Insulin drives nutrients into cells, it maintains muscle-promoting anabolism for lean gains, it drives prostaglandin output to influence recovery rate from training, it influences nitric oxide regulation and, yes, insulin efficiency keeps the thermogenic fat cells involved in fat elimination in the ON position.
Insulin resistance is common amongst us but most people battling this compromised insulin and metabolic state don’t know it. A compromised reaction by the insulin responsive cells (muscle cells) of the body due to desensitization by these cells forces the pancreas to pump out more insulin to compensate for the desensitized state. In the insulin resistant state, blood sugar and other nutrients can accumulate in blood to induce oxidation and damage to tissues. The body responds to this compromised signaling by pumping out more insulin than normal to clear sugar and other nutrients from blood where they can cause harm.
When insulin levels are elevated beyond healthy levels, an enzyme called the COX enzyme is accelerated to increase the amounts of PGE2 in the body. PGE2 is a pro-inflammatory autocrine hormone; it’s the hormone we block when we use COX-inhibitors like aspirin (ASA) to counter inflammatory pain and swelling.
Research now shows irrefutably that insulin inefficiency generates a proportional increase in downstream prostaglandins (namely PGE2) that can block the signal to thermogenic cells. Each meal then prompts an elevated insulin response, and in turn an elevated prostaglandin hormone state that creates an inflammatory cloud throughout the body. Interestingly, each of us lives with differing degrees of insulin efficiency which dictates how these downstream metabolic activities work for us. In conjunction with thyroid activity, these factors influence metabolic rate, shape our body and even influence mind and workload needed to reach our physique goals.
The inflammatory hormones that rise out of insulin’s influence interfere with your natural adrenergic activation of brown fat cells by blocking norepnephrine’s signal on the brown fat cell membrane surface. Inflammation turns down your thermogenic fat furnaces. It is this PGE2 activity that is blocked when one uses a non-steroidal anti-inflammatory drug like ASA as part of the ECA stack.
This elevated subclinical inflammation created by a lower insulin efficiency also interferes with recovery from training, increasespost workout soreness, and ultimately results in slower lean muscle gains. It also reduces your ability to resist and quickly recover from muscle and joint strains. Research shows that this underlying inflammation is even a factor that ages us prematurely.
In this insulin inefficient state, every mouthful of food triggers an insulin response that is conducive to fat accumulation at multiple compounding levels beyond thermogenic shut down. Insulin is pretty much a ‘storage’ hormone so it tends to quickly push energy substrates from blood into cells for storage. Unhealthy elevation of insulin in response to the meal in the presence of those muscle cells that cannot respond fast enough to insulin’s signal increases the chance of dietary nutrients reaching fat stores before they can be used for anabolism by muscle cells.
If the cells that make up your lean muscle mass are desensitized or simply less sensitive to insulin’s signal than your leaner, more muscular buddy’s, then your attempts to feed your lean muscle mass building blocks through protein-rich nutrition are simply delivering less than maximum results. In other words, the gateways on the cell membranes of your lean muscle cells may not be opening fast enough and wide enough to allow these building blocks to enter the cells and saturate them. The consequence is the cells gasp for more nutrition to recover from your workload, and the liver has to convert and then shuttle the precious nutrients to fat stores.
There are additional biological factors to compound fat accumulation when the metabolism is altered by this desensitization to insulin. That compromised reaction by the insulin responsive cells (muscle cells) of the body forces the pancreas to pump out more insulin to compensate for the desensitized state of the cells. The nutrients have no where to go but to storage as fat. Research also shows that this excess insulin, itself, is converted to triglycerides (fat) as the body engages in an effort to remove the dangers that the elevated insulin response represents to the body.
Multiple metabolic prompts cause dietary nutrients and calories to be shuttled to fat storage if insulin efficiency is compromised. The body becomes so inefficient that these fat-burning brown fat cells eventually start acting like white adipose fats cells to store more fat when their primary design is to help you burn away fat! The amount of work you need to do in the gym to put on mass and keep lean might just be proportional to this state of insulin efficiency.
Many resort to using aggressive thermogenic activators like the ECA (Ephedrine Caffeine Aspirin) stack when all else fails to keep that unwanted layer fat off. Again, the reason for the ASA is to reduce levels of that prostaglandin hormone so that the adrenergic activity of ephedrine (E in the ECA stack) can do its brown fat-activating job. You cant stay on theECA stack indefinitely or cardiovascular health risks will become a reality. BUT what happens when you stop using the stack? REBOUND!!
Typically when on the rebound fat starts to accumulate with a torturous momentum because the metabolism has not been reset by this incomplete ECA stack to maximize insulin efficiency. If insulin efficiency were to be optimized the ECA stack wouldn’t be necessary or required again after the initial fat loss goal was achieved. RESETTING the metabolism with an insulin reset keeps the metabolism running lean.
Although multiple hormones and biological systems (thyroid/thyroxin, cortisol, insulin, steroid hormones) in the body contribute to or regulate metabolic rate, anabolic efficiency and thermogenesis, insulin works much like the primary gear in your car influencing a plethora of downstream endocrine and autocrine hormones. Insulin efficiency
also cycles back to influence how these other modifiers of metabolism effect the fat mass and lean mass management.
Your state of insulin influences how dietary nutrients such a protein, fat and carbs are used and stored. It also has a lot of influence over how much protein is used to make muscle and how much gets turned back for conversion to glycogen or fat.
Although degrees of insulin resistance that might be dysfunctional are more likely to cripple the metabolism when we’re older ( > 30 yrs old), each of us has a metabolism that idles at slightly different rates based on how sensitive your cells are to insulin’s and thyroxin’s signal and how effective the pancreas and the thyroid are at producing the hormones on demand.
Fine tuning insulin efficiency to amplify the signal even slightly will maximize results from thermogenic supplements, anabolic agents and promote long term fat management and lean muscle preservation.
author: Prof Franco Cavaleri BSc NB; Mr IFBB North America