Excessive accumulation of lipids inside the muscle is a hallmark of insulin resistance; the harbinger of diabetes, obesity and heart disease. In fact, one way that researchers create insulin resistance in the lab is to inject free fatty acids into study subjects’ bloodstreams.
Think of lipid buildup inside muscles like the TV show in which people hoard things. A little storage is good, but when you don’t throw anything away, it’s easy to be paralyzed by your own belongings.
Because skeletal muscle is a major contributor to having a high metabolic rate, and is also the body’s primary fat-burning furnace, fatty muscle is a bad thing. Emerging research links leptin resistance to impaired fat burning.
— Mike Mutzel MSc (@MikeMutzel) January 13, 2015
Leptin Resistance Impairs Fatty Acid Oxidation Inside Muscle
As the body’s main energy gauge, high levels of leptin suggest high fuel capacity, which under normal conditions, triggers the body to stop eating and increases energy expenditure. (Leptin not only has receptors in the brain, it also has receptors inside skeletal muscle, where it promotes fatty acid oxidation (fat burning) and reduces fatty acid storage, at least in lean people.)
A recent study revealed that leptin resistance in the muscle tissue of obese subjects lead to increase uptake of fats (inside the muscle) and reduced fatty acid oxidation, when compared to lean, leptin sensitive subjects. 
Since muscle tissue is body’s primary site of fatty acid oxidation, and since leptin (along with adrenaline) is one of the main triggers of skeletal muscle fatty acid oxidation, it’s safe to say that leptin resistance sets up a huge road block in the fat burning process.
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Why Fatty Muscle Is a Bad Thing (if you'd like to stay lean)
Hoarding of lipids inside muscle tissue is beneficial for a cyclist riding in the Tour de France, because they are actually burning the fat. However, this isn’t the case for the twenty-first-century couch potato. This was recently demonstrated by researchers from the Netherlands. They found that an intravenous infusion of lipids had little to no effect on insulin functioning in trained athletes, yet reduced insulin sensitivity by 63 percent in untrained people. It was noted that trained athletes had 32 percent higher mitochondrial capacity compared to sedentary study subjects.
Fatty muscle, insulin resistance, and mitochondrial dysfunction go hand in hand. Research studies have reported a 30 percent reduction in mitochondrial function among insulin-resistant individuals compared to metabolically healthy counterparts.
Researchers at the University of Colorado found that lipid deposits inside muscle tissue correlate strongly with abdominal fat and an increase in the ratio of triglyceride to heart-healthy cholesterol in adolescents prior to and during puberty. This suggests that lipid accumulation in muscle tissue is an early event contributing to metabolic imbalances.
Activating Mitochondrial Pathways Are Key To Burning Fat Inside Muscle
A hot area of research today involves tweaking the molecular switches to make energy currency more available to mitochondria to make them more efficient fat-burners. AMPK and PGC-1α (peroxisome proliferator-activated receptor γ coactivator 1α) both stimulate the mitochondria to burn fat and sugar more efficiently. When increased by fasting, exercise, cold temperatures, and certain natural compounds, the AMPK and PGC-1α pair also instruct the mitochondria to divide, a process known as mitochondrial biogenesis. In brief, these molecular signaling hubs guide our mitochondria to burn more fat and carbohydrates for fuel.
You can think of AMPK as a fuel gauge, monitoring the energy status in your cells. If cells are filled with fat and sugar—as in obesity and diabetes—AMPK will diminish, and the energy factories, your mitochondria, will not be able to burn fat or sugar. When AMPK is increased, mitochondria in your liver and muscles function better, so toxic fat spillover from fat cells is reduced and overall insulin sensitivity improves. AMPK is so powerful that a low level may be the reason why some overweight people gain strength and stamina on an exercise program, but still don’t lose weight or improve their sensitivity to insulin.
One way to keep your cellular powerhouses burning fatty acids and sugar and churning out energy is regular exercise. One study reported that athletes can increase the amount of energy burned inside their mitochondria over 54 percent higher when compared to their sedentary counterparts. This is the kind of fat burning that also improves insulin sensitivity. Scientists have reported that feeding animals high-fat, high-carbohydrate diets reduces the expression of AMPK and PGC-1α by up to 46 percent. (This suggests yet another way in which diet can influence our gut microflora). It can have a ricochet effect on our metabolism, reducing fat burning.
The Best Natural Ways to Increase Fatty Acid Oxidation Inside the Mitochondria
1) Dynamic Weight Training. Aim for 20 minutes of dynamic resistance training five to seven days per week.
2) Aerobic (cardio) Based Training. Studies show that 30 minutes, five days per week is the sweet spot for keeping the capillary network and fat-burning machinery in high-gear. Try cardio-based training first thing in the morning on an empty stomach, with coffee or green tea.
3) Phytonutrients. Herbs and botanicals such as resveratrol, pterostilbene, green tea and berberine work wonders for your mitochondria
4) Carnitine and Alpha-Lipoic Acid (ALA). Studies show these two nutrients increase fatty acid transport inside the mitochondria and also stimulate the mitochondria’s ability to burn fat.
Related Reading:How to Increase the 3 Major Steps of the Fat Loss Process
1) Mutzel, M. (2014). Belly Fat Effect: The Real Secret About How Your Diet, Intestinal Health, and Gut Bacteria Help You Burn Fat. Wilsonville Media. ISBN: 9780991070312
2) Steinberg, G. R., Parolin, M. L., Heigenhauser, G. J. F., & Dyck, D. J. (2002). Leptin increases FA oxidation in lean but not obese human skeletal muscle: evidence of peripheral leptin resistance. Am J Physiol Endocrinol Metab, 283(1), E187–92. doi:10.1152/ajpendo.00542.2001