Effects of exercise and physical fitness on the pituitary-thyroid axis and on prolactin secretion in male runners.

The effects of acute exercise and thyrotropin-releasing hormone on the pituitary-thyroid axis were examined in men placed into three well-defined categories of physical fitness. There were 20 sedentary men, 22 joggers (running four to 20 miles per week) and 18 marathoners (running 30 to 100 miles per week) who participated. During treadmill exercise, the mean VO2 max differed among all groups, being 38.5, 45.0, and 60.3 mL/kg . min in the sedentary, jogger, and marathon groups, respectively. Serum was obtained before, immediately after, and one hour after exercise for measurement of thyroxine (T4), triiodothyronine (T3), reverse T3, thyrotropin (TSH), and prolactin. Basal values of all hormones did not differ among the groups. Maximal short-term treadmill exercise produced no change in serum T4, T3, reverse T3, or TSH. Prolactin rose significantly by a similar amount in all three subject groups. On a separate day, ten individuals from each group received thyrotropin releasing hormone (TRH; 500 micrograms IV). Neither the peak TSH response nor the total TSH secreted during two hours after TRH differed among groups. The mean total prolactin secretion in the joggers and marathoners was 48% and 45% greater, respectively, than in the sedentary men. Five subjects in each group also underwent a TRH test immediately postexercise. Similar to the results on the nonexercise day, the integrated TSH response to TRH was similar in all three groups, whereas the integrated PRL response to TRH was increased by 52% and 78% in the two conditioned groups. Post-TRH sera from one subject in each group were fractionated on a Sephadex G-100 column.(ABSTRACT TRUNCATED AT 250 WORDS)

3'-Monoiodothyronine degradation in rat liver homogenate: enzyme characteristics and documentation of deiodination by high-pressure liquid chromatography.

Characteristics of 3'-monoiodothyronine (3'-T1) degradation were examined in vitro in rat tissue homogenates. In rat liver homogenates, 3'-T1 degradation was optimal at pH 7.4, and was dependent upon time, temperature, and tissue concentration. The Michaeli's constant (Km) = 0.84 mumol/L. 3'-T1 degradation was enhanced by dithiothreitol and inhibited by propylthiouracil, sodium ipodate, ANS, and sodium azide but not by methimazole. Animals that fasted for three days had significant reductions in both hepatic T4 to T3 conversion (199 +/- 12 v 116 +/- 12 pg T3 generated/mg protein; P less than 0.001) and 3'-T1 degradation (588 +/- 31 v 148 +/- 53 pg 3'-T1 degraded/mg protein; P less than 0.001). To document that 3'-T1 degradation was occurring by deiodination, both liver and kidney homogenates were incubated with 125I-3'-T1 (approximately 3 microCi; 13.1 nmol/L). The reaction products were separated on a reverse-phase high pressure liquid chromatography (HPLC) column. In both tissues an iodide peak was generated, and no other radiolabeled peaks appeared except for 125I-3'-T1. These data suggest that 3'-T1 is metabolized by phenolic-ring monodeiodination and is enzymic in nature.

The effects of pyridoxine on pituitary hormone secretion in amenorrhea-galactorrhea syndromes.

Six patients with amenorrhea, five of whom had galactorrhea and elevated PRL levels, were evaluated on a metabolic ward. All had normal sella tomograms, normal thyroid functions, and routine laboratory evaluations. None of the patients had taken any medication in the previous 6 months. On alternate days, five patients received 500 microgram of TRH iv with the measurement of PRL, TSH, FSh, LH, and hGH; 500 mg L-dopa orally with the measurement of PRL, FSH, and LH; a bolus infusion of 300 mg pyridoxine (B6) with measurement of PRL, hGH, TSH, FSH, and LH; and 25 mg chlorpromazine (CPZ) im with the measurement of PRL, LH, and FSH. The patients were then discharged on 600 mg oral pyridoxine/day and were readmitted for a repeat of the complete protocol 21 days later. The patients were continued on 600 mg oral pyridoxine for 3-4 months with monthly evaluations of serum PRL, LH, and FSH levels. These evaluations continued for 3 months after discontinuing pyridoxine. There was no demonstrable change in serum PRL after acute or chronic B6 therapy, mor was there a significant change in the response of PRL to CPZ, L-dopa, or TRH. The mean basal PRL was 97.5 +/- 9.7 ng/ml and after 3-4 months of oral pyridoxine was 97.1 +/- 14.8. In addition, there was no significant change in LH or FSH levels in response to acute or chronic B6, TRH, L-dopa, or CPZ. Neither acute B6 infusion nor chronic B6 therapy had any effect on TSH or the TSH response to TRH. Finally, acute B6 infusion had no effect on hGH levels and there were no paradoxical hGH responses to TRH. Two patients began having regular menses while on chronic pyridoxine. Their hormonal responses did not differ from those of the group, however.

Pituitary and thyroid function in male cynomolgus monkeys.

In four male cynomolgus monkeys, serum thyroxine was 6.2 +/- 0.9 micrograms/dl, and triiodothyronine was 207 +/- 12 ng/dl (mean +/- SE). Kinetic studies using 131I-thyroxine and 125I-triiodothyronine showed that the disappearance of both hormones was non-linear and best fit a biexponential equation. The metabolic clearance rates and production rates for thyroxine were 21.5 +/- 0.6 ml/kg/day and 1.34 +/- 0.23 micrograms/kg/day, respectively, and T1/2(beta) = 29.6 +/- 2.0 hours. For triiodothyronine, the metabolic clearance rate was 156.6 +/- 12.0 ml/kg/day, the production rate was 0.33 +/- 0.04 micrograms/kg/day, and T1/2 (beta) was 13.3 +/- 1.3 hours. Basel serum thyrotropin levels in five euthyroid animals were 1.4 +/- 0.6 microU/ml and increased after thyrotropin-releasing hormone to 6.7 +/- 2.2 microU/ml. Serum prolactin was 5.8 +/- 0.7 ng/ml, and it increased to 26.6 +/- 4.5 ng/ml after thyrotropin-releasing hormone. Four animals received chronic dexamethasone therapy (1 mg twice daily for 5.5 months). While baseline and thyrotropin-releasing hormone stimulated thyrotropin values were lower (0.8 +/- 0.2 microU/ml and 3.2 +/- 0.5 microU/ml, respectively), these reductions were not significant.

Nature of suppressed TSH secretion during undernutrition: effect of fasting and refeeding on TSH responses to prolonged TRH infusions.

TSH responses to 4-hr continuous TRH infusions of approximately 0.8 microgram/min were assessed during feeding (1500 Kcal), fasting, and refeeding (1500 Kcal) intervals in 9 euthyroid obese subjects. The total area under the TSH response curve was 1854 +/- 322 muU/ml . 4-hr during feeding, decreased to 1359 +/- 199 muU/ml . 4-hr (p less than 0.01) on the 10th day of fasting, and remained low, being 1405 +/- 185 muU/ml . 4-hr, despite refeeding a 1500 Kcal diet (40% carbohydrate, 40% fat, 20% protein) for 5 days. Baseline serum T3 concentrations were 167 +/- 11 ng/dl during feeding, 86 +/- 8 ng/dl during fasting, and 119 +/- 12 ng/dl during refeeding. The observed decreases in TSH release appeared to correlate with decreased biologic action on the thyroid gland since the net rise in T3 during the infusion was less in fasting and refeeding than in the control (fed) period. Basal serum rT3 levels were 42 +/- 5 ng/dl during feeding, rose as expected to 56 +/- 5 ng/dl during fasting (p less than 0.005), and were completely restored to normal during refeeding (36 +/- 5 ng/dl). These data suggest that: (1) TSH responsiveness to prolonged TRH infusion is diminished during fasting and does not return to control (fed) values despite 5 days of refeeding a 1500 Kcal diet; (2) net T3 increases observed during the TRH infusion are greater in the fed period than in the fasting or refeeding periods; and (3) 5 days of refeeding a 1500 Kcal diet (40% carbohydrate, 40% fat, 20% protein) did not return the T3 to its original fed value whereas rT3 was completely restored to control values. Lastly, since the TSH response was lower both during the early and late phases of the infusion, the decrease in delta TSH to a bolus of TRH during fasting appears to represent one manifestation of a more general suppression of TSH neogenesis associated with caloric deprivation.