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Exhalation (or expiration) is the flow of the breath out of an organism. In humans it is the movement of air from the lungs out of the airways, to the external environment during breathing.

This happens due to elastic properties of the lungs, as well as the internal intercostal muscles which lower the rib cage and decrease thoracic volume; as the thoracic diaphragm relaxes during exhalation it causes the tissue it has depressed to rise superiorly and put pressure on the lungs to expel the air. During forced exhalation, as when blowing out a candle, expiratory muscles including the abdominal muscles and internal intercostal muscles generate abdominal and thoracic pressure, which forces air out of the lungs.

Exhaled air is rich in carbon dioxide, a waste product of cellular respiration during the production of energy, which is stored as ATP. Exhalation has a complementary relationship to inhalation which together make up the respiratory cycle of a breath.

Exhalation and gas exchange[edit]

The main reason for exhalation is to rid the body of carbon dioxide, which is the waste product of gas exchange in humans. Air is brought in the body through inhalation. During this process air is taken in through the lungs. Diffusion in the alveoli allows for the exchange of O2 into the pulmonary capillaries and the removal of CO2 and other gases from the pulmonary capillaries to be exhaled. In order for the lungs to expel air the diaphragm relaxes, which pushes up on the lungs; the air then flows through the trachea then through the larynx and pharynx to the nasal cavity and oral cavity where it is expelled out of the body.[1] Exhalation takes longer than inhalation since it is believed to facilitate better exchange of gases. Parts of the nervous system help to regulate respiration in humans; the exhaled air isn’t just carbon dioxide; it contains a mixture of other gases. Human breath contains volatile organic compounds (VOCs); these compounds consist of methanol, isoprene, acetone, ethanol and other alcohols. The exhaled mixture also contains ketones, water and other hydrocarbons.[2][3]

It is during exhalation that the olfaction contribution to flavor occurs in contrast to that of ordinary smell which occurs during the inhalation phase.[4]


Spirometry is used to measure lung function; the total lung capacity (TLC), functional residual capacity (FRC), residual volume (RV), and vital capacity (VC) are all values that can be tested using this method. Spirometry is used to help detect, but not diagnose, respiratory issues like COPD, and asthma, it is a simple and cost effective screening method.[5] Further evaluation of a person's respiratory function can be done by assessing the minute ventilation, forced vital capacity (FVC), and forced expiratory volume (FEV); these values differ in men and women because men tend to be larger than women.

TLC is the maximum amount of air in the lungs after maximum inhalation. In men the average TLC is 6000 ml, and in women it is 4200 ml. FRC is the amount of air left in the lungs after normal exhalation. Men leave about 2400 ml on average while women retain around 1800 ml. RV is amount of air left in the lungs after a forced exhalation; the average RV in men is 1200 ml and women 1100 ml. VC is the maximum amount of air that can be exhaled after a maximum inhalation. Men tend to average 4800 ml and women 3100 ml.[citation needed]

Asthma, COPD, and smokers have reduced airflow ability. People who suffer from asthma and COPD show decreases in exhaled air due to inflammation of the airways; this inflammation causes narrowing of the airways which allows less air to be exhaled. Numerous things cause inflammation some examples are cigarette smoke and environmental interactions such as allergies, weather, and exercise. In smokers the inability to exhale fully is due to the loss of elasticity in the lungs. Smoke in the lungs causes them to harden and become less elastic, which prevents the lungs from expanding or shrinking as they normally would.[citation needed]

Dead space can be determined by two types of factors which are anatomical and physiological; some physiological factors are having non-perfuse but ventilated alveoli, such as a pulmonary embolism or smoking, excessive ventilation of the alveoli, brought on in relation to perfusion, in people with chronic obstructive lung disease, and “shunt dead space,” which is a mistake between the left to right lung that moves the higher CO2 concentrations in the venous blood into the arterial side.[6] The anatomical factors are the size of the airway, the valves, and tubing of the respiratory system.[6] Physiological dead space of the lungs can affect the amount of dead space as well with factors including smoking, and diseases. Dead space is a key factor for the lungs to work because of the differences in pressures, but it can also hinder the person.[citation needed]

One of the reasons we can breathe is because of the elasticity of the lungs; the internal surface of the lungs on average in a non-emphysemic person is normally 63m2 and can hold about 5lts of air volume.[7] Both lungs together have the same amount of surface area as half of a tennis court. Disease such as, emphysema, tuberculosis, can reduce the amount of surface area and elasticity of the lungs. Another big factor in the elasticity of the lungs is smoking because of the residue left behind in the lungs from the smoking; the elasticity of the lungs can be trained to expand further.[citation needed]

Brain involvement[edit]

Brain control of exhalation can be broken down into voluntary control and involuntary control. During voluntary exhalation, air is held in the lungs and released at a fixed rate. Examples of voluntary expiration include: singing, speaking, exercising, playing an instrument, and voluntary hyperpnea. Involuntary breathing includes metabolic and behavioral breathing.[citation needed]

Voluntary expiration[edit]

The neurological pathway of voluntary exhalation is complex and not fully understood. However, a few basics are known; the motor cortex within the cerebral cortex of the brain is known to control voluntary respiration because the motor cortex controls voluntary muscle movement.[8] This is referred to as the corticospinal pathway or ascending respiratory pathway;[8][9] the pathway of the electrical signal starts in the motor cortex, goes to the spinal cord, and then to the respiratory muscles. The spinal neurons connect directly to the respiratory muscles. Initiation of voluntary contraction and relaxation of the internal and external internal costals has been shown to take place in the superior portion of the primary motor cortex.[8] Posterior to the location of thoracic control (within the superior portion of the primary motor cortex) is the center for diaphragm control.[8] Studies indicate that there are numerous other sites within the brain that may be associated with voluntary expiration; the inferior portion of the primary motor cortex may be involved, specifically, in controlled exhalation.[8] Activity has also been seen within the supplementary motor area and the premotor cortex during voluntary respiration; this is most likely due to the focus and mental preparation of the voluntary muscular movement.[8]

Voluntary expiration is essential for many types of activities. Phonic respiration (speech generation) is a type of controlled expiration that is used every day. Speech generation is completely dependent on expiration, this can be seen by trying to talk while inhaling.[10] Using airflow from the lungs, one can control the duration, amplitude, and pitch.[11] While the air is expelled it flows through the glottis causing vibrations, which produces sound. Depending on the glottis movement the pitch of the voice changes and the intensity of the air through the glottis change the volume of the sound produced by the glottis.[citation needed]

Involuntary expiration[edit]

Involuntary respiration is controlled by respiratory centers within the medulla oblongata and pons; the medullary respiratory center can be subdivided into anterior and posterior portions. They are called the ventral and dorsal respiratory groups respectively; the pontine respiratory group consists of two parts: the pneumotaxic center and the apneustic center.[9] All four of these centers are located in the brainstem and work together to control involuntary respiration. In our case, the ventral respiratory group (VRG) controls involuntary exhalation.

The neurological pathway for involuntary respiration is called the bulbospinal pathway, it is also referred to as the descending respiratory pathway.[9] “The pathway descends along the spinal ventralateral column. The descending tract for autonomic inspiration is located laterally, and the tract for autonomic expiration is located ventrally.”[12] Autonomic Inspiration is controlled by the pontine respiratory center and both medullary respiratory centers. In our case, the VRG controls autonomic exhalation. Signals from the VRG are sent along the spinal cord to several nerves; these nerves include the intercostals, phrenic, and abdominals.[9] These nerves lead to the specific muscles they control; the bulbospinal pathway descending from the VRG allows the respiratory centers to control muscle relaxation, which leads to exhalation.


Yawning is considered a non-respiratory gas movement. A non-respiratory gas movement is another process that moves air in and out of the lungs that don't include breathing. Yawning is a reflex that tends to disrupt the normal breathing rhythm and is believed to be contagious as well;[13] the reason why we yawn is unknown, but some think we yawn as a way to regulate the body’s levels of O2 and CO2. Studies done in a controlled environment with different levels of O2 and CO2 have disproved that hypothesis. Although there isn’t a concrete explanation as to why we yawn, others think people exhale as a cooling mechanism for our brains. Studies on animals have supported this idea and it is possible humans could be linked to it as well.[14] What is known is that yawning does ventilate all the alveoli in the lungs.


Several receptor groups in the body regulate metabolic breathing; these receptors signal the respiratory center to initiate inhalation or exhalation. Peripheral chemoreceptors are located in the aorta and carotid arteries, they respond to changing blood levels of oxygen, carbon dioxide, and H+ by signaling the pons and medulla.[9] Irritant and stretch receptors in the lungs can directly cause exhalation. Both sense foreign particles and promote spontaneous coughing, they are also known as mechanoreceptors because they recognize physical changes not chemical changes.[9] Central chemoreceptors in the medulla also recognize chemical variations in H+. Specifically, they monitor pH change within the medullary interstitual fluid and cerebral spinal fluid.[9]

See also[edit]


  1. ^ Sahin-Yilmaz, A.; Naclerio, R. M. (2011). "Anatomy and Physiology of the Upper Airway". Proceedings of the American Thoracic Society. 8 (1): 31–9. doi:10.1513/pats.201007-050RN. PMID 21364219.
  2. ^ Fenske, Jill D.; Paulson, Suzanne E. (1999). "Human Breath Emissions of VOCs". Journal of the Air & Waste Management Association. 49 (5): 594–8. doi:10.1080/10473289.1999.10463831. PMID 10352577.
  3. ^ Weisel, C. P. (2010). "Benzene exposure: An overview of monitoring methods and their findings". Chemico-Biological Interactions. 184 (1–2): 58–66. doi:10.1016/j.cbi.2009.12.030. PMC 4009073. PMID 20056112.
  4. ^ Masaoka, Yuri; Satoh, Hironori; Akai, Lena; Homma, Ikuo (2010). "Expiration: The moment we experience retronasal olfaction in flavor". Neuroscience Letters. 473 (2): 92–6. doi:10.1016/j.neulet.2010.02.024. PMID 20171264.
  5. ^ Kivastik, Jana; Kingisepp, Peet-Henn (2001). "Spirometric reference values in Estonian schoolchildren". Clinical Physiology. 21 (4): 490–7. doi:10.1046/j.1365-2281.2001.00352.x. PMID 11442581.
  6. ^ a b Hedenstierna, G; Sandhagen, B (2006). "Assessing dead space. A meaningful variable?". Minerva Anestesiologica. 72 (6): 521–8. PMID 16682925.
  7. ^ Thurlbeck, W. M. (1967). "Internal surface area and other measurements in emphysema". Thorax. 22 (6): 483–96. doi:10.1136/thx.22.6.483. PMC 471691. PMID 5624577.
  8. ^ a b c d e f McKay, L. C.; Evans, K. C.; Frackowiak, R. S. J.; Corfield, D. R. (2003). "Neural correlates of voluntary breathing in humans". Journal of Applied Physiology. 95 (3): 1170–8. doi:10.1152/japplphysiol.00641.2002. PMID 12754178.
  9. ^ a b c d e f g Caruana-Montaldo, Brendan (2000). "The Control of Breathing in Clinical Practice". Chest. 117: 205–225. CiteSeerX doi:10.1378/chest.117.1.205.
  10. ^ Newman, D. "The Physiology of Speech Production" (PDF). Retrieved 31 March 2012.
  11. ^ Heman-Ackah, Yolanda D. (2005). "Physiology of voice production: considerations for the vocal performer". Journal of Singing. 62 (2): 173–6.
  12. ^ Homma, Ikuo; Masaoka, Yuri (2008). "Breathing rhythms and emotions". Experimental Physiology. 93 (9): 1011–21. doi:10.1113/expphysiol.2008.042424. PMID 18487316.
  13. ^ Sarnecki, John (2008). "Content and Contagion in Yawning". Philosophical Psychology. 21 (6): 721–37. doi:10.1080/09515080802513292.
  14. ^ Corey, Timothy P.; Shoup-Knox, Melanie L.; Gordis, Elana B.; Gallup, Gordon G. (2012). "Changes in Physiology before, during, and after Yawning". Frontiers in Evolutionary Neuroscience. 3. doi:10.3389/fnevo.2011.00007. PMC 3251816.

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