Monday, December 3, 2012

Myths, Metabolism, & Appetite Part 2a

Part 2-The human guide to metabolism

In part 1 of this article, we discussed some of the common myths that get passed off to you from the fitness and medical establishments.  In Part 2, we discuss the science behind how we use our food and where we need to direct our attention to avoid the metabolic disadvantages our environment puts us in.  If you get nothing from this article, realize that this is a far more complicated issue than energy balance.  We are dealing with a lot more “what’s” and “how’s” than “how much”.  Let’s start with your muscles.

Muscle fiber type and characteristics
There are 2 broad categories of muscle fibers(Also called cells), Type I muscle fibers and Type II muscle fibers.  The Type I muscle fibers have a low contraction threshold which means they are recruited for very low force activities like walking.  They take a while to fatigue and also contract more slowly which is why they are referred to as Slow-twitch fibers.  The Type II fibers have a high contraction threshold which means they are recruited for high force activities like sprinting, jumping, and climbing.  They also fatigue quickly and have a fast contraction velocity which is why they are often referred to as Fast-twitch fibers.  The Type II muscle fibers can also be broken down in to IIa and IIx fibers.  The IIa fibers are considered intermediate in that they are recruited for moderate forces, fatigue more slowly, and burn significant amounts of fat and glucose, while the IIx fibers have the highest force threshold and use mostly ATP that is recharged with glucose.  Type I fibers, on the other hand, recharge most of their ATP with fat.

The easiest way to differentiate between the 3 is that Type I fibers are recruited for low force movements, Type IIa fibers are recruited for moderate forces, and Type IIx are recruited for high force movements.  What’s interesting about this is that in order to recruit the Type IIx fibers, you MUST recruit the Type I and Type IIa fibers first.  So, during low force activities you are only recruiting Type I fibers while during high force movements you are recruiting all 3.  Since Force=Mass x Acceleration, in order to increase force you have to either increase the mass of what you are moving, or increase how fast you move it. 

Muscle activity and fuel
Given what you learned about the properties of glucose and fatty acids in the first part of this article and the fiber type characteristics, you could probably have figured out on your own that Type I fibers use more fat to recharge ATP stores, Type IIa fibers use both glucose and fat, and Type II fibers use more glucose.  So, obviously the appropriate fuel for someone who spends most of their time generating high forces like lifting heavy weights or sprinting is carbohydrate while the appropriate fuel for someone who spends most of their time generating low forces like walking is fat.  So what happens when the fuel a person eats doesn’t match the fuel they burn?

When a person’s diet is primarily fat and they try to perform very intense activities, they are limited to what their body can do because they can’t generate force quickly enough with fat.  If they have had significant carbohydrate in recent days they will burn through their stored glucose (Called glycogen) and once those stores are gone they fatigue rapidly.  Therefore, if you try to sprint as fast as you can but you don’t have enough glycogen to recharge ATP stores, your speed drops off very quickly as the higher threshold fibers fatigue and stop contracting.  If you rest for a bit these fibers will be recharged and you may be able to go again, but only if you rest long enough to recharge ATP.

When a person’s diet consists mostly of carbohydrate and they stick to low intensity activities, the situation is quite different.  Since the glucose that carbohydrates break down in to provides a quick form of energy, performing low intensity activity is still an option because you are not limited by the speed of energy production, you have a conscious choice in the type of activity you perform because the energy will either be used immediately or stored for later use.  While on the surface this sounds great, your ability to store glucose is very limited, especially when compared to what you can store as fat. 

Blood glucose and glycogen storage
A trained individual can store 100g of glucose as glycogen in the liver and up to 400g of glycogen in their muscle cells, which is equivalent to 2,000 calories of stored glycogen.  This number has been shown in studies to be 25% lower in untrained individuals, reducing the muscle glycogen storage capacity to 300g.  In comparison, 10lbs of body fat contains 35,000 calories and 10lbs is certainly not an upper limit in the amount of fat you can store.  What happens when you exceed your body’s ability to store glycogen?  It’s sent to the liver where it is converted to fat, but let’s dig a little deeper.

When you eat a mixed meal, the broken down food eventually enters your small intestine to be absorbed in to your bloodstream.  Depending on how many carbohydrates you eat your blood glucose levels begin to rise because carbohydrates break down in to glucose.  Your blood glucose is tightly regulated to be a little less than 1 teaspoon of glucose in your entire blood volume, any more is toxic and any less could lead to passing out.  There are 3 primary tissues that will take up this glucose to lower blood levels; the brain, the liver, and the muscles.  The primary role of liver glycogen is to maintain blood glucose levels, as blood levels drop the liver breaks down stored glycogen and releases it in to the bloodstream to maintain stable blood glucose.  The brain uses only about 150g of glucose to fulfill it’s energy needs so the primary site of glucose removal will happen in the muscle fibers, provided they are used.  In order for glucose to enter these tissues you need glucose transporters(GLUT) within the cells to move to the cell membrane and bring the glucose in.  Different cells have different GLUT that are given a number while some cells have multiple types, here we just refer to them in general for simplicity. 

There are only 2 scenarios where GLUT will move to the cell membrane of a muscle fiber; exercise or insulin.  Insulin is a hormone secreted by the pancreas to lower blood glucose.  It does this by causing GLUT in liver, brain, and muscle tissue to pull glucose in.  Since carbohydrates break down in to glucose, carbohydrate consumption increases insulin levels the most, followed by protein, while fat causes little to no insulin response.  Obviously, if you are exercising, GLUT moves the glucose in to the cell for burning without the aid of insulin, so exercise reduces insulin secretion.  Since GLUT is pulling glucose in to the muscle fiber you are lowering blood glucose so the pancreas will not be triggered to secrete insulin unless you stop and glucose continues to be absorbed from the small intestine.  If you rely on insulin as the transport method in to the cell the glucose will be stored as glycogen for later use. 

The glycogen that is stored in a muscle fiber can only be used by that fiber, it doesn’t enter circulation to be burned elsewhere.   Therefore, you must activate that muscle fiber to lower glycogen levels inside of it.  If you are an active person who performs intense physical activity you will eventually exhaust these glycogen stores and everything goes on peachy keen.  If you do not perform intense physical activity, eventually these muscle cells will reach storage capacity and stop listening to insulin.  As such, the glucose needs to go somewhere else or insulin levels will continue to rise. 

At this point, the glucose will go to the liver and be stored as glycogen until the liver’s stores are full.  Once the liver’s glycogen stores are full, insulin levels will increase further, leading to hyperinsulinemia (Too much insulin in relation to glucose) and the conversion of glucose in to fat.  The high insulin levels make it easy for this fat to be stored in fat cells because insulin also increases fatty acid entry in to fat cells.  You are now insulin resistant until your liver or muscle glycogen stores are depleted.  What this means is that insulin will circulate, but since there are no places for the glucose to go, it must be converted to fat and stored.  Insulin resistance is a bad scene as another aspect of insulin is that high levels prevent body fat from being released or fat from being oxidized.  If this doesn’t grab your attention, maybe the condition that insulin resistance eventually leads to will, Type 2 Diabetes. 

Mechanisms of insulin resistance
When you look at the data, it seems as though insulin resistance is not something that happens all at once, but over time.  In fact, there is compelling evidence that insulin resistance isn’t a system wide issue that happens all at once, it happens gradually as muscle fibers that don’t get used atrophy and become insulin resistant.  You become more insulin resistant as parts of you become insulin resistant, it doesn’t just happen in an instant.  This is supported by what we know about aging and muscle atrophy, not to mention the risk of getting diabetes increases dramatically with age(1 in 10 people over 20 years old have it, 1 in 4 over the age of 65) right alongside IIx muscle atrophy.  There is also compelling scientific data that supports this as well.
 A recent study showed that binding a leg in a cast for 48 hours led to a drop in insulin sensitivity in that leg with no change in the insulin sensitivity of the other(1).  Obviously if restricting the use of 1 leg leads to a drop in insulin sensitivity in that leg, there would also be a drop in insulin sensitivity of the upper body in people who do not perform significant activity with those muscles.  It is painfully obvious that your primary goal should be to activate as many of your muscle fibers as possible.  This not only includes fiber type and location, but also with respect to the joint angle. 

When you perform an exercise with limited range of motion, you only contract a portion of the muscle fibers within the muscle groups being used.  If you do a bicep curl with 50% range of motion, you are not using all of the muscle fibers in the biceps, regardless of the amount of force required.  If you always do the bicep curl with that range of motion, you will continually use the same muscle fibers while neglecting the remaining, increasing the chance a proportion of the fibers within that group will become insulin resistant.

The science obviously supports the use it or lose it notion that you need to use a muscle fiber for it to maintain benefit to you.  In fact, we are starting to see some studies roll in that are providing support for the notion that intense exercise is very beneficial for people with Type 2 Diabetes.  In a study conducted in 2002 at the International Diabetes Institute in Victoria, Australia, subjects who weight trained AND lost weight improved their blood glucose control more than subjects who just lost weight despite the weight loss only group losing more weight (2).  HbA1c, a 3 month average of blood glucose, fell by .7% in the weight training/weight loss group while it fell .06% in the weight loss only group.  A person with HbA1c above 6.0% is considered diabetic.

In a study looking at exercise intensity and improvements in insulin sensitivity in women with Type 2 diabetes, researchers found that improvements in insulin sensitivity were related to the intensity of the exercise while improvements in blood glucose levels were related to the volume, or amount, of exercise (3).  The problem with studies like this one, however, is that the modality of exercise is almost always aerobic in nature.  So even though there are varying levels of intensity, the intensity is never sufficient enough to recruit the IIx fibers, which you’ll see is very important.  The bulk of our research on exercise focuses on aerobic/cardiovascular training, which is a problem because any single exercise modality carried out for more than 60 seconds at a time cannot be considered high intensity with regard to the muscle fibers it activates because these fibers fatigue quicker than that.  In addition, the muscle fiber adaptation that this type of exercise causes will atrophy the fibers that tend to be insulin resistant since they are never used, making them useless in blood glucose disposal.

In another study involving overweight Latino adolescent males, researchers found that a 16 week resistance training protocol improved insulin sensitivity by 45%, far above the 25% typically attributed to cardiovascular exercise.  In addition, this effect remained in place even when accounting for the decrease in fat mass, meaning that adaptations other than a reduction in fat mass or increase in muscle mass were at play.  (4)  So how does low intensity, aerobic exercise come in to play?

There are countless studies showing improved insulin sensitivity with aerobic exercise.  I do not discount any of these studies and agree that aerobic exercise improves insulin sensitivity as well.  However, the mechanisms by which aerobic exercise improve insulin sensitivity are not the same as the mechanisms that high intensity, anaerobic exercise improve insulin sensitivity.  With aerobic exercise like long distance running, you are not activating a significant number of type IIa or IIx muscle fibers in the lower body, and you certainly are not activating a large number of any muscle fibers in the upper body given wind is the only resistance and acceleration during long distance running is negligible.  There is little to no effect on the more glycolytic, Type IIx fiber type.  So, in addition to long distance running, you still have to perform strength training to maintain activation of the IIx fibers and to prevent the muscle fiber adaptation from long distance running that runs counter to this.  It’s kind of like digging a hole, then digging another hole and filling in the first hole with the dirt from that one.

The improvements in insulin sensitivity from aerobic style training would be limited to emptying out glycogen stores of the lower threshold fibers which typically aren’t insulin resistant anyway, while also emptying the liver of glycogen stores in order to maintain stable blood glucose levels.  This would allow greater consumption of carbohydrate before conversion to fat given the triggers for the liver to convert glucose to fat are full glycogen stores and high insulin levels.  In addition, you would get an increase in the glycogen storage capacity of these muscle fibers, but they aren’t glycolytic in nature anyway so the increase would be small.  What you would get that is significant is something you wouldn’t want if you were genetically prone to obesity, insulin resistance, or Type 2 Diabetes…atrophy of the higher threshold, more glycolytic, type IIx muscle fibers.

Type 2 Diabetes and insulin resistance
Type 2 Diabetes is a “disease” that was once called Adult-onset Diabetes.  It was called this because only adults came down with it, now 13 year olds get it.  The reason I refer to it as a “disease” is because it is actually not a full-blown disease in most of the people diagnosed with it, it’s just a metabolic state that can be reversed and sent in to remission fairly easily using the available science.  Every time we eat we become resistant to insulin to some degree, and any time our glycogen stores are full we are insulin resistant at that time.  Your body also has a natural circadian rhythm of insulin sensitivity with healthy people being more insulin resistant at night and less insulin resistance in the morning.  Once you exercise you become more sensitive to insulin, how sensitive is in direct relation to how much of your glycogen stores you empty out with physical activity.  Type 2 Diabetes (T2D) ensues once you’ve been chronically insulin resistant for a number of years and your blood glucose isn’t regulated properly.  It is a product of inactivity AND diet, not one or the other.  That is not to say that T2D is only caused by this mechanism, but it is probably the greatest contributing factor.

Type 2 diabetes is diagnosed with a fasting blood glucose>125mg/dL and people are considered pre-diabetic with fasting blood glucose>100mg/dL.  As this metabolic state progresses, or more appropriately gets ignored, the cells in your pancreas responsible for secreting insulin, the beta cells, wear out and die.  The beta cells cannot replicate and your ability to secrete insulin becomes impaired.  As it progresses further the patient becomes reliant on insulin injections.  At this point it is a disease reminiscent of it’s sister disease, Type 1 Diabetes. 

When Type 1 diabetics are young their beta cells are destroyed by their immune system so they cannot make insulin at all.  Until Type 2 diabetics wear out their beta cells, their problem is too much insulin.  This state is induced by excessive carbohydrate intake as well as a lack of physical activity.  However, the susceptibility to Type 2 Diabetes is genetic, some people will never get the disease just as some people will never become obese. 

Gary Taubes, a science writer, has done a very good job of bringing the dietary characteristics that promote insulin resistance to light.  His 2 books, Good Calories Bad Calories and Why We Get Fat, are a must read to understand what is one of the primary drivers of insulin resistance...Diet.  His view, while on point, is just a bit too myopic for my taste.  While he promotes exercise for many of the health benefits associated with it, his view on exercise for fat loss seems to be that it is a waste of time.  He also points out, rightfully so, that exercise can increase appetite.  While this is true, this is dictated by the amount and type of exercise.  I believe this is a product of him looking at exercise in terms of calories in vs calories out and not with regard to the effect on insulin sensitivity.    When we look at some of the physiological characteristics of people prone to obesity and Type 2 Diabetes, this notion becomes clearer.  One interesting trait that makes a person susceptible to Type 2 Diabetes that has been staring us right in the face for over a decade.

Part 2b