The diving reflex, also known as the diving response and mammalian diving reflex is a response to immersion that overrides the basic homeostatic reflexes, which is found in all air-breathing vertebrates. It optimizes respiration by preferentially distributing oxygen stores to the heart and brain which allows staying underwater for extended periods of time. It is exhibited strongly in aquatic mammals (seals, otters, dolphins, muskrats), but exists in other mammals, including humans, in particular babies up to 6 months old (see Infant swimming). Diving birds, such as penguins, have a similar diving reflex. It may be the evolutionary development of a more primitive response to hypoxia exhibited by fishes. The diving reflex is triggered specifically by chilling the face and breath-hold. The most noticeable effects are on the cardiovascular system, which displays peripheral vasoconstriction, slowed pulse rate, redirection of blood to the vital organs to conserve oxygen, release of red blood cells stored in the spleen, and, in humans, heart rhythm irregularities.
Although aquatic animals have evolved profound physiological adaptations to conserve oxygen during submersion, the apnea and breath-holding duration, bradycardia, vasoconstriction, and redistribution of cardiac output occur also in terrestrial animals as a neural response, but the effects are more profound in natural divers.
When the face is submerged, receptors that are sensitive to cold within the nasal cavity and other areas of the face supplied by the fifth (V) cranial nerve (the trigeminal nerve) relay the information to the brain and then innervate the tenth (X) cranial nerve, (the vagus nerve), which is part of the autonomic nervous system. This causes bradycardia and peripheral vasoconstriction. Blood is diverted from the limbs and all organs but the heart and the brain (and lungs), concentrating flow in a heart–brain circuit and allowing the animal to conserve oxygen.
In humans, the diving reflex is not induced when limbs are introduced to cold water. Mild bradycardia is caused by subjects holding their breath without submerging the face in water. When breathing with face submerged the reflex strength increases proportionally to decreasing water temperature. However the greatest bradycardia effect is induced when the subject is holding breath with face submerged. Both apnea and facial cooling are triggers of this reflex, but actual water contact with the face appears to be unimportant.
The diving response in humans varies considerably depending on level of exertion, and also varies with age and breath-hold diving acclimatisation. Diving bradycardia is relatively strong in infants younger than a year old and may be a survival response to hypoxic exposures around the time of birth. The response reduces with age and is more strongly developed in breath-hold divers. The reduction in oxygen consumption seems to be in proportion to the pulse rate and the effect is relatively stronger during exercise.
Children tend to survive longer than adults when deprived of oxygen underwater. The exact mechanism for this effect has been debated and may be a result of brain cooling similar to the protective effects seen in patients treated with deep hypothermia.
Upon initiation of the reflex, changes occur:
Bradycardia and cardiac outputEdit
Bradycardia is the response to facial contact with cold water: the human heart rate slows down ten to twenty-five percent. Seals experience changes that are even more dramatic, going from about 125 beats per minute to as low as 10 on an extended dive. During breath-holding, humans also display reduced left ventricular contractility and diminished cardiac output, effects that may be more severe during submersion due to hydrostatic pressure.
Slowing the heart rate reduces the cardiac oxygen consumption, and compensates for the hypertension due to vasoconstriction. However, breath-hold time is reduced when the whole body is exposed to cold water as the metabolic rate increases to compensate for accelerated heat loss even when the heart rate is significantly slowed.
Preliminary evidence indicates that the bilateral carotid bodies detect the decreasing oxygen and rising carbon dioxide levels in blood during breath-holding, then send signals to the brain to regulate the entire cardiovascular response of the diving reflex.
The spleen contracts in response to lowered levels of oxygen and increased levels of carbon dioxide, releasing red blood cells and increasing the oxygen capacity of the blood. This may start before the bradycardia.
Blood shift is a term used when blood flow to the extremities is redistributed to the head and torso during a breathhold dive. Peripheral vasoconstriction occurs during submersion by resistance vessels limiting blood flow to muscles, skin, and viscera, regions which are "hypoxia-tolerant", thereby preserving oxygenated blood for the heart, lungs, and brain. The increased resistance to peripheral blood flow raises the blood pressure, which is compensated by bradycardia, conditions which are accentuated by cold water. Aquatic mammals have blood volume that is some three times larger per mass than in humans, a difference augmented by considerably more oxygen bound to hemoglobin and myoglobin of diving mammals, enabling prolongation of submersion after capillary blood flow in peripheral organs is minimized.
Cardiac arrhythmias are a common characteristic of the human diving response. As part of the diving reflex, increased activity of the cardiac parasympathetic nervous system not only regulates the bradycardia, but also is associated with ectopic beats which are characteristic of human heart function during breath-hold dives. Arrhythmias may be accentuated by neural responses to face immersion in cold water, distension of the heart due to central blood shift, and the increasing resistance to left ventricular ejection (afterload) by rising blood pressure. Arrhythmias commonly measured in the electrocardiogram during human breath-hold dives include ST depression, heightened T wave, and a positive U wave following the QRS complex, measurements associated with reduced left ventricular contractility and overall depressed cardiac function during a dive.
Adaptations of aquatic mammalsEdit
Diving mammals have an elastic aortic bulb thought to help maintain arterial pressure during the extended intervals between heartbeats during dives, and have high blood volume, combined with large storage capacity in veins and retes of the thorax and head in seals and dolphins. Chronic physiological adaptations of blood include elevated hematocrit, hemoglobin, and myoglobin levels which enable greater oxygen storage and delivery to essential organs during a dive. Oxygen use is minimised during the diving reflex by energy efficient swimming or gliding behaviour, and regulation of metabolism, heart rate, and peripheral vasoconstriction.
Aerobic diving capacity is limited by available oxygen and the rate at which it is consumed. Diving mammals and birds have a considerably greater blood volume than terrestrial animals of similar size, and in addition have a far greater concentration of haemoglobin and myoglobin, and this haemoglobin and myoglobin is also capable of carrying a higher oxygen load. During diving, the haematocrit and haemoglobin are temporarily increased by reflex splenic contraction, which discharges a large additional amount of red blood cells. The brain tissue of diving mammals also contains higher levels of neuroglobin and cytoglobin than terrestrial animals.
Aquatic mammals seldom dive beyond their aerobic diving limit, which is related to the myoglobin oxygen stored. The muscle mass of aquatic mammals is relatively large, so the high myoglobin content of their skeletal muscles provides a large reserve. Myoglobin-bound oxygen is only released in relatively hypoxic muscle tissue, so the peripheral vasoconstriction due to the diving reflex makes the muscles ischaemic and promotes early use of myoglobin bound oxygen.
The diving reflex is used in clinical practice as a means to treat supraventricular tachycardia. This is an example of a vagal maneuver, whereby the vagus nerve is stimulated in order to block the atrioventricular node, which interrupts the abnormal electrical circuit taking place in a supraventricular tachycardia. This is especially useful in infants in whom the diving reflex is well-preserved, allowing the valsalva maneuver or carotid sinus massage to be more appropriate.[clarification needed]
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