To investigate the effect of the increase in glucocorticoids during exercise on endurance, rats were either sham operated (SO) or adrenalectomized. All adrenalectomized rats were given a subcutaneously implanted corticosterone pellet at the time of adrenalectomy. Adrenalectomized rats were injected with corticosterone (ADX Cort) or corn oil (ADX) 5 min before exercise. Rats were killed at rest or after running on a treadmill (21 m/min, 15% grade) until exhaustion. SO rats ran 138 +/- 6 min compared with 114 +/- 9 min for ADX Cort and 89 +/- 8 min for ADX. All differences in run times were significant (P less than 0.05). Corticosterone levels were similar in exhausted SO and ADX Cort groups. ADX exhausted rats had corticosterone levels similar to resting values in SO and ADX rats. Inhibition of the rise in glucocorticoids during exercise had no effect on liver glycogen, liver adenosine 3',5'-cyclic monophosphate, plasma insulin, blood glucose, lactate, glycerol, or 3-hydroxybutyrate, plasma norepinephrine, or red quadriceps and soleus glycogen. Plasma free fatty acids were significantly depressed at exhaustion in ADX rats compared with SO. These data show that glucocorticoids exert effects within the time frame of a prolonged exercise bout and play a role in increasing endurance.

Abstract— The effects of thiamine deprivation and of treatment with the thiamine antagonists, oxythiamine and pyrithiamine, on the storage and synthesis of acetylcholine were studied in rats. Rats treated with pyrithiamine always developed ataxia and convulsions, and they died in an average of 36 ± 5.0 hr after onset of convulsions. Injections of sublethal doses of eserine after onset of convulsions had no effect or shortened survival time. If injections were started before the onset of convulsions, the survival time was increased to 56 ± 3.3 hr. The content of total acetylcholine‐like compounds, measured by bioassay, in the brain was decreased in all three types of thiamine deficiency. On the other hand, the amount of parenterally administered [14C]pyruvate converted to [14C]acetylcholine in vivo was affected only by treatment with pyrithiamine. The increase found was probably due to an increased permeability of the blood‐brain barrier to the pyruvate. Conversion of [14C]pyruvate to [14C]acetylcholine in vitro was decreased significantly in homogenates of brains from both oxythiamine and pyrithiamine‐treated animals.

The purpose of this study was to determine the metabolic function of the marked increase in plasma epinephrine which occurs in fasted rats during treadmill exercise. Fasted adrenodemedullated (ADM) and sham-operated (SHAM) rats were run on a rodent treadmill (21 m/min, 15% grade) for 30 min or until exhaustion. ADM rats were infused with saline, epinephrine, glucose, or lactate during the exercise bouts. ADM saline-infused rats showed markedly reduced endurance, hypoglycemia, elevated plasma insulin, reduced blood lactate, and reduced muscle glycogenolysis compared with exercising SHAM's. Epinephrine infusion corrected all deficiencies. Glucose infusion restored endurance run times and blood glucose to normal without correcting the deficiencies in blood lactate and muscle glycogenolysis. Infusion of lactate partially corrected the hypoglycemia at 30 min of exercise, but endurance was not restored to normal and rats were hypoglycemic at exhaustion. We conclude that in the fasted exercising rat, actions of epinephrine in addition to provision of gluconeogenic substrate are essential for preventing hypoglycemia and allowing the rat to run for long periods of time.

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