The influence of varying inspired fractions of O2 and CO2 on the development of involuntary breathing movements during maximal apnoea

Brešković, Toni; Lojpur, Mihajlo; Maslov, Petra Zubin; Cross, Troy J.; Kraljević, Jasenka; Ljubković, Marko; Marinović, Jasna; Ivančev, Vladimir; Johnson, Bruce D.; Dujić, Željko

doi:10.1016/j.resp.2012.03.007

Cited by 16 publications

(10 citation statements)

References 22 publications

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“…The largest increase in oxygen stores before breath-holding is attained by having subjects breathe pure oxygen (inspired oxygen fraction, FIO 2 , of 1) before the performance of maximal breathholds. The investigations of breath-holding in hyperoxia are scanty and rarely using pure oxygen (Bjurström and Schoene, 1987;Breskovic et al, 2012;Klocke and Rahn, 1959;Lin, 1987;Otis et al, 1948). None of them studied the cardiovascular responses to apnoea on a beat-by-beat basis.…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

Fagoni

Sivieri

Antonutto

et al. 2015

Respiratory Physiology & Neurobiology

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a b s t r a c tPurpose: We hypothesized that the third dynamic phase ( 3) of the cardiovascular response to apnoea requires attainment of the physiological breaking point, so that the duration of the second steady phase ( 2) of the classical cardiovascular response to apnoea, though appearing in both air and oxygen, is longer in oxygen. Methods: Nineteen divers performed maximal apnoeas in air and oxygen. We measured beat-by-beat arterial pressure, heart rate (f H ), stroke volume (SV), cardiac output (Q ). Results: The f H , SV andQ changes during apnoea followed the same patterns in oxygen as in air. Duration of steady 2 was 105 ± 37 and 185 ± 36 s, in air and oxygen (p < 0.05), respectively. At end of apnoea, arterial oxygen saturation was 1.00 ± 0.00 in oxygen and 0.75 ± 0.10 in air. Conclusions:The results support the tested hypothesis. Lack of hypoxaemia during oxygen apnoeas suggests that, if chemoreflexes determine 3, the increase in CO 2 stores might play a central role in eliciting their activation.

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Section: Introductionmentioning

confidence: 99%

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

Fagoni

Sivieri

Antonutto

et al. 2015

Respiratory Physiology & Neurobiology

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“…The individual factors contributing to volitional breath-hold duration are relatively well known. However, understanding how these mechanisms interact to determine the break point of a breath hold remains a challenging area of integrative physiology (3,12,25).…”

Section: Introductionmentioning

confidence: 99%

The ins and outs of breath holding: simple demonstrations of complex respiratory physiology

Skow

Day

Fuller

et al. 2015

Advances in Physiology Education

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The physiology of breath holding is complex, and voluntary breath-hold duration is affected by many factors, including practice, psychology, respiratory chemoreflexes, and lung stretch. In this activity, we outline a number of simple laboratory activities or classroom demonstrations that illustrate the complexity of the integrative physiology behind breath-hold duration. These activities require minimal equipment and are easily adapted to small-group demonstrations or a larger-group inquiry format where students can design a protocol and collect and analyze data from their classmates. Specifically, breath-hold duration is measured during a number of maneuvers, including after end expiration, end inspiration, voluntary prior hyperventilation, and inspired hyperoxia. Further activities illustrate the potential contribution of chemoreflexes through rebreathing and repeated rebreathing after a maximum breath hold. The outcome measures resulting from each intervention are easily visualized and plotted and can comprise a comprehensive data set to illustrate and discuss complex and integrated cardiorespiratory physiology.

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“…The beginning of the second period, the ‘struggle’ phase, is marked by the onset of involuntary respiratory contractions that increase in both magnitude and frequency until the breaking point of apnoea is reached [2], [3]. Several factors are known to influence the apnoea breakpoint, these factors include: the degree of hypoxaemia and hypercapnia; lung volume and rate of alveolar gas-exchange; and afferent information originating within the diaphragm during contraction [4]–[7]. In addition to these factors, the ability to maintain adequate delivery of O 2 to the cerebral tissues must necessarily impact on breath holding performance [8], [9], insofar as brain hypoxia/hypercapnia may induce cognitive impairment, unconsciousness and, in some cases, may result in fatality [10], [11].…”

Section: Introductionmentioning

confidence: 99%

The Effects of Involuntary Respiratory Contractions on Cerebral Blood Flow during Maximal Apnoea in Trained Divers

et al. 2013

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The effects of involuntary respiratory contractions on the cerebral blood flow response to maximal apnoea is presently unclear. We hypothesised that while respiratory contractions may augment left ventricular stroke volume, cardiac output and ultimately cerebral blood flow during the struggle phase, these contractions would simultaneously cause marked ‘respiratory’ variability in blood flow to the brain. Respiratory, cardiovascular and cerebrovascular parameters were measured in ten trained, male apnoea divers during maximal ‘dry’ breath holding. Intrathoracic pressure was estimated via oesophageal pressure. Left ventricular stroke volume, cardiac output and mean arterial pressure were monitored using finger photoplethysmography, and cerebral blood flow velocity was obtained using transcranial ultrasound. The increasingly negative inspiratory intrathoracic pressure swings of the struggle phase significantly influenced the rise in left ventricular stroke volume (R 2 = 0.63, P<0.05), thereby contributing to the increase in cerebral blood flow velocity throughout this phase of apnoea. However, these contractions also caused marked respiratory variability in left ventricular stroke volume, cardiac output, mean arterial pressure and cerebral blood flow velocity during the struggle phase (R 2 = 0.99, P<0.05). Interestingly, the magnitude of respiratory variability in cerebral blood flow velocity was inversely correlated with struggle phase duration (R 2 = 0.71, P<0.05). This study confirms the hypothesis that, on the one hand, involuntary respiratory contractions facilitate cerebral haemodynamics during the struggle phase while, on the other, these contractions produce marked respiratory variability in blood flow to the brain. In addition, our findings indicate that such variability in cerebral blood flow negatively impacts on struggle phase duration, and thus impairs breath holding performance.

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The influence of varying inspired fractions of O2 and CO2 on the development of involuntary breathing movements during maximal apnoea

Cited by 16 publications

References 22 publications

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

Cardiovascular responses to dry resting apnoeas in elite divers while breathing pure oxygen

The ins and outs of breath holding: simple demonstrations of complex respiratory physiology

The Effects of Involuntary Respiratory Contractions on Cerebral Blood Flow during Maximal Apnoea in Trained Divers

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