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
Part 2b
