Mammalian diving reflex

The mammalian diving reflex is a reflex in mammals which optimizes respiration to allow staying underwater for extended periods of time. It is exhibited strongly in aquatic mammals (seals,[1] otters, dolphins, etc.), but exists in weaker versions 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. Every animal's diving reflex is triggered specifically by cold water contacting the face.[2]


Upon initiation of the reflex, three changes happen to a body, in this order:

  1. Bradycardia is the first response to submersion. Immediately upon facial contact with cold water, the human heart rate slows down ten to twenty-five percent.[2] Seals experience changes that are even more dramatic, going from about 125 beats per minute to as low as 10 on an extended dive.[1][3] Slowing the heart rate lessens the need for bloodstream oxygen, leaving more to be used by other organs.
  2. Next, peripheral vasoconstriction sets in. When under high pressure induced by deep diving, capillaries in the extremities start closing off, stopping blood circulation to those areas. Note that vasoconstriction usually applies to arterioles, but in this case is completely an effect of the capillaries. Toes and fingers close off first, then hands and feet, and ultimately arms and legs stop allowing blood circulation, leaving more blood for use by the heart and brain. Human musculature accounts for only 12% of the body's total oxygen storage, and the body's muscles tend to suffer cramping during this phase. Aquatic mammals have as much as 25 to 30% of their oxygen storage in muscle, and thus they can keep working long after capillary blood supply is stopped.
  3. Last is the blood shift. Peripheral vasoconstriction in the extremities starts as soon as the body enters the water, pushing blood into the thoracic organs, particularly the lungs. This engorges the alveolar capillaries, increasing intra-alveolar gas pressure, the pressure inside the chest, and opposing submergence pressure on the chest. As depth increases, peripheral vasoconstriction and hydrostatic pressure on the extremities continue to drive the blood shift. When depth increases to the point where chest compression limits are reached, the blood shift accelerates. This is due to the rapidly increasing difference between hydrostatic pressure on the extremities and intra-alveolar gas pressure. The blood shift keeps pressure inside the chest high enough to allow the diver to proceed deeper without the chest collapsing. There is a risk, however - "A sufficient pressure difference between the blood pressure in the pulmonary capillaries and the intra-alveolar gas pressure may cause stress failure with leakage of fluid and blood into the lungs" (pulmonary edema or lung squeeze).[4] Blood freely flows back into the extremities as the diver heads back to the surface. This stage of the diving reflex has been observed in humans (such as accomplished freediver Bret Gilliam) during deep (over 90 metres or 300 ft) dives.[5] An incorrect impression exists among some that during the blood shift, blood and plasma pass freely throughout the thoracic cavity and into the alveoli. This is not normal, but rather a type of lung barotrauma. Blood in the alveoli is called pulmonary edema, and is dangerous at best and deadly at worst.

Thus, both a conscious and an unconscious person can survive longer without oxygen under cold water than in a comparable situation on dry land. 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.[6][7]

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 cranial nerve X (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, creating a heart–brain circuit and allowing the mammal to conserve oxygen.

In humans, the mammalian 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 within water.[6] When breathing with face submerged this causes a diving reflex which increases proportionally to decreasing water temperature.[2] Activating the diving reflex with cold water can be used to treat supraventricular tachycardia.[8] However the greatest bradycardia effect is induced when the subject is holding breath with face submerged.

Medical application

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.[9] This is especially useful in infants. A towel soaked in ice-cold water may be applied to the 'snout' region of the face. In children, the valsalva maneuver or carotid sinus massage is more appropriate.[10]

See also


  1. 1 2 Zapol WM, Hill RD, Qvist J, Falke K, Schneider RC, Liggins GC, Hochachka PW (September 1989). "Arterial gas tensions and hemoglobin concentrations of the freely diving Weddell seal". Undersea Biomed Res. 16 (5): 363–73. PMID 2800051. Retrieved 2008-06-14.
  2. 1 2 3 Speck DF, Bruce DS (March 1978). "Effects of varying thermal and apneic conditions on the human diving reflex". Undersea Biomed Res. 5 (1): 9–14. PMID 636078. Retrieved 2008-06-14.
  3. Thornton SJ, Hochachka PW (2004). "Oxygen and the diving seal". Undersea Hyperb Med. 31 (1): 81–95. PMID 15233163. Retrieved 2008-06-14.
  4. Peter Lindholm; Claes EG Lundgren. "Journal of Appied Physiology - The physiology and pathophysiology of human breath-hold diving". Retrieved 4 April 2015.
  5. Gilliam B (2011). "A practical discussion of nitrogen narcosis". Tech Diving Mag. Retrieved 2013-10-05.
  6. 1 2 Lundgren, Claus EG; Ferrigno, Massimo (eds). (1985). "Physiology of Breath-hold Diving. 31st Undersea and Hyperbaric Medical Society Workshop.". UHMS Publication Number 72(WS-BH)4-15-87. Undersea and Hyperbaric Medical Society. Retrieved 2009-04-16.
  7. Mackensen GB, McDonagh DL, Warner DS (March 2009). "Perioperative hypothermia: use and therapeutic implications". J. Neurotrauma. 26 (3): 342–58. doi:10.1089/neu.2008.0596. PMID 19231924.
  8. Mathew PK (January 1981). "Diving reflex. Another method of treating paroxysmal supraventricular tachycardia". Arch. Intern. Med. 141 (1): 22–3. doi:10.1001/archinte.141.1.22. PMID 7447580.
  9. Grahame IF, Hann IM (June 1978). "Use of the diving reflex to treat supraventricular tachycardia in an infant.". Arch Dis Child. 53 (6): 515–6. doi:10.1136/adc.53.6.515.
  10. Gardiner M, Eisen S, Murphy C. Training in paediatrics: the essential curriculum. Oxford University Press, Oxford 2009.
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