Modeling the diving bradycardia: Toward an “oxygen-conserving breaking point”?

Costalat, Guillaume; Pichon, Aurélien; Joulia, Fabrice; Lemaître, Frédéric

doi:10.1007/s00421-015-3129-5

Cited by 25 publications

(37 citation statements)

References 40 publications

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“…A significant increase in blood pressure was seen after 40 % of individual maximal apnea time. This is in parallel with other studies, showing a bi-or even tri-phasic change in blood pressure and bradycardia [11,27,36].…”

Section: Blood Pressure Apnea Duration and Cosupporting

confidence: 91%

“…The diving response caused by apnea is mostly described as peripheral vasoconstriction due to sympathetic activity, resulting in hypertension and vagally induced bradycardia with reduction of cardiac output [29]. It is believed that the diving response aims to reduce oxygen consumption by inducing peripheral vasoconstriction [2,4,11]. This leads to redistribution of blood flow and ensures adequate oxygen supply for hypoxia sensible organs such as CNS [23].…”

Section: Differential Modulation Of Blood Flow Following Apneamentioning

confidence: 99%

“…Hypoxia and hypercapnia are known to increase sympathetic nerve activity (MSNA). MSNA leads to peripheral vasoconstriction and thereby to hypertension [7,20,22,28] and bradycardia [11,15,38] during breath holding. On the contrary, isolated hypoxia is accompanied by vasodilation and an increase in heart rate [1,6,7].…”

Section: Introductionmentioning

confidence: 99%

“…On the contrary, isolated hypoxia is accompanied by vasodilation and an increase in heart rate [1,6,7]. Bradycardia is described as an oxygen-saving mechanism [2,4,11] and may be part of the diving response, but baroreflex-activation due to increased blood pressure following acute hypercapnia [24] and stimulated chemoreceptors also seem to play an important role in influencing bradycardia [29,30].…”

Section: Introductionmentioning

confidence: 99%

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Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

et al. 2016

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Prolonged breath-hold causes complex compensatory mechanisms such as increase in blood pressure, redistribution of blood flow, and bradycardia. We tested whether apnea induces an elevation of catecholamine-concentrations in well-trained apneic divers.11 apneic divers performed maximal dry apnea in a horizontal position. Parameters measured during apnea included blood pressure, ECG, and central, in addition to peripheral hemoglobin oxygenation. Peripheral arterial hemoglobin oxygenation was detected by pulse oximetry, whereas peripheral (abdominal) and central (cerebral) tissue oxygenation was measured by Near Infrared Spectroscopy (NIRS). Exhaled O and CO, plasma norepinephrine and epinephrine concentrations were measured before and after apnea.Averaged apnea time was 247±76 s. Systolic blood pressure increased from 135±13 to 185±25 mmHg. End-expiratory CO increased from 29±4 mmHg to 49±6 mmHg. Norepinephrine increased from 623±307 to 1 826±984 pg ml and epinephrine from 78±22 to 143±65 pg ml during apnea. Heart rate reduction was inversely correlated with increased norepinephrine (correlation coefficient -0.844, p=0.001). Central (cerebral) O desaturation was time-delayed compared to peripheral O desaturation as measured by NIRS and SpO.Increased norepinephrine caused by apnea may contribute to blood shift from peripheral tissues to the CNS and thus help to preserve cerebral tissue O saturation longer than that of peripheral tissue.

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Section: Blood Pressure Apnea Duration and Cosupporting

confidence: 91%

Section: Differential Modulation Of Blood Flow Following Apneamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

et al. 2016

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“…Throughout the last years, apneic diving has become increasingly popular, and apneic divers have been pushing their limits of performance beyond expected boundaries. Prolonged apnea leads to the so‐called diving response, which includes vasoconstriction, elevated mean arterial blood pressure, bradycardia, and increased cerebral blood flow . In the case of apnea, these compensatory mechanisms secure an adequate oxygen supply of the brain due to blood redistribution …”

Section: Introductionmentioning

confidence: 99%

Sustained apnea induces endothelial activation

Eichhorn

Dolscheid‐Pommerich

Erdfelder

et al. 2017

Clinical Cardiology

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Background Apnea diving has gained worldwide popularity, even though the pathophysiological consequences of this challenging sport on the human body are poorly investigated and understood. This study aims to assess the influence of sustained apnea in healthy volunteers on circulating microparticles (MPs) and microRNAs (miRs), which are established biomarkers reflecting vascular function. Hypothesis Short intermittent hypoxia due to voluntary breath‐holding affects circulating levels of endothelial cell‐derived MPs (EMPs) and endothelial cell‐derived miRs. Methods Under dry laboratory conditions, 10 trained apneic divers performed maximal breath‐hold. Venous blood samples were taken, once before and at 4 defined points in time after apnea. Samples were analyzed for circulating EMPs and endothelial miRs. Results Average apnea time was 329 seconds (±103), and SpO2 at the end of apnea was 79% (±12). Apnea was associated with a time‐dependent increase of circulating endothelial cell‐derived EMPs and endothelial miRs. Levels of circulating EMPs in the bloodstream reached a peak 4 hours after the apnea period and returned to baseline levels after 24 hours. Circulating miR‐126 levels were elevated at all time points after a single voluntary maximal apnea, whereas miR‐26 levels were elevated significantly only after 30 minutes and 4 hours. Also miR‐21 and miR‐92 levels increased, but did not reach the level of significance. Conclusions Even a single maximal breath‐hold induces acute endothelial activation and should be performed with great caution by subjects with preexisting vascular diseases. Voluntary apnea might be used as a model to simulate changes in endothelial function caused by hypoxia in humans.

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A School Goes into Depth

Ferretti

2023

Perspectives in Physiology

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Modeling the diving bradycardia: Toward an “oxygen-conserving breaking point”?

Abstract: In addition to accurately fitting the HR kinetics, the most striking finding is an "oxygen-conserving breaking point" highlighted by the model, which might be interpreted as unique adaptive feature against hypoxic damages in the human diving bradycardia.

Cited by 25 publications

References 40 publications

Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

Sustained apnea induces endothelial activation

A School Goes into Depth

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