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Advanced Theories of Hypertrophy & Anabolism(Muscle Growth)
By Ross Erstling
By Ross Erstling
Exercise increases muscle protein synthesis and plasma levels of Follistatin, Interleukin-5, IGF-1, MGF, HGH, Testosterone, and androgen receptor sensitivity. Anabolic steroids increase follistatin expression.
EXERCISE itself seems to be the ultimate KEY to regulating plasma levels of growth factors(and their expression) in the body, which lends credence to the notion that more frequent bouts of exercise will induce greater hypertrophy(and hyperplasia) in a the enhanced athlete. OVETRAINING? No, just UNDER-eating and inadequate resting.
You must VARY the type of STIMULUS; heavy weight, light weight, higher rep and lower rep. Remember, every time that you EXERCISE you cause a CASCADE of accute biochemical and hormonal responses that increase hypertrophy. ONLY exercise can induce these changes, and it seems logical that if executed properly, with sufficient feeding and resting, the more you can exercise, the more you can increase muscle protein synthesis, Follistatin levels and expression, IGF-1 levels and expression, interleukin-5 levels and expression, androgen-receptor sensitivity and testosterone-uptake–which equates to signficantly greater hypertrophy.
Exercise Induces a Marked Increase in Plasma Follistatin: Evidence That Follistatin Is a Contraction-Induced Hepatokine
Jakob Hansen,
Claus Brandt,
Anders R. Nielsen,
Pernille Hojman,
Martin Whitham,
Mark A. Febbraio,
Bente K. Pedersen and
Peter Plomgaard
- Author Affiliations
The Centre of Inflammation and Metabolism (J.H., C.B., A.R.N., P.H., B.K.P., P.P.), Department of Infectious Diseases and Copenhagen Muscle Research Center, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 2100 Copenhagen, Denmark; Department of Oncology (P.H.), Copenhagen University Hospital Herlev, 2730 Herlev, Denmark; and Cellular and Molecular Metabolism Laboratory (M.W., M.A.F.), Baker International Diabetes Institute, Heart and Diabetes Institute, Melbourne, 3004 Victoria, Australia
Address all correspondence and requests for reprints to: Peter Plomgaard, Rigshospitalet, Centre of Inflammation and Metabolism, 7641, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. E-mail: [email protected], Centre of Inflammation and Metabolism.
Abstract
Follistatin is a member of the TGF-β super family and inhibits the action of myostatin to regulate skeletal muscle growth. The regulation of follistatin during physical exercise is unclear but may be important because physical activity is a major intervention to prevent age-related sarcopenia. First, healthy subjects performed either bicycle or one-legged knee extensor exercise. Arterial-venous differences were assessed during the one-legged knee extensor experiment. Next, mice performed 1 h of swimming, and the expression of follistatin was examined in various tissues using quantitative PCR. Western blotting assessed follistatin protein content in the liver. IL-6 and epinephrine were investigated as drivers of follistatin secretion. After 3 h of bicycle exercise, plasma follistatin increased 3 h into recovery with a peak of 7-fold. No net release of follistatin could be detected from the exercising limb. In mice performing a bout of swimming exercise, increases in plasma follistatin as well as follistatin mRNA and protein expression in the liver were observed. IL-6 infusion to healthy young men did not affect the follistatin concentration in the circulation. When mice were stimulated with epinephrine, no increase in the hepatic mRNA of follistatin was observed. This is the first study to demonstrate that plasma follistatin is increased during exercise and most likely originates from the liver. These data introduce new perspectives regarding muscle-liver cross talk during exercise and during recovery from exercise.
