Thyroid hormone and estrogen regulate exercise-induced growth hormone release.

Daniele Leão Ignacio,João Paulo Albuquerque Cavalcanti-De-Albuquerque,Diego H Da S Silvestre,Denise P Carvalho,João Pedro Werneck-De-Castro,Ruy Andrade Louzada,Guillermo López Lluch

doi:10.1371/journal.pone.0122556

Abstract

Growth hormone (GH) regulates whole body metabolism, and physical exercise is the most potent stimulus to induce its secretion in humans. The mechanisms underlying GH secretion after exercise remain to be defined. The aim of this study was to elucidate the role of estrogen and pituitary type 1 deiodinase (D1) activation on exercise-induced GH secretion. Ten days after bilateral ovariectomy, animals were submitted to 20 min of treadmill exercise at 75% of maximum aerobic capacity and tissues were harvested immediately or 30 min after exercise. Non-exercised animals were used as controls. A significant increase in D1 activity occurred immediately after exercise (~60%) in sham-operated animals and GH was higher (~6-fold) 30 min after exercise. Estrogen deficient rats exhibited basal levels of GH and D1 activity comparable to those found in control rats. However, after exercise both D1 activity and serum GH levels were blunted compared to sedentary rats. To understand the potential cause-effect of D1 activation in exercise-induced GH release, we pharmacologically blocked D1 activity by propylthiouracil (PTU) injection into intact rats and submitted them to the acute exercise session. D1 inhibition blocked exercise-induced GH secretion, although basal levels were unaltered. In conclusion, estrogen deficiency impairs the induction of thyroid hormone activating enzyme D1 in the pituitary, and GH release by acute exercise. Also, acute D1 activation is essential for exercise-induced GH response.

Highlights

Overweight and obesity are epidemic diseases leading to diabetes and metabolic syndromes, and are associated with cardiovascular disorders [1], especially for women facing the menopause transition [2]
Pituitary (PIT) D1 [28] and brown adipose tissue (BAT) D2 [11] activities increase after a single running exercise session [28], and in response to a 8-week swimming exercise training program [11]. Both PIT D1 and BAT D2 activities response to exercise are blunted in trained obese estrogen deficient rats [11]. These results suggest that impairment of T4-to-T3 conversion in PIT and BAT by decreased D1 and D2 activities respectively in response to exercise could be involved in the genesis of obesity in E2 deficient rats trough (i) decreasing Growth hormone (GH) release by PIT and/or (ii) reducing BAT metabolism
The present study reveals that estrogen deficiency caused by short-term ovariectomy (Ovx) blunts growth hormone (GH) release induced by high intensity exercise (Fig 2B), as well as thyroid hormone activating enzyme D1 activity in pituitary (Fig 2A)

Summary

Introduction

Overweight and obesity are epidemic diseases leading to diabetes and metabolic syndromes, and are associated with cardiovascular disorders [1], especially for women facing the menopause transition [2]. Menopausal transition is associated with unfavorable changes in body. Hormonal Regulation of Exercise-Induced GH Release composition, abdominal fat deposition and general health outcomes [3,4,5]. Growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis regulates growth and development during childhood and adolescence, and regulates body composition, metabolism and exercise aerobic capacity throughout life [5]. Its deficiency (GHD) is associated with increased body fat and a lower lean body mass [10, 11]. These changes in body composition are associated with metabolic derangements including insulin resistance [9]

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