|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Molecular Pharmacology, Physiology and Biotechnology, Brown University, Providence, Rhode Island, United States
* To whom correspondence should be addressed. E-mail: warrend{at}anesthesia.ucsf.edu.
To test the hypothesis that submergence temperature affects the distribution of the lactate load and glycogen utilization during anoxia in turtles, we sampled a variety of tissues after 7 d, 24 h and 4 h of anoxic submergence at 5, 15 and 25°C, respectively. These anoxic durations were chosen because we found they produced similar decreases in plasma HCO3- (ca. 18-22 mequiv L-1). The sampled tissues included ventricle, liver, small intestine, carapace and the following muscles: flexor digitorum longus (FD), retrahens capitis (RC), iliofibularis (IF), and pectoralis (PT). Shell and skeleton sequestered 41.9%, 34.1% and 26.1% of the estimated lactate load at 5, 15 and 25°C. The change in plasma Ca2+ and Mg2+, relative to the estimated lactate load, decreased with increased temperature, indicating greater buffer release from bone at colder temperatures. Tissue lactate contents, relative to plasma lactate, increased with the temperature of the submergence. Glucose mobilization and tissue glycogen utilization were more pronounced at 15 and 25°C than at 5°C. We conclude that, in slider turtles, the ability of the mineralized tissue to participate in the buffering of lactic acid during anoxia is inversely related to temperature, causing the lactate burden to shift to the tissues at warmer temperatures. Muscles utilize glycogen during anoxia more at warmer temperatures.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |