will anabolic pump cause a dramatic increase in lean muscle growth or it is mainly for lipolysis. ive taken IGF-LR3 in the past and that gave me similar effects to what im reading about anabolic pump ..but i did not necessarily gain that much muscle while on IGF ..i became flat after i came off ..almost as if it were all smoke and mirrors..will this happen with anabolic pump?
The aesthetic effects may appear similar, but they are not physiologically similar compounds by any means.
IGF-1 is a polypeptide endocrine hormone, released in the presence of GH by the liver, in order to promote several intracellular processes. The so-called "carbohydrate utilization" from IGF-1 and other polypeptides results from IGF-1's powerfull activation of phosphatidylinositol 3-kinase [PI3K]-dependent Akt pathways. PI3K is part of a family of enzymes that are activated by hormones, cytokines, growth factors and so on. After being activated by IGF-1, PI3K causes the phosphorylation of Akt[2] to the membrane periphery, where it in turn phosphorylates several proteins which are involved in cell growth and function; most important to us weight-lifters, GLUT4 [glucose transport] and mTOR [protein synthesis]. Akt[2] is necessary for Insulin-induced translocation of GLUT4 to the plasma membrane of cells, and is one of three of a family of proteins that regulate cell function. By virtue of affecting the PI3K/Akt pathways, growth factors have a wide-range of physiological effects - including theoretical hyperplasia - not limited to glucose transport, and this is what separates them from Anabolic Pump.
Anabolic Pump, on the other hand, circumvents Insulin-Dependent pathways of glucose homeostasis, and instead causes increased phosphorylation of AMPk [adenosine monophosphate kinase]. AMPk, as it sounds, is a substrate of AMP [adenosine monophosphate] and is activated by a downstream messenger AMPkK [adenosine monophosphate kinase-kinase]. It is activated in response to a rising AMP:ATP ratio [AMP is produced in the consumption of ATP during skeletal muscle contraction]. The increased phosphorylation of AMPk by AMPkK also has a wide-range of intracellular effects, that are all adaptive mechanisms to meet energy demands. Phosphorylation of AMPk may inhibit lipogenesis, plasma triglyceride and cholesterol synthesis; induce lipolysis and the oxidation of fatty acids by regulating the PPAR family [controls coactivation and transcription factors] and their target genes [such as CPT-1 that controls b-oxidation of fatty acids]; as well as regulating the glycolytic processes glycolysis and increased expression of hexokinase II and translocation of GLUT4 to the plasma membrane of the cell. AMPK also regulates mTOR [protein synthesis] but not to the prominent degree it regulates glycolytic and lipolytic processes.
