Tissue lactate concentration has been reported to be a useful postmortem indicator of antemortem awareness of mortal danger. The purpose of this study was to determine further whether selected tissue metabolites could be used as postmortem markers of antemortem adrenergic stress. Sprague-Dawley albino rats were anesthetized with pentobarbital and then injected with 2.0 mg kg-1 i.p. epinephrine hydrochloride to induce experimentally a severe sympathetic response that may be associated with the awareness of mortal danger; 20 min after the injection of epinephrine, when the metabolic response was at its peak, the animals were killed by exsanguination. Samples of the following tissues were removed immediately prior to death (0 h) and 48 h postmortem: soleus, plantaris, kidney medulla, kidney cortex, liver, and heart. These samples were analyzed for glycogen, lactate, ATP, creatine phosphate, pH, and total protein concentration. Significant differences in lactate concentration were observed in all tissues except soleus at 0 h in the epinephrine-injected animals. Specific tissues also had significant reductions in glycogen, ATP, and creatine phosphate concentrations at 0 h. At 48 h postmortem, however, only the liver and soleus lactate concentrations were significantly different from the 48-h control samples. It is unlikely that these small differences found in some tissues at 48 h postmortem would be detected in an uncontrolled accident situation. We concluded from these findings that these selected tissue metabolites are not useful as long-term postmortem indicators of antemortem adrenergically induced hypermetabolism.

The purpose of this study was to determine if the perturbations in two glycolytic metabolites that occur during hemorrhagic shock can be used as discriminatory postmortem indicators of death resulting from severe hemorrhagic shock. Two groups of male albino Sprague-Dawley rats were hemorrhaged by withdrawing either 40% (Group I) or 45% (Group II) of the total blood volume. Glycogen and lactate concentrations were determined at 0 and 48 hr postmortem in the following tissues and organs: diaphragm, heart, liver, kidney cortex, and kidney medulla. The differences in lactate and glycogen in Group I at 0 hr were not significantly different from the nonhemorrhaged controls, with the exception of the lower liver glycogen concentration (58% of control). In Group II glycogen concentration was significantly reduced at 0 hr in the diaphragm (70% of control), liver (37%), and kidney medulla (55%). Lactate concentration was higher in all tissues examined by 270-640%; within 48 hr all tissues for both control and hemorrhaged animals had declined to baseline levels of glycogen concentration, whereas lactate levels had increased as much as 34-fold. There were no highly significant differences in glycogen at 48 hr between the control and hemorrhaged groups. In Group II the lactates were similar for both the control and hemorrhaged animals with the exception of the higher concentrations in the kidney cortex (54%) and medulla (41%). It was concluded from these findings that although significant metabolic perturbations are present at the time of death due to hemorrhage these differences do not persist up to 48 hr postmortem, with the possible exception of the kidney lactate concentrations.

To examine the significance of endogenous stores of glycogen in specific fiber types (I, IIa, IIb) of the costal region of the diaphragm, adult male Wistar rats performed continuous running (25 m/min, 8 degrees grade) exercise for either 30 min or until fatigue. At 30 min of exercise, glycogen loss, as measured microphotometrically using the periodic acid-Schiff technique averaged between 73 and 80% (P less than 0.05) in the different fiber types. When exercise was performed to exhaustion, representing an additional 94 min, no further reduction in glycogen was observed in any fiber type. Biochemical determinations of glycogen from the diaphragm confirmed the extensive reduction in glycogen concentration with exercise. Large reductions (P less than 0.05) in glycogen were also noted in the soleus, plantaris, and vastus lateralis red. Although significant depletion (P less than 0.05) occurred in the vastus lateralis white, it was not as pronounced as in these other muscles. Repletion to preexercise glycogen concentration was complete by 4 h of recovery in all muscles except the vastus lateralis white. It is concluded that endogenous glycogen is a significant substrate in all muscles sampled regardless of fiber composition. In the case of the costal region of the diaphragm, the increased work of breathing resulting from heavy exercise leads to the recruitment of all fiber types, and each fiber type depends on glycogen as a substrate at least early in the exercise.

Some controversy exists in the literature as to whether or not diaphragmatic glycogen is utilized during exercise. In this study male Sprague-Dawley rats were used to determine whether prolonged treadmill exercise would result in a significant reduction of glycogen concentration in the respiratory muscles. Untrained rats were run to exhaustion at a speed of 24 m/min, up a 10% grade. Run time averaged 48:30 min. After exercise a significant reduction in glycogen was observed in the diaphragm (43% of control), intercostals (43%), heart (39%), and plantaris (76%). In the diaphragm a significant reduction was shown in both types I and II fibers using the periodic acid-Schiff (PAS) stain for glycogen. These findings show that muscles with vastly different aerobic capacities utilize endogenous glycogen during moderately intense submaximal endurance exercise and that the costal diaphragm muscle is not an exception as has recently been suggested.