IGF-1 LR3 is a polypeptide chain that is comprised of 83 amino acids. It has a molecular structure of C990H1528N262O300S7, and it contains a molecular mass of 9200. It is sometimes known as Long r3 igf-1, and can occasionally gets confused with the peptide chain Long r2 ifg-1 because it has a similar molecular build and structural property.
IGF-1 LR3 at a Glance
Scientific study that has been based on animal test subjects has indicated that IGF-1 LR3’s basic functionality can be linked to two bodily organs; the pancreas and the liver. More to the point, its overall operation mechanics can be broken down to a secretion level, as it has been shown that it specifically works in conjunction with the following two secretions:
- Insulin – This peptide hormone, which is secreted by the beta cells of the pancreas, is essentially responsible for ensuring that cells in the liver, skeletal muscles and fat tissue absorb glucose from the bloodstream properly.
- IGF–1 – Also known as Insulin-like Growth Factor-1 or Somatomedin C, this liver-secreted peptide hormone is shown to be highly reactive in its nature. What this means is, its expression is responsible for promoting the construction and repair of various muscular and skeletal tissues throughout an animal test subject’s body through a series of chemical reaction of complex molecules.
It has been shown that IGF-1 LR3’s relationship with insulin is that it has the ability to boost the transport of the secretion through the bloodstream. This enables the secretion to interact on a cellular level within an animal test subject on a far more efficient basis. This would include the liver, the organ that secretes IGF-1. The problem with IGF-1 and its reactive tendencies is that they do not last all that long. Scientific study based on animal test subjects has determined that this particular secretion has a rapid half-life of just around 20 minutes. This causes the peptide to have a very limited effectiveness. However, it has been shown that IGF-1 LR3 has the capacity to boost this half-life in dramatic fashion; extending it to over a period of 20 days. This extended half-life, when paired up with the peptide’s ability to boost the rate of insulin transport, can lead to a host of boosted processes. Some of these boosted processes include an increase in RNA synthesis, and increase in protein synthesis, an increase in glucose transport, and an increase in amino acids to cells. Furthermore, its abilities also have been shown to cause a decrease in protein degradation, thus making its properties of synthesis even stronger.
Benefits Tied to IGF-1 LR3
The relationship that IGF-1 LR3 has with insulin and IGF-1 and the elevated processes that it can cause has led scientific study based on animal test subjects to determine that the peptide can be linked to host of hypothetical benefits. The first of these benefits relates to an increase in muscle retention. Because IGF-1 LR3 has been shown to boost the half life of IGF-1, it is thought that the reactive effects that are associated with the secretions can also increase. This has led to the notion that these heightened effects can cause an animal test subject to maintain and preserve its muscular shape and tone at a substantially more efficient rate. Another benefit that is associated with this boost in half-life pertains to the notion of increasing the rate of recovery from a muscle or skeletal-related injury. Because IGF-1’s reactive nature has been shown to play a role in muscle and skeletal repair, it is thought that IGF-1 LR3’s ability to extend the functionality of the secretion’s effectiveness could lead to an animal test subject’s overall healing processes to improve. Further studies have indicated that the presence of IGF-1 LR3 can lead to a boost of endurance. The rationale behind this concept stems from its ability to boost protein synthesis and prohibit protein degradation. It is thought that these dual processes can enable an animal test subject to experience a more consistent level of performance for a longer period of time before the negative effects of fatigue manifest.