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Introduction
Lots of bodybuilders use Insulin and it may seem complicated at first but i will simplify it
Also don't be afraid of going hypo, that only happens if you're making dumb decisions
Insulin Secretion
Insulin is a peptide hormone that contains two chains of amino acids that are connected by 2 disulfide bridges. It is secreted by pancreatic β cells in response to blood glucose levels changing from protein/carbs and is used by the body to regulate the glucose.
Once blood glucose rises, insulin is secreted from the β cells in the pancreas, this insulin then binds to insulin receptors on the outside of cells in the liver, skeletal muscle and adipose tissue. The IRs have two subunits, one being the outer alpha subunit that binds the hormone and the transmembrane beta subunit which is an insulin stimulated tyrosine specific protein kinase.
Intake of carbs → blood glucose rises → pancreatic β cells sense the increase in glucose and GLUT1 and GLUT3 transporters allow glucose into the cell → elevated ATP/APD ratio inhibits ATP sensitive potassium channel → depolarization that leads to calcium gates ion channels to open allowing a large influx of calcium into the cell → calcium interacts with the insulin containing vesicles and translocates them to the membrane → insulin secretion into blood
Biosynthesis of Insulin
Insulin is first introduced in the β cells of the pancreas as preproinsulin which is a 110 amino acid chain that is inactive. This is then brought to the rough endoplasmic reticulum where the signal peptide is removed from the N terminal via signal peptidase. The result of this and the folding of the protein in the RER creates proinsulin which is then transported into the golgi apparatus. In the golgi the proinsulin is packaged into secretary vessels and the c peptide is destroyed by pro protein convertase 1 and 3 and protein convertase 2. Then the proinsulin has 2 pairs amino acids cut off the ends via carboxypeptidase E which results in active insulin
Preproinsulin → Proinsulin (RER) → Transported to golgi (c peptide removal/secretary vessels) → active insulin with two disulfide bonds
Mechanisms on Muscle/liver/adipose tissue
Muscle
Insulin binds to the insulin receptor that autophosphorylates upon binding. From here PI3K gets phosphorylated and then helps formation of PIP. The PIP activates AKT via downstream cascade. AKT activates mTOR which leads to protein synthesis. AKT also makes the GLUT4 vesicles migrate to the cell membrane causing a large uptake of glucose into the muscle cell resulting in increased glycogen stores. Insulin inhibits GSK3, normally GSK3 keeps glycogen synthase off but by inhibiting it glycogen synthesis is able to commence thus leading to more glucose molecules being added to glycogen particles.
Increased glycogen stores result in a lot more water retention in the muscle. Each gram of glycogen binds to ~3g of water so naturally higher glycogen stores means more water retention which equates to bigger muscles. Is anti catabolic as well by keeping mTOR activated. Increased eNOS levels means more vascularity which is perfect for pumps
Adipose
Insulin is used in adipocytes for fat storage and inhibits lipolysis. Adipocytes do not express the glycerol kinase gene and depend on glycolysis for glycerol 3 phosphate. G3P is made when the G3P dehydrogenase acts on glycolytic intermediate and glyceraldehyde 3 phosphate. Also glucose → acetyl-CoA conversion allows for fatty acid synthesis. Only 5% gets stored as glycogen and the rest is used for fatty acid synthesis.
This is why when you're using insulin you want to keep dietary fats low so that those fats don't build up in your adipocytes excessively
Liver
Insulin induces glycolysis and lipogenesis in the liver to be used for energy through glycolytic enzymes. Firstly the insulin binds IR on hepatocytes and then activates AKT, the activated AKT then activates PDE3B and that then reduces cAMP which reduces PKA. The decreased PKA leads to dephosphorylation of pyruvate kinase and PFK2, the active PFK2 creates fructose 2,6 bisphosphate which activates PFK1. F2,6BP inhibits F1,6BP which inhibits gluconeogenesis. Glycolysis is increased and glucose 6 phosphate activity decreases this decreasing glucose output.
Reducing cAMP and increased phosphoprotein phosphatase deactivate glycogen phosphorylase and activate glycogen synthase thus adding to glycogen stores
When glycolysis is promoted the glucose is converted to pyruvate which then enters the mitochondria and goes through the pyruvate dehydrogenase complex and turns into acetyl-CoA which is then used for fatty acid synthesis which are then used for lipids
Insulin IR binding → AKT activation → PDE3B activation → reduced cAMP levels → dephosphorylation of PKF2 and pyruvate kinase → those two get rendered active/increased activity → PFK2 converts fructose 6 phosphate into fructose 2,6 bisphosphate → f26bp activates glycolytic enzyme, PFK1 and reduces gluconeogenesis via inhibiting of f16bp and also phosphatases PP1 → Increase in glycolysis
Glucose conversion to pyruvate → pyruvate dehydrogenase complex in mitochondria → acetyl-CoA for fatty acid synthesis
This basically makes energy stores for your body and they get used for when you exercise. However, excessive lipogenesis can lead to fat gain.
Insulin Types
For this section I will go over one brand of insulin for each type and discuss the ideal way to use them. Dosing varies so I will be using example dosages so you get the idea of when to use them. You should figure out what dose is best for you via your carb/iu ratio + Insulin sensitivity
Rapid acting → Short acting → Intermediate acting → Long acting
Humalog
Rapid acting insulin that has an onset of 10-15 minutes, peak effect at 1-2 hours and duration of 2-4 hours. For example, pin 4iu humalog 10-15 minutes before your pre workout carb load, workout and have your intra workout fast acting carbs on deck. Crazy pump inbound
Novolin R
Onset is 30-60 minutes, effects peak around 2-4 hours and the duration lasts roughly 5-8 hours. Rule of thumb is 10-15 carbs for every 1 iu of insulin. For example, 10iu pre workout eat your carbs roughly 30 minutes after you pin, have your intra workout carbs, 10iu post workout + meal to shuttle glucose and amino acids to myocytes
Novolin N
Onset of 1-2 hours, peak effects at 4-8 hours and duration of 12-18 hours. For example, 15-25iu in the morning with breakfast
Lantus
Long acting insulin that is best taken in the morning with your first meal. Has no peak effect and lasts roughly all day so you would pin this once. For example, 15-25iu in the morning and then make sure to eat a consistent carb amount
Bodybuilders usually use rapid acting slin to shuttle all that nutrients into muscle very quickly. Another thing, make sure your pre workout meals have the right amount of potassium and sodium
Hypoglycemia
This is low blood glucose and many people are reasonably scared of it because it can be fatal. Other side effects include clumsiness, trouble speaking, confusion, feeling of hunger, seizures, sweating, weakness, loss of consciousness.
Make sure you have a fast acting glucose source on hand like glucose tablets and make sure to measure your blood glucose
Conclusion
Insulin is nice and anabolic, anti catabolic and can get you some nice pump pics
Second thread coming soon —------------->
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@saccharinesaint @xorsizm @copevictim @Dearpleasehelpme @submissivechud @giga.mia
I fucking struggled making this tbh
