Calorie Partitioning
by Lyle McDonald
Introduction: The following is a chapter excerpt from my Ultimate Diet 2.0, dealing with calorie partitioning. It deals with what controls where calories go when you eat them, and what determines where they come from when you diet. If you read my previous article on AMPk: Master Regulator, it may explain some of the underlying physiology for what's discussed in this chapter. Of course, the rest of the book details an integrated system of nutrition and training to take advantage of this information, to make sure that you pull calories out of fat cells when you diet, and put them back into muscle when you overfeed; with the goal of losing fat while maintaining or gainin muscle at the same time.
Chapter 4: Why is it so hard (Part 2)
Partitioning
At a very fundamental level, the problem natural bodybuilders and athletes have is one of partitioning. At its simplest, partitioning refers to where the calories go (into muscle or fat cells) when you eat more of them or come from (from muscle or fat cells) when you eat less of them.
In an ideal universe, every calorie you ate would go to muscle tissue, with none going into fat cells; you'd gain 100% muscle and no fat. In that same ideal universe, every calorie used during dieting would come from fat stores; you'd lose 100% fat and no muscle. Unfortunately, we don't live in an ideal universe.
As I mentioned early in this book, some hapless individuals will lose as much as one pound of muscle for every 2-3 pounds of fat that they lose when they diet. Typically, those same individuals will put on about the same amount of fat and muscle when they gain weight. Thus is the balance of the universe maintained. More genetically advantaged individuals tend to put more calories into muscle (meaning less into fat) when they overeat and pull more calories out of fat cells (and less out of muscle) when they diet. They stay naturally lean and have few problems dieting. Once again, you aren't one of them, or you wouldn't be reading this book.
When talking about calorie partitioning, researchers refer to something called the P-ratio. Essentially, P-ratio represents the amount of protein that is either gained (or lost) during over (or under) feeding. So a low P-ratio when dieting would mean you used very little protein and a lot of fat. A high P-ratio would mean that you used a lot of protein and very little fat. It looks like, for the most part, P-ratio is more or less the same for a given individual: they will gain about same amount of muscle when they overfeed as they lose when they diet. P-ratio can vary between individuals, of course, but for any given person, it appears to be relatively constant.
So what controls P-ratio? As depressing as this is, the majority of of the P-ratio is out of our control; it's mostly genetic. We can control maybe 15-20% of it with how we eat or train. Supraphysiological amounts of certain compounds (supplements) and, of course, drugs, can also affect the P-ratio. Exercise is perhaps the most significant weapon we have in battling with our body and affecting P-ratio.
So what are the main determinants of calorie partitioning? Hormones are crucially important. High testosterone levels tend to have positive partitioning effects (more muscle, less fat) while chronically high levels of cortisol have the opposite effect (less muscle, more fat). Thyroid and nervous system activity affect not only metabolic rate but also fat burning. Thyroid also affects protein synthesis. Optimal levels of these hormones not only mean better fat loss (and less muscle loss) when you diet but better muscular gains (and less fat gain) when you gain weight. Unfortunately, levels of these hormones are basically "set" by our genetics; the only way to change them significantly is with supplements or drugs. Beyond that, there's not a whole lot we can do to control them.
Another factor controlling P-ratio is insulin sensitivity which refers to how well or how poorly a given tissue responds to the hormone insulin. High insulin sensitivity means that a small amount of insulin will generate a large response; insulin resistance indicates that it takes more insulin to cause the same effects to occur.
Now, insulin is a storage hormone, affecting nutrient storage in tissues such as liver, muscle and fat cells. In that same ideal world, we'd have high insulin sensitivity in skeletal muscle (as this would tend to drive more calories into muscle) and poor insulin sensitivity in fat cells (making it harder to store calories there). This is especially true when you're trying to gain muscle.
When you diet, it's actually better to be insulin resistant (note that two of the most effective diet drugs, GH and clenbuterol/ephedrine cause insulin resistance). By limiting the muscle's use of glucose for fuel, insulin resistance not only spares glucose for use by the brain, but also increases the muscles use of fatty acids for fuel.
In addition to hormonal advantages, it's likely that the genetic elite have high skeletal muscle insulin sensitivity. They store tremendous amounts of calories in their muscles, which leaves less to go to fat cells. Their bodies also don't have to release as much insulin in response to food intake.
In contrast, individuals with poor skeletal muscle insulin sensitivity tend to overproduce insulin, don't store calories in muscle well (this is part of why they have trouble getting a pump: poor glycogen storage in muscle cells) and tend to spill calories over to fat cells more effectively.
So what controls insulin sensitivity? As always, there are a host of factors. One is simply genetic, folks can vary 10 fold in their sensitivity to insulin even if everything about them is the same. Another is diet. Diets high in carbohydrates (especially highly refined carbohydrates), saturated fats and low in fiber tend to impair insulin sensitivity. Diets with lowered carbohydrates (or less refined sources), healthier fats (fish oils and monounsaturated fats like olive oil) and higher fiber intakes tend to improve insulin sensitivity.
Another major factor is activity which influences insulin sensitivity in a number of ways. The first is that muscular contraction itself improves insulin sensitivity, facilitating glucose uptake into the cell. Glycogen depletion (remember this, it's important) improves insulin sensitivity as well.
So what else controls the P-ratio? As it turns out, the primary predictor of P-ratio during over- and underfeeding is bodyfat percentage. The more bodyfat you carry, the more fat you tend to lose when you diet (meaning less muscle loss) and the leaner you are, the less fat you tend to lose (meaning more muscle loss). The same goes in reverse: naturally lean (but not folks who have dieted down) individuals tend to gain more muscle and less fat when they overfeed and fatter individuals tend to gain more fat and less muscle when they overfeed.
The question is why, why does bodyfat percentage have such a profound impact on P-ratio? There are a few easy answers. One is that bodyfat and insulin sensitivity tend to correlate: the fatter you get, the more insulin resistant you tend to get and the leaner you are the more insulin sensitive you tend to be.
A second is that, the fatter you are, the more fatty acids you have available for fuel. In general, when fatty acids are available in large amounts, they get used. This spares both glucose and protein. By extension, the leaner you get, the more problems you tend to have; as it gets harder to mobilize fatty acids, the body has less to use. Since there is less glucose available (because you're dieting) this increases the reliance on amino acids (protein) for fuel.
The original Ultimate Diet advocated medium chain triglycerides (a special type of fatty acid that is used more easily for fuel than standard fats) and this can be a good strategy under certain circumstances. I'll mention some other options later on in the book.
But that's not all. It turns out that bodyfat percentage is controlling metabolism to a much greater degree than just by providing fatty acids. Research over the past 10 years or so has identified fat cells as an endocrine tissue in their own right, secreting numerous hormones and proteins that have major effects on other tissues. Perhaps the most important, and certainly the one most talked about is leptin, but that's far from the only one.
Tumor necrosis factor-alpha, the various interleukins, adiponectin and other compounds released from fat cells are sending signals to other tissues in the body which affect metabolism.
Without getting into all of the nitpicky details (many of which haven't been worked out yet), I just want to talk a little about leptin (if you read my last book, this will all be familiar ground).
To be con't.
by Lyle McDonald
Introduction: The following is a chapter excerpt from my Ultimate Diet 2.0, dealing with calorie partitioning. It deals with what controls where calories go when you eat them, and what determines where they come from when you diet. If you read my previous article on AMPk: Master Regulator, it may explain some of the underlying physiology for what's discussed in this chapter. Of course, the rest of the book details an integrated system of nutrition and training to take advantage of this information, to make sure that you pull calories out of fat cells when you diet, and put them back into muscle when you overfeed; with the goal of losing fat while maintaining or gainin muscle at the same time.
Chapter 4: Why is it so hard (Part 2)
Partitioning
At a very fundamental level, the problem natural bodybuilders and athletes have is one of partitioning. At its simplest, partitioning refers to where the calories go (into muscle or fat cells) when you eat more of them or come from (from muscle or fat cells) when you eat less of them.
In an ideal universe, every calorie you ate would go to muscle tissue, with none going into fat cells; you'd gain 100% muscle and no fat. In that same ideal universe, every calorie used during dieting would come from fat stores; you'd lose 100% fat and no muscle. Unfortunately, we don't live in an ideal universe.
As I mentioned early in this book, some hapless individuals will lose as much as one pound of muscle for every 2-3 pounds of fat that they lose when they diet. Typically, those same individuals will put on about the same amount of fat and muscle when they gain weight. Thus is the balance of the universe maintained. More genetically advantaged individuals tend to put more calories into muscle (meaning less into fat) when they overeat and pull more calories out of fat cells (and less out of muscle) when they diet. They stay naturally lean and have few problems dieting. Once again, you aren't one of them, or you wouldn't be reading this book.
When talking about calorie partitioning, researchers refer to something called the P-ratio. Essentially, P-ratio represents the amount of protein that is either gained (or lost) during over (or under) feeding. So a low P-ratio when dieting would mean you used very little protein and a lot of fat. A high P-ratio would mean that you used a lot of protein and very little fat. It looks like, for the most part, P-ratio is more or less the same for a given individual: they will gain about same amount of muscle when they overfeed as they lose when they diet. P-ratio can vary between individuals, of course, but for any given person, it appears to be relatively constant.
So what controls P-ratio? As depressing as this is, the majority of of the P-ratio is out of our control; it's mostly genetic. We can control maybe 15-20% of it with how we eat or train. Supraphysiological amounts of certain compounds (supplements) and, of course, drugs, can also affect the P-ratio. Exercise is perhaps the most significant weapon we have in battling with our body and affecting P-ratio.
So what are the main determinants of calorie partitioning? Hormones are crucially important. High testosterone levels tend to have positive partitioning effects (more muscle, less fat) while chronically high levels of cortisol have the opposite effect (less muscle, more fat). Thyroid and nervous system activity affect not only metabolic rate but also fat burning. Thyroid also affects protein synthesis. Optimal levels of these hormones not only mean better fat loss (and less muscle loss) when you diet but better muscular gains (and less fat gain) when you gain weight. Unfortunately, levels of these hormones are basically "set" by our genetics; the only way to change them significantly is with supplements or drugs. Beyond that, there's not a whole lot we can do to control them.
Another factor controlling P-ratio is insulin sensitivity which refers to how well or how poorly a given tissue responds to the hormone insulin. High insulin sensitivity means that a small amount of insulin will generate a large response; insulin resistance indicates that it takes more insulin to cause the same effects to occur.
Now, insulin is a storage hormone, affecting nutrient storage in tissues such as liver, muscle and fat cells. In that same ideal world, we'd have high insulin sensitivity in skeletal muscle (as this would tend to drive more calories into muscle) and poor insulin sensitivity in fat cells (making it harder to store calories there). This is especially true when you're trying to gain muscle.
When you diet, it's actually better to be insulin resistant (note that two of the most effective diet drugs, GH and clenbuterol/ephedrine cause insulin resistance). By limiting the muscle's use of glucose for fuel, insulin resistance not only spares glucose for use by the brain, but also increases the muscles use of fatty acids for fuel.
In addition to hormonal advantages, it's likely that the genetic elite have high skeletal muscle insulin sensitivity. They store tremendous amounts of calories in their muscles, which leaves less to go to fat cells. Their bodies also don't have to release as much insulin in response to food intake.
In contrast, individuals with poor skeletal muscle insulin sensitivity tend to overproduce insulin, don't store calories in muscle well (this is part of why they have trouble getting a pump: poor glycogen storage in muscle cells) and tend to spill calories over to fat cells more effectively.
So what controls insulin sensitivity? As always, there are a host of factors. One is simply genetic, folks can vary 10 fold in their sensitivity to insulin even if everything about them is the same. Another is diet. Diets high in carbohydrates (especially highly refined carbohydrates), saturated fats and low in fiber tend to impair insulin sensitivity. Diets with lowered carbohydrates (or less refined sources), healthier fats (fish oils and monounsaturated fats like olive oil) and higher fiber intakes tend to improve insulin sensitivity.
Another major factor is activity which influences insulin sensitivity in a number of ways. The first is that muscular contraction itself improves insulin sensitivity, facilitating glucose uptake into the cell. Glycogen depletion (remember this, it's important) improves insulin sensitivity as well.
So what else controls the P-ratio? As it turns out, the primary predictor of P-ratio during over- and underfeeding is bodyfat percentage. The more bodyfat you carry, the more fat you tend to lose when you diet (meaning less muscle loss) and the leaner you are, the less fat you tend to lose (meaning more muscle loss). The same goes in reverse: naturally lean (but not folks who have dieted down) individuals tend to gain more muscle and less fat when they overfeed and fatter individuals tend to gain more fat and less muscle when they overfeed.
The question is why, why does bodyfat percentage have such a profound impact on P-ratio? There are a few easy answers. One is that bodyfat and insulin sensitivity tend to correlate: the fatter you get, the more insulin resistant you tend to get and the leaner you are the more insulin sensitive you tend to be.
A second is that, the fatter you are, the more fatty acids you have available for fuel. In general, when fatty acids are available in large amounts, they get used. This spares both glucose and protein. By extension, the leaner you get, the more problems you tend to have; as it gets harder to mobilize fatty acids, the body has less to use. Since there is less glucose available (because you're dieting) this increases the reliance on amino acids (protein) for fuel.
The original Ultimate Diet advocated medium chain triglycerides (a special type of fatty acid that is used more easily for fuel than standard fats) and this can be a good strategy under certain circumstances. I'll mention some other options later on in the book.
But that's not all. It turns out that bodyfat percentage is controlling metabolism to a much greater degree than just by providing fatty acids. Research over the past 10 years or so has identified fat cells as an endocrine tissue in their own right, secreting numerous hormones and proteins that have major effects on other tissues. Perhaps the most important, and certainly the one most talked about is leptin, but that's far from the only one.
Tumor necrosis factor-alpha, the various interleukins, adiponectin and other compounds released from fat cells are sending signals to other tissues in the body which affect metabolism.
Without getting into all of the nitpicky details (many of which haven't been worked out yet), I just want to talk a little about leptin (if you read my last book, this will all be familiar ground).
To be con't.
