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Physiological discoveries

By the late 19th century, as salvage operations became deeper and longer, an unexplained malady began afflicting the divers; they would suffer breathing difficulties, dizziness, joint pain and paralysis, sometimes leading to death. The problem was already well known among workers building tunnels and bridge footings operating under pressure in caissons and was initially called caisson disease; it was later renamed the bends because the joint pain typically caused the sufferer to stoop. Early reports of the disease had been made at the time of Charles Pasley 's salvage operation, but scientists were still ignorant of its causes.

French physiologist Paul Bert was the first to understand it as decompression sickness (DCS). His work, La Pression barométrique (1878), was a comprehensive investigation into the physiological effects of air pressure, both above and below the normal. He determined that inhaling pressurised air caused nitrogen to dissolve into the bloodstream; rapid depressurisation would then release the nitrogen into its gaseous state, forming bubbles that could block the blood circulation and potentially cause paralysis or death. Central nervous system oxygen toxicity was also first described in this publication and is sometimes referred to as the "Paul Bert effect".

John Scott Haldane designed a decompression chamber in 1907, and he produced the first decompression tables for the Royal Navy in 1908 after extensive experiments with animals and human subjects. These tables established a method of decompression in stages – it remains the basis for decompression methods to this day. Following Haldane's recommendation, the maximum safe operating depth for divers was extended to 61 metres (200 ft).

The US Navy continued research into decompression, and in 1915 the first Bureau of Construction and Repair decompression tables were developed by French and Stilson. Experimental dives were conducted in the 1930s, forming the basis for the 1937 US Navy air decompression tables. Surface decompression and oxygen use were also researched in the 1930s. The US Navy 1957 tables were developed to correct problems found in the 1937 tables.

In 1965 Hugh LeMessurier and Brian Andrew Hills published their paper, A thermodynamic approach arising from a study on Torres Strait diving techniques, which suggested that decompression following schedules based on conventional models results in asymptomatic bubble formation which must then be re-dissolved at the decompression stops before it can be eliminated. This is slower than allowing the gas to be eliminated while it is still in solution, and indicates the importance of minimising bubble phase gas for efficient decompression.

M.P. Spencer showed that Doppler ultrasonic methods can detect venous bubbles in asymptomatic divers, and Dr Andrew Pilmanis showed that safety stops reduced bubble formation. In 1981 D.E. Yount described the Varying Permeability Model, proposing a mechanism of bubble formation. Several other bubble models followed. The pathophysiology of decompression sickness is not yet fully understood, but decompression practice has reached a stage where the risk is fairly low, and most incidents are successfully treated by therapeutic recompression and hyperbaric oxygen therapy. Mixed breathing gases are used to reduce the effects of the hyperbaric environment on ambient pressure divers.

Efficient decompression requires the diver to ascend fast enough to establish as high a decompression gradient, in as many tissues as safely possible, without provoking the development of symptomatic bubbles. This is facilitated by the highest acceptably safe oxygen partial pressure in the breathing gas, and avoiding gas changes that could cause counterdiffusion bubble formation or growth. The development of schedules that are both safe and efficient has been complicated by the large number of variables and uncertainties, including personal variation in response under varying environmental conditions and workload.