What Is Muscular Fat and Why Does It Matter?

Muscular fat is fat that accumulates in and around your skeletal muscles, and growing evidence links it to insulin resistance, reduced physical function, worse surgical outcomes, and accelerated age-related decline. Unlike the fat you can pinch under your skin, muscular fat sits where you cannot see or feel it, nestled between and even within muscle fibers. Researchers use the term “myosteatosis” to describe the broader phenomenon, and it turns out to be far more biologically active than anyone appreciated a few decades ago.

The Different Types of Fat Inside and Around Muscle

When researchers talk about muscular fat, they are usually referring to two or three related but distinct things. The first is intermuscular adipose tissue, commonly called IMAT. This is actual adipose (fat) tissue that sits between individual muscles or between bundles of muscle fibers. It shows up clearly on CT and MRI scans. The second is intramyocellular lipid, or IMCL, which refers to tiny fat droplets stored inside the muscle cells themselves. These droplets are extremely small and serve as a local fuel source for muscle contraction. A third category, sometimes grouped with IMCL, involves specific lipid species like diacylglycerols and ceramides that accumulate within muscle tissue and can interfere with insulin signaling.

The distinction matters because these fat types behave differently. IMAT acts much like visceral belly fat in terms of its metabolic impact. Gene expression studies in both pigs and humans have shown that IMAT and visceral fat share similar inflammatory and immune-related gene activity, and an increase in IMAT poses a comparable threat to insulin sensitivity as visceral fat does.¹ Meanwhile, IMCL can be either helpful or harmful depending on context, which leads to one of the most interesting puzzles in this area of research.

The Athlete’s Paradox

If fat inside muscle were simply bad, you would expect endurance athletes to have very little of it. The opposite is true. Endurance-trained athletes have elevated levels of intramyocellular lipid, sometimes matching or exceeding the levels seen in people with type 2 diabetes, yet their muscles are highly insulin-sensitive and their metabolic health is excellent.² Researchers named this the “athlete’s paradox,” and it has been a productive puzzle for over two decades.

The resolution comes down to where the fat sits within the cell and how the cell uses it. In trained athletes, lipid droplets tend to be numerous, small, and located deep within the muscle fiber near the energy-producing machinery. In people with type 2 diabetes, the same total amount of fat is stored in fewer, larger droplets clustered near the outer edge of the fiber, predominantly in fast-twitch fibers that are less metabolically active.³ Athletes also have much higher oxidative capacity, meaning their muscles burn fat efficiently as fuel rather than letting it accumulate in forms that disrupt cell signaling.⁴

The practical takeaway is that the total amount of fat in your muscles tells only part of the story. What matters just as much is whether your muscles have the machinery to burn that fat and whether the fat is stored in a pattern that supports rather than disrupts normal muscle function. Training builds that machinery. Inactivity and metabolic disease erode it.

How Muscular Fat Damages Metabolism

The metabolic harm from muscular fat operates through several channels. IMAT, the fat tissue sitting between muscle fiber bundles, can trigger local inflammation by releasing inflammatory signaling molecules directly onto nearby muscle fibers.⁵ This is not just a general inflammatory state drifting through the bloodstream. The proximity of IMAT to muscle fibers means those inflammatory signals hit the muscle at high concentrations, like a loudspeaker right next to your ear rather than across the room.

Research directly quantifying what IMAT secretes has found it to be remarkably inflammatory. Compared to subcutaneous fat (the fat under your skin) and visceral fat, IMAT released significantly more of multiple inflammatory cytokines, chemokines, and eicosanoids in laboratory analysis.⁶ Experiments using human tissue have also confirmed that factors secreted from IMAT directly reduce muscle insulin sensitivity, likely through inflammatory signaling and by increasing local fatty acid concentrations.⁷

Within muscle cells themselves, certain lipid species are more disruptive than others. Diacylglycerols and ceramides can impair the molecular cascade through which insulin tells a muscle cell to take up glucose, and acylcarnitines reflect inefficient fat-burning by mitochondria. The intramuscular lipid profile, meaning which specific fats accumulate and where, is a telling indicator of insulin resistance.⁸

The Mitochondrial Connection

A recurring theme in muscular fat research is that the problem is often not too much fat coming in but too little being burned. Mitochondria, the structures inside cells that produce energy by burning fuel, play a central role. When researchers investigated why fat accumulates in myosteatosis, they found that mitochondrial dysfunction and reduced fatty acid oxidation were likely driving the buildup, rather than an oversupply of fat from the diet alone.⁹ This aligns with the athlete’s paradox: trained athletes have abundant mitochondria that efficiently oxidize fat, keeping intramuscular lipids in a healthy, dynamic state. Sedentary or metabolically impaired individuals have fewer and less efficient mitochondria, so fat that enters the muscle tends to stay and accumulate in harmful forms.

Muscle cells do have a protective mechanism. A family of proteins called perilipins coat the surface of lipid droplets within cells and help regulate when and how fat is released. This “packaging” of fat into specific compartments acts as a compensatory strategy, isolating potentially harmful lipid species from the rest of the cell.¹⁰ When this packaging system works well, intramuscular fat stays contained and available as fuel. When it breaks down, lipid intermediates spill into parts of the cell where they interfere with insulin signaling and energy production.

Muscular Fat and Aging

Myosteatosis increases with age in virtually everyone, and this is one of the key reasons muscle quality deteriorates even in people who maintain a stable weight. A workshop convened at the National Institute on Aging described myosteatosis as an ectopic fat depot that grows with aging and negatively correlates with muscle mass, strength, mobility, and metabolic health.¹¹

The effects compound. As muscular fat increases with age, it contributes to increased passive muscle stiffness, reduced force production, and greater systemic inflammation. The age-related decline in sex hormones and the development of anabolic resistance, where muscles become less responsive to the signals that normally trigger growth, amplify these effects.¹² You can think of it as a feedback loop: less activity leads to more muscular fat, which impairs muscle quality, which makes activity harder, which leads to still more fat infiltration.

This matters for everyday function in older adults. Research on very old adults (nonagenarians) found that higher-quality muscle fibers, specifically those with lower fat infiltration in the quadriceps, were associated with better gait performance in terms of step regularity and symmetry.¹³ In middle-aged women with knee osteoarthritis, increased intramuscular fat in the thigh was associated with reduced knee strength and slower walking and stair-climbing speeds.¹⁴ The relationship between fat-infiltrated muscle and impaired gait is clinically relevant because unsteady walking is one of the strongest predictors of falls in older people.

Why Surgeons and ICU Doctors Care About Myosteatosis

Muscular fat has emerged as a surprisingly powerful predictor of who does well and who does poorly after surgery or critical illness. Surgeons can measure myosteatosis from routine CT scans by looking at the density of muscle tissue on the images. Fattier muscle appears darker, and the difference is measurable in Hounsfield units.

In kidney transplant recipients, myosteatosis was the only independent risk factor for postsurgical complications, with patients who had it facing roughly four and a half times the odds of complications compared to those without it.¹⁵ In critically ill surgical patients, myosteatosis was independently associated with higher 90-day mortality, longer time on mechanical ventilation, and longer ICU stays.¹⁶ And in gastric cancer patients undergoing robotic surgery, myosteatosis independently predicted nearly triple the odds of overall complications and significantly poorer long-term survival.¹⁷

These findings are reshaping how clinicians assess risk before surgery. Traditional measures like body mass index miss myosteatosis entirely. Someone can have a normal BMI yet harbor significant fat infiltration in their muscles, leaving them poorly equipped for the metabolic stress of surgery or critical illness. The growing recognition of myosteatosis as a prognostic marker is one of the more actionable developments in this field.

Muscular Fat and Fatty Liver Disease

The relationship between muscular fat and non-alcoholic fatty liver disease is another area gaining attention. Among people with fatty liver disease, intermuscular fat was significantly higher than in those without the condition. In obese individuals specifically, IMAT was independently correlated with fatty liver, and among those who already had fatty liver, higher IMAT was independently associated with a greater risk of advanced liver fibrosis.¹⁸ A separate study of middle-aged and older adults with type 2 diabetes found that the ratio of fat to muscle mass was an independent predictor of fatty liver, with the association being especially strong in men.¹⁹

This makes physiological sense. When muscles are poor at burning fat, surplus fatty acids circulate back to the liver, contributing to hepatic fat storage. Muscular fat and liver fat may be downstream manifestations of the same underlying metabolic dysfunction: impaired fatty acid oxidation, chronic low-grade inflammation, and insulin resistance feeding each other across organs.

What Exercise Does to Muscular Fat

Exercise is the most consistently effective intervention against muscular fat, and it works through several routes simultaneously. In a study of elderly men with impaired glucose tolerance, an endurance training program reduced intramuscular triglyceride levels, increased fatty acid oxidation capacity, improved the glucose transporter protein expression in muscle, and increased capillary density around the muscle fibers that specialize in endurance work.²⁰ In other words, training did not just reduce the fat; it rebuilt the machinery that burns fat and takes up glucose.

Both aerobic exercise and resistance training appear to help, though they may work through partially different mechanisms. Aerobic training improves mitochondrial oxidative capacity, meaning your muscle cells get better at using fat as fuel. Resistance training builds muscle mass and can physically displace some of the fat that has infiltrated the tissue. For older adults especially, the combination is likely most beneficial since the problem is both too much fat and too little functional muscle.

The challenge is that the people who stand to benefit most from exercise are often those least able to do it. Heavy myosteatosis impairs muscle force production and increases stiffness, making movement harder and less comfortable. Starting with low-intensity activities and gradually building is a reasonable approach, though the research on optimal exercise prescriptions for reversing myosteatosis specifically is still developing.

How Diet Influences the Fat Inside Your Muscles

The type of dietary fat you eat appears to influence what ends up stored in your muscles, not just how much. In mice fed high-fat diets, a diet rich in unsaturated fatty acids (from sources like sunflower oil) prevented the accumulation of both triglycerides and diacylglycerols in muscle, while a saturated-fat-heavy diet did not. The fatty acid composition of the stored muscle lipids reflected what the animals ate.²¹ In rats, a diet enriched in polyunsaturated fat kept muscle ceramide levels stable, while a diet high in saturated fat increased ceramide content by roughly half in certain muscle types.²²

These are animal studies, so the direct applicability to human diets requires some caution. But the pattern is consistent with broader nutritional research: saturated fat tends to worsen insulin resistance and inflammatory markers, while replacing it with unsaturated fat tends to improve them. The idea that the specific fats reaching your muscles depend on what you eat adds a layer of granularity beyond simply counting total fat intake.

GLP-1 Medications and Muscle Quality

The rapid adoption of GLP-1 receptor agonist medications for weight loss has raised concerns about muscle loss alongside fat loss. A review of the evidence found that skeletal muscle changes with these drugs appear to be adaptive rather than destructive. Reductions in muscle volume seem proportional to what would be expected given the amount of weight lost, and improvements in insulin sensitivity and muscle fat infiltration likely contribute to improved muscle quality even as overall volume decreases.²³

This is an important nuance. A muscle that loses volume but also loses its fat infiltration can end up functionally better, pound for pound, than the larger but fattier muscle it replaced. Think of it as trading a marbled steak for a leaner cut. The total mass is less, but the tissue that remains is more purely contractile. Whether this holds up across all patient populations and durations of treatment is still being studied, and combining these medications with resistance exercise is widely recommended to preserve as much functional muscle as possible.

Who Is Most Susceptible

Susceptibility to myosteatosis is not evenly distributed. Age is the single largest factor, but sex, ethnicity, and genetic background all play a role.²⁴ Women tend to store more intramuscular fat than men, though the metabolic consequences can differ. Sleep also appears relevant: research has found that reduced sleep duration and poor sleep quality are associated with lower skeletal muscle mass, potentially through disruption of circadian rhythms that regulate muscle maintenance and repair.²⁵

Chronic diseases accelerate the process. People with type 2 diabetes, obesity, cancer, and conditions that force extended bed rest are all at heightened risk. Frailty and inactivity create a vicious cycle with muscular fat. In frail older adults, higher intramuscular fat correlates with higher local inflammation, which contributes to further muscle and mobility dysfunction.²⁶

Intramuscular Fat in Animals Versus Humans

If the term “marbling” came to mind while reading this, the connection is not accidental. Intramuscular fat is the same tissue prized in beef cattle for flavor and tenderness. Cattle have an unusually high capacity to accumulate intramuscular fat compared to other species, partly because of abundant fatty acid sources for triglyceride synthesis. In cattle, intramuscular fat develops later and grows more slowly than other fat depots like subcutaneous fat.²⁷

In humans, intramuscular fat within the muscle cells themselves is normally modest and primarily serves as local fuel. The kind of visible marbling you see in a well-fed steer would be considered pathological in a human thigh. It is worth noting that when meat scientists talk about intramuscular fat as a positive quality trait, they are describing a consumer preference for flavor and texture in food, not a health outcome for the animal. In your own body, the same tissue is working against you, interfering with the very functions muscle is supposed to perform.