Action of GH on skeletal muscle function: molecular and metabolic mechanisms.

نویسندگان

  • Viral Chikani
  • Ken K Y Ho
چکیده

Skeletal muscle is a target tissue of GH. Based on its anabolic properties, it is widely accepted that GH enhances muscle performance in sports and muscle function in the elderly. This paper critically reviews information on the effects of GH on muscle function covering structure, protein metabolism, the role of IGF1 mediation, bioenergetics and performance drawn from molecular, cellular and physiological studies on animals and humans. GH increases muscle strength by enhancing muscle mass without affecting contractile force or fibre composition type. GH stimulates whole-body protein accretion with protein synthesis occurring in muscular and extra-muscular sites. The energy required to power muscle function is derived from a continuum of anaerobic and aerobic sources. Molecular and functional studies provide evidence that GH stimulates the anaerobic and suppresses the aerobic energy system, in turn affecting power-based functional measures in a time-dependent manner. GH exerts complex multi-system effects on skeletal muscle function in part mediated by the IGF system.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Responses of Muscle Mitochondrial Function to Physical Activity: A Literature Review

Skeletal muscles play an active role in regulating the metabolic homeostasis through their ability for relating to adipose tissue and endocrine hormones. Contraction of the skeletal muscle leads to increased release of several myokines, such as irisin, which is able to interact with the adipose tissue. Physical activity promotes the irisin mechanism by augmenting the peroxisomes (PGC1-α) in the...

متن کامل

Growth hormone regulation of metabolic gene expression in muscle: a microarray study in hypopituitary men.

Muscle is a target of growth hormone (GH) action and a major contributor to whole body metabolism. Little is known about how GH regulates metabolic processes in muscle or the extent to which muscle contributes to changes in whole body substrate metabolism during GH treatment. To identify GH-responsive genes that regulate substrate metabolism in muscle, we studied six hypopituitary men who under...

متن کامل

Effects of ionic parameters on behavior of a skeletal muscle fiber model

All living cells have a membrane which separates inside the cell from it's outside. There is a potential difference between inside and outside of the cell. This potential difference will change during an action potential. It is quite common to peruse action potentials of skeletal muscle fibers with the Hodgkin-Huxley model. Since Hodgkin and Huxley summarized some controlling currents like inwa...

متن کامل

Biomonitoring the skeletal muscle metabolic dysfunction in knee osteoarthritis in older adults: Is Jumpstart Nutrition® Supplementation effective?

Background: This study aimed to investigate the efficacy of Jumpstart Nutrition® dietary supplement (JNDS) for enhancing the skeletal muscle metabolism and function of older adults with knee osteoarthritis (KOA) by evaluating the biomarkers of aberrant levels of serum tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), C-reactive protein (CRP), creatine kinase-muscle (CK-MM), and aldol...

متن کامل

Myostatin is a skeletal muscle target of growth hormone anabolic action.

Myostatin is a cytokine that has recently been shown to selectively and potently inhibit myogenesis. To investigate the mechanisms of anabolic actions of GH on skeletal muscle growth, we examined the in vitro and in vivo effects of GH on myostatin regulation. Twelve GH-deficient hypopituitary adult subjects were treated with recombinant GH (5 micro g/kg.d) in a double-blind, placebo-controlled ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Journal of molecular endocrinology

دوره 52 1  شماره 

صفحات  -

تاریخ انتشار 2014