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Sarcopenic Obesity – Definition and Background

The term “sarcopenic obesity” has been proposed to describe obesity characterized by reduced skeletal muscle mass and function.

There is currently no consensus on the definition of sarcopenic obesity, but the diagnosis should include criteria for both sarcopenia and obesity. The diagnosis of sarcopenia is based on low muscle mass, low muscle strength, and poor physical performance.

Sarcopenia is more common in women than in men. Reducing excess adipose tissue, which is the cornerstone of treatment for people living with obesity, often results in a concomitant reduction in muscle mass.

Low muscle mass can lead to progressive weakness, disability, increased morbidity and mortality.

Clinical relevance and observations

However, the understanding of the importance of skeletal muscle preservation seems to be largely limited to its effect on aging patients and less so in the obese patient group. The change in skeletal muscle mass is not homogeneous in obese individuals, while the heterogeneous phenotypes of these individuals seem to contribute to its even less recognition.

The literature confirms the positive correlation between body mass index (BMI) and lean mass.

Modest increases in skeletal muscle mass occur as a result of the higher muscular work required by increased body weight as well as the potential direct anabolic effects of higher dietary protein intake.

Mechanisms of Muscle Metabolic Changes

However, it is becoming increasingly clear that changes in skeletal muscle metabolism may occur in obesity, leading to a body composition with higher fat mass and a significant loss of muscle mass. Several complex interrelated mechanisms may contribute to these changes.

The primary metabolic abnormalities found in obesity, such as persistent subclinical inflammation, including through adipokines secretion from adipose tissue, oxidative stress, and insulin resistance, can foster a myocatabolic potential and promote a kind of “anabolic resistance” in skeletal muscle, blunting the response of muscle protein synthesis to nutrients.

Ectopic fat accumulation in muscle, as a result of excessive availability, is also associated with systemic insulin resistance. Similarly, the observed, in later stages, mitochondrial dysfunction in skeletal muscle of obese patients exacerbates oxidative stress and the associated metabolic cascades that lead to insulin resistance and catabolism.

It is possible that the reduction in ATP production leads to low muscle strength and endurance. Another possible mechanism involved in limiting the maintenance of skeletal muscle mass involves the dysfunction of muscle progenitor cells, which can undergo differentiation into adipocytes.

Factors that aggravate the condition

In addition, low physical activity is a fundamental associated factor, which often evolves in parallel with the progression of the disease (increase in body weight) due to the worsening of musculoskeletal complications of obesity and the inability of patients to exercise.

Also, common comorbidities of obesity, such as type 2 diabetes mellitus, chronic heart failure, chronic kidney disease, malignancies, etc. may act aggravatingly by causing catabolic changes through common pathways mentioned above such as increased oxidative stress, proinflammatory lesions but also through reduced vascular perfusion (atherosclerotic disease, increased epicardial fat, etc.) but also due to reduced physical activity due to them.

In conclusion, multiple mechanisms are responsible for the metabolic changes of muscle tissue in obesity, especially in individuals with longer disease duration, complications and comorbidities, as well as in elderly individuals who may undergo additional muscle changes due to aging. Most mechanisms directly reduce muscle anabolism, while others seem to have a negative effect on muscle quality, i.e. strength per muscle unit and endurance.

The latter include muscle fat accumulation that reduces muscle density and quality, mitochondrial dysfunction with reduced ATP production and maximal oxygen consumption leading to reduced strength and endurance.

Diagnosis and clinical limitations

The identification of sarcopenic obesity has limitations in the methodology used to determine its characteristics (body composition analysis, muscle strength or cardiorespiratory fitness and physical capacity). However, it remains important as we know that individuals with obesity and low muscle mass had a higher risk of developing weakness and disability and therefore poor quality of life, while this risk seems to be significantly higher than that observed in lean individuals with similar muscle changes.

Low or declining muscle mass is emerging as a negative prognostic factor associated with higher morbidity and mortality in obese patients suffering from chronic diseases.

Clinical examples and prognostic significance

For example, low physical activity capacity in individuals with obesity and heart failure predicted poor outcome, while in individuals with chronic kidney disease, changes in muscle mass were a determinant of survival independent of changes in total body weight.

This highlights the important role of muscle mass in the morbidity and mortality of obese patients and, correspondingly, the potential improvement in obesity-related morbidity and mortality when measures to prevent and/or treat changes in muscle mass are implemented.

When should it be assessed?

The risk of skeletal muscle loss and dysfunction should be assessed in obese individuals, especially in the presence of advanced age (>65 years) or when concomitant metabolic complications, chronic diseases and/or acute complications occur. Sarcopenic obesity may be involved in the occurrence of T2DM, non-alcoholic fatty liver disease, dyslipidemia, arterial hypertension and cardiovascular disease, etc.

Finally, monitoring skeletal muscle function and mass is important in order to prevent or minimize muscle loss in patients undergoing metabolic surgery (including due to rapid weight loss).

Therapeutic approach and endpoints

Sarcopenic obesity remains largely undiagnosed. The pathogenesis of sarcopenic obesity appears to be multifactorial (interaction of aging, reduced physical activity, insulin resistance, inflammation, oxidative stress, etc.), resulting in a quantitative and qualitative decrease in muscle mass and an increase in fat mass.

Hypocaloric diet, exercise and adequate protein intake are the cornerstones of the proper management of these patients. Weight loss without exercise in individuals with sarcopenic obesity results in a reduction in fat mass but inevitably a reduction in lean mass is observed, thus worsening sarcopenia.

The best type of exercise has not yet been determined, but available data suggest that resistance exercise or a combination of aerobic and resistance exercise may be the best option.