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

机译:在训练有素的潜水员最大呼吸暂停期间非自愿呼吸收缩对脑血流的影响

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摘要

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.
机译:目前尚不清楚非自愿性呼吸收缩对最大呼吸暂停的脑血流反应的影响。我们假设,尽管呼吸收缩可能会增加搏斗阶段的左心室搏动量,心输出量并最终增加脑血流量,但这些收缩会同时导致流向大脑的血液明显“呼吸”变化。在最大的“屏气”屏气期间,对十名训练有素的男性呼吸暂停者的呼吸,心血管和脑血管参数进行了测量。通过食道压力估算胸腔内压力。使用手指光体积描记法监测左心室搏动量,心输出量和平均动脉压,并使用经颅超声检查来获取脑血流速度。搏斗期的吸气胸腔内压力波动越来越负,这显着影响了左心室搏动量的升高(R 2 = 0.63,P <0.05),从而在整个此过程中促进了脑血流速度的增加。呼吸暂停阶段。然而,这些收缩也导致挣扎期左心室搏动量,心输出量,平均动脉压和脑血流速度明显变化(R 2 = 0.99,P <0.05)。有趣的是,脑血流速度的呼吸变异性大小与搏斗阶段持续时间呈负相关(R 2 = 0.71,P <0.05)。这项研究证实了以下假设:一方面,非自主呼吸收缩在搏斗阶段促进了脑血流动力学,而另一方面,这些收缩在流向大脑的血液中产生了明显的呼吸变异性。此外,我们的发现表明,脑血流的这种变化对搏斗阶段持续时间有负面影响,因此会削弱屏气表现。

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