Prevention of sarcopenia should begin in adulthood, as the loss of muscle mass and function begins around the age of thirty and becomes more prominent after the age of fifty. Prevention is based on maintaining a high level of physical activity in daily life, specific endurance exercise, proper nutrition and avoidance of risky behaviors (smoking, drinking alcohol). Establishing these habits can delay the onset of sarcopenia, possibly by more than a decade, depending on the age at which the changes begin.
It is probably worth using screening tests to detect sarcopenia in this population, although there is still no agreement on what age to start looking for sarcopenia, nor has population screening been shown to improve relevant clinical outcomes.
An alternative is to look for sarcopenia in certain care settings or at-risk populations. The elderly admitted to hospitals, nursing homes or rehabilitation centers, and those attending Geriatrics consultations are particularly at-risk groups; repeated falls, those who appear to walk more slowly, those with prolonged limitation of physical activity, those who use a cane or crutch, or those who have trouble getting out of a chair.
Treatment of sarcopenia
Treatment of sarcopenia must necessarily include resistance exercises and improvement of the diet, increasing protein intake to 1.2-1.5 g/kg/day and covering caloric requirements. In some cases, it will also be necessary to resort to nutritional supplements, which may contain leucine, HMB and vitamin D to optimize their effects on muscle.
A proportionate distribution of proteins throughout the day is also recommended, with emphasis on ingesting proteins immediately after exercise, since the muscle seems to have priority at that time to receive the ingested proteins.
Medications to treat sarcopenia are not yet available.
Pathophysiology of sarcopenia
The pathophysiology of sarcopenia is very complex, including both muscular processes and endocrine and neurological regulatory processes.
With normal aging, the quality of muscle fibers deteriorates, reducing their maximum power, shortening speed and elasticity.
Anatomical changes also occur, with a reduction in the number and activation of muscle satellite cells, a reduction in the number of muscle fibers (especially type IIA) and fatty infiltration of the muscle. Circulating levels of myostatin also increase with age, and the regulation of various genes that regulate muscle protein metabolism is modified.
On the other hand, the neurological control of movement is also affected.