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Understanding Sarcopenia

Sarcopenia, or age-realted skeletal muscle decline, can't be stopped. But, fitness professionals can explain the effects of sarcopenia to their older adult clients, as well as help them to reverse sarcopenia's effects and slow its process.

One inevitable aspect of aging is a steady decline in strength due, in large part, to a gradual loss of skeletal muscle. Generally, we continue to gain strength up to age 30,1 which is about the age when elite athletes reach their peak performance. After 30 years of age, we lose, on average, about 0.5 percent in muscle mass per year until the age of 50, after which the decline is more rapid. The average 50-year-old can expect to lose an additional 30 percent of their muscle mass by the time they are 70 years old, and a further 30 percent between 70 and 80 years of age.2 Note that this is a mean rate of decline - there is considerable variability that depends on genetics and environmental factors, such as activity status. Sedentary individuals lose muscle mass and strength at a faster rate than those who are more physically active.
The medical expression for this age-related skeletal muscle decline is sarcopenia, a Greek term meaning "poverty of flesh."11 The effect of sarcopenia on physical capacity is so gradual that it goes unnoticed for decades unless there is a reason to document physical performance on a regular basis.Master athletes, for example, are painfully aware of their declining physical prowess every time they participate in an organized competitive event. While sarcopenia affects everyone, regardless of gender, ethnicity, income, disease states or health behavior,9 fitness professionals can help clients control its effects.While master athletes are affected by sarcopenia, they retain more muscle mass, strength and endurance than their sedentary counterparts, because of their regular physical activity.5 Most of your clients will have a narrow understanding about how and why physical activity is "good for them," because the marketing messages they are exposed to are superficial. Often, the messages promote basic heart health or desirable body weight. There is hardly ever any reference about how aging affects the metabolic health of skeletal muscle, and how the decline in its quantity and quality relates to heart health, changes in body composition and the so-called "diseases of aging," including osteoporosis, insulin insensitivity and chronic fatigue. The message is this: Sarcopenia is a normal part of aging and, left unchecked, it can lead to weakness, disability, chronic diseases, falls and loss of independence.Aerobic and resistance training can slow sarcopenia, and even reverse its abnormal acceleration due to sedentary behavior, thus helping to maintain overall good health well into old age.11 Fitness professionals who cater to an older population can help educate them about sarcopenia. Clients will appreciate knowing something about the science of aging, as it helps them appreciate the true benefits of exercise.

Men vs. women

Some fitness professionals might suspect that sarcopenia is more of a "female" problem because women inherently have a lower skeletal muscle mass to begin with, they live longer and they have higher rates of disability than men.11 Like bone loss, the menopausal years are a period of accelerated skeletal muscle loss for women, and the abrupt reduction of estrogen during menopause is the probable cause. But sarcopenia occurs in both sexes. Men face declining testosterone levels with age, which removes the key anabolic stimulation for protein synthesis. Between the ages of 25 and 75 years, men lose between 30 and 50 percent of their testosterone - and the decline continues past the age of 75.111

Why muscle is important

Besides its role in locomotion, skeletal muscle has at least four other important functions. 1. It is a depository site for protein. Protein is not stored in the same way fat is stored. The body stores fat that is not in immediate use in special depository sites for future use. Proteins that are not being directly used for body functioning, such as muscle contractile material, enzymes, the immune system, etc., are discarded from the body. This presents a potential problem, because a body that is low in protein is at risk during illness, when nitrogen must be mobilized from muscle tissue to provide amino acids to the immune system.Without adequate nitrogen, the body's capacity to withstand an acute illness declines. Low levels of muscle protein are thought to be related to the poor recovery process older people experience after illness and disease states.10 2. Skeletal muscle affects metabolic rate. A low skeletal muscle mass means that there are fewer metabolically active muscle cells, and this results in a lower resting metabolic rate (RMR).2 There is an estimated 15-percent decline in RMR from 30 to 80 years of age, which translates into using 250 fewer kilocalories each day. This might not seem like much, but keep in mind that an individual who feels weak and tired, and has a low level of endurance, will minimize daily physical activity. A lower daily physical activity level reduces total daily energy expenditure even further, since the body adjusts by eliminating its excess metabolic capacity, so there is a compensatory decline in skeletal muscle - and the cycle continues. 3. Healthy skeletal muscle is a major factor in resisting fatigue. The gradual decline in muscle contributes to a reduction in aerobic exercise tolerance as measured by VO2max. Even master athletes who continue to train lose 5.5 percent of their VO2 max per decade. Sedentary individuals have a 12-percent reduction in VO2 max per decade.2 An inability of the muscle cells to consume sufficient quantities of oxygen efficiently causes early fatigue while performing even the most basic daily activities. 4. Muscle is a disposal site for glucose and fatty acids. After a person eats a meal, their muscle cells will absorb fatty acids and the glucose needed for energy production. A lower number of muscle fibers reduces the immediate need for fatty acids and glucose. Consequently, these substrates will circulate in the blood until they can be removed and stored in adipose tissue. Older individuals often have a hyperglycemic effect after a meal because of the higher levels of glucose in the blood that are not removed at a normal rate. Such high levels of unabsorbed glucose circulating in the blood raises insulin levels and stresses the glucose transport mechanism of the muscle cells, which can contribute to insulin resistance in the long term. For this reason, it has been suggested that post-meal hyperglycemia is a potential risk factor for type 2 diabetes.13 Excess fatty acids and glucose will ultimately be stored as fat in adipose tissue, but while they are circulating in the blood, they can cause substantial damage to the muscle cell and general body composition. In addition to its locomotion function, skeletal muscle is important to efficient body metabolism. Any reduction in muscle size or number of fibers has a negative effect on metabolic capacity.6 The causes of sarcopenia are not clearly understood. Hypotheses include damage to the mitochondrial DNA, reduced protein synthesis, changes in the composition of the muscle fibers and the muscle as a whole, inactivity, hormonal changes and inadequate nutrition. Following is a brief summary of the key research findings related to some possible causes of sarcopenia, which can help you educate your older clients about the condition.

Muscle fiber type, number and size

There are two categories of fibers in skeletal muscle, which are referred to as type I and type II fibers. Type I fibers, commonly called slow-twitch fibers, have a high oxidative capacity, mitochondrial content and capillary density that makes them resistant to fatigue. In contrast, type II fibers, commonly referred to as fasttwitch fibers, are designed for speed and power and are not very rich in mitochondria or blood supply. Between the ages of 20 and 80, there is a variable reduction in muscle fiber size, about a 50-percent reduction in total fiber numbers, and an increase in fat and connective tissue.7 The decline in the number of muscle fibers is particularly rapid after the age of 50.2 From a training perspective, once clients have lost fibers, they can only compensate for this loss by training the remaining fibers. While the generation of new fibers might be possible in humans, it is probably only to a limited extent.8 Sarcopenia affects both types of fibers, but, because type I fibers remain in regular use throughout the life span, they are less affected than the type II fibers. The average sedentary individual hardly ever uses type II fibers, and this results in their atrophy.3 Regular endurance exercise does not protect the fast-twitch fibers from atrophy, but does provide some protection for the type I slow-twitch fibers.14 Strength training, on the other hand, provides protection for type II fibers, and may also provide some protection to type I fibers. Why people lose muscle fibers with age remains a puzzle, but may be related to the death of motor units that innervate the fibers. When motor units die, those that remain will attempt to reinnervate some of the abandoned or dying muscle fibers through the process of collateral sprouting.Young muscle has a mosaic "look" to it because the arrangement of type I and type II fibers are randomly distributed throughout the muscle. In older muscle, similar types of fibers are clumped together so that type I and type II fibers are situated next to each other rather than being dispersed randomly throughout the muscle. In essence, a muscle from an older person looks quite different from that of a young person. The fiber types are clumped together, there is more fat and connective tissue, there are fewer type II fibers and the remaining fibers are smaller.

Protein synthesis

Skeletal muscle repair requires a delicate balance between synthesis of new proteins and a disposal of damaged proteins. The efficient synthesis of new proteins maintains muscle mass and the replacement of damaged protein maintains muscle quality. To maintain muscle mass, the breakdown rates cannot exceed the synthesis rates. Any imbalance between protein synthesis and disposal rates of damaged protein could certainly be an important cause for the loss of muscle mass if the muscle fails to keep pace with its needed repair. Whether older muscle loses its ability to synthesize new protein, or if the breakdown rates are accelerated, is unclear. Some research indicates that synthesis rates are actually higher in older muscle, 15 and that aging muscle is simply slow to respond to stimuli that are anabolic in young muscle. That is, older muscle remains capable of normal synthesis rates but does not respond adequately to anabolic stimuli to do so. Other research suggests that older muscle loses its ability to synthesize new protein quickly enough to match disposal rates. There is a 30-percent synthesis reduction with age, 7 but this could be due to either a slowing of the synthesis production process or to a lack of anabolic stimulation. The only thing certain is that as people get older, there is a gradual failure of the protein synthesis machinery to replace worn-out muscle cells. While confusion in this area persists, it is known that strength training has an anabolic effect on older muscle, and muscle hypertrophy is possible well into old age. In other words, exercisers can positively alter the balance between protein breakdown and protein synthesis through resistance training, even though the stimulus might not be as effective as it was in younger muscle.

Mitochondrial dysfunction

The mitochondria are the prime energy production sites for the muscle cell. An adequate number of healthy mitochondria is crucial to the viability of the muscle fiber. Synthesis of mitochondrial proteins in human skeletal muscle declines with advancing age,12 and this decline is thought to account for fatigue, reduced endurance capacity and possible loss of strength. Because mitochondrial DNA is continually exposed to free radicals, it is speculated that cumulative mitochondrial DNA damage may account for mitochondrial dysfunction. DNA is the template for synthesis of mitochondria, and any change in the DNA has an effect on the ability of the cell to manufacture good quality mitochondria. Older people have significantly higher oxidative damage to their mitochondrial DNA,12 possibly because the antioxidant defense enzymes cannot keep up with DNA repair requirements. In the older body, there are dramatic losses of antioxidant proteins.4 Age-related sarcopenia could, therefore, be due to mitochondrial DNA damage, a reduction in mitochondrial protein synthesis and a reduction in the total number of available mitochondria that collectively affects the ability of mitochondria to produce adequate energy for the muscle fiber. These changes are more rapid in muscles that are underused. The DNA oxidation damage concept is consistent with the oxidative theory of aging.

Hormones and sarcopenia

Several hormones, including testosterone, growth hormone (GH), insulin-like growth hormone-1 (IGF-1) and dehydroepiandrosterone (DHEA), are important regulators of muscle protein turnover. The effect of reduced testosterone and estrogen on skeletal muscle was previously discussed. Age-related growth hormone and IGF-1 changes also play a role. Secretion of growth hormone from the pituitary stimulates increased peripheral production of IGF-1. Circulating levels of growth hormone and IGF-1 both decrease with age, thereby removing an important anabolic effect on skeletal muscle while, at the same time, stimulating the storage of fat.2 DHEA is a hormone produced by the adrenal cortex, and, after age 20, there is a progressive decline in DHEA levels at the rate of about 10 percent per decade until age 80, when the decline becomes more rapid. But the biological role of DHEA is not well defined.Athletes use DHEA supplementation for performance enhancement; however, research about the effect of DHEA on muscle growth is mixed. With age comes a decreased synthesis of hormones that have an anabolic effect on the muscle.Reduction of these growth factors probably contributes to the decreased fiber size and overall muscle strength in older people. Some of these growth factors are also responsible for the repair of muscle tissue. A reduced ability to repair implies that the muscle quality is poor, and this could contribute to the progressive loss of strength and muscle fiber speed of contraction with age.

Training program implications

Understanding the mechanisms behind age-related muscle loss is important from a fitness training standpoint. Preventing or slowing down the rate of muscle loss before it occurs is an important intervention to long-term individual health. Older sedentary individuals have less strength and lean mass than do active counterparts, don't live as long and do not recover as well after illness. Convincing evidence of the importance of physical activity as an intervention strategy comes from the demonstrated capacity of exercise to reverse sarcopenia and to slow its progress.9 Aerobic training and resistance training go hand-in-hand, and both should be prescribed. Aerobic training is associated with increased mitochondrial health in both young and older people.14 A resistancetraining program is particularly important for the maintenance of muscle fiber size and number, due to profound anabolic effects that can help counteract the reduction of anabolic hormones. Skeletal muscle in older participants clearly adapts to chronic endurance and resistance training, both structurally and metabolically. The greatest benefits are likely to be seen if aerobic and resistance training is incorporated well before 50 years of age, and maintained for as long as possible. Endurance training or strength training alone will not affect all the age-related changes in skeletal muscle, because each form of training has different metabolic effects on skeletal muscle. Older endurance-trained athletes are similar in muscle mass and strength to older sedentary individuals. Their mitochondria and muscle capillary perfusion is, however, superior to their sedentary counterparts.5 It is important for your clients to understand that the appropriate training program can slow the relentless effects of aging on muscle structure and function, but will not prevent sarcopenia completely.5 It does, however, provide the essential stimulus for maintenance. Like a new car that runs well initially, as time passes, parts wear out. If we do not replace the worn-out parts, the car will stop running. Your clients can help their bodies repair themselves by providing them with the necessary stimulus so that the maximum number of possible repairs can take place in a timely manner. Both aerobic and resistance training stimulate the building blocks for this repair process. References 1. Bortz, W.M. Nonage vs. age. Journal of Gerontology: Medical Sciences 56(9): M527-M528, September 2001. 2. Greenlund, L.J., and K.S. Nair. Sarcopenia: Consequences, mechanisms and potential therapies. Mechanisms of Ageing and Development 124(3): 287-299,March 2003. 3. Harridge, S.D. Ageing and local growth factors in muscle. Scandinavian Journal of Medicine & Science in Sports 13(1): 34-39, February 2003. 4. Haseler, L.J., A.P. Lin and R. S. Richardson. Skeletal muscle oxidative metabolism in sedentary humans: 31P-MRS assessment of O2 supply and demand limitations. Journal of Applied Physiology 97(3): 1,077-1,081, September 2004. 5. Hawkins, S.A, R.A. Wiswell and T.J. Marcell. Exercise and the master athlete: A model of successful aging? Journal of Gerontology: Medical Sciences 58(11): 1,009-1,011, November 2003. 6. Kohrt, W.M., and J. O. Holloszy. Loss of skeletal muscle mass with aging: Effect on glucose tolerance. Journal of Gerontology: Medical Sciences 50 Spec No.: 68-72, November 1995. 7. Larsson, L., and B. Ramamurthy.Aging-related changes in skeletal muscle: Mechanisms and interventions. Drugs and Aging 17(4): 303-316, October 2000. 8. Luff, A. Age-associated changes in the innervation of muscle fibers and changes in the mechanical properties of motor units. Annals of the New York Academy of Sciences 854: 92-101, November 1998. 9. Lynch, G.S. Tackling Australia's future health problems: Developing strategies to combat sarcopenia - age-related muscle wasting and weakness. Internal Medicine Journal 34(5): 294-296, May 2004. 10. Roubenoff, R., and C. Castaneda. Sarcopenia: Understanding the dynamics of aging muscle. Journal of the American Medical Association 286(10): 1,206-1,212, September 2001. 11. Roubenoff, R., and V. Hughes. Sarcopenia: Current concepts. Journal of Gerontology: Medical Sciences 55(12): M716-724, December 2000. 12. Short, K.R., M.L. Bigelow, J. Kahl, R. Singh, J. Coenen-Schimke, S. Raghavakaimal and K.S. Nair. Decline in skeletal muscle mitochondrial function with aging in humans. Proceedings of the National Academy of Sciences of the United States of America 102(15): 5,618- 5,623, April 2005. 13. Soonthornpun, S., C. Rattarasarn, R. Leelawattana and W. Setasuban. Postprandial plasma glucose: A good index of glycemic control in type 2 diabetic patients having near-normal fasting glucose levels. Diabetes Research and Clinical Practice 46(1): 23-27, October 1999. 14. Trappe, S.W., D.L. Costill, M.D. Vukovich, J. Jones and T. Melham. Aging among elite distance runners: A 22-year longitudinal study. Journal of Applied Physiology 80(1): 285-290, January 1996. 15. Volpi, E., M. Sheffield-Moore, B.B. Rasmussen and R.R. Wolfe. Basal muscle amino acid kinetics and protein synthesis in healthy young and older men. Journal of the American Medical Association 286(10): 1,206- 1,212, September 2001.
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