Sarcopenia, the muscle loss related to aging, may start slowly in your thirties and continue progressing with growing rapidity into your seventies. It is not identified with definite biomarkers as medical practitioners prefer to use today. Sarcopenia tends to get an “I know it when I see it” sort of diagnosis.
Although this difficulty in diagnosing sarcopenia is understandable considering the mental picture of the frailty associated with aging, loss of muscle mass is a major health issue.
- With a loss of muscle comes a loss of strength
- It is more difficult to get around, climb stairs, or walk long distances
- It leads to falls and serious injuries including broken bones
- When injuries occur, it takes longer to heal
- Surgeries may be less successful and infections take hold more readily
Unless measures are taken to stop it, sarcopenia may lead to prolonged hospitalizations, nursing homes, and possibly even death.
Anabolism and Catabolism
Our bodies are in the constant process of remodeling. We build and rebuild molecules, break down old cells and tissues to make way for the new, and dispose of or reuse the molecules. When we are young the rate at which we rebuild (anabolism) exceeds the rate at which we break down (catabolism). There are multiple factors that trigger more catabolism than anabolism as we age, including:
- Changes in neurochemistry
- Hormone imbalances
- Production of inflammatory cytokine (cells produced by the immune system that act on other cells)
- Inadequate nutrition
- Environmental hazards
- Declining physical activity
Muscle is composed of many different cell types. Muscle stem cells are called satellite cells. Satellite cells are located on the outside membrane of the muscle cells and next to the blood vessels. These cells are not active unless there is some stimulus from injury to the muscle or from the environment carried in the blood stream. When activated, these satellite cells become new muscle cells.
Estradiol and Testosterone
Sarcopenia develops with the decline of sex hormones. Research in the last decade reveals that the satellite cells have receptors for–and respond to—estrogens (such as estradiol) and androgens (such as testosterone). Studies support that estradiol has beneficial effects on muscle strength.
Most muscle cell types have receptors for testosterone, but testosterone receptors predominate in satellite cells. Administration of testosterone increases the number of satellite cells, and also directly inhibits inflammatory cytokines. Higher testosterone levels contribute to increased strength and mass; since women generally have less testosterone than men, this might explain why women tend to develop sarcopenia at twice the rate as men.
DHEA and Human Growth Hormone
Adrenal DHEA, another androgen, also declines with age, and may affect muscle strength via a number of mechanisms. DHEA is converted to estrogens and testosterone in the body, which may have a direct effect on receptors. Also, DHEA increases sensitivity to insulin, another anabolic hormone, which may also increase levels of IGF-1 (the active metabolite of growth hormone). Increased IGF-1 may indicate increased levels of growth hormone. Growth hormone has been shown to increase muscle mass in many studies.
The Triad of Frailty
In their article Frailty and the Older Man, Drs. Jeremy Walston and Linda Fried proposed looking at the concept of frailty in the elderly as a triad:
- With aging the hypothalamic responses to stress change, cortisol levels increase, and the signals to produce sex hormones and growth hormone decline
- The immune system is affected, producing fewer antibodies and more inflammatory cytokines
- Both of these effects contribute to sarcopenia
All three systems are interdependent: the endocrine system, the immune system, and the muscular system participate together in a spiral of decline.