Fatty muscle SKELETAL MUSCLES ARE the large muscle groups, such as the biceps, triceps, quadriceps, trunk, and gluteal muscles, that we use to move our limbs voluntarily.
This differentiates them from smooth muscles, muscles such as the heart or diaphragm, which are largely not under voluntary control.
Skeletal muscles burn the bulk of the glucose available after meals and store their own supply of glycogen to provide quick bursts of energy.
This muscle glycogen is not available for use by other organs of the body.
Normally, little fat is found in skeletal muscle.
Fat cells are specialized for fat storage; muscle cells are not.
With hyperinsulinemia and excess sugar, the liver creates new fat by DNL and distributes these triglycerides throughout the body.
When adipocytes (fat storage cells) become overwhelmed, skeletal muscles also take up the fat, leading ultimately to fat deposits between muscle fibers.
The technical term is intramyocyte lipid accumulation, but it could easily be called fatty muscle.
We can see this process of developing fatty muscle more clearly in farm-raised cattle, where the accumulation of fat between muscle fibers is called delicious!
The streaks of fat are clearly visible as marbling, the intermingling of fat with lean muscle.
As the meat cooks, the fat melts, making the beef more tender, moist, and flavorful, as it literally bastes itself.
For this reason, well-marbled beef commands a premium price.
Kobe beef, the ultra-premium Japanese delicacy, is prized for its high degree of marbling.
The United States Department of Agriculture grades beef based on the degree of marbling.
Prime beef, the highest and most expensive grade, has the most marbling.
Cattle ranchers know that marbling depends almost entirely on diet.
Cows are ruminants, which means they normally eat grass and do not develop marbling.
The result is a more flavorful but less tender steak.
However, a grain-heavy diet increases the growth rate as well as the marbling.
For this reason, many grass-fed cows are “finished” with a period of corn feeding to develop the desired fatty muscle, or marbling.
Carbohydrate-heavy diets cause fatty muscle.
It’s no secret in cattle, and it works just as well in humans.
Fatty liver produces insulin resistance in the liver.
In the same manner, fatty muscle produces insulin resistance in skeletal muscles.
Hyperinsulinemia forces too much fat and glucose inside the skeletal muscles.
They become completely full, so insulin cannot push any more inside.
This is the same overflow phenomenon.
Since the skeletal muscles are so large, they contribute significantly to overall insulin resistance in the body.24 Fat deposition in skeletal muscles, obesity, and severity of insulin resistance are closely related.25 Muscles from obese subjects take up fatty acid at an equal rate to lean subjects but burn it at only half the speed, leading to greater accumulation of fat within the muscles.
Weight loss can partially rectify this problem.
Why can’t the muscle just burn off this fat?
The answer lies in the biochemical process known as the Randle cycle.
The Randle cycle DR.
PHILIP RANDLE first described the glucose, fatty acid, or Randle, cycle in 1963.26 Working with isolated heart and skeletal muscle cell preparations, Randle demonstrated that cells burning glucose could not burn fat and vice versa.
Furthermore, this phenomenon did not require the assistance of insulin or any other hormones.
Your body simply cannot use both fuels simultaneously.
You either burn sugar or fat, but not both.
Most cells can use fat directly for energy but certain key cells, notably the brain, cannot.
During the fasting state, large organs such as the liver, heart, pancreas, and skeletal muscles burn fat to conserve what little glucose is available for the brain.
This essential survival mechanism maximizes the time humans can survive without eating.
Since the liver cannot produce enough new glucose by the process of gluconeogenesis for the entire body, the Randle cycle helps conserve glucose for where it
is needed the most.
The liver also produces ketone bodies from fat, which provides up to 75 percent of the brain’s energy requirements, and further conserves glucose.
The body’s ability to block the use of glucose by relying on fatty acids instead has also been called physiological insulin resistance.
When the body is mostly burning fat, such as during very low, carbohydrate diets or fasting, it cannot burn glucose.
Therefore, if you start to eat carbohydrates, the cells temporarily cannot handle the glucose load and your blood glucose levels rise.
This phenomenon looks like insulin resistance but is not really the same mechanism at all.
As insulin rises, the body switches to burning glucose and the blood glucose levels fall back.
The opposite is also true.
When the body is burning glucose, it cannot burn fat, but saves stored fat for later consumption.
The Randle cycle ensures the skeletal muscle cells cannot simply burn off the excess fat when they are fully saturated with glucose.
They are burning glucose, not fat, so it accumulates.
Voilà!
Fatty muscle and insulin resistance.
Fatty muscle and fatty liver lead to rising insulin resistance, provoking the compensatory hyperinsulinemia that keeps blood glucose normal.
But as we’ve seen, this cycle eventually leads to the development of more insulin resistance in a classic, self-reinforcing cycle.
Over time, the insulin levels march relentlessly higher, as does the insulin resistance.
Ultimately, something’s gotta give.
Enter phase 2.
PHASE 2: BETA CELL DYSFUNCTION
BLOOD GLUCOSE RISES quickly when the pancreatic beta cells responsible for insulin production cannot keep pace with rising insulin resistance.
When this compensatory mechanism fails, it only takes one to two years before a diagnosis of full-blown type 2 diabetes.
Over time, insulin production peaks and eventually starts to fall.27 The progressive decline in insulin production is often called beta cell dysfunction, or sometimes pancreatic burnout.
But what causes this burnout?
Many researchers suggest hyperglycemia destroys beta cells.
But there’s an obvious and insurmountable problem with this theory.
As insulin resistance develops, blood glucose stays relatively controlled.
Glucose doesn’t rise significantly until after beta cells fail.
The beta cell
dysfunction causes the high blood glucose, not the other way around.
The prevailing hypothesis is that the beta cells are simply worn out from overproducing insulin for so long.
Like a rickety old engine that has been revved too many times, the excessive chronic workload has caused irreversible damage.
However, three main problems exist with this paradigm of chronic progressive scarring of the pancreas.
First, beta cell function has been proven to be fully reversible.
Dr.
Roy Taylor of Newcastle University in the U.K. demonstrated pancreatic function recovery with an ultra-low calorie diet.28 The fact that weight loss can reverse type 2 diabetes also implies reversibility to the beta cell function.
Simply, the beta cells are not burnt out.
Second, with excessive use, the body generally responds with increased, not decreased, function.
If you exercise a muscle, it gets stronger; it doesn’t burn out.
With overactive secretion, glands generally get larger, not smaller.
If you think and study a lot, you increase your knowledge; your brain doesn’t burn out.
The same holds true for the insulin-producing cells.
They should grow larger (hypertrophy), not smaller (atrophy).
Finally, beta cell burnout implies that damage occurs only due to longstanding excessive use.
It takes many decades of overactivity to produce scarring and fibrosis.
The rising epidemic of type 2 diabetes in children and adolescents clearly proves this concept false.
With type 2 diabetes now being diagnosed in children as young as three years old, it is inconceivable that any part of their body has already burned out.
What causes the beta cell dysfunction?
Since this defect naturally follows insulin resistance, Ockham’s razor suggests that the beta cell dysfunction should share the same basic mechanism as the insulin resistance.
Specifically, the problem is fatty infiltration of organs, and recent research has identified the likely culprit.
During the first phase, fatty liver and fatty muscles create increased insulin resistance.
In the second phase, fatty pancreas creates beta cell dysfunction.
The pancreas is not burnt out; it is merely clogged with fat.