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Kay Tetzlaff, Holger Schöppenthau and 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.

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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.

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Matthew J. Barlow, Antonis Elia, Oliver M. Shannon, Angeliki Zacharogianni and Angelica Lodin-Sundstrom

Competitive apnea also known as free diving or breath-hold diving is an increasingly popular sport in which individuals attempt to achieve the greatest possible stationary breath-hold duration (i.e., static apnea) or maximal underwater distance or depth (i.e., dynamic apnea). During apnea, oxygen

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Sam Lowings, Oliver Michael Shannon, Kevin Deighton, Jamie Matu and Matthew John Barlow

Nitrate supplementation appears to be most ergogenic when oxygen availability is restricted and subsequently may be particularly beneficial for swimming performance due to the breath-hold element of this sport. This represents the first investigation of nitrate supplementation and swimming time-trial (TT) performance. In a randomized double-blind repeated-measures crossover study, ten (5 male, 5 female) trained swimmers ingested 140ml nitrate-rich (~12.5mmol nitrate) or nitrate-depleted (~0.01mmol nitrate) beetroot juice. Three hours later, subjects completed a maximal effort swim TT comprising 168m (8 × 21m lengths) backstroke. Preexercise fractional exhaled nitric oxide concentration was significantly elevated with nitrate compared with placebo, Mean (SD): 17 (9) vs. 7 (3)p.p.b., p = .008. Nitrate supplementation had a likely trivial effect on overall swim TT performance (mean difference 1.22s; 90% CI -0.18–2.6s; 0.93%; p = .144; d = 0.13; unlikely beneficial (22.6%), likely trivial (77.2%), most unlikely negative (0.2%)). The effects of nitrate supplementation during the first half of the TT were trivial (mean difference 0.29s; 90% CI -0.94–1.5s; 0.46%; p = .678; d = 0.05), but there was a possible beneficial effect of nitrate supplementation during the second half of the TT (mean difference 0.93s; 90% CI 0.13–1.70s; 1.36%; p = .062; d = 0.24; possibly beneficial (63.5%), possibly trivial (36.3%), most unlikely negative (0.2%)). The duration and speed of underwater swimming within the performance did not differ between nitrate and placebo (both p > .30). Nitrate supplementation increased nitric oxide bioavailability but did not benefit short-distance swimming performance or the underwater phases of the TT. Further investigation into the effects of nitrate supplementation during the second half of performance tests may be warranted.