IGF1 and Muscular Development
Growth hormone goes from the pituitary gland to the liver and that stimulates the production of insulin-like growth factors which are polypeptide protein hormones known as (IGFs). There are a number of varieties, the various IGFs, IGF1 weightlifters are most interested in because it's anabolic, muscle-building effects. It is comprised of 70 different inter-connected amino acids and is produced when growth hormone levels in the bloodstream rise, increasing the production of binding proteins. IGF1 is known to be the mediator of growth hormone anabolic effects. The interconnected relationship between IGF1 and growth hormone is referred to as the Growth Hormone/IGF1 Axis.
The growth of the skeletal muscle cells (hypertrophy) is mostly regulated by at least three identified processes,
satellite cell activity
, gene transcription,
protein translation.
IGF1 can influence the 3 above mechanisms. Research has shown that an increase of IGF1 in the bloodstreams spurs growth and regeneration by the body’s cells particularly among skeletal muscle cells, where it is shown to positively impact muscle strength, size and efficiency. Specifically, it contributes to skeletal muscle growth (hypertrophy) by provoking the synthesis of protein while helping to block muscle atrophy.
Other cells that are affected by IGF1 include cartilage, liver, kidney, skin tissue, lung, nerve and bone. IGF1 deficiencies can result in stunted growth and many of other health problems. Because it can activate insulin receptors, IGF1 has the ability to enhance insulin’s effects on muscle development. Because IGF1 levels are tied to growth hormone levels, lower levels of growth hormone in the bloodstream correlate to similar reductions in the production of IGF1. Growth hormone, IGF1 production peaks during childhood and adolescence and declines as we get older.
We know that muscle cells get bigger and stronger because of the result of their capacity to continuously adapt to the stress of resistance training with weights. To accomplish this feat it is attributed to muscle precursor cells that reside in and around skeletal muscle cells. These cells are often called satellite cells. These cells are dormant until they are called into duty by hormones such as IGF1.
When activated by IGF1 the cells divide and become genetically similar to those found in skeletal muscle cells. This is known as differentiation. Once the satellite cells’ nuclei become similar to those of skeletal muscle cells they become critical to muscle growth and development. This is because skeletal muscle cells must increase their number of nuclei in order to grow larger and repair themselves. The larger the muscle, the more nuclei it requires.
IGF1 also interacts with a number of different stress-activated proteins that help in the muscle cells that maintenance, repair and growth. When IGF1 binds with these various protein receptors it stimulates a host of biological processes that contribute to and regulate muscle cell growth and development.
There are a number of strategies to stimulate production of IGF1 in your body. Because it stimulates a strong hormonal response, resistance training with weights will boost production of IGF1. In particular, it induces its most potent anabolic state in skeletal muscle cells during the intense physical stress generated by heavy weight lifting. This is due in part to the fact that lifting heavy weights stimulates the production of growth hormone, which in turn signals the liver to produce IGF1.
Nutrition has a very strong effect on the body to make IGF1. IE, a regimen that includes occasional fasting combined with periods of undereating has been shown to have a positive impact on the body’s production of IGF1. Carb intake has a influence on IGF1 production. Evidence shows that carb intake should be minimized to one meal per day or immediately after an exercise session. It is important to maintain enough calorie intake and increase omega-3 fatty acids. Omega 3 not only enhances anabolic actions but it also assists in protecting against insulin resistance.