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Caloric restriction dramatically reduces serum levels of IGF-1 yet at the same time increases GH release. This mechanism effectively helps the individual adapt metabolically without having anabolic actions which would potentially hasten death by starvation. It is important to understand that GH can either be anabolic or catabolic. When nutrient intake is high, GH secretion is increased leading also to increased levels of IGF-1, IGFBP3 and insulin. The main role of GH under these conditions is to increase anabolism through local growth factors like IGF-1 and insulin. Conversely, when nutrient intake is low, GH is again increased. But this time there is no concomitant increase in IGF-1, IGFBP3, or insulin. Under these circumstances GH is acting as a catabolic hormone increasing the utilization of fat for fuel thus sparing body glucose yet having no muscle building effects. This behavior of the GH/IGF-1 axis is part of what makes it so difficult to build muscle while dieting. It should be noted that locally produced IGF-1 in skeletal muscle responds normally to training while dieting. This makes heavy poundages a must when trying to get ready for a show without the use of drugs.
The Somatomedin hypothesis states that GH is released from the pituitary and then travels to the liver and other peripheral tissues where it causes the synthesis and release of IGFs. IGFs got there name because of there structural and functional similarity to proinsulin. This hypothesis dictates that IGFs work as endocrine growth factors, meaning that they travel in the blood to the target tissues after being released from cells that produced it, specifically the liver in this case. Indeed, many studies have followed showing that in animals that are GH deficient, systemic IGF-1 infusions lead to normal growth. The effects were similar to those observed after GH administration. Interestingly, additional studies also followed that showed IGF-1 to be greatly inferior as an endocrine growth factor requiring almost 50 times the amount to exert that same effects of GH (Skottner, 1987). Recently rhIGF-1 has become widely more available and is currently approved form the treatment of HIV associated wasting. This increased availability allowed testing of this hypothesis in humans. Studies in human subjects with GH insensitivity (Laron syndrome) has consistently validated the somatomedin hypothesis (Rank, 1995; Savage, 1993).
The second theory as to how GH produces anabolic effects is called the Dual Effector theory (Green, 1985). This theory states that GH itself has anabolic effects on body tissues without the need of IGF-1. This theory has been supported by studies injecting GH directly into growth plates. Further evidence supporting this theory lies in genetically altered strains of mice. When comparing mice who genetically over express GH and mice who over express IGF-1, GH mice are larger. This evidence has been sited by some to support the dual effector theory. Interestingly, when IGF-1 antiserum (it destroys IGF-1) is administered concomitantly with GH, all of the anabolic effects of GH are abolished.
During puberty there is a disruption in your body’s ability to accurately regulate GH levels leading to increased GH, IGF-1, and insulin levels. This combined with elevated testosterone production characterizes puberty. Research has shown that this disruption is caused by the aromatization of testosterone as well as some direct actions of androgens.4,5,6,7,8 In a recent study by Fryburg9 the effects of testosterone and stanozolol were compared for their effects on stimulating GH release. Testosterone enanthate (only 3 mg per kg per week) increased GH levels by 22% and IGF-1 levels by 21% whereas oral stanozolol (0.1mg per kg per day) had no effect whatsoever on GH or IGF-1 levels. A couple of notes about this study. It was only 2-3 weeks long and although stanozolol did not effect GH or IGF-1 levels, it had a similar effect on urinary nitrogen levels. Urinary nitrogen is fraught with confounding variables when used to determine skeletal muscle anabolism and/or catabolism and thus should not be considered an accurate indicator of skeletal muscle growth. Using labeled tracer amino acids as well as 3-methylhistidine is a far more reliable way of determining actual contractile protein synthesis and breakdown respectively. Nevertheless, this study may well explain the observation that many bodybuilders do not respond as well to testosterones with complete estrogenic blockade.
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