Fatty Liver Disease in Athletes: Causes and the Link with Training Load and Pharmacology

Fatty liver disease has long been considered a disease of sedentary, obese people, and regular training really is among the best ways to prevent it. Yet active people are not insured against it either: weightlifters in a “bulk,” athletes in strength sports with a large body mass, lovers of sweet drinks, and users of hormonal drugs have their own risk factors. The editorial team examines how load and pharmacology are connected with the accumulation of fat in the liver.

What fatty liver disease is

Fatty liver disease, or hepatic steatosis, is a condition in which fat accumulates in more than 5% of liver cells (hepatocytes). In most cases it is associated with metabolic disorders and for a long time was called non-alcoholic fatty liver disease (NAFLD).

In 2023 international hepatology societies proposed new terminology: metabolic dysfunction-associated steatotic liver disease (MASLD). The diagnosis is made when steatosis is combined with at least one cardiometabolic risk factor — excess body weight or waist circumference, impaired glucose metabolism, elevated blood pressure, high triglycerides, or low HDL cholesterol (Rinella et al., 2023).

The disease has a spectrum of forms: from simple steatosis without inflammation to steatohepatitis (MASH), when fat is accompanied by inflammation and cell damage, and further — to fibrosis and cirrhosis. The most important prognostic factor is exactly the degree of fibrosis.

MASLD is the most common chronic liver disease in the world, and its frequency is rising along with the prevalence of obesity and type 2 diabetes. In most people it proceeds asymptomatically for years and is detected by chance on ultrasound or by elevated liver tests.

The main causes and mechanisms

A central role is played by insulin resistance. When tissues respond poorly to insulin, more fatty acids are released from adipose tissue and enter the liver, while the liver itself more actively synthesizes fat from carbohydrates. The removal of fat in the form of lipoproteins does not keep pace with its intake.

Visceral fat — fat around the internal organs — is especially closely associated with fatty liver disease. So even an athlete with a normal body mass index but an increased waist may have steatosis. And conversely, in weightlifters and representatives of strength sports with a large body mass, it is exactly the ratio of muscle to visceral fat that determines the risk.

Dietary factors are a persistent excess of calories, a large amount of added sugar, and especially fructose from sweet drinks, juices, and “gainers” with simple carbohydrates. Fructose is metabolized mainly in the liver and actively stimulates fat synthesis there. A period of “dirty bulking” with a chronic calorie surplus creates exactly such conditions.

Among other causes are alcohol (with significant consumption we already speak of alcoholic or mixed disease), genetic variants (for example, in the PNPLA3 gene), rapid weight loss during fasting, certain medications, and endocrine conditions — hypothyroidism, polycystic ovary syndrome, growth hormone deficiency.

Training: protection, not a cause

Physical activity is among the most proven ways to reduce the fat content in the liver. A meta-analysis by Keating and co-authors (2012) showed that regular training reduces liver fat even without significant weight loss. This effect is attributed to increased insulin sensitivity and greater use of fatty acids by the muscles.

Both aerobic and strength training have a positive effect. For people who find it hard to do long cardio sessions, strength loads are a full-fledged alternative. The clinical guidelines of EASL and AASLD consider physical activity a cornerstone of treatment along with dietary change.

So the training process itself does not cause fatty liver disease. The risk in athletes is associated with what happens around training: with nutrition during periods of mass gain, with alcohol “after competitions,” with long breaks after injuries, when eating habits persist while energy expenditure drops sharply.

A separate case is former strength-sport athletes and weightlifters after finishing their careers. The high caloric content of the diet, usual for the competition period, in combination with a drop in activity, quickly leads to the accumulation of visceral fat and steatosis.

• the risk rises: a prolonged calorie surplus, sweet drinks, alcohol, a large waist size;
• the risk rises: an abrupt cessation of training without dietary correction;
• the risk decreases: regular aerobic or strength training, a moderate calorie deficit in case of excess weight.

Pharmacology and the liver

Anabolic-androgenic steroids, especially oral 17-alpha-alkylated ones, are known for their hepatotoxicity, but their typical “liver” profile is different — cholestasis (impaired outflow of bile), peliosis hepatis, adenomas, and in rare cases tumors (Pope et al., 2014). At the same time, steroids worsen the lipid profile, reduce HDL, and can affect insulin sensitivity, that is, exactly the metabolic factors that underlie MASLD.

Systemic glucocorticoids are classic drugs that cause steatosis: they raise glucose levels, promote insulin resistance, and redistribute fat. Athletes receive them for injuries, asthma, or allergies; short courses are usually safe, while long-term intake requires monitoring.

Growth hormone has a twofold connection with the liver. Its deficiency is associated with fatty liver disease, while its excess, in particular with self-directed use, causes insulin resistance and can disrupt carbohydrate metabolism. Among other drugs associated with steatosis are amiodarone, methotrexate, tamoxifen, and some antiretroviral drugs.

Supplements should not be forgotten either. The LiverTox database of the US National Institutes of Health describes cases of liver damage from concentrated green tea extracts, some herbal “fat burners,” and multi-component supplements. This is no longer fatty liver disease but toxic damage, yet it adds a burden to a liver that already has steatosis.

The trap of liver tests in athletes

Elevated ALT and AST often become the first signal that something is wrong with the liver. However, in people who train, these enzymes are not of liver origin alone: they are also found in muscles. After a heavy strength workout their level can rise significantly and remain elevated for several days.

Pettersson and co-authors (2008) showed that in healthy men who had not previously done strength training, ALT and AST after a session with weights rose to values that could be regarded as pathological and remained so for at least a week. In parallel, creatine kinase — a marker of muscle damage — rose sharply.

So for a correct assessment of liver tests, before the test it is worth taking a break from heavy training and at the same time taking creatine kinase and GGT. It is also important to remember the reverse: normal liver enzymes do not rule out fatty liver disease, which often proceeds with normal ALT and AST.

Editorial conclusions

Fatty liver disease is a metabolic disease whose basis is insulin resistance, visceral fat, and an excess of calories, especially from sugar and fructose. Regular training protects the liver rather than harms it.

In athletes the risks are associated with nutrition during mass gain, alcohol, cessation of training without dietary correction, as well as with hormonal drugs and glucocorticoids that worsen the metabolic profile. Anabolic steroids, in addition, have their own hepatotoxicity.

Elevated ALT and AST after training are easily confused with liver damage, so tests are taken after rest and together with creatine kinase and GGT.

We also recommend reading our materials on the prevention and diagnosis of fatty liver disease, on liver tests when using pharmacology, and on creatine kinase in athletes.

References

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2. European Association for the Study of the Liver (EASL), European Association for the Study of Diabetes (EASD), European Association for the Study of Obesity (EASO). EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016;64(6):1388–1402.
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4. Keating SE, Hackett DA, George J, Johnson NA. Exercise and non-alcoholic fatty liver disease: a systematic review and meta-analysis. J Hepatol. 2012;57(1):157–166.
5. Pettersson J, Hindorf U, Persson P, et al. Muscular exercise can cause highly pathological liver function tests in healthy men. Br J Clin Pharmacol. 2008;65(2):253–259.
6. Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
7. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases.