Going to Extremes of Lung Physiology–Deep Breath-Hold Diving

2021 ◽  
Vol 12 ◽  
Kay Tetzlaff ◽  
Frederic Lemaitre ◽  
Christof Burgstahler ◽  
Julian A. Luetkens ◽  
Lars Eichhorn

Breath-hold diving involves environmental challenges, such as water immersion, hydrostatic pressure, and asphyxia, that put the respiratory system under stress. While training and inherent individual factors may increase tolerance to these challenges, the limits of human respiratory physiology will be reached quickly during deep breath-hold dives. Nonetheless, world records in deep breath-hold diving of more than 214 m of seawater have considerably exceeded predictions from human physiology. Investigations of elite breath-hold divers and their achievements revised our understanding of possible physiological adaptations in humans and revealed techniques such as glossopharyngeal breathing as being essential to achieve extremes in breath-hold diving performance. These techniques allow elite athletes to increase total lung capacity and minimize residual volume, thereby reducing thoracic squeeze. However, the inability of human lungs to collapse early during descent enables respiratory gas exchange to continue at greater depths, forcing nitrogen (N2) out of the alveolar space to dissolve in body tissues. This will increase risk of N2 narcosis and decompression stress. Clinical cases of stroke-like syndromes after single deep breath-hold dives point to possible mechanisms of decompression stress, caused by N2 entering the vasculature upon ascent from these deep dives. Mechanisms of neurological injury and inert gas narcosis during deep breath-hold dives are still incompletely understood. This review addresses possible hypotheses and elucidates factors that may contribute to pathophysiology of deep freediving accidents. Awareness of the unique challenges to pulmonary physiology at depth is paramount to assess medical risks of deep breath-hold diving.

2006 ◽  
Vol 101 (3) ◽  
pp. 799-801 ◽  
Leigh M. Seccombe ◽  
Peter G. Rogers ◽  
Nghi Mai ◽  
Chris K. Wong ◽  
Leonard Kritharides ◽  

One technique employed by competitive breath-hold divers to increase diving depth is to hyperinflate the lungs with glossopharyngeal breathing (GPB). Our aim was to assess the relationship between measured volume and pressure changes due to GPB. Seven healthy male breath-hold divers, age 33 ( 8 ) [mean (SD)] years were recruited. Subjects performed baseline body plethysmography (TLCPRE). Plethysmography and mouth relaxation pressure were recorded immediately following a maximal GPB maneuver at total lung capacity (TLC) (TLCGPB) and within 5 min after the final GPB maneuver (TLCPOST). Mean TLC increased from TLCPRE to TLCGPB by 1.95 (0.66) liters and vital capacity (VC) by 1.92 (0.56) liters ( P < 0.0001), with no change in residual volume. There was an increase in TLCPOST compared with TLCPRE of 0.16 liters (0.14) ( P < 0.02). Mean mouth relaxation pressure at TLCGPB was 65 (19) cmH2O and was highly correlated with the percent increase in TLC ( R = 0.96). Breath-hold divers achieve substantial increases in measured lung volumes using GPB primarily from increasing VC. Approximately one-third of the additional air was accommodated by air compression.

1981 ◽  
Vol 51 (2) ◽  
pp. 313-316 ◽  
F. Ruff ◽  
R. R. Martin ◽  
J. Milic-Emili

By use of 133Xe, the regional distribution of residual volume (RV) was measured in six seated healthy men, following a fast vital capacity (VC) expiration a) without and b) with a breath hold at residual volume of approximately 30 s and c) following a slow (greater than 30 s) VC expiration from total lung capacity (TLC) without a breath hold at RV. After the breath hold at RV, regional RV/TLC in the lower lung zones decreased significantly compared wih results obtained with fast expiratory VC and no breath hold at RV. At lung top the opposite was true. The distribution of regional RV/TLC was the same following the slow VC expiration with no breath hold at RV as with the fast expiration with the breath hold at RV. The different regional distribution of RV in b and c relative to a was probably due mainly to collateral ventilation, i.e., during the breath hold at RV and the slow expiration some of the gas that was trapped in the dependent lung zones behind closed airways escaped into the upper regions of the lung where the small airways had remained patent, leading to increased expansion of upper alveoli.

2017 ◽  
Vol 12 (2) ◽  
pp. 268-271 ◽  
Kay Tetzlaff ◽  
Holger Schöppenthau ◽  
Jochen D. Schipke

Context:It has been widely believed that tissue nitrogen uptake from the lungs during breath-hold diving would be insufficient to cause decompression stress in humans. With competitive free diving, however, diving depths have been ever increasing over the past decades.Methods:A case is presented of a competitive free-diving athlete who suffered stroke-like symptoms after surfacing from his last dive of a series of 3 deep breath-hold dives. A literature and Web search was performed to screen for similar cases of subjects with serious neurological symptoms after deep breath-hold dives.Case Details:A previously healthy 31-y-old athlete experienced right-sided motor weakness and difficulty speaking immediately after surfacing from a breathhold dive to a depth of 100 m. He had performed 2 preceding breath-hold dives to that depth with surface intervals of only 15 min. The presentation of symptoms and neuroimaging findings supported a clinical diagnosis of stroke. Three more cases of neurological insults were retrieved by literature and Web search; in all cases the athletes presented with stroke-like symptoms after single breath-hold dives of depths exceeding 100 m. Two of these cases only had a short delay to recompression treatment and completely recovered from the insult.Conclusions:This report highlights the possibility of neurological insult, eg, stroke, due to cerebral arterial gas embolism as a consequence of decompression stress after deep breath-hold dives. Thus, stroke as a clinical presentation of cerebral arterial gas embolism should be considered another risk of extreme breath-hold diving.

Guido Ferretti

This article discusses the limits of deep breath-hold diving in humans. After a short historical introduction and a discussion of the evolution of depth records, the classical theories of breath-hold diving limits are presented and discussed, namely that of the ratio between total lung capacity and residual volume and that of blood shift, implying an increase in central blood volume. Then the current vision is introduced, based on the principles of the energetics of muscular exercise. The new vision has turned the classical vision upside down, moving the discussion to a different level. A direct consequence of the new theory is the importance of having large lung volumes at the start of a dive, in order to increase body oxygen stores. I finally discuss the role of anaerobic lactic metabolism as a possible mechanism of oxygen preservation, thus prolonging breath-hold duration.

1972 ◽  
Vol 42 (2) ◽  
pp. 117-128 ◽  
B. Bake ◽  
A. R. Fugl-Meyer ◽  
G. Grimby

1. The regional distribution of ventilation was studied with 133Xe techniques in the sitting position in six patients with complete traumatic transection of the cervical spinal cord, 3–40 months after the lesion, and in four normal subjects. The relative contributions of the rib cage and abdomen to ventilation were determined from chest-wall motions. 2. Total lung capacity (TLC) was decreased and residual volume increased in the patients. After correction for the decreased TLC, the distribution of the regional functional residual capacity in the tetraplegic patients was similar to that of the normal subjects. In the patients, where the abdomen contributed to about half of the tidal volume, decreased ventilation of basal regions was demonstrated from measurements of regional tidal volumes (Vtr) and regional 133Xe wash-in curves. 3. The distribution of ventilation in normal persons, however, was not changed by varying the relative contributions of the rib cage and abdomen to the tidal volume, as shown from Vtr and regional 133Xe wash-out measurements. 4. The results in the tetraplegic patients are interpreted as evidence of ‘small airway disease’, presumably from infection of the air way and impairment of the cough.

1993 ◽  
Vol 36 (3) ◽  
pp. 516-520 ◽  
Jeannette D. Hoit ◽  
Nancy Pearl Solomon ◽  
Thomas J. Hixon

This investigation was designed to test the hypothesis that voice onset time (VOT) varies as a function of lung volume. Recordings were made of five men as they repeated a phrase containing stressed /pi/ syllables, beginning at total lung capacity and ending at residual volume. VOT was found to be longer at high lung volumes and shorter at low lung volumes in most cases. This finding points out the need to take lung volume into account when using VOT as an index of laryngeal behavior in both healthy individuals and those with speech disorders.

2017 ◽  
Vol 7 (1) ◽  
Jia-yi Hu ◽  
Bei-bei Liu ◽  
Yi-peng Du ◽  
Yuan Zhang ◽  
Yi-wei Zhang ◽  

Abstract Smoking is a dominant risk factor for chronic obstructive pulmonary disease (COPD) and emphysema, but not every smoker develops emphysema. Immune responses in smokers vary. Some autoantibodies have been shown to contribute to the development of emphysema in smokers. β2-adrenergic receptors (β2-ARs) are important targets in COPD therapy. β2-adrenergic receptor autoantibodies (β2-AAbs), which may directly affect β2-ARs, were shown to be increased in rats with passive-smoking-induced emphysema in our current preliminary studies. Using cigarette-smoke exposure (CS-exposure) and active-immune (via injections of β2-AR second extracellular loop peptides) rat models, we found that CS-exposed rats showed higher serum β2-AAb levels than control rats before alveolar airspaces became enlarged. Active-immune rats showed increased serum β2-AAb levels, and exhibited alveolar airspace destruction. CS-exposed-active-immune treated rats showed more extensive alveolar airspace destruction than rats undergoing CS-exposure alone. In our current clinical studies, we showed that plasma β2-AAb levels were positively correlated with the RV/TLC (residual volume/total lung capacity) ratio (r = 0.455, p < 0.001) and RV%pred (residual volume/residual volume predicted percentage, r = 0.454, p < 0.001) in 50 smokers; smokers with higher plasma β2-AAb levels exhibited worse alveolar airspace destruction. We suggest that increased circulating β2-AAbs are associated with smoking-related emphysema.

1987 ◽  
Vol 62 (3) ◽  
pp. 1179-1185 ◽  
R. B. Filuk ◽  
N. R. Anthonisen

Twelve stable adult asthmatics slowly inhaled boluses of He at 20, 40, or 60% vital capacity (VC); these volumes were achieved either by expiring from total lung capacity (TLC) or by inspiring from residual volume (RV). Inspirations were continued to TLC and then were followed by slow expirations to RV while expired He was measured as a function of expired volume. At 20% VC slopes of alveolar plateaus (phase III) were positive, at 40% VC they were flat, and at 60% VC they were negative; at 20 and 60% VC the slopes were steeper than those in normals. When boluses were administered at 40 and 60% VC, He washout curves were independent of lung volume history. However at 20% VC the slope of phase III was significantly less positive when boluses were given after inspiration from RV than after expiration from TLC. In eight subjects, who were given inhaled beta-agonists, slopes of all He washouts decreased and became independent of volume history at 20% VC. We conclude that in asthmatics at low lung volumes the airways that determine ventilation distribution behave as though they have less hysteresis than the lung parenchyma probably due to increased airway tone.

1992 ◽  
Vol 73 (1) ◽  
pp. 151-159 ◽  
D. C. Poole ◽  
O. Mathieu-Costello

To determine the potential range of diaphragm sarcomere lengths in situ and the effect of changes in sarcomere length on capillary and fiber geometry, rat diaphragms were perfusion fixed in situ with glutaraldehyde at different airway pressures and during electrical stimulation. The lengths of thick (1.517 +/- 0.007 microns) and thin (1.194 +/- 0.048 microns) filaments were not different from those established for rat limb muscle. Morphometric techniques were used to determine fiber cross-sectional area, sarcomere length, capillary orientation, and capillary length and surface area per fiber volume. All measurements were referenced to sarcomere length, which averaged 2.88 +/- 0.08 microns at -20 to -25 cmH2O airway pressure (residual volume) and 2.32 +/- 0.05 microns at +20 to +26 cmH2O airway pressure (total lung capacity). The contribution of capillary tortuosity and branching to total capillary length was dependent on sarcomere length and varied from 5 to 22%, consistent with that shown previously for mammalian limb muscles over this range of sarcomere lengths. Capillary length per fiber volume [Jv(c,f)] was significantly greater at residual volume (3,761 +/- 193 mm-2) than at total lung capacity (3,142 +/- 118 mm-2) and correlated with sarcomere length [l; r = 0.628, Jv(c,f) = 876l + 1,156, P less than 0.01; n = 18]. We conclude that the diaphragm is unusual in that the apparent in situ minimal sarcomere length is greater than 2.0 microns.(ABSTRACT TRUNCATED AT 250 WORDS)

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