For diving and exercise physiologists, `venting your spleen' has a whole different meaning than it does to the layman. In diving mammals and heavy exercisers, the spleen serves as an oxygen reservoir, storing highly viscous `thick blood', rich in red blood cells, during periods of rest, and injecting these stored red blood cells into the general circulation when oxygen levels are stressed and increased transport is required. Such injections of oxygenated red blood cells occur during periods of heavy exercise in some mammals, such as horses, and are particularly well developed in diving mammals. The spleen of the Arctic Weddell seal contains so much extra oxygenated blood that it often is referred to as a SCUBA tank; in fact, the release of red blood cells into the circulation is so tightly regulated that arterial oxygen content doesn't decrease for the first 15–18 min underwater. Splenic emptying under these circumstances is due to an active contraction of the spleen triggered by adreneric innervation; spleen volume in some diving seals may reduce by as much as 85%! However, in general, humans have a less well-developed dive response and a relatively small splenic reservoir (about 8% of total body red blood cells versus more than 20 litres of sequestered RBCs in the Weddell seal), and the human spleen is poorly innervated by adrenergic fibers. It has thus been suggested that the observed decrease in human spleen volume following sympathetic activity is due to passive collapse as blood supply to the spleen decreases rather than to an adaptive, active contraction. Recent work by D. Bakovic and coworkers set out to investigate whether splenic contraction is part of the human dive response too.

The team began examining spleen volume and blood flow during simulated human dives in which volunteers submerged their faces while holding their breath. They reasoned that a decrease in spleen volume, caused by a decreased arterial inflow and increased or unaltered venous outflow, would indicate passive collapse. Conversely, an active contraction would result in increased venous outflow without changing arterial inflow. Their results showed that over five successive periods of breath-holding, the diameter of the splenic artery was not altered, whereas the diameter of the splenic vein increased after the first apnea and then gradually returned to baseline. Spleen volume decreased by 14–18% after the first apnea and did not change significantly during subsequent breath-holds.

While the decrease in spleen volume during human `diving' thus appears to be an active process, rather than a passive collapse, the question of its functional significance remains. Does an injection of red blood cells from the human spleen during apnea increase how long you can hold your breath? For this, the authors looked at dive length in trained apneic divers (members of the Croatian national apneic diving team, no less!), in untrained individuals and in persons who had undergone a complete splenectomy at least 2 years previously. Apneic periods were longer during subsequent dives than for the first dive in both trained and untrained individuals but not in splenectomized persons. As the spleen did not relax in the 2-min recovery periods between apneas, the splenic emptying of the first dive thus increased circulating red blood cells for subsequent dives, without a further reduction in spleen volume. The authors suggest that subsequent apneas were longer because there were more red blood cells and thus a higher oxygen carrying capacity from the outset, although they were unable to definitively measure blood gases.

While numerous other factors, including experience, can increase apneic `dive time' over sequential trials, these other factors apparently did not extend repeat dive times in splenectomized individuals, leaving the intriguing possibility that, as with other facets of the dive response, humans share similar, if less well developed, adaptations exemplified by such champion mammalian divers as Weddell and elephant seals.