Some species of seals can perform dives that last for a staggering 2 hrs. To achieve this they store large amounts of oxygen in a large volume of hemoglobin-rich blood and in myoglobinrich skeletal muscles, and economize with these stores through a selective down-regulation of tissue perfusion and metabolism. Hematocrit values that may approach 75% make their blood highly viscous, thereby potentially imposing an increased work load on their heart, but the diving-associated profound bradycardia relieves this burden to the extent that coronary blood flow may, in fact, drop to only 10% of pre-dive values. Red blood cells (RBC) of seals also have properties that reduce aggregation/sedimentation and a subsequent additional rise in viscosity, under the stasis-like conditions that may prevail in their large central venous compartments during dives. In situations where a high oxygen-carrying capacity is not needed, such as during haul-out, hematocrit values drop due to temporary storage of RBC in their large spleen, which fully dilated may hold 25–30% of all RBC. The diving-induced redistribution of blood serves the purpose of securing hypoxia-sensitive tissues (primarily the brain) with adequate oxygen supply, while most other tissues must subsist on locally stored oxygen and/or anaerobiosis, and apparently also may enter into a hypometabolic state. Despite these measures, arterial oxygen tension slowly drops and eventually may fall below 15 mmHg. Under such conditions of severe hypoxemia the integrity of brain tissue seems to be preserved due to the combined effect of a high capillary density, a blood-borne brain cooling by up to 4°C, a high capacity for anaerobic metabolism and an unusual organisation of oxidative metabolism between glia and neurons, and a high inherent neuronal hypoxia tolerance which is based on still poorly understood mechanisms but which seems to involve hypoxia-induced hypometabolism.