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.
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.
Endurance-trained rats utilize liver glycogen at a reduced rate during exercise compared to nontrained rats. We have compared liver cAMP responses to exercise in trained and nontrained rats in an attempt to elucidate the mechanism of this adaptation. Rats were trained on a motor-driven rodent treadmill 5 days/wk for 12 wk. On the day of the test, trained and nontrained rats were quickly anesthetized after running at 21 m/min up a 15% grade for periods up to 90 min. After 45 min of running, liver cAMP had increased from 0.60 +/- 0.01 to 0.90 +/- 0.03 pmol/mg in nontrained rats whereas no significant increase had occurred in livers of trained rats. Plasma glucagon and norepinephrine levels were significantly lower in trained rats at this point. At the end of 90 min hepatic cAMP was 1.28 +/- 0.12 in nontrained compared to 0.83 +/- 0.06 pmol/mg in trained rats. Plasma glucagon was markedly elevated in nontrained but not in trained rats at this time. The lower rate of liver glycogen utilization in trained rats is consistent with the lower cAMP levels maintained early in exercise.
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