Cold shock response

The physiological response to a sudden immersion in cold water may be divided in three or four discrete stages, with different risks and physiological changes, all being part of an entity labelled as Cold Water Immersion Syndrome. Although this process is a continuum, the 4 phases was initially described in the 1980s as it follows:[3][4]

The first stage of cold water immersion syndrome, the cold shock response, includes a group of reflexes lasting under 5 min in laboratory volunteers and initiated by thermoreceptors sensing rapid skin cooling. Water has a thermal conductivity 25 times and a volume-specific heat capacity over 3000 times that of air; subsequently, surface cooling is precipitous. The primary components of the cold shock reflex include gasping, tachypnea, reduced breath-holding time, and peripheral vasoconstriction, the latter effect highlighting the presumed physiologic principle (i.e., warmth preservation via central blood shunting). The magnitude of the cold shock response parallels the cutaneous cooling rate, and its termination is likely due to reflex baroreceptor responses or thermoreceptor habituation.

The mammalian diving reflex consists of a series of adaptive reflexes which occur after submersion in cold water. The physiologic purpose of the diving reflex is not well understood, but is believed to be oxygen conservation, a quality evident in diving mammals, in which the response is most pronounced. The diving reflex encompasses bradycardia (cardiac parasympathetic control), expiratory apnea (respiratory control center), peripheral vasoconstriction (vasomotor control center), adrenal catecholamine release, and vascular splenic contraction.[3]

Early models of cold water immersion syndrome focused primarily on sympathetic responses, however recent research suggests sympathetic and parasympathetic coactivation (autonomic conflict) may be responsible for some cold water immersion deaths. Although reciprocal activation between sympathetic (cold shock) and parasympathetic (diving response) systems is commonly adaptive (follow one another), simultaneous activation appears to be associated with ectopic beats or arrhythmias. Cold water induced rhythm disturbances are common, albeit frequently asymptomatic. In most humans, head-out cold-water immersion results in sympathetically driven sinus tachycardia with variable ectopic beats and supraventricular or junctional arrhythmias. These cold water immersion induced arrythmias appear to be accentuated by parasympathetic stimulation resulting from facial submersion or breath holding. Even vagally dominant diving bradycardia caused by isolated cold water facial immersion frequently is interrupted by supraventricular arrhythmias or premature beats. In theory, atrioventricular blockade or sinus arrest due to profound parasympathetic dominance might result in syncope or sudden cardiac death, but these rhythms tend to be rapidly reversed by lung stretch receptor activation associated with breathing. As such, a vagally produced arrest scenario is likelier during entrapment submersion than in flush drowning.[3][4]

Cold shock has been described in several species and at least part of the physiology is similar, as described above in the Diving Reflex.

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.[6] Both prokaryotic and eukaryotic cells are capable of undergoing a cold shock response.[7] The effects of a cold shock in bacteria include:[8]

• 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.[7] 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).[9] The volume of the cold shock proteins produced will depend on the severity of the temperature decrease.[10] 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.[7]

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.[8] 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.[10] 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.[10]

Once the initial shock of the temperature decrease has been dealt with, the production of cold shock proteins is slowly tapered off.[8] 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.[6]

Cold shocks cause the repression of several hundreds of genes in the bacterium E. coli. Many of these genes are repressed quickly after the decrease in temperature, while others are only affected several hours after this event.[11] The repression mechanism is described in.[12] Shortly, during cold-shocks, cellular energy levels decrease. This hampers the efficiency by which DNA gyrases remove positive supercoils produced by transcription events, whose accumulation eventually blocks future transcription events.

Many of the genes repressed during cold shock are involved in cell metabolism. By knowing the mechanism by which these genes respond, one can potentially tune it, in genetically modified bacteria, to modify at which temperature is the response to cold shock activated. This modification could reduce the energy costs of bioreactors.[12]