Extreme human breath-hold diving

Department of Physiology, University Medical Centre, 1 Rue Michel Servet, 1211 Geneva 4, Switzerland.
Arbeitsphysiologie (Impact Factor: 2.19). 05/2001; 84(4):254-71. DOI: 10.1007/s004210000377
Source: PubMed


In this paper, the respiratory, circulatory and metabolic adjustments to human extreme breath-hold diving are reviewed. A survey of the literature reveals that in extreme divers, adaptive mechanisms take place that allow prolongation of apnoea beyond the limits attained by non-diving subjects, and preservation of oxygen stores during the dives. The occurrence of a diving response, including peripheral vasoconstriction, increased arterial blood pressure, bradycardia and lowered cardiac output, is strongly implicated. Some peripheral regions may be excluded from perfusion, with consequent reliance on anaerobic metabolism. In addition, extreme breath-hold divers show a blunted ventilatory response to carbon dioxide breathing, possibly as a consequence of frequent exposure to high carbon dioxide partial pressures during the dives. These mechanisms allow the attainment of particularly low alveolar oxygen (< 30 mmHg) and high alveolar carbon dioxide (> 50 mmHg) partial pressures at the end of maximal dry breath-holds, and reduce oxygen consumption during the dive at the expense of increased anaerobic glycolysis (rate of blood lactate accumulation > 0.04 mM.s-1). The current absolute world record for depth in breath-hold diving is 150 m. Its further improvement depends upon how far the equilibrium between starting oxygen stores, the overall rate of energy expenditure, the fraction of energy provided by anaerobic metabolism and the diving speed can be pushed, with consciousness upon emersion. The ultimate limit to breath-hold diving records may indeed be imposed by an energetic constraint.

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    • "Η βύθιση του ̟ροσώ̟ου σε κρύο νερό µειώνει την καρδιακή συχνότητα, ενώ ̟αράλληλα ̟ροκαλεί αύξηση στην αρτηριακή ̟ίεση (Ferretti, 2001). Ε̟ισηµαίνουµε ότι, η έκθεση σe κρύο νερό χωρίς ά̟νοια, ενεργο̟οιεί την α̟όκριση στο κρύο (Tipton, 1989). "
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    ABSTRACT: Apnea provokes a number of physiological responses especially with face immersion. We examine for the first time the cardio respiratory responses after sub-maximal apnea in ten swimmers. Apnea was performed during face immersion in cold water (10±1.050C) and with pre-determined duration of 40 seconds. The room temperature was maintained at 250C. The heart rate average value at rest was 80.95±17.75 (bpm) whereas after the apnea 64.35±14.56 and the difference is statistically significant (p<0.02). The systolic blood pressure at rest was 124±8.76 (mmHg) and after the apnea 138±6.33 (p<0.000). The oxygen consumption at rest was 375.6±118.51 (ml/min) whilst after the apnea 598.3±155.38 (p=0.009). The carbon dioxide production at rest was 377.7±208.31 (ml/min) and after the apnea 621.7±130.28 (p < 0.015). Results support the notion of the activation of the dive reflex after face immersion in the aforementioned physiological parameters.
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    • "Hypoxia preconditioning refers to a period of hypoxia followed by a period of time during which there is a protection against asphyxia (Sharp et al. 2004). Apnoea training induced intermittent hypoxia and ischaemia (Manley 1990, Ferretti 2001). Then, the BHD's apnoea response could be not only the result of an enhancement of the 'diving reflex' but also a hypoxia preconditioning effect. "
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    • "The mammalian diving response is a powerful autonomic response comprising at least three simpler reflexes that activate the parasympathetic, sympathetic, and respiratory systems (Kooyman et al., 1981; Butler and Jones, 1982, 1997; Blix and Folkow, 1983; Elsner and Gooden, 1983; de Burgh Daly, 1984; Kooyman and Ponganis, 1998; Ferretti, 2001; Davis et al., 2004; Foster and Sheel, 2005). These simple reflexes independently can be dissociated peripherally to block the different systems associated with the response. "
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    ABSTRACT: The mammalian diving response is a powerful autonomic adjustment to underwater submersion greatly affecting heart rate, arterial blood pressure, and ventilation. The bradycardia is mediated by the parasympathetic nervous system, arterial blood pressure is mediated via the sympathetic system and still other circuits mediate the respiratory changes. In the present study we investigate the cardiorespiratory responses and the brainstem neurons activated by voluntary diving of trained rats, and, compare them to control and swimming animals which did not dive. We show that the bradycardia and increase in arterial blood pressure induced by diving were significantly different than that induced by swimming. Neuronal activation was calculated after immunohistochemical processing of brainstem sections for Fos protein. Labeled neurons were counted in the caudal pressor area, the medullary dorsal horn, subnuclei of the nucleus tractus solitarii (NTS), the nucleus raphe pallidus (RPa), the rostroventrolateral medulla, the A5 area, the nucleus locus coeruleus, the Kölliker-Fuse area, and the external lateral and superior lateral subnuclei of the parabrachial nucleus. All these areas showed significant increases in Fos labeling when data from voluntary diving rats were compared to control rats and all but the commissural subnucleus of the NTS, A5 area, and RPa were significantly different from swimming rats. These data provide a substrate for more precise experiments to determine the role of these nuclei in the reflex circuits driving the diving response.
    Frontiers in Physiology 05/2012; 3:111. DOI:10.3389/fphys.2012.00111 · 3.53 Impact Factor
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