| Summary: | To examine the physiological and biochemical changes that occur during diving, northern elephant seal pups were subjected to forced dive protocols while undergoing Magnetic Resonance Imaging and Spectroscopic analysis. Splenic volume measurements were obtained in the predive, dive and postdive state. Splenic contraction was initiated immediately upon facial immersion, reducing to 14.0 - 17.8% of its predive volume by minute 3 of the dive. A corresponding increase in hepatic sinus volume occurred, suggesting a direct shift of blood from the spleen to the sinus. In the postdive period, the spleen gradually dilated, achieving its maximum volume at 18-22 minutes after the dive (3.35% of body mass; n = 5). Stroke volume (SV) measurements were obtained during diving using phase contrast MR imaging. Mean resting SV was 104.94 mis ± 4.12 SEM, while SV during the dive increased significantly to a mean value of 126.12 ± 3.93 SEM. These data are in contrast to the findings of previous studies on pinnipeds, which indicate either the maintenance or decline of stroke volume during the dive. Pre-dive, postdive or diving heart rates did not correlate with mass or with stroke volume during any state. However, diving SV correlated with the ratio of diving HR to predive HR (P = 0.01, R = 0.99). These findings indicate that the effect of diving on stroke volume is altered by the degree of bradycardia rather than the absolute HR. MR spectroscopy analysis was used to investigate changes in locomotory muscle phosphocreatine (PCr) levels during diving. End-dive PCr levels ranged from 36.84 - 103.93% of resting (average 80.85% ± 5.89 SEM). Animals who exhibited a significant decrease in PCr during diving showed a correlation between end-dive PCr and intracellular pH values. Plasma lactate levels indicated that all dives were within the aerobic diving limit. This study demonstrates that in northern elephant seals, PCr hydrolysis does occur during aerobic dives, indicating that the depletion of [PCr] is driven by an alteration in muscle [H⁺] rather than by changes in [adenylate]. The decrease in muscle pH is attributed to respiratory acidosis caused by significant CO₂ accumulation during hypoperfusion. Science, Faculty of Zoology, Department of Graduate
|
|---|