Sarcopenia comes from the Greek words sacra, "flesh", and penia, "poverty". More specifically, sarcopenia is the gradual loss of muscle mass and strength with age. It's not a disease, not a condition, and not a syndrome, but rather an unfortunate consequence of the natural aging process. Not to be confused with cachexia (accelerated muscle loss secondary to a disease such as cancer), sarcopenia is slow, progressive, and unnervingly unsuspecting. The 0.5-1% loss of muscle mass each year is deceptive, and unlike many of the consequences of aging, sarcopenia actually starts when we are quite young, generally around the age of 30. The loss of muscle mass and strength has profound consequences on day-to-day living.
Sarcopenia alters muscle structure and function in many different ways. First and foremost with sarcopenia comes muscle atrophy. Muscle atrophy is the shrinking of individual muscle cells, called muscle fibers. So while you do not lose a substantial number of muscle fibers, the smaller diameter muscle fibers result in reduced strength and mass. Interestingly, not all muscle undergoes atrophy equally. Muscle fibers can be separated based on size, contraction properties, and metabolic abilities, into different "fiber types". With sarcopenia, the larger more powerful muscle fibers preferentially undergo atrophy and contribute to the loss in overall strength. However, the loss of muscle size is not the only factor that contributes to a loss in muscle strength. A change in muscle quality also occurs with sarcopenia. Healthy muscle is just that, muscle. However, with sarcopenia, muscle becomes increasingly infiltrated with alternative cells types such as fibroblasts (cells that contribute to tissue structure) or adipocytes (fat cells).
How and whether these two physiological processes, loss in muscle size and loss in muscle quality, interact is not entirely known. One theory involves the muscle satellite cells or muscle stem cells. Normally, when muscle fibers are damaged muscle precursor cells that hang out next to the muscle fibers and wait to be called into action replace them. With aging however these muscle stem cells can become dysfunctional and instead of muscle replacing muscle, pesky fibroblast or adipocytes either show up or may be produced by the muscle stem cells (the jury is still out). A number of labs (Campisi Lab, Rando Lab, Blau lab, Conboy lab) in the Bay Area are studying how muscle stem cells function normally and in disease.