Patrician Alexander, Spajić Boris, Gasho Christopher, Caldwell Hannah G, Dawkins Tony, Stembridge Michael, Lovering Andrew T, Coombs Geoff B, Howe Connor A, Barak Otto, Drviš Ivan, Dujić Željko, Ainslie Philip N
Center for Heart, Lung & Vascular Health, University of British Columbia - Okanagan, Kelowna, BC, Canada.
Faculty of Kinesiology, University of Zagreb, Zagreb, Croatia.
Exp Physiol. 2021 Apr;106(4):1120-1133. doi: 10.1113/EP089176. Epub 2021 Mar 12.
What is the central question of this study? How does deep breath-hold diving impact cardiopulmonary function, both acutely and over the subsequent 2.5 hours post-dive? What is the main finding and its importance? Breath-hold diving, to depths below residual volume, is associated with acute impairments in pulmonary gas exchange, which typically resolve within 2.5 hours. These data provide new insight into the behaviour of the lungs and pulmonary vasculature following deep diving.
Breath-hold diving involves highly integrative and extreme physiological responses to both exercise and asphyxia during progressive elevations in hydrostatic pressure. Over two diving training camps (Study 1 and 2), 25 breath-hold divers (recreational to world-champion) performed 66 dives to 57 ± 20 m (range: 18-117 m). Using the deepest dive from each diver, temporal changes in cardiopulmonary function were assessed using non-invasive pulmonary gas exchange (indexed via the O deficit), ultrasound B-line scores, lung compliance and pulmonary haemodynamics at baseline and following the dive. Hydrostatically induced lung compression was quantified in Study 2, using spirometry and lung volume measurement, enabling each dive to be categorized by its residual volume (RV)-equivalent depth. From both studies, pulmonary gas exchange inefficiency - defined as an increase in O deficit - was related to the depth of the dive (r = 0.345; P < 0.001), with dives associated with lung squeeze symptoms exhibiting the greatest deficits. In Study 1, although B-lines doubled from baseline (P = 0.027), cardiac output and pulmonary artery systolic pressure were unchanged post-dive. In Study 2, dives with lung compression to ≤RV had higher O deficits at 9 min, compared to dives that did not exceed RV (24 ± 25 vs. 5 ± 8 mmHg; P = 0.021). The physiological significance of a small increase in estimated lung compliance post-dive (via decreased and increased/unaltered airway resistance and reactance, respectively) remains equivocal. Following deep dives, the current study highlights an integrated link between hydrostatically induced lung compression and transient impairments in pulmonary gas exchange efficiency.
本研究的核心问题是什么？深度屏气潜水如何在急性情况下以及潜水后的2.5小时内影响心肺功能？主要发现及其重要性是什么？屏气潜水至残气量以下深度与肺气体交换的急性损伤有关，这种损伤通常在2.5小时内恢复。这些数据为深度潜水后肺和肺血管系统的行为提供了新的见解。
屏气潜水涉及在静水压力逐渐升高期间对运动和窒息的高度整合且极端的生理反应。在两个潜水训练营（研究1和研究2）中，25名屏气潜水员（从休闲潜水员到世界冠军）进行了66次潜水，深度达57±20米（范围：18 - 117米）。利用每位潜水员的最深潜水，在基线和潜水后使用无创肺气体交换（通过氧亏指数）、超声B线评分、肺顺应性和肺血流动力学评估心肺功能的时间变化。在研究2中，使用肺活量测定法和肺容积测量对静水压力引起的肺压缩进行量化，从而能够根据每个潜水的等效残气量（RV）深度对其进行分类。从两项研究来看，肺气体交换效率低下（定义为氧亏增加）与潜水深度相关（r = 0.345；P < 0.001），出现肺挤压症状的潜水表现出最大的氧亏。在研究1中，尽管B线从基线翻倍（P = 0.027），但潜水后心输出量和肺动脉收缩压未发生变化。在研究2中，与未超过RV的潜水相比，肺压缩至≤RV的潜水在9分钟时氧亏更高（分别为24±25与5±8mmHg；P = 0.021）。潜水后估计肺顺应性略有增加（分别通过降低和增加/不变的气道阻力和电抗）的生理意义仍不明确。深度潜水后，本研究突出了静水压力引起的肺压缩与肺气体交换效率的短暂损伤之间的综合联系。
