Part 1: What Happens To Your Body When You Fast? – Energy Production
Today, we Skribit. The question of the day, with 184 votes, is a very interesting one. It is:
Physiological processes during fasting
As you know, I’m a big fan of intermittent fasting, but this is an area of it that I’ve never really looked at. I’m going to break this into several posts because there’s a lot going on here and I don’t want to burden everyone with a novella. Today, we’ll look at how the body handles energy production during the fasting period, a good starting point given that, when you get down to it, an energy source and water are the only two requirements for the body to operate.
First things first, let’s define fasting. A simple timeline showing the various states of the body will be useful here (baseline is the end of the previous meal):
- Up to about 3 hours: the “fed” state
- From 3 to about 12-18 hours: the “postabsorptive” or “early fasting” state
- Up to about 2 days: the “fasting” state
- Beyond 2 days: “starvation” state or “long-term fasting”
We know what happens in the “fed” state. The body is digesting the food consumed in the previous meal, generating energy from the carbohydrates and fats ingested and depositing excess as stored glycogen and fat. Where our interest today lies is in what happens after those three or so hours of digestion and energy storage.
So let’s turn our attention to what goes on from about 3 hours post-meal onward. At a base level, the body begins digging into stored forms of energy to supply its needs. The three forms of stored energy in the mammalian body are glycogen, amino acids (protein), and adipose tissue (fat).
I’m sure I’m not surprising anyone here by noting that the body stores glycogen. Glycogen is a polysaccharide form of glucose, stored in both the liver and in the muscles. Due to the lack of the glucose-6-phosphatase enzyme, muscle glycogen is only available to the muscle in which it is stored (i.e., the biceps cannot tap into the glycogen stored in the triceps or the calves), but liver glycogen is readily available to any body cells. The brain is a prodigious consumer of glucose, gobbling up nearly 60% of the body’s blood sugar.
After digestion, the liver begins releasing its stored glycogen to the body for use in running the brain and other systems. A study in rats showed a marked decrease in liver glycogen (see Table 3) during a 24-hour fast. In fact, rats on a normal ad libitum feeding schedule showed a more than 100-fold difference in liver glycogen stores (138.4 mg vs 1.3 mg for the fasted rats). Muscle glycogen is also somewhat depleted during a fast as glucose is used to fuel daily activity. Simple 24-hour fasting, without inducement of exercise to deplete muscle glycogen, brought muscle glycogen down by about 50%.
In humans, just the overnight fast of sleeping is enough to nearly deplete liver glycogen. That big brain doesn’t stop working and sucking up glucose just because you’re unconscious.
When the body runs out of glycogen in the liver to fuel the brain, it turns to amino acids. Through the process of gluconeogenesis, the liver breaks down these proteins to create glucose. Before the bodybuilders in the crowd pass out at the thought of losing a single ounce of their hard-earned muscles, the interesting thing here is that the body isn’t necessarily using muscle proteins at this stage. The liver is able to meet most of its glucose needs by recycling lactate and alanine.
Around the eighteen hour mark, when we move into the “fasting” state, muscle proteins become the chief source of amino acids to fuel gluconeogensis. The breakdown of fat stores through lipolysis (next section) also provides glycerol, which the liver converts into glucose. While I can’t find anything on this, I don’t think a bit of muscle protein breakdown is necessarily a bad thing, so long as your lifestyle is typically anabolic. I’d think that allowing the muscles to consume worn out proteins allows for better rebuilding of new muscle fibers, clearing out cellular junk. I may also be completely out in left field (Anyone have anything on this? Bueller? Bueller?).
To continue this ramble, another interesting thing is that not all amino acids are broken down for glucose. Some are known as ketogenic amino acids. In humans, the two aminos that are always converted to energy through ketogenesis are leucine and lysine. Threonine, isoleucine, phenylalanine, tryptophan, and tyrosine can go either way, being broken down for either ketones or glucose as needed.
I, and many others around the CrossFit and Performance Menu forums, have found an increase in muscle mass and a decrease in fat mass during our experiments with fasting. I have to wonder if a low-carb diet with fasting versus a typical high-carb diet with fasting has any effect. Low-carb diets tend to be protein-sparing. While the body still needs glucose, the increased protein intake on a low-carb diet supplies the necessary amino acids to generate adequate glucose.
Lipolysis is the process of mobilizing fat from the body’s adipose stores for breakdown into usable energy. There are essentially five main hormones controlling this process: epinephrine, norepinephrine, glucagon, and adrenocorticotropic hormone (ACTH), along with insulin. Insulin is the great regulator; as we know from our biochemistry textbook (or from Good Calories, Bad Calories), when insulin is up, fat mobilization is down. The other four hormones are lipolysis inducers.
First, let’s look at the regulator, insulin. During fasting, insulin drops due to the lack of incoming calories from the gut. Along with that, blood glucose levels decrease to baseline. With no influx of glucose and fatty acids coming from the gut, there is no need for the storage hormone.
What about the other four hormones, the ones stimulating lipolysis? We see an increase in ACTH, along with an increase in cortisol, at least in Ramadan-style fasting of eating breakfast before sun-up and dinner after sun-down with nothing in between, a fast of approximately 13-14 hours. We also get an increase in epinephrine, further driving lipolysis. Norepinephrine is much less potent in stimulating lipolysis than is epinephrine and from what I’ve found, levels of norepinephrine don’t appear to change much during fasting.
Throughout the animal kingdom, fasting increases glucagon levels. It happens in humans (Page 242). It happens in rats. The garden warbler, a bird (and therefore, not a mammal), also sees an increase in glucagon during fasting. That means absolutely nothing to two-legged, non-flying mammals like ourselves, but it is interesting that Nature uses similar mechanisms throughout its branches to alleviate the same issues.
The really exciting part of this is that we’re seeing these hormonal changes around 12-14 hours of the fasting period. Once the body has digested and stored or burned the previous meal, it begins cranking up other methods of meeting its energy needs. I think this is why so many are seeing positive effects from regular fasts of 15-24 hours. The body uses all of its energy systems, taps into stored fat, and never gets too much time to tear into the muscles. As I understand it though, these short fasts don’t allow the body to get fully into ketosis with a full switch to lipolysis for energy. Again though, I wonder how a low-carb diet affects the rate at which the body turns up the lipolysis.
I’ve tried to simplify this to a level that both you and I can understand. I’m not 100% sure that I digested what I read and spit it back out entirely correctly. If I’m off on something, please correct me. What did I miss? What questions does this generate?