What Is Sarcopenia, and Can We Turn Back the Clock?
How to confront three forces that weaken muscle cells in the elderly.
What makes us weaken with age? The prime culprit is sarcopenia—age-related loss of muscle mass, strength, power and function (Sayer et al. 2013; Morley 2012). Morley (2012) says 5%–13% of 60- to 70-year-olds and 11%–50% of people in their 80s have sarcopenia, which means “poverty of flesh.”
A 2002 report from the United Nations Second World Assembly on Ageing (United Nations 2002) outlined why fitness and wellness professionals need to learn more about age-related muscle loss. The report predicted that the world’s over-60 population would more than triple from 2000 to 2050, with the over-80 population increasing fivefold.
A major theme of that U.N. assembly was how to provide older people with health care and support, including preventive and rehabilitative care. Exercise professionals need to recognize that the coming exponential growth of the older population is likely to influence clientele
demographics, requiring a much more in-depth understanding of sarcopenia and of the best interventions for managing it.
What Causes Sarcopenia?
While several factors play a role in sarcopenia, three major contributors will be discussed here:
- reduction in muscle innervation (activation)
- oxidative damage from reactive oxygen species
- nutritional factors associated with age (Doria et al. 2012; Sayer et al. 2013)
Reduced Muscle Innervation
The “use-it-or-lose-it” principle explains one of the main causes of sarcopenia—a reduction in muscle innervation. Morley (2012) says the most dominant cause of sarcopenia is inactivity, both in the elderly and in the overall population. Muscle motor units—motor nerves and the muscle fibers they innervate—are codependent, implying that when the motor neurons begin to die as a result of age and/or inactivity, denervation (interruption of the nerve connection) of the muscle fibers causes atrophy (wasting away) of the muscle cells.
As people become less active with age, they lose some of their motor neurons and face diminished function of those that remain (Sayer et al. 2013). Importantly, muscle contractions from exercise trigger the release of muscle growth factors, including insulin growth factor and mechano-growth factor (Morley 2012). These growth factors activate specialized cells in muscle (called satellite cells) that promote protein synthesis.
Cardiovascular and resistance exercises play a major role in preventing the muscle-innervation problems that lead to sarcopenia. While no accepted exercise guidelines have been adopted to protect against sarcopenia, the sidebar “Physical Activity Guidelines for Adults and Older Adults” offers a good starting point.
Reactive Oxygen Species
Reactive oxygen species (ROS) are chemically active molecules that contain oxygen. Produced naturally by all tissues of the body during aerobic metabolism, ROS help with the cells’ homeostasis (balance) regulation and cell messaging. Because ROS are reactive, if they are overproduced (owing to a functional deterioration of the mitochondria, the cells’ power generators) they may start attacking other molecules in cells, especially in muscle (Doria et al. 2012).
ROS are thought to play a key role in the development of sarcopenia (Sayer et al. 2013). That makes sense, given that skeletal muscle is the body’s largest consumer of oxygen and is vulnerable to ROS buildup. ROS can cause oxidative damage to mitochondrial proteins, cell membranes and even DNA. This damage impairs the function of ATP (adenosine triphosphate, the energy “currency” of the cell) and prevents cells from carrying out many necessary metabolic functions. Apoptosis (self-destruction of a cell) can also result from an accumulation of ROS
within the mitochondria (Doria et al. 2012). The great news is that moderate- and high-intensity exercise will promote the production of powerful antioxidant enzymes that combat the accumulation of ROS (Gomez-Cabrera, Domenech & Viña 2008).
Sayer et al. (2013) summarize literature indicating that diet also has an important influence on sarcopenia, with the most consistent evidence pointing to the roles of protein, vitamin D and anti-oxidant nutrients. The authors say the loss of appetite and hunger response as a result of aging causes an average 25% decrease in food intake between the ages of 40 and 70. This decrease in consumption leads to insufficient protein intake and low micronutrient levels.
Many vitamins and minerals play key roles in healthy muscular and neural functioning. Sayer and colleagues say there is a fourfold increase in the likelihood of frailty in elderly populations with low vitamin D status, thus implicating the association with vitamin D insufficiency and sarcopenia. Interestingly, Sayer et al. note that meta-analysis (statistical analyses of multiple studies) suggests vitamin D supplementation (700–1,000 International Units per day) reduces the risk of falls in older people.
It is clear that sarcopenia is a prevalent and debilitating disorder with several causes, effects and counteractions. Moderate- and high-intensity cardiovascular exercise and resistance training can counteract neural decay and produce the antioxidants needed to fight the reactive oxygen species. An exercise program coupled with a proper nutritional plan provides a meaningful strategy that can make the difference between debilitation and a healthy, active lifestyle. As personal trainers, it is our responsibility to see that the elderly we train are given the tools to enjoy the quality of life they have worked so hard to earn.
|cardiovascular exercise||150 minutes (2.5 hours) per week||moderate 4–5 on a 1–10 scale|
|cardiovascular exercise||75 minutes per week||vigorous 7–8 on a 1–10 scale|
|cardiovascular exercise for greater benefit||300 minutes (5 hours) per week||moderate 4–5 on a 1–10 scale|
|cardiovascular exercise for greater benefit||150 minutes (2.5 hours) per week||vigorous 7–8 on a 1–10 scale|
|muscle-strengthening activities||at least twice per week||moderate or high, involving all major muscle groups|
Doria, E., et al. 2012. Relationship between human aging muscle and oxidative system pathway. Oxidative Medicine and Cellular Longevity, doi:10.1155/2012/830257.
Gomez-Cabrera, M.C., Domenech, E., & Vin╠âa, J. 2008. Moderate exercise is an antioxidant: Upregulation of antioxidant genes by training. Free Radical Biology & Medicine, 44 (2), 126ÔÇô31.
HHS (U.S. Department of Health and Human Services). 2008. Office of Disease Prevention and Health Promotion. 2008 Physical Activity Guidelines for Americans. www.health.gov/PAGuidelines/pdf/paguide.pdf; accessed Nov. 14, 2013.
Morley, J.E., 2012. Sarcopenia in the elderly. Family Practice, 29 (1 Suppl.), i44ÔÇôi48.
Sayer, A.A., et al. 2013. New horizons in the pathogenesis, diagnosis and management of sarcopenia. Age and Ageing, 42 (2), 145ÔÇô50.
United Nations (2002). Political Declaration and Madrid International Plan of Action on Ageing. Second World Assembly on Ageing, Madrid, Spain. www.un.org/en/events/pastevents/pdfs/Madrid_plan.pdf; accessed Nov. 14, 2013.