Introduction: The spleen serves as a repository of erythrocytes that can be jettisoned into circulation following sympathetic stimulation, such as hypoxia or apnea. Evidence supports that there may be a functional benefit to spleen contraction during breath-hold diving, likely by increasing oxygen carrying and pH buffering capacities. However, the magnitude of apnea-induced spleen contraction during immersion, and the corresponding hematological changes, have not been quantified. We have recently identified that spleen volume increases after 30 min of thermoneutral head out water immersion (HOWI), likely due to initial hydrostatic pressure-induced increases in central blood volume, and remains elevated through 135 min, despite immersion-induced diuresis. Whether these HOWI-induced changes in spleen volume modify the magnitude of apnea-induced spleen contraction is unknown. Cross-sectional observations indicate that there is a positive relation between baseline spleen volume and the magnitude of apnea-induced spleen contraction.
Purpose: Test the hypothesis that the magnitude of apnea-induced spleen contraction increases during thermoneutral HOWI.
Methods: Spleen volume was measured pre- and post- a set of five apneas in eight healthy adults (3 women; 27 ± 4 y) before, during (at 30 and 135 min) and 20 min following thermoneutral (36 ± 1°C) HOWI. At each timepoint, spleen length, width, and thickness were measured via ultrasound and spleen volume was calculated using the Pilström equation (test-retest CV: 2 ± 2%). Hemoglobin concentration ([Hb]) and hematocrit were measured pre- and post- each set of apneas via capillary blood samples. Urine was collected at 60 min and 120 min of HOWI. Data are presented as mean ± SD.
Results: Compared to pre-HOWI (97 ± 32 s), average apnea times were higher at 30 min (115 ± 36 s, p=0.02) and 135 min (120 ± 43 s, plt;0.01) of HOWI, but returned to pre- levels at post-HOWI (103 ± 38 s, p=0.70). [Hb] increased from pre- to post- apneas (main effect: plt;0.01), but the magnitude of the increase did not differ between timepoints (pre-HOWI: +0.4 ± 0.3, 30 min of HOWI: +0.3 ± 0.5, 135 min of HOWI: +0.3 ± 0.5, post-HOWI: +0.2 ± 0.2 g/dL, p=0.68). Hematocrit did not change from pre- to post- apneas (main effect: p=0.72), and the magnitude of changes from pre- to post- apneas did not differ between timepoints (p=0.43). Spleen volume decreased from pre- to post-apneas at each timepoint (plt;0.01). The reduction in spleen volume was greater than pre-HOWI (-41 ± 18 mL) at 30 min of HOWI (-65 ± 26 mL, p=0.03), but did not differ from pre-HOWI at 135 min of HOWI (-50 ± 12 mL, p =0.44), despite marked diuresis (urine volume: 425 ± 193 mL), or at post-HOWI (-40 ± 13 mL, p=0.99).
Conclusion: Apnea-induced spleen contraction was acutely increased at 30 mins of HOWI. However, following immersion-induced diuresis the magnitude of spleen contraction at 130 min of HOWI returned to pre-HOWI levels. Increases in [Hb], which were presumably caused by spleen contraction, were not modified by HOWI, suggesting the hematological response to apnea-induced spleen contraction is not modified by immersion.
Supported by Office of Naval Research award N00014-20-1-2593.
