Luft et al. (26) clearly demonstrated the glycaemic control to deteriorate following exposure to a single supraphysiological dose of human GH in hypophysectomised adults with type 1 diabetes mellitus. Somewhat surprisingly, only modest effects of GH on glucose metabolism were recorded in the first metabolic balance studies involving adult hypopituitary patients (27, 28). More recent studies on glucose homeostasis in GH deficient adults have generated results, which at first glance may appear contradictory. Insulin resistance may be more prevalent in untreated GH deficient adults (29, 30), whereas the impact of GH replacement on this feature seems to depend on the duration and the dose. Below, some of the metabolic effects of GH in human subjects, with special reference to the interaction between glucose and lipid metabolism, will be reviewed. Studies In Normal Adults Almost forty years ago it was shown that infusion of high dose GH into the brachial artery of healthy adults reduced forearm glucose uptake in both muscle and adipose tissue (31). This was parallelled by a drop in RQ and an increase in muscle uptake of FFA, both of which suggest oxidation of FFA by the muscle. This pattern was opposite that of insulin, and co-administration of insulin and GH resulted in only minimal changes in net fluxes of glucose and FFA across the forearm bed. These studies clearly indicated direct insulin antagonistic effects of GH on muscle and adipose tissue. The introduction of reliable radioimmunoassays for GH revealed the pulsatile and episodic nature of GH release (32) now known to be generated by alternating secretion of GHRH and SST. A GH pulse is released roughly every second hour with a mean daily secretion of 0.5 mg (33). Apart from a circadian variation in terms of elevated nocturnal GH levelsduring the early hours of sleep, GH secretion is amplified during fasting and stress, whereas meals suppress GH release. We studied the metabolic effect of a
Growth Hormone Rating: (1 being the lowest, 5 being the highest) Strength-4 Weight Gain-4 Fat Loss-4 Side Effects-2 Keep Gains--4 What HGH therapy can do: Reduce excess body fat, especially abdominal fat. (The reduction of abdominal fat is the single most profound effect of HGH replacement in many people.) Increase muscle mass (and physical strength if combined with moderate exercise). Reduce wrinkling of the skin and some other effects of skin aging. Re-grow certain internal organs that have atrophied with age. Increase bone density. Strengthen the immune system. Reverse cognitive decline. Stimulate production of the bone marrow cells that produce red blood cells. Reduce the probability that you will spend the last years of your life in a nursing home. HGH slows the progression of cardiovascular disease, and reduces the risk of death from cardiovascular disease, in individuals with natural growth hormone levels that are below average for the age of the individual. HGH can also slow the progression of cardiovascular disease by improving one's cholesterol profile. There is increasing evidence over the past year or two that maintaining healthy growth hormone levels results in a stronger heart. Individuals with low growth hormone levels have an overall increased risk of death due to cardiovascular disease. Low growth hormone levels cause a particularly large increase in the risk of stroke as compared with individuals receiving growth hormone replacement. Uses of HGH in sports and bodybuilding: (Minimum effective dosages seem to start at 4 I.U. per day). 1) Human growth hormone provides a potent anabolic effect; it builds muscle. Without turning this into a biochem lesson – especially since that’s way over my head – suffice to say that HGH increases the body’s ability to synthesize protein, and that this allows for muscle tissue to be built. Human growth hormone use produces the holy grail of all anabolic benefits, hyperplasia. Hyperplasia is the permanent increase in the amount of muscle
Drugs that can increase GH include: amphetamines, arginine, dopamine, estrogens, glucagon, histamine, insulin, levodopa, methyldopa, and nicotinic acid ect. The following is a chart adapted from Basic and Clinical Endocrinology, 5th Edition depicting other factors influencing the GH secretion spike: Factors Increasing GH Secretion: Factors Decreasing GH Secretion: Physiological: Physiological: Sleep Hyperglycemia Fasting Elevated Blood Free Fatty Acids Exercise Obesity High Amino Acids in the Blood Hyper or Hypothyroidism Low Blood Sugar Pharmacologic Pharmacologic Any hypoglycemic agent GH itself Estrogens Somatostatin Alpha-agonists Alpha antagonists (yohimbine) Beta antagonists Beta agonists (ephedrine, clenbuterol) Serotonin Serotonin antagonists Dopamine Dopamine antagonists GABA HGH and Exercise: Exercise Stimulates Natural HGH Production Regular exercise is the best way to naturally increase you HGH production and with weaker muscles, lower bone mass and less flexibility; therefore making stretching (like yoga) a part of your daily routine. Several studies have shown that exercise prolongs life, decreases heart disease, and lowers high blood pressure and stroke rates. Aerobic exercise is very important for maintaining a healthy vascular system, which is a central factor in longevity, vitality and health. (L-DIHYDROXYPHENYLALANINE) L-Dopa: Growth hormone releaser:
Keywords: Parkinson's disease; Levodopa; GH; Exercise INHIBITORY EFFECT OF CIMETIDINE ON L-DOPA-STIMULATED GROWTH HORMONE RELEASE IN NORMAL MAN A. ZANOBONI, G. GALMOZZI, S. MARINONI, WANDA ZANOBONI-MUCIACCIA SUMMARY Some evidence suggests the existence of a histaminergic influence on GH secretion in animals and man. We used cimetidine, a specific H2-receptor antagonist, to study the possible interference of H2-receptor blockade on plasma GH release by L-dopa and on PRL inhibition by L-dopa in normal man. Seven healthy normal male volunteers aged 23–36 years received a single oral dose of L-dopa (500 mg) or an i.v. bolus of cimetidine (300 mg) or both (L-dopa 30 min before cimetidine). Blood samples were taken at various times over 2 h and plasma GH and PRL levels measured. Cimetidine alone did not alter basal plasma GH values; L-dopa elicited the well-known GH releasing effect with peak values at 75 min (15.65 ± 2.8 ng/ml); cimetidine injected 30 min after L-dopa ingestion significantly blunted the GH response to L-dopa and peak values (4.7 ± 1.6 ng/ml) were delayed to 105 min. Cimetidine provoked a rapid rise in plasma PRL with the peak value of 15 ± 3 ng/ml at 15 min, followed by a return to near basal values in min. L-Dopa completely inhibited the PRL response to cimetidine. We conclude that there is an inhibitory influence of the H2-receptor antagonist cimetidine on GH release by L-dopa. This, together with the action of cimetidine on PRL secretion (with or without L-dopa), suggests a possible antidopaminergic effect of H2-receptor blockade at the level of the central nervous system.