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.

Several methods, giving values essentially in agreement, are now available to determine the iodine content-of plasma. Attempts to quantitate the iodine content of tissues have not yielded consistent results. The purpose of our paper is to report the application to this problem of a method based on isotopic equilibrium and using 1125 as a radioactive tracer. With this procedure, it is possible to measure the concentration of total iodine, iodide, thyroxine, triiodothyronine, and some unidentified iodine-containing substances in plasma, selected tissues, and excreta of the rat. METHODSDiets. Rats were fed two separate diets differing in their iodine content. The first, designated "high-iodine," consisted of a standard laboratory diet 1 containing 1.7 ,ug of iodine 2 per g of ration; the second, designated "low-iodine," was a special low-iodine ration 3 containing 0.06 /Ag of iodine 2 per g. To avoid the possibility of producing iodine deficiency (1), we added enough potassium iodide to raise the iodine content to 0.22 /Ag per g. The amount of iodine added to the diets as I"5 was negligible. The two diets, therefore, differed approximately tenfold in iodine concentration. Enough feed was obtained from the manufacturers to complete all the experiments with one lot, avoiding variations in the stable-iodine content.

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