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

Eichhorn, Lars; Erdfelder, Felix; Kessler, F. J.; Dolscheid‐Pommerich, Ramona; Zur, Berndt; Hoffmann, Uwe; Ellerkmann, R. Ellerkmann; Meyer, Rainer

doi:10.1055/s-0042-107351

Cited by 21 publications

(27 citation statements)

References 41 publications

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“…The rising glucose levels are likely a consequence of adrenalineinduced glucose mobilization and underline the exceptional metabolic and mental challenge of prolonged breath-hold. 37 The correlative venous pO 2 analyses documented pathologically low O 2 levels after 5 minutes of breath-hold (down to 60% SpO 2 ) and corroborated similarities of this breath-hold experiment with clinical settings of hypoxemia. On the other hand, untrained persons may encounter life-threatening consequences under these circumstances, while freedivers face hypoxemia under voluntary and trained conditions.…”

Section: Discussionsupporting

confidence: 67%

Cerebrovascular Reactivity during Prolonged Breath-Hold in Experienced Freedivers

Keil¹,

Eichhorn²,

Mutsaerts

et al. 2018

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE: Experienced freedivers can endure prolonged breath-holds despite severe hypoxemia and are therefore ideal subjects to study apnea-induced cerebrovascular reactivity. This multiparametric study investigated CBF, the spatial coefficient of variation as a correlate of arterial transit time and brain metabolism, dynamics during prolonged apnea. MATERIALS AND METHODS: Fifteen male freedivers (age range, 20-64 years; cumulative previous prolonged breath-holds Ͼ2 minutes and 30 seconds: 4-79,200) underwent repetitive 3T pseudocontinuous arterial spin-labeling and 31 P-/ 1 H-MR spectroscopy before, during, and after a 5-minute breath-hold (split into early and late phases) and gave temporally matching venous blood gas samples. Correlation of temporal and regional cerebrovascular reactivity to blood gases and cumulative previous breath-holds of Ͼ2 minutes and 30 seconds in a lifetime was assessed. RESULTS: The spatial coefficient of variation of CBF (by arterial spin-labeling) decreased during the early breath-hold phase (Ϫ30.0%, P ϭ .002), whereas CBF remained almost stable during this phase and increased in the late phase (ϩ51.8%, P ϭ .001). CBF differed between the anterior and the posterior circulation during all phases (eg, during late breath-hold: MCA, 57.3 Ϯ 14.2 versus posterior cerebral artery, 42.7 Ϯ 10.8 mL/100 g/min; P ϭ .001). There was an association between breath-hold experience and lower CBF (1000 previous breath-holds reduced WM CBF by 0.6 mL/100 g/min; 95% CI, 0.15-1.1 mL/100 g/min; P ϭ .01). While breath-hold caused peripheral lactate rise (ϩ18.5%) and hypoxemia (oxygen saturation, Ϫ24.0%), cerebral lactate and adenosine diphosphate remained within physiologic ranges despite early signs of oxidative stress [Ϫ6.4% phosphocreatine / (adenosine triphosphate ϩ adenosine diphosphate); P ϭ .02]. CONCLUSIONS: This study revealed that the cerebral energy metabolism of trained freedivers withstands severe hypoxic hypercarbia in prolonged breath-hold due to a complex cerebrovascular hemodynamic response. ABBREVIATIONS: ATP ϭ adenosine triphosphate; ASL ϭ arterial spin-labeling; ASL-sCoV ϭ spatial coefficient of variation of CBF (by ASL); ATT ϭ arterial transit time; CVR ϭ cerebrovascular reactivity; HR ϭ heart rate; P i ϭ inorganic phosphates; PCr ϭ phosphocreatine; pO 2 ϭ partial pressure of oxygen; SpO 2 ϭ oxygen saturation

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Section: Discussionsupporting

confidence: 67%

Cerebrovascular Reactivity during Prolonged Breath-Hold in Experienced Freedivers

Keil¹,

Eichhorn²,

Mutsaerts

et al. 2018

AJNR Am J Neuroradiol

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“…We found a decrease in HR (76 ± 23 bpm vs. 61 ± 12 bpm) and an increase in LVSV (75.6 ± 16.9 ml vs. 95.1 ± 32.6 ml) in this study. Using a previously reported increase of systolic and diastolic blood pressure from 135 ± 13 mmHg to 185 ± 25 mmHg [ 16 ], the estimated myocardial oxygen demand using the modified pressure work index [ 15 ] increases from 8.51 ml/min/100 g to 9.48 ml/min/100 g (increase of 11%) during apnoea.…”

Section: Resultsmentioning

confidence: 99%

Cardiovascular magnetic resonance assessment of acute cardiovascular effects of voluntary apnoea in elite divers

Eichhorn

Doerner

Luetkens

et al. 2018

Journal of Cardiovascular Magnetic Resonance

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BackgroundProlonged breath holding results in hypoxemia and hypercapnia. Compensatory mechanisms help maintain adequate oxygen supply to hypoxia sensitive organs, but burden the cardiovascular system.The aim was to investigate human compensatory mechanisms and their effects on the cardiovascular system with regard to cardiac function and morphology, blood flow redistribution, serum biomarkers of the adrenergic system and myocardial injury markers following prolonged apnoea.MethodsSeventeen elite apnoea divers performed maximal breath-hold during cardiovascular magnetic resonance imaging (CMR). Two breath-hold sessions were performed to assess (1) cardiac function, myocardial tissue properties and (2) blood flow. In between CMR sessions, a head MRI was performed for the assessment of signs of silent brain ischemia. Urine and blood samples were analysed prior to and up to 4 h after the first breath-hold.ResultsMean breath-hold time was 297 ± 52 s. Left ventricular (LV) end-systolic, end-diastolic, and stroke volume increased significantly (p < 0.05). Peripheral oxygen saturation, LV ejection fraction, LV fractional shortening, and heart rate decreased significantly (p < 0.05). Blood distribution was diverted to cerebral regions with no significant changes in the descending aorta. Catecholamine levels, high-sensitivity cardiac troponin, and NT-pro-BNP levels increased significantly, but did not reach pathological levels.ConclusionCompensatory effects of prolonged apnoea substantially burden the cardiovascular system. CMR tissue characterisation did not reveal acute myocardial injury, indicating that the resulting cardiovascular stress does not exceed compensatory physiological limits in healthy subjects. However, these compensatory mechanisms could overly tax those limits in subjects with pre-existing cardiac disease. For divers interested in competetive apnoea diving, a comprehensive medical exam with a special focus on the cardiovascular system may be warranted.Trial registrationThis prospective single-centre study was approved by the institutional ethics committee review board. It was retrospectively registered under ClinicalTrials.gov (Trial registration: NCT02280226. Registered 29 October 2014).Electronic supplementary materialThe online version of this article (10.1186/s12968-018-0455-x) contains supplementary material, which is available to authorized users.

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“…The mean SpO 2 levels of the study subjects dropped to 79% at the end of apnea and to even lower levels within the first seconds after onset of respiration. This delay in desaturation is a result of the physiological diving response and has previously been described for apneic divers . Peripheral chemoreflex regulation, sympathetic nerve activity, and a norepinephrine increase leads to peripheral vasoconstriction and hypertension .…”

Section: Discussionmentioning

confidence: 61%

“…This delay in desaturation is a result of the physiological diving response and has previously been described for apneic divers. 5,7 Peripheral chemoreflex regulation, sympathetic nerve activity, 1 and a norepinephrine increase 7 leads to peripheral vasoconstriction and hypertension. 1,4 The increase in partial pressure of carbon dioxide (pCO 2 ) leads to an elevated cerebral blood flow, which ensures adequate oxygen supply to the brain, compared to the periphery.…”

Section: Discussionmentioning

confidence: 99%

“…5 Breath-holding burdens the cardiovascular system due to extreme peripheral vasoconstriction 6 and catecholamine release. 7 But apart from scientific interest in and public fascination with the sport, cardiac arrhythmias are commonly seen in people performing apnea. 8 Studies focusing on cardiac function under apnea show progressive hindrance to diastolic filling.…”

Section: Introductionmentioning

confidence: 99%

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

Cited by 21 publications

References 41 publications

Cerebrovascular Reactivity during Prolonged Breath-Hold in Experienced Freedivers

Cerebrovascular Reactivity during Prolonged Breath-Hold in Experienced Freedivers

Cardiovascular magnetic resonance assessment of acute cardiovascular effects of voluntary apnoea in elite divers

Sustained apnea induces endothelial activation

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