Both exercise MPI and exercise echocardiography have high NPVs for primary and secondary cardiac events. The prognostic utility of both modalities is similar for both men and women.
Endurance exercise training produces major adaptations in hormonal and metabolic responses to exercise. This study was designed to determine whether the differences in hormone response persist in the fasted condition when liver glycogen is depleted. Rats were run on a motor-driven rodent treadmill 5 days/wk for periods up to 2 h/day for 10 wk. Trained and nontrained rats were then fasted 24 h and were run for periods ranging from 0- to 60 min. At the end of 60 min of exercise muscle glycogen was higher in trained rats (2.9 +/- 0.3 vs. 1.1 +/- 0.1 mg/g). Blood glucose was maintained at higher levels in trained rats throughout the course of the exercise (3.2 +/- 0.1 vs. 2.3 +/- 0.1 mM after 60 min). Plasma concentrations of glucagon and epinephrine increased in both groups during the exercise but were significantly lower in trained animals. Differences between trained and nontrained animals in stress hormone responses to exercise persist in the fasted state and appear to be a consequence of the capacity of trained animals to maintain higher blood glucose levels.
Endurance-trained animals and human subjects have been reported to exhibit a lesser degree of postexercise ketosis than nontrained controls. We have studied the mechanism of this adaptation. Trained (2 h/day, 6 wk) and nontrained rats were fasted overnight and then run at 16 m/min up a 15% grade for 90 min. Trained rats had lower blood 3-hydroxybutyrate during exercise and during a 90-min postexercise period than nontrained rats. Liver malonyl coenzyme A (CoA), carnitine, and glycogen were not significantly different in the two groups at any time during and after exercise. Therefore these factors cannot be responsible for the difference in ketonemia. Plasma free-fatty acids and hepatic adenosine 3',5'-cyclic monophosphate were elevated in nontrained rats with respect to trained rats. These two differences could conceivably be responsible for a different ketogenic rate. In addition, 3-ketoacid CoA transferase activity of gastrocnemius muscle was increased by training. The increase in ketone oxidizing enzymes of muscle may also be partially responsible for the training-induced attenuation of postexercise ketonemia in these fasted rats.
We have examined the roles of liver glycogen and malonyl coenzyme A (CoA) in determining the degree of postexercise ketosis in endurance-trained and nontrained rats. Three groups of rats were run on a treadmill for 90 min: trained (2 h/day, 6 wk) and food restricted to 5.5 g/100 g body wt the night before the 90-min exercise bout (group 1), nontrained fed ad libitum (group 2), and nontrained food restricted (same as trained) (group 3). Liver glycogen was 34 +/- 5, 24 +/- 2, and 7 +/- 2 mg/g in groups 1, 2, and 3, respectively, at the end of exercise. At the end of exercise and during the postexercise period the blood 3-hydroxybutyrate concentration in group 3 was significantly higher than in groups 1 or 2. No difference was observed between groups 1 and 2 in blood 3-hydroxybutyrate. Hepatic malonyl CoA was decreased to the same extent in all rats during exercise but remained depressed only in the glycogen-depleted group 3 rats in the postexercise period. These data suggest that the differences in degree of ketonemia in the postexercise period (but not during exercise) were due to lower hepatic malonyl CoA in group 3 rats.
The existence of the sympathetic innervation of the liver has been known for many years, but the role of this system in regulation of liver metabolism is unclear. The purpose of these experiments was to identify physiological conditions for activation of liver sympathetics. Liver norepinephrine (NE) was measured in normal resting rats and in rats exposed to swimming, treadmill running, fasting, and insulin-induced hypoglycemia. Liver NE decreased significantly in response to swimming (-71% of control), treadmill running (-53% of control), and hypoglycemia (-24% of control). Rats that are endurance trained by daily bouts of treadmill running for 3 mo show no decrease in liver NE in response to a 60-min run on the treadmill, whereas nontrained rats show a 50% decrease in liver NE with the same amount of exercise. We conclude that the liver sympathetics are activated in response to swimming, treadmill exercise and hypoglycemia, and that endurance training causes a reduction in the degree of exercise-induced activation of these neurons.
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