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Saturation Diving; Physiology and Pathophysiology

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In saturation diving, divers stay under pressure until most of their tissues are saturated with breathing gas. Divers spend a long time in isolation exposed to increased partial pressure of oxygen, potentially toxic gases, bacteria, and bubble formation during decompression combined with shift work and long periods of relative inactivity. Hyperoxia may lead to the production of reactive oxygen species (ROS) that interact with cell structures, causing damage to proteins, lipids, and nucleic acid. Vascular gas‐bubble formation and hyperoxia may lead to dysfunction of the endothelium. The antioxidant status of the diver is an important mechanism in the protection against injury and is influenced both by diet and genetic factors.

The factors mentioned above may lead to production of heat shock proteins (HSP) that also may have a negative effect on endothelial function. On the other hand, there is a great deal of evidence that HSPs may also have a “conditioning” effect, thus protecting against injury.

As people age, their ability to produce antioxidants decreases. We do not currently know the capacity for antioxidant defense, but it is reasonable to assume that it has a limit. Many studies have linked ROS to disease states such as cancer, insulin resistance, diabetes mellitus, cardiovascular diseases, and atherosclerosis as well as to old age. However, ROS are also involved in a number of protective mechanisms, for instance immune defense, antibacterial action, vascular tone, and signal transduction. Low‐grade oxidative stress can increase antioxidant production.

While under pressure, divers change depth frequently. After such changes and at the end of the dive, divers must follow procedures to decompress safely. Decompression sickness (DCS) used to be one of the major causes of injury in saturation diving. Improved decompression procedures have significantly reduced the number of reported incidents; however, data indicate considerable underreporting of injuries. Furthermore, divers who are required to return to the surface quickly are under higher risk of serious injury as no adequate decompression procedures for such situations are available.

Decompression also leads to the production of endothelial microparticles that may reduce endothelial function. As good endothelial function is a documented indicator of health that can be influenced by regular exercise, regular physical exercise is recommended for saturation divers.

Nowadays, saturation diving is a reasonably safe and well controlled method for working under water. Until now, no long‐term impact on health due to diving has been documented. However, we still have limited knowledge about the pathophysiologic mechanisms involved. In particular we know little about the effect of long exposure to hyperoxia and microparticles on the endothelium. © 2014 American Physiological Society. Compr Physiol 4:1229‐1272, 2014.

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Figure 1. Figure 1. An underwater work site. To the left is the diving bell used by the diver to “commute” to the work place.
Figure 2. Figure 2. Dust levels during a hyperbaric welding trial shift showing mass concentration of PM2.5 and concentration of particles with a mean diameter of 10‐240 nm. The mean diameter of particles observed was 25‐30 nm (120).
Figure 3. Figure 3. Particle aerodynamic diameter observed during hyperbaric welding operations. Local extraction ventilation was used only during welding, and the peak concentrations shown represent periods of high speed grinding when local extraction was not used (120).
Figure 4. Figure 4. Drilling mud burn showing a dermatitis affecting the ankle and forefoot.
Figure 5. Figure 5. Temperature of thermal comfort in hyperbaric helium, adapted from (364).
Figure 6. Figure 6. The synthesis of NO and NO from diet (256).
Figure 7. Figure 7. Left shows bubble formation, right shows dive profiles, upper panel shows a U.S. Navy profile, and the bottom shows short periods of recompression (282).
Figure 8. Figure 8. Bubbles appear as high‐intensity signals in carotid artery (brain circulation) 4‐23 h after decompression is complete. The intensity is a measure of the size and shows that after 23 h there still are small gas bubbles in blood vessels supplying the brain (54).
Figure 9. Figure 9. Mass stranding of whales. From Der Spiegel 21, 2013.
Figure 10. Figure 10. Imbalance or dysregulation of defense against oxidative stress (124).
Figure 11. Figure 11. Modifiable risk factors that can be influenced by the diver (383).
Figure 12. Figure 12. The principle of systems epidemiology (189).

Figure 1. An underwater work site. To the left is the diving bell used by the diver to “commute” to the work place.

Figure 2. Dust levels during a hyperbaric welding trial shift showing mass concentration of PM2.5 and concentration of particles with a mean diameter of 10‐240 nm. The mean diameter of particles observed was 25‐30 nm (120).

Figure 3. Particle aerodynamic diameter observed during hyperbaric welding operations. Local extraction ventilation was used only during welding, and the peak concentrations shown represent periods of high speed grinding when local extraction was not used (120).

Figure 4. Drilling mud burn showing a dermatitis affecting the ankle and forefoot.

Figure 5. Temperature of thermal comfort in hyperbaric helium, adapted from (364).

Figure 6. The synthesis of NO and NO from diet (256).

Figure 7. Left shows bubble formation, right shows dive profiles, upper panel shows a U.S. Navy profile, and the bottom shows short periods of recompression (282).

Figure 8. Bubbles appear as high‐intensity signals in carotid artery (brain circulation) 4‐23 h after decompression is complete. The intensity is a measure of the size and shows that after 23 h there still are small gas bubbles in blood vessels supplying the brain (54).

Figure 9. Mass stranding of whales. From Der Spiegel 21, 2013.

Figure 10. Imbalance or dysregulation of defense against oxidative stress (124).

Figure 11. Modifiable risk factors that can be influenced by the diver (383).

Figure 12. The principle of systems epidemiology (189).
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Further Reading

Brubakk AO and Neuman TS (eds). The physiology and medicine of diving 5th edition, Saunders, Edinburgh 2003.

Brubakk AO, Eftedal OS, Wisloff U. Endothelium and diving. In: Endothelial Biomedicine. Aird WC (ed). Cambridge University Press Cambridge 2007, pp. 497-505.

Wisloff U, Haram GM, Brubakk AO. Exercise and the endothelium. In: Endothelial Biomedicine. Aird WC (ed). Cambridge University Press Cambridge 2007, pp. 506-515.

Brubakk AO, Flook V, Vik A. Gas bubbles and the lungs. In: Lundgren CEG, Miller JN (eds) The lung at depth. Marchel Dekker New York 1999, pp 236-294.

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How to Cite

Alf O. Brubakk, John A.S. Ross, Stephen R. Thom. Saturation Diving; Physiology and Pathophysiology. Compr Physiol 2014, 4: 1229-1272. doi: 10.1002/cphy.c130048