Yawn comes from Old English 'Ginian' and 'Gionian' meaning to 'Open the mouth wide, gape', which in turn comes from the Proto-Germanic base gin-. Yawning is a spontaneous, stereotyped and often repetitive motor act characterized by gaping of the mouth accompanied by a long inspiration, a brief acme followed by a short expiration.
It is not just a matter of opening one’s mouth, but a generalized stretching of muscles, those of the respiratory tract (diaphragm, intercostal), the face and the neck. It may be seen as a part of the generalized stretch, named pandiculation, with which it is generally associated.Evidence that yawning and stretching may be related comes from the observation that if you try to stifle or prevent a yawn by clenching your jaws shut, the yawn is somewhat "unsatisfying." For some reason, the stretching of jaw and face muscles is necessary for a good yawn.
Until now, no specific cerebral structure has been identified as a yawning center. A good number of clinical and pharmacological arguments indicate that yawning involves the hypothalamus (particularly the paraventricular nucleus, PVN), the bulbus and pontic regions, with frontal region connections in primates and to the cervical medulla. The PVN is an integration center between the central and peripheral autonomic nervous systems. It is involved in numerous functions ranging from feeding, metabolic balance, blood pressure and heart rate, to sexual behavior and yawning.
The paraventricular nucleus of the hypothalamus contains a group of oxytocinergic neurons originating in this nucleus and projecting to extra-hypothalamic brain areas (hippocampus, medulla oblongata, and spinal cord) controls yawning. Activation of these neurons by dopamine and its agonists, excitatory amino acids (N-methyl-D-aspartic acid) or oxytocin itself, or by electrical stimulation leads to yawning, while their inhibition by gamma-amino-butyric acid and its agonists or by opioid peptides and opiate-like drugs inhibits yawning. The activation of these neurons is secondary to the activation of nitric oxide synthase, which produces nitric oxide. Nitric oxide in turn causes, by a mechanism that is as yet unidentified, the release of oxytocin in extra hypothalamic brain areas. Other compounds modulate yawning by activating central oxytocinergic neurons: sexual hormones, serotonin, hypocretin and endogenous peptides (adrenocorticotropin-melanocyte-stimulating hormone). Oxytocin activates cholinergic neurotransmission in the hippocampus and the reticular formation of the brainstem.
Acetylcholine induces yawning via the muscarinic receptors of effectors from which the respiratory neurons in the medulla, the motor nuclei of the Vth,VIIth, IXth, Xth, and XIIth cranial nerves, the phrenic nerves (C1–C4) and the motor supply to the intercostal muscles.
There are reciprocal connections between insula and thalamus, hypothalamus, reticular activating system (RAS), the locus coeruleus. After a yawn, humans experience an unfolding feeling of well-being. Physical movement (somatic motor system) and respiratory activity are coordinated by interactions involving brainstem mechanisms and structures such as the nucleus of the solitary tract, the PVN, and the RAS. Visceral somatic sensations are functionnally and anatomically linked. Subjectively experienced feelings as well as emotions might be bases on higher-order re-representations of homeostatic afferent sensory activity in human forebrain. Direct ascending projections from these sites activate insular cortex by way of the basal (parasympathetic) and posterior (sympathetic) parts of the ventromedial nucleus of the thalamus. These modality-specific, topographically organized projection pathways are phylogenetically distinct to primates and are well-developed only in humans. These pathways progressively activate higher-order homeostatic afferent re-representations in more anterior portions of the insula. The anterior insula (particularly right, non dominant) is activated predominantly by homeostatic afferents. Indeed, the insular cortex is involved in higher somatic integration, in relation to both somatic, autonomic and limbic systems. The ventral anterior insula is most important for core affect, a term that describes broadly-tuned motivational states with associated subjective feelings.
(Yawning: unsuspected avenue for a better understanding of arousal and interoception, 2006)
Why do we yawn?
• Yawn and oxygen
One commonly held notion is that yawning functions to modify levels of oxygen and carbon dioxide in the blood: yawning occurs when one's blood contains increased amounts of carbon dioxide and therefore becomes in need of the influx of oxygen (or expulsion of carbon dioxide) that a yawn can provide.
In 1987, Provine corrected this theory: in his study, he subjected participants to air with higher than normal levels of CO2 (3% to 5% versus the usual 0.03%). The experiment showed that neither elevated carbon dioxide nor depressed oxygen levels in the blood caused the frequency of yawning in subjects to change. In a second study, Provine found that having subjects exercise hard enough to double their breathing rate also had no effect on yawning. Together, the studies prove that yawning is not a primary respiratory function. However, need of oxygen continues to be considered a possible cause of yawn. (Yawning: no effect of 3-5% CO2, 100% O2, and exercise,1987)
Analysing variations in physiology, it has been observed an increase of respiration period and so a decrease of respiratory rate during and after a yawn.
Slowed breathing persisted for ~15s following peak inhalation; arguing against the hypothesis that yawning acts as a respiratory mechanism to regulate the amount of oxygen and carbon dioxide in the blood. Rather, this finding suggests a decrease in post yawning oxygen intake, due to the decreased breathing rate. Nor is the decreased breathing rate compensated for by deeper breaths. While respiration period was significantly decreased at 10 and 15s after a yawn, tidal volume returned to baseline approximately 5s following yawning, demonstrating that breathing rate slowed without compensatory change in lung volume. Thus, any surplus oxygen achieved by the deep inhalation associated with yawning would appear to be nullified by the subsequent decrease in respiratory rate. This is in agreement with the observations of Provine showing that yawning frequency is not influenced by oxygen and CO2 levels. (Changes in Physiology before, during, and after Yawning, 2012)
• Yawn and arousal
According to another theory, the significance of yawning is to increase the alert status of the individual during a change. The release in the brain of the same neurotransmitters that control emotions, appetite and mood would increase the frequency of yawn. All of the accepted characteristics of yawning - hunger, boredom, lethargy - have something in common: they are associated with change. When animals change between behaviours, they are not merely responding in a passive way to conditions of the environment, but they are following internally generated signals produced by homeostasis procedures originating from the hypothalamus (suprachiasmatic nucleus, SCN, and paraventricular nucleus, PVN, of the hypothalamus).
This internal rhythm has the ability to anticipate the transitions and triggers behavioural and physiological changes in accordance with those transitions. Yawning is a behaviour which shares these characteristics and appears to be associated with transitions between periods of high and low activity or arousal. Matikainen and Elo proposed a proximate mechanism to support this theory, suggesting that yawning mechanically stimulates the carotid artery, promoting an increase in cortical arousal via neck compressions that accompany yawning. The carotid body is highly vascularized and compressions may increase circulation, resulting in stimulation by hormones such as adenosine or catecholamines (Does yawning increase arousal through mechanical stimulation of the carotid body?, 2008).
• Yawn and brain temperature
Another hypothesis, supported by Gallup, is that yawning is a brain cooling mechanism. This is the actual most accreditated theory: consistent with the role of the hypothalamus and the PVN, evidence from diverse sources suggests that yawning may be a thermoregulatory mechanism. Yawning is triggered by an increase in brain temperature, and that the physiological reactions following a yawn promote a return to brain thermal homeostasis. Recent research directly measured cortical temperature in rats and found a distinctive association between brain temperature and yawning . By continuously monitoring cortical temperatures during the 3-min prior to and following a yawn, these researchers found a significant increase in temperature leading up to the onset of a yawn, followed by a significant decrease in temperature and return to baseline in the 3-min following the yawn.
The slope of temperature regressed against time changed significantly surrounding the onset of a yawn, first shifting in a positive direction at 1min prior to yawning and then in a negative direction at the time of yawning. The changes in temperature that portend the occurrence of yawning (Y)/stretching(S) occur well in advance of the act itself, and the changes in temperature that follow the act continue for several minutes afterward. Both yawning and stretching may be responses to, or symptoms of transient brain hyperthermia. These behaviors may be acting either independently or in tandem to counter intermittent increases in brain temperature and promote thermal homeostasis. Differences in the nature of these behaviors, however, suggest that stretching may facilitate more widespread cooling compared to direct brain and head cooling associated with yawning. (Yawning and stretching predict brain temperature changes in rats: support for the thermoregulatory hypothesis, 2010)
Analysing changes in physiology before, during and after yawning, it has been observed a significant increase in heart rate at the peak of yawning compared to baseline, 10s post yawn, and 15s post yawn.
Comparing variation of some physiological parameters during a yawn and an inhale, it is also been observed an increase in both skin conductance levels (SCL) and in skin conductance response (SCR) during and after a yawn.
This heightened heart rate may lead to an increase in circulation, including blood flow to the brain and turnover therein, as it is demonstrated by an increase of skin conductance.
The rate of blood flow to the brain is one of the key factors in determining the temperature of the brain. In humans, brain temperature averages approximately 37°C, with circadian fluctuations of up to ±0.5°C. Brain temperature is primarily determined by metabolic heat production, temperature of the blood supply, and rate of blood flow. Physiological cooling mechanisms affecting the blood supply to the brain include convection, conduction, and evaporation. Increased blood flow during body stretching, neck and facial stretching, or increased heart rate variability during yawning would enable this cooler blood to pass trough the warmer brain tissue more rapidly, increasing convective brain cooling. Introduction of cool air into the nasal cavity can effectively lower brain surface temperature and during periods of induced mild hyperthermia, nasal breathing produces a rapid (0.1°C per minute) drop in frontal lobe temperature of up to 0.8°C. During a yawn, deep inhalation may similarly invoke evaporative cooling of the venous blood draining from the nasal and oral orifices into the cavernous sinus. This process would effectively cool the area surrounding the internal carotid artery, which supplies blood to the rest of the brain.
(Changes in Physiology before, during, and after Yawning, 2012)
Cooling is primarily the result of enhanced cerebral blood flow and countercurrent heat exchange with ambient air. Accordingly, the incidence of yawning in humans was influenced by seasonal variation in climate conditions; the temperature of the ambient air is what gives a yawn its utility. Thus yawning should be counterproductive – and therefore suppressed – in ambient temperatures at or exceeding body temperature, as taking a deep inhalation of air would no longer promote cooling. In other words, there should be a “thermal window” or a relatively narrow range of ambient temperatures in which to expect highest rates of yawning.
Across seasonal trials yawning was associated with lower ambient temperatures, and in particular, yawning was less frequent in the summer condition when temperatures were higher and humidity was lower. Furthermore, the proportion of individuals yawning in the summer dropped greatly as the length of time spent outside increased, suggesting that the expression of social yawning may reflect a compromise with thermal effects. On the other hand, there was a positive relationship between time spent outdoors prior to testing and yawning in the winter condition. (Contagious yawning and seasonal climate variation, 2011)
Yawn and sleep
A circadian rhythm has been found in spontaneous yawning. In normal, unstressed humans daily peaks of yawning are associated with transitions from sleeping to waking and from waking to sleeping. The association between yawning and sleep can be further understood from a thermoregulatory viewpoint. Yawning occurs most frequently in the morning after waking, and in the evening just prior to sleep. Brain temperature is highest before sleep, while lowest during sleep. Yawning stops during sleep, but yawning upon waking may be due to an increase in metabolic activity.
The state-change associated with waking, and the increased arousal that accompanies waking may require an immediate change in blood flow, and temperature regulation as well.
According to the theory of Walusinski, yawning is part of interoceptiveness, or sensitivity to events happening within the body. Yawning plays an important role in the link between REM sleep and arousal. Behavioral pattern continuity from prenatal to postnatal life shows a strict parallelism between the ontogeny of REM sleep and yawning. Basically, REM sleep in the human declines from 50% of total sleep time (8 h) and a frequency of 30/50 yawns per day, in the newborn, to 15% of total sleep time (1 h) and less than 20 yawns per day, in the adult.
It has been shown that upon waking, yawning and stretching reverse the total muscle relaxation that characterizes REM sleep. Stretching corrects the loss of conscious imagery—the impaired sense of the position of various body parts in relation to neighboring parts—and yawning resets the mental self-image, thus increasing arousal and self-awareness. (Yawning: unsuspected avenue for a better understanding of arousal and interoception, 2006)
Yawn and fatigue
Tiredness due to physical exercise or mental concentration on tasks is often referred to as ‘fatigue’. Yawning is seen when humans (and animals) become fatigued. Blood cortisol levels are known to rise during stress and fatigue; yawning may occur when we are under stress or tired. We do not know whether cortisol levels fluctuate during yawning. Potentially, yawning and cortisol levels may provide a valuable diagnostic tool and warning of untoward underlying neurological problems. (Born to yawn? Cortisol linked to yawning: a new hypothesis, 2011)
Yawning after eating
After a big meal, excessive yawning often appears. This could be explained by the fact that in our digestive system there is a real nervous system, called enteric nervous system, formed by 100 million of neurons. When we overeat, interoceptors of our viscera, presented in this enteric system, are activated and can cause yawning.
Poor posture can cause yawning. When a person is in a slouched position, pressure is put on the lungs, which will not allow them to fill with air while breathing. This is even more evident after eating. The stomach is full, which will put pressure on the lungs from the abdominal area. After a big meal, the body may relax to a slumped position, which puts pressure on the lungs from the ribs and chest area. When a person has overeaten, and is very full, this puts even more pressure on the lungs and may cause excessive yawning after eating.
The tiredness or drowsy feeling you get after eating a full meal will also affect your blood-sugar level. This, too, may cause excessive yawning by creating a chemical imbalance in the body. The yawing and sleepy sensations may continue until the body has a chance to level out the sugar imbalance and return the sugar levels to normal.
One pathological condition that can cause excessive yawning after eating is helicobacter pylori. This infection has been closely linked to gastric disorders such as cancer and ulcers. Once the problem has been diagnosed and it has been found that helicobacter pylori is present, antibiotics are given and the excessive yawning after eating should cease.
In humans, yawning is often triggered by others yawning (seeing a person yawning, reading or thinking about yawning, talking to someone on the phone who is yawning) and is a typical example of positive feedback. Clinical, psychological, and neurobiological clues suggest a link between yawn contagion and empathy in humans.
“Yawning is so contagious that virtually anything having to do with yawning will trigger it, even thinking about it or reading about it,” Provine says. “Someone reading your story will have yawns triggered, [just] by virtue of reading it.”
The proximate cause for contagious yawning may lie with mirror neurons in the frontal cortex of certain vertebrates, which, upon being exposed to a stimulus from conspecific (same species) and occasionally interspecific organisms, activates the same regions in the brain. Mirror neurons are a particular class of visual-motor neurons, originally discovered in area F5 of the premotor cortex of the macaque that are activated both when the monkey performs a certain action, and when it observes another individual (monkey or man) made a similar action. These neurons are also present in humans in the pre-frontal cortex, premotor cortex, supplementary motor area, in the cingulate cortex, parietal cortex, and cerebellum, constituting the mirror neuron system (MNS).
Haker, Rössler et al., in their recent study, used functional magnetic resonance imaging to assess brain activity during contagious yawning (CY). Through an fMRI, signal-dependent changes in blood oxygen levels (BOLD) were compared when subjects viewed videotapes of yawning faces as opposed to faces with a neutral expression. In response to yawning, subjects showed unilateral activation of their Brodmann’s area 9 (BA 9) portion of the right inferior frontal gyrus, a region of the MNS. In this way, two individuals could share physiological and associated emotional states based on perceived motor patterns.
When the two conditions (yawning vs. neutral) were contrasted, it was found only right-sided activation: besides activation of the middle temporal gyrus, it was found specific activation in the BA 9 portion of the right IFG and in the right superior frontal gyms.
The BA 9 is involved in higher social cognitive functioning such as mentalizing. Thus, activation of this area might represent the effect of contagiousness, possibly linking the MNS to higher cognitive functions such as cognitive empathy. This involvement of an area associated with higher cognitive functions, which are not developed at birth, may explain why CY is ontogenetically seen only in later stages of a person's development. (Mirror neuron activity during contagious yawning-an fMRI study, 2012)
The discovery of mirror neurons has shown that the motor system can be activated both in a "on-line" during the execution of the act, both in a state "off line" during the observation or imagination of an act. Mirror neurons have been proposed as a driving force for imitation which lies at the root of much human learning such as language acquisition. Yawning may be an offshoot of the same imitative impulse. Young children with autism spectrum disorders do not increase their yawning frequency after seeing other people yawning, in contrast to typically developing children. In fact, the autistic children actually yawned less during the videos of yawning than during the control videos. This supports the claim that contagious yawning is related to empathic capacity.
In a recent study conducted by Norscia and Palagi, it has been revealed that - among other variables such as nationality, gender, and sensory modality - only social bonding predicted the occurrence, frequency, and latency of yawn contagion. As with other measures of empathy, the rate of contagion was found to be greatest in response to kin, then friends, then acquaintances, and lastly strangers. Hence, yawn contagion appears to be primarily driven by the emotional closeness between individuals.(Yawn contagion and empathy in Homo sapiens, 2011)
Yawn during the life
Yawning and stretching have related phylogenetic old origins. In the human embryo, yawning occurs as early as 12 weeks after conception and remains relatively unchanged throughout life. Children don’t fall prey to contagious yawning until about three, four years of age. From birth, when spontaneous yawns are very frequent (50-60 per day), to adolescence the number of them decreases daily (10-20 per day). From adult age to old age, the number of yawns decreases lightly, disappearing completely only in presence of a pathology, connected with neurological dysfunctions, like Parkinson disease, because of a decrese of dopamine, or motor problems. The decrease of yawning in the elderly suggests an associated decrease of dopaminergic activity.
(Le bâillement: naissance, vie et sénescence, 2006)
Excessive yawning and pathology
Yawning also needs to be considered when dealing with cases of excessive yawning, and yawning related medical symptoms.
In 1888 Jean-Martin Charcot presented, during one of his celebrated Tuesday gatherings at La Salpêtrière, the case of a young woman inconvenienced by 8 yawns a minute, that is 480 per hour! He qualified this as a form of hysteria, despite his examination revealing binasal hemianopsia, right-side cheirobrachial skin insensitivity to all stimuli and loss of smell. Given our contemporary knowledge, this points to a pituitary adenoma.
If a person yawns four times within one minute, it is considered to be excessive. If the yawning persists and occurs in an abnormal amount of time, you will need to seek medical attention to rule out a more serious condition.
There is evidence linking painful headaches and a variety of thermoregulatory disorders with excessive yawning. The yawning experienced during these times may be due to circulatory dysfunction. This coupled with evidence that yawning has medical implications for a variety of disorders suggests that aberrant yawning is symptomatic of thermoregulatory dysfunction.
Of short duration, excessive yawning may predict a vasovagal reaction or neurovegetative disorders (dyspepsia, migraine-like syndromes). All insults to the intra-cranial central nervous system or the hypothalamo-hypophyseal region may be involved: tumors with intracranial hypertension, infections, temporal epilepsy, strokes, etc. Multiple sclerosis, epilepsy, encephalitis, supranuclear palsy, schizophrenia, treatment for opiate withdrawal, sleep deprivation, migraine headaches, stress and anxiety, and central nervous system damage are all related to thermoregulatory dysfunction and each of these conditions is associated with atypical yawning. Excessive yawning appears to be symptomatic of conditions that increase brain and/or core temperature, such as central nervous system damage, sleep deprivation, and specific serotonin reuptake inhibitors. (Yawning and thermoregulation, 2008). Drugs that cause an increase of brain temperature are connected with excessive yawning, while drugs that lead to hypothermia (e.g., opioids) inhibit yawning. Nasal breathing and forehead cooling, which have been identified as specific brain cooling mechanisms, diminish the incidence of yawning. The development of psychotropic drugs has given rise to a rich iatrogenic pathology: serotoninergic agents, apomorphine, acetylcholinesterase inhibitors, sismotherapy and opiate withdrawal are triggers of yawn clusters. Excessive sleepiness with excessive yawning should also suggest examination for an obstructive sleep apnea syndrome. Thus, excessive yawning could be clinically associated with thermoregulatory/circulatory/neurological distress/dysfunction, and could be used as a diagnostic indicator. (Yawn, 2008)
Finally excessive yawning is one of the most frequent causes of the dislocation of the jaw. A painful yawn may also reveals a pathology of the temporomandibular joint. In 2012, in Korea, it has been observed a case of fracture of the first rib after an excessive act of pandiculation (Juvenile First Rib Fracture Caused by Morning Stretching).
Yawning is a physiological, spontaneous and stereotyped act that continues to be at the center of actual debate and research. Today, the most accreditated theory remains the brain cooling mechanism. In fact this thermoregulative function is at the base of lots of aspects connected with yawning:
• changes in physiology before, during and after yawning can be explained with this necessity to regulate and maintain brain homeostasis
• yawning associated with transitions from sleeping to waking and from waking to sleeping is based on variation of brain temperature
• excessive yawning is often symptomatic of pathologies connected with an increase of brain and/or core temperature; drugs that cause hyperthermia cause a major yawn frequency, while drugs that lead to hypothermia inhibit yawning.
Finally, an interesting aspect is contagious yawning, based on empathy. Researches have investigated what specific cerebral areas are stimulated when we see, hear or read about yawning and have demonstrated the contagiousness is linked to mirror neurons.
Development of scientific and medical knowledge and future researches will contribute to find more and more detailed explanations of mechanisms that lead yawning.