Cold shock response

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Cold shock response is a series of cardio-respiratory responses caused by sudden immersion in cold water.

In cold water immersions, cold shock response is perhaps the most common cause of death,[1] such as by falling through thin ice. The immediate shock of the cold causes involuntary inhalation, which, if underwater, can result in drowning. The cold water can also cause heart attack due to vasoconstriction,[2] where the heart has to work harder to pump the same volume of blood throughout the body. For people with existing cardiovascular disease, the additional workload can result in cardiac arrest. Inhalation of water (and thus drowning) may result from hyperventilation. Some people are much better able to survive swimming in very cold water due to body or mental conditioning.[1]

Physiological response[edit]

The physiological response results in temporary breathlessness and vasoconstriction. Vasovagal stimulation which leads to cardiac arrest

Conditioning against cold shock[edit]

It is possible to undergo physiological conditioning to reduce the cold shock response, and some people are naturally better suited to swimming in very cold water. Adaptations include the following:

  1. having an insulating layer of body fat covering the limbs and torso without being overweight;[1]
  2. ability to experience immersion without involuntary physical shock or mental panic;[1]
  3. ability to resist shivering;[1]
  4. ability to raise metabolism (and, in some cases, increase blood temperature slightly above the normal level);[citation needed]
  5. a generalized delaying of metabolic shutdown (including slipping into unconsciousness) as central and peripheral body temperatures fall.[citation needed]

In these ways, winter swimmers can survive both the initial shock and prolonged exposure. Nevertheless, the human organism is not suited to freezing water: the struggle to maintain blood temperature (by swimming or conditioned metabolic response) produces great fatigue after thirty minutes or less.[3]

Conditioning against the cold shock response is an effective and cost efficient way to prevent drowning.[4] Those who benefit the most from the habituation of a cold shock response are athletes, soldiers and those who are at risk of cold water immersion.[4]

Cold shock response in bacteria[edit]

A cold shock is when bacteria undergo a significant reduction in temperature, likely due to their environment dropping in temperature. To constitute as a cold shock the temperature reduction needs to be both significant, for example dropping from 37 °C to 20 °C, and it needs to happen over a short period of time, traditionally in under 24 hours.[5] Both prokaryotic and eukaryotic cells are capable of undergoing a cold shock response.[6] The effects of a cold shock in bacteria include:[7]

  • Decreased cell membrane fluidity
  • Decreased enzyme activity
  • Decreased efficiency of transcription and translation
  • Decreased efficiency of protein folding
  • Decreased ribosome function

The bacteria uses the cytoplasmic membrane, RNA/DNA, and ribosomes as cold sensors in the cell, placing them in charge of monitoring the cell's temperature.[6] Once these sensors send the signal that a cold shock is occurring, the bacteria will pause the majority of protein synthesis in order to redirect its focus to producing what are called cold shock proteins (Csp).[8] The volume of the cold shock proteins produced will depend on the severity of the temperature decrease.[9] The function of these cold shock proteins is to assist the cell in adapting to the sudden temperature change, allowing it to maintain as close to a normal level of function as possible.[6]

One way cold shock proteins are thought to function is by acting as nucleic acid chaperones. These cold shock proteins will block the formation of secondary structures in the mRNA during the cold shock, leaving the bacteria with only single strand RNA.[7] Single strand is the most efficient form of RNA for the facilitation of transcription and translation. This will help to counteract the decreased efficiency of transcription and translation brought about by the cold shock.[9] Cold shock proteins also affect the formation of hairpin structures in the RNA, blocking them from being formed. The function of these hairpin structures is to slow down or decrease the transcription of RNA. So by removing them, this will also help to increase the efficiency of transcription and translation.[9]

Once the initial shock of the temperature decrease has been dealt with, the production of cold shock proteins is slowly tapered off.[7] Instead, other proteins are synthesized in their place as the cell continues to grow at this new lower temperature. However, the rate of growth seen by these bacterial cells at colder temperatures is often lower than the rates of growth they exhibit at warmer temperatures.[5]

Cold shock response in humans[edit]

In humans, the temperature to initiate a cold shock response begins at <15 °C (59 °F).[10] Within the first three minutes of cold water immersion, the skin begins to cool.[10] Within thirty minutes, the human body begins to experience neuromuscular cooling, and then, after thirty minutes, the human body experiences hypothermia.[10]

Benefits of cold shock[edit]

Cold water immersion tactics are often employed by athletes to reduce the chance of heat illness and is employed to speed up muscle recovery and reduce soreness.[10]

See also[edit]

  • Diving reflex – The physiological responses to immersion of air-breathing vertebrates
  • Hypothermia – Human body core temperature below 35.0 °C
  • Cold water immersion – Respiratory impairment resulting from being in or underneath a liquid


  1. ^ a b c d e "Exercise in the Cold: Part II - A physiological trip through cold water exposure". The science of sport. 29 January 2008. Retrieved 2010-04-23.
  2. ^ Staff. "4 Phases of Cold Water Immersion". Beyond Cold Water Bootcamp. Canadian Safe Boating Council. Archived from the original on 3 December 2013. Retrieved 8 November 2013.
  3. ^ Janský, L.; Janáková, H.; Ulicný, B.; Srámek, P.; Hosek, V.; Heller, J.; Parízková, J. (1996). "Changes in thermal homeostasis in humans due to repeated cold water immersions". Pflügers Archiv: European Journal of Physiology. 432 (3): 368–372. doi:10.1007/s004240050146. PMID 8765994. S2CID 21614210.
  4. ^ a b Eglin, Clare M; Butt, George; Howden, Stephen; Nash, Thomas; Costello, Joseph (14 September 2015). "Rapid habituation of the cold shock response". Extreme Physiology & Medicine. 4 (S1): A38, 2046–7648–4-S1-A38. doi:10.1186/2046-7648-4-S1-A38. ISSN 2046-7648.
  5. ^ a b Shires, K.; Steyn, L. (2001). "The cold-shock stress response in Mycobacterium smegmatis induces the expression of a histone-like protein". Molecular Microbiology. 39 (4): 994–1009. doi:10.1046/j.1365-2958.2001.02291.x. ISSN 1365-2958. PMID 11251819.
  6. ^ a b c Phadtare, S., Alsina, J., & Inouye, M. (1999). “Cold-shock response and cold-shock proteins”. Current Opinion in Microbiology. 2(2), 175-180. doi:10.1016/S1369-5274(99)80031-9
  7. ^ a b c Phadtare, Sangita (2004). "Recent developments in bacterial cold-shock response". Current Issues in Molecular Biology. 6 (2): 125–136. ISSN 1467-3037. PMID 15119823.
  8. ^ Di Pietro, Fabio; Brandi, Anna; Dzeladini, Nadire; Fabbretti, Attilio; Carzaniga, Thomas; Piersimoni, Lolita; Pon, Cynthia L; Giuliodori, Anna Maria (2013). "Role of the ribosome-associated protein PY in the cold-shock response of Escherichia coli". MicrobiologyOpen. 2 (2): 293–307. doi:10.1002/mbo3.68. ISSN 2045-8827. PMC 3633353. PMID 23420694.
  9. ^ a b c Keto-Timonen, Riikka; Hietala, Nina; Palonen, Eveliina; Hakakorpi, Anna; Lindström, Miia; Korkeala, Hannu (2016). "Cold Shock Proteins: A Minireview with Special Emphasis on Csp-family of Enteropathogenic Yersinia". Frontiers in Microbiology. 7: 1151. doi:10.3389/fmicb.2016.01151. ISSN 1664-302X. PMC 4956666. PMID 27499753.
  10. ^ a b c d Tipton, M. J.; Collier, N.; Massey, H.; Corbett, J.; Harper, M. (2017-11-01). "Cold water immersion: kill or cure?: Cold water immersion: kill or cure?". Experimental Physiology. 102 (11): 1335–1355. doi:10.1113/EP086283. PMID 28833689.