Competitive apnoea divers dive repetitively to depths >50 m. During the final portions of ascent, divers experience significant hypoxaemia. Additionally, hyperbaria during diving increases thoracic blood volume while simultaneously reducing lung volume and increasing pulmonary artery pressure. We hypothesized that divers would have exaggerated hypoxic pulmonary vasoconstriction, leading to increased right heart work owing to their repetitive hypoxaemia and hyperbaria, and that the administration of sildenafil would have a greater effect in reducing pulmonary resistance in divers. We recruited 16 divers (Divers) and 16 age-and sex-matched non-diving control subjects (Controls). Using a double-blinded, placebo-controlled, cross-over design, participants were evaluated for normal cardiac and lung function, then their cardiopulmonary responses to 20-30 min of isocapnic hypoxia (end-tidal partial pressure of O 2 = 50 mmHg) were measured 1 h after ingestion of 50 mg sildenafil or placebo. Cardiac structure and cardiopulmonary function were similar at baseline. With placebo, Divers had a significantly smaller increase in total pulmonary resistance than Controls after 20-30 min isocapnic hypoxia (change −3.85 ± 72.85 vs. 73.74 ± 91.06 dyns cm −5 , P = 0.0222). With sildenafil, Divers and Controls had similar blunted increases in total pulmonary resistance after 20-30 min of hypoxia.Divers also had a significantly lower systemic vascular resistance after sildenafil in normoxia. These data indicate that repetitive apnoea diving leads to a blunted hypoxic pulmonary vasoconstriction. We suggest that this is a beneficial adaption allowing for increased cardiac output with reduced right heart work and thus reducing cardiac oxygen utilization in hypoxaemic conditions.

No abstract

Hypoxia (low oxygen) induces a reversible form of pulmonary hypertension which can be studied to elucidate the etiology of pulmonary hypertension and right heart dysfunction. Breath‐hold divers (BHD) routinely place themselves into extremely hypoxemic (low blood oxygen) conditions and therefore repeatedly expose themselves to acute intermittent hypoxia and bouts of pulmonary hypertension and increased right heart work. The purpose of this study was to 1) determine if pulmonary arterial pressure and right heart dysfunction in hypoxia were greater in BHD compared to controls, and 2) determine the role of a pulmonary vasodilator in alleviating the increased pulmonary pressure in response to hypoxia. The hypotheses under hypoxic conditions were as followed 1) Right heart dysfunction will be the most severe amongst subjects with the greatest degree of pulmonary hypertension, regardless of group and 2) Sildenafil administration will result in a reduction of pulmonary arterial pressure compared to a placebo during hypoxia, regardless of group. Subjects (n=24, 12 BHD, 12 Control) completed two 30‐minute isocapnic normobaric hypoxic breathing challenges, after receiving either 50mg sildenafil or placebo, with a 48‐hour minimum washout period between visits. Pulmonary arterial systolic pressure (PASP) and right heart function via tricuspid anular plane systolic excursion (TAPSE) measures were made using Doppler ultrasound, and total pulmonary resistance (TPR) was calculated as PASP / cardiac output (Qt). Compared to placebo, BHD had a reduction in TPR with sildenafil in normoxia placebo (312.5 ± 92.8 vs 385 ± 122.6 dynes/sec/cm‐5, respectively, p = .04). Compared to normoxia, PASP was increased with hypoxia in BHDc with placebo (22.9±6.0 vs. 32.4±8.9 mm Hg, respectively, p=0.0002) but not with sildenafil. Conversely, BHD had no changes in PASP with placebo, but had an increase in PASP from normoxia to hypoxia with sildenafil (22.3±4.8 vs. 31.5±6.9 mm Hg, respectively, p=0.0002). There was no effect of group or treatment on TAPSE. Our data suggests breath hold divers may have a previously unrecognized chronic pulmonary vasoconstriction in room air that is prevented with administration of sildenafil.