Abstract
In order to further define O(2) store utilization during dives and understand the physiological basis of the aerobic dive limit (ADL, dive duration associated with the onset of post-dive blood lactate accumulation), emperor penguins (Aptenodytes forsteri) were equipped with either a blood partial pressure of oxygen (P(O(2))) recorder or a blood sampler while they were diving at an isolated dive hole in the sea ice of McMurdo Sound, Antarctica. Arterial P(O(2)) profiles (57 dives) revealed that (a) pre-dive P(O(2)) was greater than that at rest, (b) P(O(2)) transiently increased during descent and (c) post-dive P(O(2)) reached that at rest in 1.92+/-1.89 min (N=53). Venous P(O(2)) profiles (130 dives) revealed that (a) pre-dive venous P(O(2)) was greater than that at rest prior to 61% of dives, (b) in 90% of dives venous P(O(2)) transiently increased with a mean maximum P(O(2)) of 53+/-18 mmHg and a mean increase in P(O(2)) of 11+/-12 mmHg, (c) in 78% of dives, this peak venous P(O(2)) occurred within the first 3 min, and (d) post-dive venous P(O(2)) reached that at rest within 2.23+/-2.64 min (N=84). Arterial and venous P(O(2)) values in blood samples collected 1-3 min into dives were greater than or near to the respective values at rest. Blood lactate concentration was less than 2 mmol l(-1) as far as 10.5 min into dives, well beyond the known ADL of 5.6 min. Mean arterial and venous P(N(2)) of samples collected at 20-37 m depth were 2.5 times those at the surface, both being 2.1+/-0.7 atmospheres absolute (ATA; N=3 each), and were not significantly different. These findings are consistent with the maintenance of gas exchange during dives (elevated arterial and venous P(O(2)) and P(N(2)) during dives), muscle ischemia during dives (elevated venous P(O(2)), lack of lactate washout into blood during dives), and arterio-venous shunting of blood both during the surface period (venous P(O(2)) greater than that at rest) and during dives (arterialized venous P(O(2)) values during descent, equivalent arterial and venous P(N(2)) values during dives). These three physiological processes contribute to the transfer of the large respiratory O(2) store to the blood during the dive, isolation of muscle metabolism from the circulation during the dive, a decreased rate of blood O(2) depletion during dives, and optimized loading of O(2) stores both before and after dives. The lack of blood O(2) depletion and blood lactate elevation during dives beyond the ADL suggests that active locomotory muscle is the site of tissue lactate accumulation that results in post-dive blood lactate elevation in dives beyond the ADL.