The Effects of Hypoxia‐Induced Central Sleep Apnea on Splenic Contraction and Oxygen Carrying Capacity

Central sleep apnea (CSA) begins developing above 3000m due to respiratory control system instability in hypoxia, and represents a series of short‐duration, end‐expiratory apneas during sleep. Previous studies demonstrate that splenic contraction is induced by both sustained hypoxia and apnea, ejecting of a store of red blood cells (RBCs) into the systemic circulation, with associated elevations in [hemoglobin] ([Hb]) and arterial oxygen content (CaO 2 ). Therefore, we aimed to assess whether the apneas associated with CSA in the context of high altitude ascent elicit splenic contraction, contributing to hematological acclimatization early in ascent to high altitude. We recruited two groups of participants for two protocols, one lab‐based (1045m; Part A) and one during rapid ascent and residence at high altitude (3800m; Part B). For Part A, 15 participants (6 females) performed five intermittent voluntary end‐expiratory apneas (15‐sec; separated by 1‐min) in normobaric hypoxia (F I O 2 0.15‐0.16) in a seated position. Splenic volume was measured via ultrasonography prior to and immediately following apneas. Capillary blood samples for [Hb] and peripheral pulse oximetry (SpO 2 ) was collected before and immediately following apneas. For Part B, 21 participants (8 females) ascended rapidly by car to 3800m over 5‐6 hours, and CSA was assessed via portable polysomnography on night two, with capillary [Hb] samples and SpO 2 collected before sleep (pm) and after waking (am). In Part A, splenic volume decreased from normoxia (201±83 mL) to hypoxia (172±62 mL; Δ29±30 mL, 95% CI [11.7–46.1 mL], P=0.003), and decreased further following apneas (151±61 mL, Δ21±17 mL, 95% CI [5.3–36.4], P=0.005) compared to hypoxia baseline. However, [Hb] and CaO 2 were unchanged following apneas. At 3800m, the apnea‐hypopnea index increased from 3.4±3.5 before ascent (1045m) to 12.3±14.5 events/hour at 3800m (P=0.002), suggesting CSA. [Hb] was elevated from 143±11 g L ‐1 (night 2) to 152±12 g L ‐1 (morning 3; Δ9±15 g L ‐1 , 95% CI [2.6–16.2 g L ‐1 ] P=0.01), which resulted in increases in CaO 2 from 16.9±1.3 to 18.5±1.5 ml dl ‐1 (Δ1.6±2 ml dl ‐1 , 95% CI [0.6–2.6 ml dl ‐1 ], P=0.003). Our data suggest that CSA‐mediated intermittent apneas in the context of early high altitude ascent results in functional splenic contraction and ejection of RBCs into the systemic circulation, increasing [Hb] and CaO 2 . This is the first demonstration that CSA‐induced splenic contraction may contribute to hematological acclimatization and increased oxygen carrying capacity early in ascent to high altitude, before the known time‐course of erythropoietin‐induced increases in [Hb] with sustained high altitude exposure.

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