My spring cut is going extremely well and I’m approaching the point where the fat that’s left to go is “stubborn fat”. This isn’t just a myth, not all fat is the same. But first a little general background on fat cells*.
All cells have little receptors sticking out from their surface (picture a ham riddled with cloves), kind of like how you have ears sticking out from your head. These receptors “listen” for “signals” from the body. The signals come in the form of molecules that are attracted by charge and snap into these receptors sending a cascade of chemical reactions into the cell.
The reaction I’m working to signal by controlling my environment (diet & activity) is to release the maximum possible amount of fat energy out of fat cells to fuel my metabolism. I’m also working to send my body the signal to prefer fat and NOT release energy from lean body mass (muscle loss), but that’s another post.
Some of the “loudest” molecules to signal the release of fat energy from fat cells are known as catecholamines (a group of hormones that include adrenaline). When these compounds snap into the fat cell’s receptors the resulting chemical cascade activates hormone sensitive lipase (and other compounds) inside fat cells, starting and driving a reaction in the cell that packages-up and moves fat out of the cell so the body can use it for fuel.
But here’s where it gets frustrating. Fat cells don’t only have receptors that drive the cell to release fat. They also have receptors that do the opposite, stop the cell from releasing fat. b2 receptors message for releasing fat, a2 receptors stop fat release (do note this is a great simplification). The proportion of b2:a2 receptors on fat cells is what determines how stubborn fat is to remove from the cell. If a fat cell has more a2 than b2 receptors then it’s a “stubborn” fat cell; the message to release fat can easily be drowned-out by the “louder” message to keep fat.
For those horrid a2 receptors a potent “do not lose fat” message comes from the presence of insulin (another hormone) snapping into them. This makes sense once you understand a little about insulin. Insulin is elevated in the presence of elevated food intake. It’s seems logical to me that the body should stop using fat for energy when you have food energy available. Recently there’s been a sharp rise of insulin nutrition mythology, but most of the insulin-fear-mongering out there seems to come from just misunderstanding the role this little wonder-hormone plays (here’s some great info on common insulin myths).
So to summarize here are two things that contribute interconnectedly to fat loss (FYI this is not the whole story):
- The magnitude & amplitude of the signal to mobilize fat; the amount of catecholamines and/or insulin present and the length of time their levels are elevated.
- How receptive fat cells are to this signal; how many and type of receptors are on the surface of the fat cells.
Obviously stubborn fat is the last to go when dieting. The amount and where you have stubborn fat is largely genetic. Men typically have it concentrated in the lower abdominal area & lower back, while women tend to carry it on their hips & thighs.
If you can’t change how much stubborn fat you have, what’s the most effective way to keep insulin low and catecholamines levels high? Don’t eat. Fasting minimizes the fat-loss-blocking a2-receptor activity due to more time spent in a low-insulin state. The catecholamine b2-receptor signal to release fat is therefore relatively maximized.
I’m using intermittent fasting, eating all my daily calories in an 8 hour window, fasting the other 16 hours. See more info here on this approach, here is another sound approach, and here’s a great review of several approaches to intermittent fasting.
I also try to add low impact steady state (LISS) activity when nearing the end of the fast. This could be a 45 min walk, a casual bike ride, even cleaning the house. It’s important not to work too hard, as higher intensity exercise will shift your metabolism away from using fat as a fuel. The LISS is mostly to drive more blood flow to those stubborn body fat areas, maximizing exposure to the catecholamine signals to release fat energy.
As I get down to the very last bit of stubborn fat, I may add a dose of yohimbine prior to my LISS. Yohimbine is a known a2-receptor inhibitor, increases blood flow, is very safe when used responsibly, and has a very short half-life.
So to summarize and list my tactics to tackle stubborn body fat, in order of effectiveness:
- Fast to minimize the “save-fat” a2-receptor activity due to more time spent in a low-insulin state.
- Do low impact steady state (LISS) activity near the end of my fast, when “lose-fat” b2-receptor messaging is most effective.
- Strategically dose supplements shown to aid in stubborn fat loss.
Most people won’t ever get down to the stubborn fat. The average guy needs to approach or even be under 10% bodyfat before stubborn body fat makes up the majority of what’s left. It’s also very important that the above is pretty much useless outside excellent fundaments; appropriate diet & training. But if you’re looking to go from pretty lean to truly shredded, the above is valuable information.
*disclaimer – I am but a humble but voracious enthusiast. I am not a medical doctor or biochemist. The above is my current understanding and is likely incomplete, but I am very confident it is accurate.