Blunted hypoxic pulmonary vasoconstriction in apnoea divers

 Competitive apnoea divers repetitively dive to depths beyond 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, increasing pulmonary artery pressure. We hypothesized that Divers would have exaggerated hypoxic pulmonary vasoconstriction leading to increased right-heart work due 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 and 16 age and sex matched non-diving controls (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 minutes of isocapnic hypoxia (end-tidal PO2 = 50 mm Hg) were measured one hour following 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 minutes isocapnic hypoxia (Δ -3.85 ± 72.85 vs 73.74 ± 91.06 dynes/sec/cm–5, p = .0222). With sildenafil, Divers and Controls had similarly blunted increases in total pulmonary resistance after 20–30 minutes of hypoxia. Divers also had a significantly lower systemic vascular resistance following sildenafil in normoxia. These data indicate that repetitive apnoea diving leads to a blunted hypoxic pulmonary vasoconstriction. We suggest this is a beneficial adaption allowing for increased cardiac output with reduced right heart work and thus reducing cardiac oxygen utilization under hypoxemic conditions.