Muscle fiber type distribution in Type 2 Diabetics
One of the more intriguing attributes of people with obesity
and Type 2 Diabetes is that they have a higher percentage of Type IIx muscle
fibers and a lower percentage of Type I fibers (5, 6, 7, 8, 9, 10). When we look at the 3 muscle fiber types, the
IIx fibers are the most insulin resistant, followed by the IIa and, finally,
the type I fibers are the least resistant to insulin(11). Obviously a person with a higher percentage
of muscle fibers that are insulin resistant will be more prone to insulin
resistance and the conditions associated with it. Looking at this merely on the surface, one
would be inclined to believe that people born with a higher percentage of Type
IIx muscle fibers may be particularly prone to these conditions. While the data shows that genetics probably
plays a large role in your percentage of Type I vs Type II fibers, it probably
has little to do with Type IIx fiber distribution. When you look at all of the information that
is out there, it appears more likely that this is an adaptive response by the
body to the environment presented to it.
In other words, it is a classic gene/environment interaction that
develops within people who have a higher percentage of Type II muscle fiber
types.
Muscle Fiber Type Conversion
It has been well established that all training, whether it
be cardiovascular/aerobic or resistance training/anaerobic, causes a change in
type IIx muscle fibers by either converting them to type IIa fibers or causing
them to take on the characteristics of the more intermediate IIa fibers(12,13). This is a positive adaptation in that it
allows you to do more work before fatigue sets in by increasing the amount of
energy the fiber can store and the amount of energy it can make. In addition, once training ceases for more
than a week, the IIa fibers revert back to IIx fibers. In fact, all sedentary people experience this
conversion whether they are prone to diabetes/obesity or not.
Knowing that the IIx fibers are primarily driven directly by
ATP and have low glycogen, it makes sense that they would be insulin resistant
because they fill up with glycogen faster.
As an adaptive response to training, they increase glycogen storage and
mitochondria content while at the same time receiving an increase in blood flow
via an increase in capillaries serving the fiber, which is basically the same
thing as taking on IIa fiber characteristics.
This improves their insulin sensitivity both by using the glycogen
content of the fibers as well as increasing their capacity to store glycogen,
improving their ability to dispose of glucose from the blood. It also improves their ability to generate
ATP from fatty acids given that is the primary role of the mitochondria. In other words, they burn more fat.
So, what drives this adaptation, is it simply a use it or
lose it scenario or is it caused by some environmental factor? Interestingly enough, it appears this
adaptation may be driven hormonally, specifically by our good friend
insulin. In a study performed on rats,
induced hyperinsulinemia caused IIa to IIx conversion (14). In another study performed on humans,
inducing hyperinsulinemia on 10 young male subjects for 3 hours increased MHC
IIx gene expression by 40% when compared to control conditions in each subject
(15). This means the subjects were
beginning to make Type IIx muscle fibers as a response to high insulin levels.
It makes sense that this could be the body adapting to the
environment you are providing it, insulin only gets high when you secrete a lot
of it. If you eat a ton of carbohydrates
and don’t exercise you will create tons of insulin to deal with that
glucose. If you eat the same amount of
carbohydrates and exercise a lot you will be using exercise as your method of
getting glucose in to cells, insulin will stay low, and this conversion will
not happen. This provides support for
the notion that Type 2 diabetes is a reversible metabolic state. If you activate IIx muscle fibers they
convert to IIa fibers, become more sensitive to insulin, and are capable of
disposing of more gulcose in the event blood glucose gets too high. If you stop using them they will convert back
to IIx fibers, become more insulin resistant, and become relatively worthless
with regard to disposing of glucose. The
end result is elevated blood insulin levels to force the glucose in to the
lower threshold Type I fibers and eventually, fat cells. A high percentage of Type II fibers in general
is a very strong risk factor for Type 2 Diabetes, and it makes sense since they
will switch from IIa fibers to the more insulin resistant IIx fibers with
disuse.
Type IIx fibers have often been referred to as the default
fiber type, but this is not something that has been studied extensively. Given that the modern diet is, by default,
high in carbohydrate, it would be interesting to see the effects of a high fat
diet on muscle fiber type conversion. Would a high fat environment induce the
opposite effect? In other words, if you
consumed more fat would this cause fiber type changes that favor fat oxidation,
a conversion to Type I fibers? While the
effect of a high fat diet on fiber type has not been studied directly, there
have been studies that show physiological adaptations via gene expression to
burning fat from a high fat diet (16) and endurance exercise (17). It is highly unlikely that eating a high fat
diet would induce a fiber type change from Type IIx to I given that IIx fibers
have a very limited blood supply, but the latter study did show an increase in
genetic expression of genes responsible for the creation of mitochondria from
exercise. A limited blood supply means
ingested fatty acids probably wouldn’t make their way to the IIx fiber, but if
these fibers converted to IIa fibers via exercise the blood supply may become
sufficient enough to go from IIx to IIa to I.
There is the possibility that a high fat diet could induce a
Type IIa to I fiber conversion given the good blood supply to IIa fibers. The general consensus is that fibers may
convert in the following ways:
Type IIx<------------>Type
IIa<------------>Type I
There is plenty of evidence of IIx to IIa and IIa to IIx
conversion in multiple studies, but the lack of studies on conversion of either
Type II fiber types to Type I fibers makes any notion that this conversion is
possible speculative at best. In
addition, given that fiber type is dictated by the type of nerve that fires the
muscle fiber, this conversion is unlikely.
Since we know people who are prone to obesity have a higher
percentage of these Type IIx fibers, getting them to convert to IIa fibers is a
potentially good intervention. In order
to get IIx fibers to take on the characteristics of the IIa fibers, you have to
activate them on a regular basis, which means meeting their force activation
threshold or fatiguing the muscles recruited before them to the point the IIx
fibers need to kick in. Given the high
force threshold for activation of IIx fibers, this is not likely to happen with
distance running or aerobics, the exercise should be glycolytic and short in
nature with appropriate rest between exercise sets. The best options that meet these criteria are
high intensity resistance training, plyometrics, and sprints. While it is certainly possible that you could
eventually activate IIx fibers via endurance exercise once the Type I and IIa
fibers run out of fuel, the speed you would need to run at or the amount of
time you would need to run for make it an unappealing option. However, no matter which dietary approach you
decide to use, low carbohydrate or low calorie, diet will have no effect on
increasing the blood supply to IIx fibers, underscoring why it is so difficult
to get rid of insulin resistance once you have it.
When we look at what happens to people as they age, we see
the same adaptation as we see in sedentary people, a conversion from IIa to IIx
muscle fibers and eventual atrophy of the IIx fibers, making them even insulin
resistant. As a result, the risk of Type
2 Diabetes doubles when you reach the age of 65 and doubles again when you
reach 80. When we look at studies
involving older people and resistance training, we see nearly identical
improvements in muscle fiber type characteristics and measures of insulin
resistance as we do in younger people (18, 19, 20) that we would not expect to
see in endurance training unless it were progressive in nature. In other words, if you can run 5 miles at a
pace of 10 minutes/mile, your fiber type characteristics will improve a little
and then stop unless you increase your speed to 9.5 minutes/mile. Then, the adaptations would stop until you
increase your speed even further. This
is something that a competitive endurance athlete does that your typical
gym-goer does not. A much better option
is to induce this fiber conversion via high intensity resistance training,
which takes less time, is more pleasant, and is unlikely to cause an overuse
injury provided it is done properly and progressively.
Glycogen depletion during exercise
During high intensity exercise, glycogen is depleted equally
among the muscle fiber types. This makes
sense given that during high intensity exercise, all muscle fiber types are
recruited. During aerobic exercise, most
of the glycogen depletion during the onset of exercise comes from the Type I
muscle fibers. Given that these fibers
have a low glycogen storage capacity, they run out of glycogen relatively
quickly. Once this happens, the Type II
fiber types will start to kick in to allow exercise to continue. But wait, we mentioned above that Type II
fibers have a high contraction threshold, why would they be activated at a
lower threshold? To provide fast acting
glucose to the Type I fibers which will fatigue without it, and the process is
actually pretty cool.
Recall that the glycogen within a muscle fiber has to be
metabolized by that fiber. If this is
the case, how can the Type II fibers provide glucose to the Type I fibers? The answer, aka loophole, is lactate. If you have ever exercised for a long period
of time, you have probably felt the burn associated with lactate/lactic
acid. This burn actually comes from the
high levels of hydrogen ions that are created alongside lactate. While glycogen cannot be passed on from fiber
to fiber, lactate can. As lactate
accumulates in a muscle fiber, it is shuttled out of the fiber and in to the
blood where it goes to the liver and is converted to glucose. Now, this glucose is free to go wherever it
is needed. But what happens once exercise
ceases?
Glycogen Storage
One concept that is important to grasp with regard to
exercise and it’s effect on insulin sensitivity is that the improvements in
insulin sensitivity are not permanent, they only last for a limited period of
time. This is probably variable based on
the amount of exercise you do, the type of exercise, and the amount of
carbohydrate you consume afterwards, but is typically about 36 hours following
exercise. During the recovery period
following exercise, the body preferentially stores glycogen while increasing
fatty acid oxidation, even when it is primarily carbohydrate being
consumed. The hormonal environment
post-exercise primes the muscles to store glucose rather than burn it (21, 22, 23).
The body’s drive to replenish glycogen is so great that even
during fasting after exercise it tries to replenish muscle glycogen stores, provided
they were used during the exercise period(22).
What the body uses to replenish glycogen stores post-exercise in the
absence of food is primarily dictated by the intensity and duration of the
exercise. If the exercise was intense
and of short duration, the lactate generated during exercise is used to
replenish glycogen. If the exercise was
of moderate intensity but long duration (Long distance running anyone?), amino
acids are the fuel, i.e., your muscles (22).
In addition, even if
you are performing physical activity, your body will replenish glycogen in the
muscle fibers you are not using (22). Active
recovery is a recovery modality where you continue to do low intensity activity
like walking or lower intensity exercise after a period more of intense
exercise. During active recovery
following exercise, even though Type I fibers are still using glucose, some of
the glucose being made in the liver from lactate is actually shuttled to the
Type II fibers that are not being used to replenish glycogen stores (22). This is, of course, contingent on those fibers
depleting their glycogen stores first.
If the intensity of exercise prior to the recovery was not sufficient
enough to engage the higher threshold IIx fibers, they will not need
glycogen. However, the Type IIa fibers,
which have a lower contraction threshold, are probably being activated to
provide the lactate that is converted in the liver to glucose to fuel the Type
I fibers, so their glycogen content would be depleted to some extent.
The science vs “conventional wisdom”
The evidence appears to support the notion that we are
dealing with a mismatch between the primary type of fuel consumed and the type
of activity performed, at least in obese people and Type 2 Diabetics. Given that obese/diabetic people have more
IIx fibers and that glycogen is preferentially directed to these fibers even
during fasting and physical activity, these fibers will typically be insulin
resistant unless used regularly. In people
with a higher percentage of these fibers that also tend to over-consume
carbohydrate and not perform physically demanding activity, it appears that we
are seeing a classic gene/environment interaction that is driving the obesity
epidemic. This same interaction occurs
in non-obese people as well via a conversion of IIa fibers to IIx.
Taking all of this data in to consideration, performing intense
physical activity on a regular basis is obviously something important for anyone
who wants to maintain insulin sensitivity throughout life. In people who are Type 2 Diabetic or obese as
well as their children, it is absolutely critical while carbohydrate is a
significant part of the diet. It is also
important to make sure this activity is performed with both the lower AND the
upper body as well as with a full range of motion. In order to improve insulin sensitivity even
further, it would also be smart to vary your exercises frequently to make sure
that you are hitting as many muscle fibers in as many muscle groups as
possible. So, let’s compare what the
science shows to the route most people are recommended to take by the medical
establishment.
If you go in to the Doctor’s office and get a diagnosis of
Pre-diabetes or Type 2 Diabetes, you are told that you need to change your diet
and start an exercise regimen. The
general theme of the discussion will center around the fact that you need to
lose weight. While this is true, the extra
weight doesn’t cause Diabetes, the extra weight is an effect of Diabetes caused
by insulin resistance.
If you lose some fat you are improving insulin sensitivity
via exercise and diet because if you weren’t you wouldn’t be able to release or
burn body fat. The problem is you are
doing it indirectly by focusing on creating an energy deficit. More often than not the exercise portion of
creating this deficit is long distance running, a spin class, or some other
aerobic activity. This will take forever
and require a massive amount of effort given the IIx fibers are not recruited for
this type of activity so they can’t convert to IIa fibers. Given that you would still have a higher
percentage of insulin resistant muscle fibers, the insulin resistance is
probably still there, and unless your diet is spot on and very low carbohydrate
you will continue to have problems with your blood glucose.
In fact, you may be able to maintain normal blood glucose
levels as long as you keep your carbohydrates low or exercise for hours per day. If you go wild and hammer in to carbohydrate-heavy
food or stop running, your blood glucose will shoot through the roof along with
your insulin levels. This doesn’t even
consider the fact that very few people who run long distances do so with a full
range of motion, progress it properly, and that running and spinning do little
to nothing for the upper body.
At this point you are probably going, “Wait a second, I know
a bunch of people who do long distance running or spinning and they aren’t
overweight.” While this is certainly
true, chances are these people aren’t prone to Type 2 Diabetes or obesity. They probably have a higher percentage of
Type I fibers so they are better suited to distance running, or they may not
have the genetic predisposition to store body fat. While the former would make them far less
likely to develop Type 2 Diabetes, neither prevents them from developing
insulin resistance. Anybody can become
insulin resistant at any time, and you don’t have to have an outwardly obese
appearance to have either Type 2 Diabetes or insulin resistance. It would certainly be much more difficult for
a person with a high percentage of Type I fibers to become insulin resistant,
but it is possible. Whether you are Type
2 Diabetic or not, insulin resistance is a bad scene. A small list of the diseases/issues
associated with insulin resistance includes cancer, heart disease, high blood
pressure, stroke, fatty liver disease, metabolic syndrome, Polycystic Ovarian
Syndrome, and Type 2 Diabetes/Obesity.
So, don’t think you’re safe just because you are lean.
Conclusion
If you get anything from part 2 of this series, it’s that
insulin sensitivity is NOT a 1- trick pony.
With exercise, you have something you can do that mimics the primary
effect of insulin while at the same time lowering your resistance to insulin
provided you do it properly. In the
context that most people approach exercise, I agree with Gary Taubes, that it
has little effect on fat loss. But, in
the proper context with the proper modalities it not only helps improve insulin
sensitivity in a way that diet cannot (You will not empty glycogen from a
muscle fiber with diet, only activating it via activity will do that), it gives
you leeway in the event you want to consume some higher carbohydrate meals.
Now that we have looked at the science behind obesity and
diabetes, it seems the exercise prescription given by the medical establishment
is way off base. While capable of
attaining short-term success, it comes at the expense of long-term health. At the end of the day, this approach is
unsustainable. You will be exercising 8
days a week and eating rice cakes all day which is not even remotely
necessary. You will be hungry,
irritable, and won’t be able to think straight.
You will be constantly preoccupied with food and tired until you just
give up. You will also enter an
overstressed state and become either sick, injured, or not be able to
sleep. Does this sound familiar? There are very specific reasons why all of
this happens, and most of it is dictated by hormones.
In Part 3 we will answer why all of this occurs and how to
adjust your diet to prevent it.
(Having problems publishing the references, I'll plug them in later today)
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