Breathing Underwater: A Guide to Diving Physiology

Breathing at the Surface

At sea level, you breathe air at 1 bar absolute pressure. The gas is approximately 21% oxygen and 79% nitrogen. Pressure gradients drive gas exchange across the alveolar membrane: oxygen diffuses from the alveoli (where PO₂ is high) into the blood (where it is lower), while CO₂ moves in the opposite direction from blood to alveoli to be exhaled.

This exchange is passive — driven entirely by partial pressure differences. No energy is spent forcing gas across the membrane. At rest, the respiratory system is working well within its capacity, and CO₂ is cleared efficiently.

How Pressure Changes Everything at Depth

Hydrostatic pressure increases by approximately 1 bar for every 10 metres of seawater. At 30 m, the absolute pressure is 4 bar. Your regulator delivers gas at ambient pressure, so every breath contains four times as many gas molecules as the same breath taken at the surface.

This has direct consequences for every stage of gas physiology.

Partial Pressures and Henry's Law

By Dalton's Law, the partial pressure of each gas component scales with total pressure. At 30 m on air:

• PO₂ = 0.21 × 4 = 0.84 bar
• PN₂ = 0.79 × 4 = 3.16 bar

Henry's Law states that the amount of gas that dissolves into a liquid is proportional to the partial pressure of that gas above the liquid. At 3.16 bar PN₂, nitrogen dissolves into blood and tissues at a rate approximately four times higher than at the surface. Oxygen also dissolves at higher rates, but because it is metabolised, it does not accumulate in the same way. Nitrogen is physiologically inert — it loads into tissues continuously throughout the dive and must be eliminated on ascent.

Gas Density and Work of Breathing

Gas density increases in direct proportion to absolute pressure. Air has a surface density of approximately 1.29 g/L. At 30 m (4 bar absolute), it is 5.16 g/L. At 40 m (5 bar), it reaches 6.45 g/L.

This density increase raises the work of breathing substantially. Drawing a denser gas through the airways and regulator requires more respiratory muscle effort. Exhalation — normally passive — also becomes active work against the resistance of a dense gas column.

Research by Mitchell and Doolette identified 6.2 g/L as the threshold above which CO₂ retention can occur even when the diver is breathing at a normal rate. For air, this threshold is crossed at approximately 40 m. At or beyond 40 m on air, the respiratory system may not be able to maintain adequate CO₂ clearance under moderate exertion.

CO₂ Retention: The Hidden Risk

CO₂ is the primary stimulus for breathing. Normal arterial PCO₂ is 35–45 mmHg. When CO₂ accumulates in the blood (hypercapnia), the stimulus to breathe increases — but at depth, the ability to respond is limited by gas density.

The sequence: dense gas increases the resistance of each breath; effective alveolar ventilation falls relative to metabolic CO₂ production; arterial PCO₂ rises; symptoms of hypercapnia develop — headache, breathlessness, anxiety, confusion. Under conditions of high PO₂ (which is the case at depth, particularly on nitrox), the CO₂ drive to breathe can be partially suppressed, meaning hypercapnia may worsen before the diver feels its urgency.

Exertion compounds the risk significantly. CO₂ production increases sharply with physical work. Swimming hard at 30–40 m combines elevated CO₂ production with the ventilation limits imposed by gas density. Skip-breathing — intentional breath-holding between respiratory cycles to conserve gas — directly suppresses CO₂ elimination and causes CO₂ to accumulate faster than with normal breathing. CO₂ is a potent proconvulsive agent: any CO₂ retained while breathing elevated PO₂ significantly lowers the CNS oxygen toxicity seizure threshold. Skip-breathing has no safe application in open-circuit diving. Rapid, shallow breathing is also counterproductive — it increases dead space ventilation (the proportion of each breath that never reaches the alveoli), meaning more breathing effort with less effective gas exchange.

Nitrogen Loading and Tissue Compartments

Different tissues absorb nitrogen at different rates. Fast compartments (blood, brain) equilibrate quickly with the ambient PN₂; slow compartments (fat, cartilage, dense bone) absorb nitrogen slowly and take much longer to off-gas. Dive algorithms model these compartments mathematically and use their calculated nitrogen loading to derive the no-decompression limit (NDL) and, beyond it, mandatory decompression stops.

The longer and deeper the dive, the more nitrogen loads into slow compartments. On a single no-decompression dive, fast compartments drive the NDL. On repetitive dives across multiple days, slow compartments accumulate residual nitrogen that does not fully clear between dives — reducing the effective NDL on each subsequent dive.

Nitrogen Narcosis

At elevated PN₂, nitrogen dissolves into the lipid-rich myelin sheaths surrounding neurons. This disrupts normal ion channel function and slows axonal conduction — an effect known as nitrogen narcosis. The Meyer-Overton hypothesis describes this as proportional to lipid solubility and partial pressure of the narcotic gas.

Narcosis typically becomes noticeable around 30 m on air (PN₂ ≈ 3.2 bar) and can cause significant cognitive impairment by 40 m. Decision-making and executive function are affected before simple motor tasks — making self-diagnosis at depth unreliable. A moderately narcotised diver can count fingers correctly while being unable to improvise solutions to novel problems.

CO₂ accumulation worsens narcosis. The two conditions overlap in symptom profile at depth, which complicates self-assessment.

What Happens on Ascent

As pressure falls on ascent, dissolved nitrogen moves out of tissues into the blood and is transported to the lungs for elimination. If ascent is too rapid, supersaturation can exceed tissue tolerance limits, and nitrogen comes out of solution as bubbles — decompression sickness (DCS).

The safety stop (3–5 minutes at 5 m) provides additional time for fast compartments to off-gas before the final pressure transition. It is not mandatory for recreational no-decompression dives, but it meaningfully reduces circulating bubble loads.

Practical Breathing Guidance

Breathe slowly and deeply — full tidal volume breaths maximise alveolar ventilation and CO₂ clearance. Never skip-breathe; the gas savings are minimal and the risk is not. Limit exertion at depth; CO₂ production is the key variable — rest before working. If you feel breathless disproportionate to gas supply, or develop a throbbing headache: stop exertion, breathe deliberately for 10–15 full breaths, signal your buddy, and ascend if symptoms do not resolve. Set your dive computer to the gas you are breathing — a nitrox dive planned on the air setting will underestimate CNS oxygen toxicity exposure.

References

• Henry W (1803) — Experiments on the quantity of gases absorbed by water at different temperatures, and under different pressures — Philosophical Transactions of the Royal Society of London
• Mitchell SJ, Doolette DJ (2013) — Selective vulnerability of the inner ear to decompression sickness in divers with right-to-left shunt: the role of tissue gas supersaturation — Journal of Applied Physiology
• Mitchell SJ, Cronjé FJ, Meintjes WAJ, Britz HC (2007) — Fatal respiratory failure during a "technical" rebreather dive at extreme pressure — Aviation, Space, and Environmental Medicine
• Ahti A et al. (2023) — Iowa Gambling Task performance at depth: narcosis impairs decision-making at recreational diving depths — Diving and Hyperbaric Medicine

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