Please see below for an introduction about Growth Hormone written by yours truly- This will allow you to build a better picture as to the information which will follow later this month.
Background
For the past 30 years scientists have researched Growth Hormone (GH) and its effects upon sports performance. Knowing the information regarding the mechanics and effects of this hormone, it really is of no surprise that this particular hormone has caused such controversial trends within the world of sport over the years; for example the abuse of growth hormone has been related to a number of pathologies yet it remains as the most abused drugs in sport (Jenkins 2001) despite its ban by the IOC and NCAA, furthermore its detection to this day of GH remains difficult.
Function
A fascinating integration of the neural and endocrine systems occurs with growth hormone release (Brooks et al 2005) and often initiates a cascade for number physiological reactions within the body (Godphrey et al 2003). For example, GH acts as a powerful anabolic hormone that affects all body systems and plays an important role in muscular hypertrophy (Macintyre 1987) initiates Lypolysis and promotes protein synthesis, therefore has a major and favorable influence on body composition (Godphrey et al, 2003). It is interesting that Growth hormone is not only related to growth it is also related to metabolism in the body thus is constituted to lean body mass, (Yang et al 2006).
Chemically there are two types of hormones; the first is steroidal hormones produced by cholesterol initiated within the adrenal and gonads, and the second category of hormones concerns the large polypeptides or small proteins which are derived from amino acids in endocrine glands (Brooks et al 2005). Growth hormone falls into the second category, and as with most other hormones in the body has a large influence upon metabolism. This means that protein carbohydrate and lipid metabolism plus the control of skeletal visceral growth are all affected by the powerful growth hormone. Growth hormone has the characteristics of all other hormones in the body whereby it is a chemical messenger that is produced and stored in glandular tissues and functions by an elaborate feedback system in the body.
Mechanics and Regulation
Growth hormone is secreted by the anterior lobe of the pituitary gland; its secretion is under tight regulation by the peptides released by the neurosecretory nuclei of the hypothalamus. As with all hormones a precise homeostatic regulation for growth hormone release is required so that normal functioning can occur under a variety of stressful situations such as exercise (Brooks et al 2005). The homeostatic role of the hormone occurs by a feedback control mechanism cleverly made possible by stimulatory and inhibitory peptides, allowing for this very necessary yet meticulous regulation within the body. A negative feedback mechanism occurs when the release of the hormone is inhibited if a particular end result of the hormonal action is achieved, and in the same instance, if a hormone secreted does not have a desired effect, then further release of the hormone is stimulated until the desired effect is achieved. Besides the fact that polypeptides allow for a regulation; upon discussing growth hormone specifically, it must be understood that physiological variables also account for the stimulation of growth hormone release such as exercise, nutrition and deep sleep.
A list has been included to allow the reader to more easily understand the stimulatory and inhibitors of growth hormone in the body working via this elaborate feedback system.
Summary of Stimulators of GH secretion include:
Peptide hormones , Growth hormone releasing hormone (GHRH also known as somatocrinin) through binding to the growth hormone releasing hormone receptor (GHRHR) ghrelin through binding to growth hormone secretagogue receptors (GHSR) sex hormone increased androgen secretion during puberty (in males from testis and in females from adrenal cortex) estrogen , clonidine and L-DOPA by stimulating GHRH release, hypoglycaemia, arginine[8] and propranolol by inhibiting somatostatin release , deep sleep, fasting & vigorous exercise
Inhibitors of GH secretion include:
somatostatin from the periventricular nucleus circulating concentrations of GH and IGF-1 (negative feedback on the pituitary and hypothalamus), hyperglycemia, glucocorticoids
GH Secretion and signaling pathways
The most potent and non pharmaceutical stimuli of growth hormone secretion are deep sleep exercise, hypoglycaemia and the infusion of amino acids (Heynes 1986). Although Growth hormone is released in a pulsatile fashion during the day with surges of secretion occur at 3- to 5-hour intervals, it is generally and largely released during circadian rhythms within the same manner, in fact studies have shown evidence for the largest growth hormone secretion peaks after the first hour of sleep (Godfrey et al 2003) plus during recovery after exercise. The pulsatile release of hGH is also clinically important because it has been shown to be amplified during periods of linear growth (Nindl et al 2001).
The secretion of growth hormone is released from the somototroph before being circulated in the blood. This release mechanism is modulated principally by two hypothalamic hormones - somatostatin and growth hormone releasing hormone (GHRH). The hypothalamus controls growth hormone secretion by means of its own secretion of two peptides; somatostatin, which inhibits secretion, and growth hormone releasing hormone, which is stimulatory Both of these hormones reach the nearby anterior pituitary through local blood vessels.
The majority of GH is bound to GH binding protein (GHBP) which is a carrier protein before being taken up by particular GH receptors located on specific target cells. GH must exert some of its effects by this specific binding process because polypeptide hormones are not fat soluble therefore they cannot penetrate sarcolemma. Once GH is bound to its target cell it activates a second messenger.
Historically, the liver has been known as a major target organ for GH as this is the focal site for insulin like growth factor (IGF-1), which in past was also known as a somatomedin. As it happens GH stimulates the production of Insulin like growth factor (IGF-1). IGF is a polypeptide protein hormone produced by the liver as an endocrine hormone and targets tissues in a paracrine/autocrine manner. IGF-1 has growth stimulating effects on a large range of tissues. IGF primarily binds to specific IGF receptors. It has been suggested that that the liver is not the only source of IGF-1. In fact, IGF- 1 synthesized by extra-hepatic tissues can also exert GH-independent autocrine/paracrine effects in the local environment (Vijayakumar et al, 2009), for example IGF1 binds to specific IGF receptors present on many cell types in many tissues, such as the liver cells, adipose cells, lymphocytes, bone, and placental membrane.
Although outside of the scope of this small project it is realised that here is a large involvement of further signalling pathways of GH, therefore a diagram been included below with reference to this point.
The diagram illustrates the signalling pathways for GH, which have been investigated in human muscle and adipose tissue, with all bold lines indicating pathways which have been shown to be activated by GH and dashed lines illustrates pathways where GH have not yet been evidenced, these are therefore only possible pathways in the effect of this hormone.
IGF 1 controls the elaborate two way feedback mechanism by which one feedback mechanism directly loops back into the anterior pituitary, inhibits further release of HGH, whilst the second feedback mechanism impedes GH releasing hormone and somatostatin release from the hypothalamus.
Apart from its’ effects on growth and development, IGF-1 also has insulin like effects on metabolism Furthermore, IGF-1 negatively regulates GH secretion through feedback mechanisms thus, small changes of IGF-1 levels are often accompanied with altered GH levels and vice versa. (Vijayakumar et al ,2009) The physiologic relevance of these effects is not known but it has been postulated that the modest increase in IGF-I might enhance post-exercise reparative processes, or that increased IGFBP-1 might protect against delayed onset hypoglycaemia (Widdowson et al 2009).
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