PubMed Health⌕ Search

PubMed · 3529282

Hormonal alterations due to exercise.

Abstract

The study of hormonal alterations due to exercise is of growing interest because of the implications for adaptation, performance, and health. The influence of the sympathoadrenal response on energy metabolism and fluid and electrolyte balance has been of primary interest in past research. Interpretation of results, however, is difficult because of the numerous factors which need to be controlled. Limitations in the interpretation of hormone levels exist because of changes in plasma volume and/or clearance rate and the influences of timing and method of blood sampling. Other factors which must be considered are the design of exercise protocols, and various subject characteristics (sex, age, fitness level, training history, diet, emotional status, diurnal and menstrual variations). Hormonal alterations during acute exercise occur primarily because of sympathoadrenal secretion of the catecholamines which initiate mobilisation of glucose and free fatty acids. This response, in turn, stimulates other endocrine glands and cells (anterior and posterior pituitary, adrenal cortex, thyroid, parathyroid, liver, pancreas, kidney) to secrete secondary hormones which potentiate fuel mobilisation and regulate water and electrolyte concentrations. As duration of exercise increases, nutrient and ion concentrations also influence hormonal responses. In recent years, research has focused on the effect of exercise-induced hormonal alterations on reproductive functioning and various endocrine-related diseases (hypopituitarism, diabetes, osteoporosis, cardiovascular disease). These topics, as well as a better understanding of mechanisms of action via receptor activity, influences on training adaptations, and implications (if any) of hormonal alterations for the growth and development of children, provide challenges for future research.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J C Bunt. Hormonal alterations due to exercise.. https://doi.org/10.2165/00007256-198603050-00003

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Neonatal hyperleptinaemia programmes adrenal medullary function in adult rats: effects on cardiovascular parameters.

Epidemiological studies have shown a strong correlation between stressful events (nutritional, hormonal or environmental) in early life and development of adult diseases such as obesity, diabetes and cardiovascular failure. It is known that gestation and lactation are crucial periods for healthy growth in mammals and that the sympathoadrenal system is markedly influenced by environmental conditions during these periods. We previously demonstrated that neonatal hyperleptinaemia in rats programmes higher body weight, higher food intake and hypothalamic leptin resistance in adulthood. Using this model of programming, we investigated adrenal medullary function and effects on cardiovascular parameters in male rats in adulthood. Leptin treatment during the first 10 days of lactation (8 microg 100 g(-1) day(-1), s.c.) resulted in lower body weight (6.5%, P < 0.05), hyperleptinaemia (10-fold, P < 0.05) and higher catecholamine content in adrenal glands (18.5%, P < 0.05) on the last day of treatment. In adulthood (150 days), the rats presented higher body weight (5%, P < 0.05), adrenal catecholamine content (3-fold, P < 0.05), tyrosine hydroxylase expression (35%, P < 0.05) and basal and caffeine-stimulated catecholamine release (53% and 100%, respectively, P < 0.05). Systolic blood pressure and heart rate were also higher in adult rats (7% and 6%, respectively, P < 0.05). Our results show that hyperleptinaemia in early life increases adrenal medullary function in adulthood and that this may alter cardiovascular parameters. Thus, we suggest that imprinting factors which increase leptin and catecholamine levels during the neonatal period could be involved in development of adult chronic diseases.

Adrenal Medulla↗

Stimulation of catecholamine synthesis via activation of p44/42 MAPK in cultured bovine adrenal medullary cells by milnacipran.

Milnacipran is a serotonin noradrenaline reuptake inhibitor (SNRI) and is used clinically as an antidepressant. We report here the effect of milnacipran on catecholamine synthesis in cultured bovine adrenal medullary cells. Incubation of adrenal medullary cells with milnacipran (300 ng/ml, 1,065 nM) for 20 min resulted in a significant increase in 14C-catecholamine synthesis from [14C]tyrosine, but not from [14C]DOPA, whereas the selective serotonin reuptake inhibitors (SSRIs), paroxetine (300 ng/ml, 800 nM) and fluvoxamine (300 ng/ml, 691 nM), had little effect. Milnacipran, but not paroxetine or fluvoxamine, increased the activity of tyrosine hydroxylase, the rate-limiting step of catecholamine biosynthesis, in a concentration-dependent manner (100-300 ng/ml, 355-1,065 nM). U0126 (1 microM), an inhibitor of p44/42 mitogen-activated protein kinase (MAPK) kinase, abolished the stimulatory effects of milnacipran on tyrosine hydroxylase activity. Furthermore, incubation of cells with milnacipran (30-100 ng/ml) for 5 min activated p44/42 MAPK, whereas paroxetine and fluvoxamine did not. The present findings suggest that milnacipran activates tyrosine hydroxylase and then stimulates catecholamine synthesis through a p44/42 MAPK-dependent pathway in cultured bovine adrenal medullary cells.

Adrenal Medulla↗

Mechanism for blockade of angiotensin subtype 1 receptors to lower plasma glucose in streptozotocin-induced diabetic rats.

AIMS: We investigated the mechanism(s) by which valsartan, a selective antagonist of angiotensin subtype 1 (AT(1)) receptor, decreased plasma glucose in streptozotocin (STZ)-induced diabetic rats. METHODS: The plasma glucose concentration was assessed by the glucose oxidase method. The concentration of beta-endorphin in plasma or medium incubating adrenal medulla was measured using an enzyme-linked immunosorbent assay. The mRNA levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver were detected by Northern blotting analysis, while the protein levels of GLUT4 in isolated soleus muscle and hepatic PEPCK were investigated using Western blotting analysis. RESULTS: A single intravenous injection of valsartan dose-dependently increased plasma beta-endorphin-like immunoreactivity (BER) in parallel with the lowering of plasma glucose concentration in STZ-induced diabetic rats. Naloxone and naloxonazine inhibited the plasma glucose-lowering action of valsartan at doses sufficient to block opioid micro-receptors. In contrast to its action in wild-type diabetic mice, valsartan failed to modify plasma glucose in opioid micro-receptor knockout diabetic mice. Bilateral adrenalectomy in STZ-induced diabetic rats eliminated both the plasma glucose-lowering action and the plasma BER-elevating action of valsartan. In the isolated adrenal medulla of STZ-induced diabetic rats, angiotensin II (Ang II) or valsartan did not affect spontaneous BER secretion. Activation of cholinergic receptors by 1.0 micromol/l acetylcholine (ACh) enhanced BER secretion from the isolated adrenal medulla of STZ-induced diabetic rats, but not in the presence of 1.0 nmol/l Ang II, while valsartan reversed this inhibition by Ang II in a concentration-dependent manner. Treatment of STZ-induced diabetic rats with valsartan (0.2 mg/kg) three times daily for 3 days resulted in an increase in gene expression of GLUT4 in soleus muscle and impeded the reduction of elevated mRNA or protein level of hepatic PEPCK. Both of these effects were blocked by opioid micro-receptor antagonist. CONCLUSIONS: The results suggest that blockade of AT(1) receptor by valsartan may enhance the adrenal beta-endorphin secretion induced by ACh, activating the opioid micro-receptors to increase glucose utilization and/or to decrease hepatic gluconeogenesis, resulting in the reduction of plasma glucose in STZ-induced diabetic rats.

Adrenal Medulla↗