Sarcopenia

Sarcopenia is a progressive and generalized skeletal muscle disorder characterized by a loss of muscle mass and strength and is associated with an increased risk of adverse outcomes, including falls, bone fractures, postoperative complications, physical disability, and mortality.^[1][2]

There are two types of sarcopenia — primary and secondary. Sarcopenia is considered primary when it results from no other underlying cause except for age.^[1] It is considered secondary when causal factors other than age are present, such as disease (e.g., cancer, advanced organ failure), malnutrition, or physical inactivity.

• History of recurrent falls
• Feeling weak
• Slow walking speed
• Difficulty rising from a chair
• Recent unintentional weight loss (> 5%)

Muscle mass, strength, and physical performance are assessed to diagnose sarcopenia.^[1] Diagnosis starts with muscle strength, usually grip strength measured using a calibrated handheld dynamometer, but lower body strength may also be assessed using the chair stand test, which measures the amount of time it takes the individual to rise five times from a seated position without using their arms. If low muscle strength is determined, muscle quantity is assessed to confirm the presence of sarcopenia. Lastly, physical performance is assessed using scores on the gait speed test, the Short Physical Performance Battery, the Timed-Up and Go test, or the 400-meter walk test to determine the severity of sarcopenia.

No specific drugs have been approved for the treatment of sarcopenia. Testosterone treatment may increase muscle mass and strength in older men with low serum testosterone levels (<200–300 ng/mL) and muscle weakness.^[3] In addition, preliminary evidence suggests that myostatin inhibitors, which block the actions of myostatin — a protein secreted by muscle cells that inhibits protein synthesis and hypertrophy — may increase muscle mass and some measures of physical performance.^[4][5] However, the medical use of myostatin inhibitors as a treatment of sarcopenia is currently limited to clinical trials.

The following supplements have been studied for the treatment of sarcopenia and have shown some efficacy in different scenarios (e.g., when combined with resistance exercise, in people with inadequate dietary intake):^[6]

• Protein
• Leucine
• Creatine
• Beta-hydroxy beta-methylbutyrate
• Omega-3 polyunsaturated fatty acids
• Vitamin D

Protein is crucial for skeletal muscle growth and maintenance, and older adults display an impaired muscle protein synthesis response to the ingestion of protein,^[7] so a large portion of the evidence base revolves around optimizing protein intake for the prevention and treatment of sarcopenia.

Total protein intake should ideally be 1.2–1.6 grams per kilogram of body weight per day, evenly distributed between 3–4 meals containing ≥ 0.4 grams of protein per kilogram of body weight.^[6]

With respect to dietary patterns, largely consistent evidence from observational studies demonstrates that higher adherence to a Mediterranean diet is associated with better physical functioning, including lower extremity functioning, mobility, and walking speed.^[8][9]

Resistance exercise is the most potent non-medical treatment for combatting skeletal muscle deterioration and improving health-related quality of life.^[10] It’s traditionally recommended that people perform 2–3 resistance training sessions per week using relatively heavy loads (i.e., 80% of 1-repetition maximum), but more recent evidence suggests that low-load resistance training (i.e., 35–50% of 1-repetition maximum) is similarly effective for increasing muscle mass and strength when performed to volitional fatigue.^[6] A combined resistance training and high-protein diet intervention seems to be more effective than either intervention alone.^[11]

In the case of primary sarcopenia, there is a wide range of factors that contribute to the development of the condition, which are not entirely understood and largely thought to be natural consequences of aging.^[2] These include decreased type II muscle fiber size, loss of motor units (i.e., a motor neuron and the muscle fibers it innervates), hormonal changes (i.e., a decline in serum levels of anabolic hormones like testosterone and insulin-like growth factor 1), anorexia (i.e., decreased or loss of appetite), decreased physical activity, anabolic resistance (i.e., a blunted muscle protein synthesis response to dietary protein and resistance exercise), systemic inflammation, insulin resistance, and increased body fat.^[12]