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Kay Tetzlaff, Holger Schöppenthau and Jochen D. Schipke


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.


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.


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.

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Bernd E. Winkler, Kay Tetzlaff, Claus-Martin Muth, Klaus Paulat and Helge Hebestreit

The purpose of this study was to monitor heart rate (HR) and rhythm during open water SCUBA dives. Nine children performed 25-min open water SCUBA dives to 8 m depth. Before, during and after these dives, ECG was recorded. Compared with predive heart rate, heart rate declined by -24 ± 8% (range -36%; -15%) during the dive. In some children a further decline in HR was observed within the last minutes of the dive. Older and taller subjects and those with a high initial HR showed a more pronounced decline in HR. Furthermore singular supraventricular and ventricular extrasystoles were observed in some children. Immersion as well as facial and skin cooling presumably account for the initial decline in heart rate. A further drop in HR within the last minutes of the dive might be related to mild hypothermia. Single supraventricular and ventricular extrasystoles might occur in healthy children during dives.

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Kai Roecker, Jule Metzger, Tobias Scholz, Kay Tetzlaff, Stephan Sorichter and Stephan Walterspacher

Specific adjustments to repeated extreme apnea are not fully known and understood. While a blunted ventilatory chemosensitivity to CO2 is described for elite breath-hold divers (BHDs) at rest, it is unclear whether specific adaptations affect their response to dynamic exercise. Eight elite BHDs with a previously validated decrease in CO2 chemosensitivity, 8 scuba divers (SCDs), and 8 matched control subjects were included in a study where markers of ventilatory response, Fowler’s dead space, partial pressure of carbon dioxide (pCO2), and blood lactate concentrations during cycle exercise were measured. Maximal power output did not differ between the groups, but lactate threshold (θL) appeared at a significantly lowered respiratory compensation point (RCP) and at a higher VO2 for the BHDs. End-tidal (petCO2) and estimated arterial pCO2 (paCO2) were significantly higher in BHDs at θL, the RCP, and maximum exhaustion. BHDs showed a significantly (P < .01) slower breathing pattern in relation to a given tidal volume at a specific work rate. In summary, BHDs presented signs of a metabolic shift from aerobic to anaerobic energy supply, decreased chemosensitivity during exercise, and a distinct ventilatory-response pattern during cycle exercise that differs from SCDs and controls.