Humans as Free Divers

You’re running on reserve tank and there’s no warning before you hit empty!

Record-holding free diver

There are two principal (and somewhat inter-related) challenges in free diving:

  1. The challenge of increasing depth, with its attendant risk of pressure-related injury to gas-containing spaces.
  2. The challenge of increasing duration, with its attendant risk of exhaustion of oxygen (O2) stores.

A third challenge that is most relevant to the more extreme exponents of free diving is the related exposure to markedly elevated gas partial pressures with related risks such gas toxicities and decompression sickness.

The challenge of increasing depth

Any anatomical or equipment gas spaces are subject to compression during descent, and their volumes may need to be compensated if barotrauma is to be avoided. Obvious examples, which are discussed elsewhere in this text, include the middle ear (see Chapter 7), sinuses (see Chapter 8) and mask. The lung is of particular relevance to free divers because, unlike divers using underwater breathing apparatus who compensate intrapulmonary pressure and volume with each breath of compressed gas, the lung volume of a free diver is progressively compressed as depth increases.

It was long believed that the limiting factor on depth in free diving would be the point at which lung volume was compressed to residual volume because compression to smaller volumes could, logically, result in trauma to the chest wall or lung itself. Thus, a diver with a total lung capacity of 6 litres and a residual volume of 1.5 litres should theoretically be able to breath-hold dive to 30 metres (4 ATA) where the total lung volume would be compressed to the residual volume (1.5 litres), a simple application of Boyle’s Law. A corollary was that divers with a larger total lung capacity and/or a smaller residual volume would be capable of greater depths before injury occurred.

The fallacy of the ‘residual volume limit’ is immediately clear when it is considered that a human has descended to 214 metres (22.4 atmospheres absolute [ATA]) without suffering obvious lung barotrauma and that free divers regularly descend to depths greater than a theoretical maximum calculated in this way. The factors that were missing from these early attempts to predict maximum depth were the distensibility of the pulmonary vasculature and the concomitant potential for intrapulmonary blood pooling to compensate for compression of lung volume, effectively allowing for compressions below predicted residual volume. The beginnings of such compensation can be seen with simple head-out immersion in an upright subject. The negative transthoracic pressure generated by having the airway open to a pressure of 1 ATA while the thorax is exposed to greater pressure (because of the surrounding water pressure) results in a shift of about 0.7 litre of blood into the thorax. A greater engorgement of the pulmonary circulation is likely if the transthoracic pressure increases further.

Notwithstanding this remarkable and fortunate mechanism for compensation, there will nevertheless come a point where pulmonary vascular capacitance is maximized and further descent will cause the lung’s remaining gas volume to develop an increasingly negative pressure relative to the environment and surrounding tissue. If this becomes excessive, then both fluid extravasation from capillaries to the alveolar space and frank haemorrhage are possible, and there is evidence from competitive free diving that both occur. This problem is referred to as pulmonary barotrauma of descent or ‘lung squeeze’. Although it is interesting and potentially of increasing importance as free diving depths are extended, this is currently a minor contributor to free diving accidents in comparison with the challenges of increasing duration underwater.

The challenge of increasing duration

It is self-evident that oxygenation is maintained from steadily dwindling O2 stores during a free dive. In contrast to marine mammals, a human’s stores are relatively small. The total O2 stores in a 70-kilogram man at resting lung volume (functional residual capacity) have been calculated to be approximately 1.5 litres. This store would be increased at total lung capacity whose value is variable among individuals. If nearly all this O2 can be extracted, one could predict that a resting man who has an O2 consumption of 300 mL per minute would completely deplete his O2 stores in 5 minutes. In reality, most untrained humans can only breath-hold for approximately 1 minute because the drive to breathe is dependent largely on rising pressures of carbon dioxide (CO2) rather than falling levels of O2 (although the two are synergistic). This inherent inability to breath-hold voluntarily to the point of critical hypoxia (an arterial partial pressure of O2 [Po2] above approximately 25 mm Hg must be maintained to avoid loss of consciousness) is clearly protective in free diving. However, it can be confounded in two important ways: by the use of hyperventilation before breath-holding and through the effects of changing ambient pressure during descent and ascent from a free dive.

Hyperventilation refers to taking a series of rapid deep breaths before breath-holding. This is often done in the mistaken belief that it significantly enhances O2 stores. Although hyperventilation does increase the alveolar O2 content to a small extent, the volume of O2 involved is effectively inconsequential. What hyperventilation can achieve is a marked lowering of arterial CO2 levels. Competitive breath-hold divers have had end-tidal CO2 pressures as low as 20 mm Hg measured at the end of their typical pre-apnoea routine. This has the effect of prolonging the breath-hold duration before the onset of a strong urge to breathe.

The obvious danger associated with hyperventilation is that it will extend the breath-hold duration closer to the point where the arterial Po2 falls below that required to maintain consciousness. There is little doubt that hyperventilation has been a contributory factor in many free diving deaths. There is also some evidence that well-practised free divers can induce a decrease in sensitivity of the medullary respiratory control centre to CO2, or they can learn to resist the uncomfortable urges to breathe that CO2 generates as its arterial pressure rises, or both. Interestingly, however, although competitors in static apnoea events (effectively breath-holding competitions without pressure change) aggressively employ hyperventilation and are highly motivated not to breathe for as long as possible, symptomatic hypoxia is not frequent as would be expected. This brings the discussion to changing ambient pressure during a free dive as an added and significant risk factor for critical hypoxia.

Arterial gas tensions during breath-hold dives change with the partial pressure of the gases in the lungs. When the breath-hold diver descends, the partial pressures of the gases in the lungs increase as their volume is decreased and gas inside is compressed. The reverse takes place during ascent back toward the surface. This leads to concomitant rises and falls in alveolar and arterial Po2.

Figure 3.1 shows alveolar pressures of the metabolic gases during (a) a breath-hold period without ambient pressure change, (b) a breath-hold dive to 10 metres and (c) a breath-hold dive to 10 metres with prior hyperventilation. In Figure 3.1 (b) and 3.1 (c), ambient and thus alveolar gas partial pressures rise during descent according to Boyle’s Law. The rise in O2 is somewhat reduced because of continued consumption. Because of the high alveolar Po2 at depth, there is a sufficient alveolar-arterial gradient to allow continuing O2 uptake for a considerable time.

In contrast, during ascent there is a rapid fall in alveolar Po2 as the lung re-expands and the volume of the alveolar gas increases. This is greater than expected from gas laws alone, thus reflecting ongoing oxygen metabolism. The dive with prior hyperventilation depicted in Figure 3.1 (c) had a longer bottom time as would be expected when prior lowering of the arterial CO2 makes the diver more comfortable remaining at depth for longer. It can be seen that a lower alveolar partial pressure of O2 develops by the time the diver reaches the surface, and such falls in alveolar and arterial Po2 during ascent would be even more dramatic on deeper dives. The obvious risk is that the diver could experience critical arterial hypoxaemia as the alveolar Po2 is rapidly falling in the latter stages of the ascent. Indeed, loss of consciousness during either the final phase of ascent or on arrival at the surface is a recurring event at free diving competitions. The dangers of breath-hold diving and hyperventilation are discussed further in Chapter 16.

In addition to hyperventilation, there are two other strategies, both controversial, that elite free divers use or manipulate in order to extend their duration underwater.

The first of these is an attempt to expedite the so-called diving reflex that can be observed in all air breathing vertebrates but that is highly developed in marine mammals (see later). This reflex is initiated by apnoea and also by facial cooling. Its principal effector arm is a marked sympathetically mediated increase in peripheral vascular resistance that increases blood pressure and in turn elicits a vagally mediated bradycardia. At the same time, there is some evidence that the sympathetic activation induces splenic contraction, increasing circulating red blood cells. Peripheral vasoconstriction has the effect of reducing the circulation of blood to the peripheries, and the bradycardia reduces O2 consumption by the heart. Central redistribution of blood makes more O2 available to vital organs. A concurrent and unwanted side effect of these processes is a predisposition to arrhythmias. This probably arises from vagal inhibition of nodal conduction combined with sympathetic sensitization of ectopic pacemakers. Not surprisingly, ventricular ectopic beats are common.

Although these are autonomically mediated phenomena, there is a strong belief among free divers that they can manipulate the process through conditioning, relaxation techniques and practice. Given that there is considerable inter-subject variability in the potency of the diving reflex, and that it tends to wane with age, it does seem plausible that it is ‘open’ to manipulation by skilled divers. In a 2014 interview William Trubridge, holder of the constant ballast no fins world depth record of 101 metres, articulated it thus:

The training I do is targeted at creating a physiology that conserves oxygen as much as possible. Whereas someone who is extremely fit would be able to supply a high amount of oxygen to their muscles very quickly, I need to shut down that oxygen flow to the muscles so that they can work anaerobically and that conserves the oxygen for the heart and the brain. Physiology for freediving is such a different set of effects to what is found in any other sport that we’re still discovering exactly what they consist of.

New Zealand Listener Magazine,
4 January 2014

Similarly, on his website Francesco “Pippin” Ferreras, a previous world record holder, described his approach in more detail:

My heart, under direct control of the Central Nervous System, begins a rapid slowdown. This diminution of my cardiac output is a result of the body’s decreasing needs for oxygen and energy consumption. This efficiency in energy conservation is of vital importance for survival in the undersea environment while in a state of apnea. As an example, when I begin my pre-immersion preparations my resting heart rate is 75 bpm, 10 minutes after entering a stare of deep relaxation it drops, to 55 bpm. As I begin my descent, in a matter of seconds it has slowed to 30 bpm. My cardiovascular performance is influenced by other factors, foremost being my physical conditioning, and mental preparation…. Once I have reached a depth of 110 m., I institute one last command to my heart to slow down. At this point my heart is down to a mere 10 to 14 bpm. On several immersions when all of the above mentioned factors are ideal I have obtained readings of an incredible 7 bpm! Obviously these findings are augmented by the power of mind over body that I have developed over the years, through the study and practice of Yoga.

The second controversial strategy used by elite free divers to extend both depth and duration underwater is so-called ‘lung packing’, more correctly referred to as glossopharyngeal insufflation. This technique involves using the glossopharyngeal muscles to pump air into the lungs, thus enabling an increase in the total lung capacity by up to 20 per cent. This extra volume potentially increases the depth at which lung compression becomes hazardous (as described earlier) and also represents an increase in the O2 stores. Adept exponents of lung packing can increase the volume of air carried by several litres, although this does not translate directly into an increase in lung volume because the gas is held in the lungs under positive pressure and is therefore compressed. Therein lies the potential problem with this strategy. There are sporadic reports of excessive packing leading to pulmonary barotrauma because of the high positive transpulmonary pressures that can reach 60 mm Hg or even more. There are also reports of hypotensive loss of consciousness resulting from profound reduction in venous return associated with high intrathoracic pressure during the act of packing. In view of these potential hazards the technique cannot be recommended. Nevertheless, it is unlikely that packing will be abandoned by extreme free divers looking for any possible edge.

Largely for completeness (and for curious interest value), there are some extreme free divers who have developed the technique of glossopharyngeal exsufflation, that is, packing in the opposite direction. This is used in those situations near terminal depth when the lungs are compressed at or below residual volume, and it is therefore impossible to generate a Valsalva manoeuvre to clear the ears or sinuses. An alternative approach to avoiding barotrauma under these conditions, and one that has been proven radiologically, is to let the sinuses (and to some extent the middle ears) flood with water!

The challenge of avoiding gas toxicities and decompression sickness

The combination of increasing depth and duration (particularly the former) during free diving opens up the possibility that extreme exponents will suffer gas toxicities and decompression sickness, complications usually associated with compressed gas diving. Neurological decompression sickness in breath-hold divers has been reported. Although some cases may be caused by arterial gas embolism following pulmonary barotrauma, predictions of inert gas tensions following repeated and closely spaced deep breath-hold dives do suggest that pathological bubble formation from dissolved inert gas is certainly possible.

Despite the extreme depths reached by free divers, overt effects of nitrogen narcosis are only rarely reported, although there may be a strong reporting bias operant here. It may also be that narcosis is not as likely as predicted on the basis of depth alone simply because the partial pressure of nitrogen in the relevant tissues takes time to equilibrate with the partial pressure of nitrogen in the lungs, and the short duration of the dives therefore limits any effect. Nevertheless, as extreme free divers are pushing deeper, there are increasing numbers of stories of strange sensations and ‘funny turns’ during these dives. It is impossible to know their exact cause, but potential explanations include nitrogen narcosis (see Chapter 15), high-pressure neurological syndrome (see Chapter 20) and cerebral O2 toxicity (see Chapter 17). Cerebral O2 toxicity seems an unlikely explanation given the very short exposures, the starting fraction of inspired O2 of 0.21 and the fact that O2 is being consumed from the moment apnoea begins. However, some reported events (e.g. facial or diaphragmatic twitching) are very typical of O2 toxicity. These sorts of problems are likely to become more common as record depths are pushed further.

Record diving

Trained free divers have been able to achieve remarkable underwater feats, and in certain societies these divers are accorded celebrity status.

Records are attempted for various categories of diving involving depth, duration and underwater distance. Because of the potential risks involved, dedicated competitions sanctioned by an umbrella society are run according to strict protocols. Physiologists and physicians need to be aware of these remarkable achievements. The records cited here are valid for January 2015 but may have been superseded at the time of reading. A complete list of current records is available at: http://www.aidainternational.org/competitive/worlds-records.

The purest form of depth record is referred to as constant weight apnoea without fins and involves return to the surface with the same weights carried down (if any) and, as the name implies, no use of fins. The record is currently 101 metres for male divers and 69 metres for female divers.

At the opposite end of the spectrum is so-called no limits free diving. This is the most extreme category in respect of depth and requires no swimming at all. Divers hold onto a weighted, rope-guided sled for descent. On reaching the target depth, they detach themselves from the sled and pull a pin that releases compressed air from a cylinder into a lift bag, which tows them back to the surface. The current record depths are 214 metres for male divers and 160 metres for female divers. The latter is the longest-standing free diving record at the present time, set by Tanya Streeter in 2002.

The absolute limit of these hazardous ‘experiments’ remains unknown, but it seems likely that depth record increments will become smaller and smaller as immutable physiological barriers are approached. Death may be precipitated at depth by pulmonary haemorrhage, pulmonary oedema or cardiac dysrhythmias. Cerebral hypoxia is an invariable development during the latter stages of ascent. Quite often these divers require rescue by standby divers because they become unconscious as a result of rapidly developing hypoxia as they approach the surface.

Records are also held for static apnoea, which is a motionless, energy-conserving head immersion exposure. The current records are a mind-boggling 11 minutes 35 seconds for male participants and 9 minutes 2 seconds for female participants.
Underwater breath-hold horizontal distances (dynamic apnoea with fins) of 281 metres (male swimmers) and 234 metres (female swimmers) have been achieved in 50-metre swimming pools with swimmers using fins for propulsion.