This study addressed the interaction between short-term adaptation to apneas with face immersion and erythrocyte release from the spleen. Twenty healthy volunteers, including ten splenectomized subjects, participated. After prone rest, they performed five maximal-duration apneas with face immersion in 10 degrees C water, with 2-min intervals. Cardiorespiratory parameters and venous blood samples were collected. In subjects with spleens, hematocrit and hemoglobin concentration increased by 6.4% and 3.3%, respectively, over the serial apneas and returned to baseline 10 min after the series. A delay of the physiological breaking point of apnea, by 30.5% (17 s), was seen only in this group. These parameters did not change in the splenectomized group. Plasma protein concentration, preapneic alveolar PCO2, inspired lung volume, and diving bradycardia remained unchanged throughout the series in both groups. Serial apneas thus triggered the hematological changes that have been previously observed after long apneic diving shifts; they were rapidly reversed and did not occur in splenectomized subjects. This suggests that splenic contraction occurs in humans as a part of the diving response and may prolong repeated apneas.

This study addressed the effects of apnea in air and apnea with face immersion in cold water (10 degrees C) on the diving response and arterial oxygen saturation during dynamic exercise. Eight trained breath-hold divers performed steady-state exercise on a cycle ergometer at 100 W. During exercise, each subject performed 30-s apneas in air and 30-s apneas with face immersion. The heart rate and arterial oxygen saturation decreased and blood pressure increased during the apneas. Compared with apneas in air, apneas with face immersion augmented the heart rate reduction from 21 to 33% (P < 0.001) and the blood pressure increase from 34 to 42% (P < 0.05). The reduction in arterial oxygen saturation from eupneic control was 6.8% during apneas in air and 5.2% during apneas with face immersion (P < 0.05). The results indicate that augmentation of the diving response slows down the depletion of the lung oxygen store, possibly associated with a larger reduction in peripheral venous oxygen stores and increased anaerobiosis. This mechanism delays the fall in alveolar and arterial PO(2) and, thereby, the development of hypoxia in vital organs. Accordingly, we conclude that the human diving response has an oxygen-conserving effect during exercise.

Diving mammals may enhance dive duration by injecting extra erythrocytes into the circulation by spleen contraction. This mechanism may also be important for apneic duration in humans. We studied the speed and magnitude of spleen volume changes evoked by serial apneas, and the associated changes in hematocrit (Hct) and hemoglobin (Hb) concentration, diving response and apneic duration. Three maximal apneas separated by 2 min rest elicited spleen contraction in all ten subjects, by a mean of 49 (27) ml (18%; P<0.001). During the same period, Hct and Hb rose by 2.2 and 2.4% respectively (P<0.01 and P<0.001), and apneic duration rose by 20 s (22% P<0.05). The mean heart rate reduction of the diving response was 15%, which remained the same throughout the apnea series. While the diving response was completely reversed between the apneas, spleen size was not recovered until 8-9 min after the final apnea corresponding with recovery of Hct and Hb. Thus, although the spleen contraction may be associated with the cardiovascular diving response, it is likely to be triggered by different mechanisms, and it may remain activated between dives spaced by short pauses. The two adjustments may provide a fast, quickly reversed, and a slow, but long-lasting, way of shifting to a diving mode in humans.