Alveolar gas exchanges and cardiovascular functions during breath holding with air.

Hong, Suk Ki; Lin, Yixin; Lally, D A; Yim, Benjamin; Kominami, N; Hong, Pu; Moore, Tom

doi:10.1152/jappl.1971.30.4.540

Cited by 96 publications

(71 citation statements)

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“…There was no detectable hemoglobin desaturation at break point in any condition. The cardiovascular changes we observed during breath holding were similar to those found previously (26,28). Averaged mean blood pressures were significantly higher at the end of breath holding [by 32 Ϯ 3 mmHg in breath holds from normocapnia (P Ͻ 0.001) and by 23 Ϯ 4 mmHg in breath holds from hypocapnia (P Ͻ 0.001)] than in eupnea (104 Ϯ 5 mmHg, n ϭ 10).…”

Section: Resultssupporting

confidence: 87%

CO₂-dependent components of sinus arrhythmia from the start of breath holding in humans

Cooper

Parkes

Clutton-Brock

2003

American Journal of Physiology-Heart and Circulatory Physiology

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A substantial portion of sinus arrhythmia in conscious humans appears to be caused by the CO2-dependent central respiratory rhythm. Under some circumstances, therefore, sinus arrhythmia might indicate the presence of the central respiratory rhythm. Humans can voluntarily modify their central respiratory rhythm (e.g., by pacing breathing or by delaying or advancing breaths), but it is not clear what happens to it from the start of breath holding. In this study, we show that sinus arrhythmia persists from the start of breath holds prolonged by preoxygenation. We also show that some of the frequency components of sinus arrhythmia start within each subject's eupneic frequency range and change when end-tidal Pco2 is lowered or raised, as we would expect if the central respiratory rhythm continues from the start of breath holding. We discuss whether sinus arrhythmia can indicate if the central respiratory rhythm continues from the start of breath holding.

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Section: Resultssupporting

confidence: 87%

CO₂-dependent components of sinus arrhythmia from the start of breath holding in humans

Cooper

Parkes

Clutton-Brock

2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, it was not feasible to measure PETCO 2 during apnoeic efforts and, in turn, we cannot comment on whether arterial hypocapnia modulated dCA during the early phase of maximal apnoea. In relation to the above, it is of note that other investigators have reported that arterial hypercapnia does not develop to any great extent within the first 60 s of voluntary breath holding [55][56][57].…”

Section: Methodological Considerationsmentioning

confidence: 91%

Dynamic Cerebral Autoregulation Is Acutely Impaired During Maximal Apnoea In Trained Divers

Cross¹,

Kavanagh²,

Brešković³

et al. 2014

Medicine & Science in Sports & Exercise

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Aims: To examine whether dynamic cerebral autoregulation is acutely impaired during maximal voluntary apnoea in trained divers.Methods: Mean arterial pressure (MAP), cerebral blood flow-velocity (CBFV) and end-tidal partial pressures of O 2 and CO 2 (PETO 2 and PETCO 2 ) were measured in eleven trained, male apnoea divers (2862 yr; 18262 cm, 7667 kg) during maximal ''dry'' breath holding. Dynamic cerebral autoregulation was assessed by determining the strength of phase synchronisation between MAP and CBFV during maximal apnoea.Results: The strength of phase synchronisation between MAP and CBFV increased from rest until the end of maximal voluntary apnoea (P,0.05), suggesting that dynamic cerebral autoregulation had weakened by the apnoea breakpoint. The magnitude of impairment in dynamic cerebral autoregulation was strongly, and positively related to the rise in PETCO 2 observed during maximal breath holding (R 2 = 0.67, P,0.05). Interestingly, the impairment in dynamic cerebral autoregulation was not related to the fall in PETO 2 induced by apnoea (R 2 = 0.01, P = 0.75).Conclusions: This study is the first to report that dynamic cerebral autoregulation is acutely impaired in trained divers performing maximal voluntary apnoea. Furthermore, our data suggest that the impaired autoregulatory response is related to the change in PETCO 2 , but not PETO 2 , during maximal apnoea in trained divers.

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“…Hypoxia increased BP during both breathhold and ventilation [141,142], despite SNA inhibition by ventilation [139]. During OSA, the relatively small and delayed BP increase of the apnoeic phase appears similar to the slow BP rise during breathholding [141], modified by the beat-by-beat oscillations dependent on the obstructed respiratory efforts [101]. During post-apnoea, the brisk BP peak may still be an effect of hypoxia, potentiated, however, by the arousal reaction [11,143], or by a yet undefined reflex elicited by the resumption of ventilation [103,126].…”

Section: Systemic Arterial Pressure (Fig 6)mentioning

confidence: 93%

“…In awake normal subjects, hypoxia increased muscle SNA, in turn causing peripheral vasoconstriction [139], while baroreceptor activation, at least partly, counteracted these hypertensive effects [140]. Hypoxia increased BP during both breathhold and ventilation [141,142], despite SNA inhibition by ventilation [139]. During OSA, the relatively small and delayed BP increase of the apnoeic phase appears similar to the slow BP rise during breathholding [141], modified by the beat-by-beat oscillations dependent on the obstructed respiratory efforts [101].…”

Section: Systemic Arterial Pressure (Fig 6)mentioning

confidence: 99%

The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms

Mr¹,

Marrone²,

Insalaco³

et al. 1994

Eur Respir J

132

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Alveolar gas exchanges and cardiovascular functions during breath holding with air.

Cited by 96 publications

References 0 publications

CO₂-dependent components of sinus arrhythmia from the start of breath holding in humans

CO₂-dependent components of sinus arrhythmia from the start of breath holding in humans

Dynamic Cerebral Autoregulation Is Acutely Impaired During Maximal Apnoea In Trained Divers

The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms

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Alveolar gas exchanges and cardiovascular functions during breath holding with air.

Cited by 96 publications

References 0 publications

CO2-dependent components of sinus arrhythmia from the start of breath holding in humans

CO2-dependent components of sinus arrhythmia from the start of breath holding in humans

Dynamic Cerebral Autoregulation Is Acutely Impaired During Maximal Apnoea In Trained Divers

The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms

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CO₂-dependent components of sinus arrhythmia from the start of breath holding in humans

CO₂-dependent components of sinus arrhythmia from the start of breath holding in humans