarros A, Brown T. The Impact of Resonance Frequency Breathing on Measures of Heart Rate Variability, Blood Pressure, and Mood. Front Public Health. 2017;5: 222.
  8. 8.0 8.1 Bains KNS, Kashyap S, Lappin SL. Anatomy, Thorax, Diaphragm. [Updated 2020 Apr 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519558/
  9. Clifton-Smith T. How We Breathe Course. Physioplus. 2020.
  10. Park H, Han D. The effect of the correlation between the contraction of the pelvic floor muscles and diaphragmatic motion during breathing. J Phys Ther Sci. 2015;27(7):2113-2115.
  11. Leanderson R, Sundberg J, von Euler C. Role of diaphragmatic activity during singing: a study of transdiaphragmatic pressures. J Appl Physiol (1985). 1987;62(1):259-270.
  12. Salomoni S, van den Hoorn W, Hodges P. Breathing and Singing: Objective Characterization of Breathing Patterns in Classical Singers. PLoS One. 2016;11(5):e0155084.
  13. Bradley H, Esformes J. Breathing pattern disorders and functional movement. Int J Sports Phys Ther. 2014; 9(1): 28-39.
  14. Finta R, Nagy E, Bender T. The effect of diaphragm training on lumbar stabilizer muscles: a new concept for improving segmental stability in the case of low back pain. J Pain Res. 2018;11:3031-3045.
  15. Terada M, Kosik KB, McCann RS, Gribble PA. Diaphragm Contractility in Individuals with Chronic Ankle Instability. Med Sci Sports Exerc. 2016;48(10):2040-2045.
  16. 16.0 16.1 Hopkins E, Sharma S. Physiology, Acid Base Balance. [Updated 2020 Aug 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507807/
  17. 17.0 17.1 17.2 17.3 Benner A, Sharma S. Physiology, Carbon Dioxide Response Curve. [Updated 2020 Apr 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538146/
  18. 18.0 18.1 18.2 Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med. 2002;347(1):43-53.
  19. Yoon S, Zuccarello M, Rapoport RM. pCO(2) and pH regulation of cerebral blood flow. Front Physiol. 2012;3:365.
  20. Giardino ND, Friedman SD, Dager SR. Anxiety, respiration, and cerebral blood flow: implications for functional brain imaging. Compr Psychiatry. 2007;48(2):103-112.
  21. Ressler KJ. Amygdala activity, fear, and anxiety: modulation by stress. Biol Psychiatry. 2010;67(12):1117-1119.
  22. 22.0 22.1 Patel AK, Benner A, Cooper JS. Physiology, Bohr Effect. [Updated 2019 Jul 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526028/
  23. Armando Hasudungan. Oxygen - Haemoglobin Dissociation Curve - Physiology. Available from: https://www.youtube.com/watch?v=BYGPkRFvzOc [last accessed 23/08/2020]
  24. 24.0 24.1 24.2 Waxenbaum JA, Reddy V, Varacallo M. Anatomy, Autonomic Nervous System. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK539845/
  25. Vaillancourt M, Chia P, Sarji S. et al. Autonomic nervous system involvement in pulmonary arterial hypertension. Respir Res. 2017; 18: 201.
  26. 26.0 26.1 AbuHasan Q, Reddy V, Siddiqui W. Neuroanatomy, Amygdala. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537102/
  27. Neuroscientifically Challenged. 2-Minute Neuroscience: Amygdala. Available from https://www.youtube.com/watch?v=JVvMSwsOXPw [last accessed: 23/08/2020]
  28. Jafari H, Courtois I, Van den Bergh O, Vlaeyen JWS, Van Diest I. Pain and respiration: a systematic review. Pain. 2017;158(6):995-1006. 
  29. 29.0 29.1 29.2 29.3 Chaitow, L., Bradley, D. and Gilbert, C. Recognizing and Treating Breathing Disorders. Elsevier, 2014
  30. Veron HL, Antunes AG, de Moura Milanesi J, Corrêa, ECR. Implications of mouth breathing on the pulmonary function and respiratory muscles. Revista CEFAC. 2016; 18(1): 242-51.
  31. Sano M, Sano S, Oka N, Yoshino K, Kato T. Increased oxygen load in the prefrontal cortex from mouth breathing: a vector-based near-infrared spectroscopy study. Neuroreport. 2013;24(17):935-940.
  32. Basheer B, Hegde KS, Bhat SS, Umar D, Baroudi K. Influence of mouth breathing on the dentofacial growth of children: a cephalometric study. J Int Oral Health. 2014;6(6):50-55.
  33. Hayes D Jr, Collins PB, Khosravi M, Lin RL, Lee LY. Bronchoconstriction triggered by breathing hot humid air in patients with asthma: role of cholinergic reflex. Am J Respir Crit Care Med. 2012;185(11):1190-6.
  34. Khosravi M, Collins PB, Lin RL, Hayes D Jr, Smith JA, Lee LY. Breathing hot humid air induces airway irritation and cough in patients with allergic rhinitis. Respir Physiol Neurobiol. 2014;198:13-19.
  35. Tsuji B, Hayashi K, Kondo N, Nishiyasu T. Characteristics of hyperthermia-induced hyperventilation in humans. Temperature (Austin). 2016;3(1):146-160.
  36. Clifton‐Smith T, Rowley J. Breathing pattern disorders and physiotherapy: inspiration for our profession. Phys Ther Rev. 2011; 16: 75–86.