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Sarcopenia: The Mystery of Muscle Loss
Chantal Vella, M.S. and Len Kravitz, Ph.D.
Introduction
Sarcopenia can be defined as the age-related loss of muscle mass, strength and function (Waters, Baumgartner & Garry 2000; Vandervoort & Symons 2001). Although there is no specific level of lean body mass or muscle mass at which one can say sarcopenia is present (Roubenoff 2001), any loss of muscle mass is of importance because there is a strong relationship between muscle mass and strength (Roth, Ferrell & Hurley 2000). Sarcopenia appears to begin in the fourth decade of life and accelerates after the age of approximately 75 years (Waters, Baumgartner & Garry 2000). With aging and inactivity, the most atrophy is seen in the fast twitch (FT) fibers which are recruited during high-intensity, anaerobic movements. Although sarcopenia is mostly seen in physically inactive individuals, it is also evident in individuals who remain physically active throughout their lives. This finding suggests that physical inactivity is not the only contributing factor to sarcopenia. Current research is finding that the development of sarcopenia is a multifactorial process. Many factors, including physical inactivity, motor-unit remodeling, decreased hormone levels, and decreased protein synthesis, may all contribute to sarcopenia. Fortunately, sarcopenia is partly reversible with appropriate exercise interventions. This article will focus on the current perspectives of sarcopenia and conclude with the importance of resistance training in preventing it.
Motor Unit Remodeling
Age related changes in the neuromuscular system may play a role in the onset of sarcopenia. With age the number of spinal cord motor neurons and functioning motor units decline (Roth, Ferrel & Hurley 2000, Roubenoff 2001). This is a continuous process throughout life and is considered irreversible (Roubenoff 2001). Human nerve cells have a predetermined life span and the decline in these cells is dependent on the location in the body, age, and presence of disease (Vandervoort & Symons 2001). It is interesting to note that nerve cells can still remain present in aged individuals yet be impaired because of biochemical changes (Vandervoort & Symons 2001). The motor neurons are responsible for sending signals from the brain to the muscles to initiate movement. A motor unit consists of the motor neuron and all of the muscle fibers that it connects to or innervates. The number of fibers that a motor neuron innervates depends on the function of that specific muscle. For example, a muscle that requires precise movements, such as muscles of the eye, will have motor units with a motor neuron innervating a few muscle fibers. Muscles that require less precise movements, such as the quadriceps muscles, will have motor units with a motor neuron innervating hundreds and possibly over a thousand muscle fibers.
The loss of muscle fibers begins with the loss of motor neurons. Motor neurons will die with age resulting in a denervation of the muscle fibers within the motor unit. This denervation causes the muscle fibers to atrophy and eventually die, leading to a decrease in muscle mass. (Roth, Ferrel & Hurley 2000). When a motor neuron dies, an adjacent motor neuron, usually a slow twitch (ST) motor neuron, may reinnervate the muscle fibers, preventing atrophy. This process is called motor unit remodeling. When compared to FT motor units, ST motor units have slower firing rates, are slower to contract, produce less muscle force and are smaller in size and fiber number. Motor unit remodeling by ST motor neurons leads to less efficient motor units. The remodeled ST motor unit will have less precise control of movements, less force production and slowing of muscle mechanics (Roth, Ferrel & Hurley 2000; Roubenoff 2001; Waters, Baumgartner & Garry 2000). This may help explain the loss of balance and speed of movement with age. In addition, denervation rates of FT muscle fibers may exceed reinnervation rates by ST motor neurons, further explaining atrophy of FT muscle fibers in the elderly (Roth, Ferrel & Hurley 2000).
Protein Synthesis/Regeneration
Another factor affecting sarcopenia is the rate of muscle protein synthesis. The quality and quantity of protein in the body is maintained by a continuous repair process, which involves both protein breakdown and synthesis (Nair 1995). The balance of protein synthesis and breakdown determines the protein content in the body (Nair 1995). With age, the changes in whole-body protein turnover reflect a decreased synthesis rate rather than an increased catabolic rate (Vandervoort & Symons 2001). Additionally, research has consistently reported that muscle protein synthesis rates are lower in older adults when compared to younger adults (Nair 1995; Yarasheski et al. 1999; Hasten et al. 2000; Roth, Ferrel & Hurley 2000). A decrease in muscle protein synthesis will result in the loss of muscle mass. It is important to note that the ability of the muscle to regenerate following injury or overload is also decreased with age. Muscle regeneration and growth of muscle tissue require the assistance of satellite cells (Roth, Ferrel & Hurley 2000). Satellite cells are specialized cells located in the basal membrane of the muscle cell and are necessary for the development of new muscle tissue. The number of satellite cells in skeletal muscle decreases as an individual ages, providing a possible mechanism for the loss of muscle mass and strength (Roth, Ferrel & Hurley 2000). All of the above are physiological explanations of why resistance training in the elderly should follow a progressive overload prescription.
Hormones
Aging is associated with several changes in hormonal levels, including a decrease in the concentrations of growth hormone (GH), testosterone (T), and insulin-like growth factor (IGF-1). A decrease in the concentrations of these hormones may be linked to the development of sarcopenia. GH and IGF-1 play a dominant role in the regulation of protein metabolism; GH and T are required for protein maintenance; and IGF-1 levels are positively correlated with muscle protein synthesis rates, specifically myofibrillar protein (actin and myosin filaments) and myosin heavy chain synthesis (part of the myosin containing cross-bridges) (Waters, Baumgartner & Garry 2000). A sustained decrease in these hormones is linked to a decrease in muscle mass and an increase in body fat (Waters, Baumgartner & Garry 2000). Although these hormones are involved in protein metabolism and maintenance, there is conflicting evidence whether hormone replacement is effective in maintaining or gaining muscle mass (Roubenoff 2001). Studies examining hormone replacement effects on lean body mass have mainly focused on GH. These studies have reported that GH replacement has not always been effective in increasing muscle mass and strength in older subjects (Roubenoff 2001; Waters, Baumgartner & Garry 2000). It has also been suggested that changes in female estrogen levels may play a role in the development of sarcopenia during menopause. However, limited research on this topic exists.
Lifestyle Factors
Sarcopenia is accelerated with a lack of physical activity, especially the lack of overload to the muscle, as in resistance exercise. The amount of physical activity generally declines with age. Physically inactive adults will see a faster and greater loss of muscle mass than physically active adults. However, sarcopenia is not completely prevented by exercise, as it is also evident, but to a lesser degree, in physically active individuals. It is possible that if the physical activity is not sufficient in intensity and duration to recruit FT muscle fibers it may lead to FT fiber atrophy and the development of sarcopenia (Roubenoff 2001). Therefore, it appears that progressive resistance training (RT) should include cycles of high-intensity/low volume training (relative to the persons fitness level). An additional factor in the development of sarcopenia may be an inadequate energy intake. Many older individuals may not be taking in enough calories and/or protein to sustain their muscle mass (Evans 1995).
Resistance Training for the Prevention of Sarcopenia
Resistance training (RT) has been shown to be a powerful intervention in the prevention and treatment of sarcopenia (Roth, Ferrel & Hurley 2000). RT has been reported to positively influence the neuromuscular system, hormone concentrations, and protein synthesis rates. According to Roubenoff (2001) and Roth et al. (2000), a properly designed RT program may increase motor neuron firing rates, improve muscle fiber recruitment, and create a more efficient motor unit. An increased motor neuron firing rate combined with an increased recruitment of muscle fibers would lead to faster muscle contractions and greater force production.
Although protein synthesis rates decrease with age, research is finding that progressive RT can increase protein synthesis rates in as little as two weeks. Hasten and others (2000) reported that following a 2-week supervised RT program muscle protein synthesis rates increased up to 182% from baseline in seven 78 to 84 year olds. Yarasheski and colleagues (1993) also found that muscle protein synthesis rates in older adults (63-66 years) increased significantly in response to 2 weeks of resistance training. In addition, Yarasheski and others (1999) reported that 3 months of supervised progressive resistance training increased the rate of muscle protein synthesis by approximately 50% in seventeen frail 76 to 92 year old men and women. These findings suggest that older men and women retain the ability to increase the rate of muscle protein synthesis in response to acute and long-term progressive resistance training. Furthermore, acute and short term RT increases the number of satellite cells in the muscle trained, leading to faster muscle regeneration (Roth, Ferrel & Hurley 2000).
Theory into Practice
It is well established that there is a progressive loss of muscle mass and muscle strength with age. In physically inactive people, after the age of 30 there is a loss of approximately 3-5% of muscle mass per decade and a parallel decline in muscle strength (Nair 1995). The development of sarcopenia is multifaceted and many of the causative factors are uncontrollable, however, the easiest and possibly the most effective treatment within our control is progressive RT. The following are general guidelines for the RT exercise prescription from the American College of Sports Medicine (Balady et al. 2000).
Screening Clients
The RT prescription needs to be individualized based on the health and/or fitness status of the participant. However, the exercise contraindications for older and frail individuals are similar to those for younger adults (Porter 2000). RT can be progressively introduced to individuals with cardiovascular disease, diabetes, dementia, pulmonary disease, chronic renal failure, peripheral vascular disease and arthritis. Clients who have uncontrolled conditions, such as hypertension, chest pain, metabolic disturbances, and acute illnesses should be medically assessed for appropriate RT participation. If any of the health-related illnesses are rapidly deteriorating, a health professional needs to be consulted immediately as this is most likely a contraindication to exercise (Porter 2000).
Number of Exercises
Complete 8 to 10 exercises for all the major muscle groups (e.g., pectorals, latissimus dorsi, deltoids, abdominals, gluteals, quadriceps and hamstrings). The selection of more multi-joint exercises is recommended, as opposed to single-joint movements (Balady 2000).
Intensity and Progression
Perform in a repetition zone of 10 to 15 repetitions that elicits a somewhat hard perceived exertion rating (12 to 13 on a Borg RPE scale). Allow for a progressive adaptation to the intensity. As the mature adult increases in strength, the progressive overload should initially increase in repetitions, followed later by an increase in resistance (Balady 2000). The usage of perceived exertion ratings for resistance exercise is contemporary, and worthy of more research from scientists and practical feedback from personal trainers in the field. Also, as indicated from this review of literature on sarcopenia, it appears that periodizing (sytematical changing) workout cycles to include higher intensity sessions with moderate intensity sessions is advisable.
Number of Sets
ACSM recommends at least 1 set per major muscle group. However, most studies with older adults have done 2 to 3 sets (Porter 2000). It is possible that multiple set programs show greater strength gains when conducted over a longer time span. However, for attaining the majority of the health benefits from RT, 1 set may be sufficient for most elderly client goals.
Frequency
RT should be preformed up to 2x per week, separating workout sessions with at least a period of 48 hours. However, the optimal frequency for the mature and frail adult has not been definitively established. It should be noted that maintenance of strength in seniors has been achieved with as little as 1 workout day per week (Porter 2000).
Safety Points
The role of the personal trainer in supervising and monitoring the workouts for the mature and frail exerciser are consequential. Many older individuals do not understand the concept of progressive overload, and must be educated and directed properly (Porter 2000).
Teaching correct lifting mechanics should be a priority with all personal trainers working with older clients.
Have clients perform exercises in a pain-free range of motion with controlled joint movements (Balady 2000).
Keep breathing patterns normal during RT exercises.
Begin a RT program with about 8 weeks of minimal resistance loads to allow adequate time for the joint connective tissues to adjust to RT (Balady 2000).
Avoid 1 RM testing unless data is being collected for research. Excessive RT loads may aggravate a pre-existing health condition (Porter 2000).
Eccentric training (lengthening muscle actions) has been shown to result in greater muscle soreness. Caution is advised in elderly RT programs that emphasize this type of training (Pollock et al. 1998).
When re-starting a resistance training regimen from a break or leave of absence, have clients begin with loads that are approximately 50% or less of the previous training intensity (Balady 2000).
To help mature clients develop better balance and muscle coordination, perform several exercise in a standing position with free weights (Porter 2000).
Plan workout time efficiently for the mature client. Sessions lasting over 60 minutes may have an unfavorable effect on exercise adherence (Balady 2000). Attempt to complete the RT workout in 20 to 30 minutes.
Clients with arthritis and other joint and bone disorders should not be permitted to do RT during periods of pain or inflammation (Balady 2000).
Closing Thoughts
For individuals that do not have access to a gym facility, RT can be accomplished with the use of therapy bands, therapy balls and using the individuals body weight as resistance. RT is a wonderful tool for preventing and partially reversing sarcopenia. Its up to us to spread the word and motivate our clients to engage in a progressive RT program for a strong and healthy life.
References
Balady, G.J, Berra, K.A., Goldling, L.A., Gordon, N.F., Mahler, D.A., Myers, J.N. and Sheldahl, L.M. (2000). ACSMS Guidelines for Exercise Testing and Prescription (Sixth Edition). Lippincott Williams and Wilkins.
Evans, W. 1995. Effects of Exercise on Body Composition and Functional Capacity of the Elderly. The Journals of Gerontology 50A: 147-154.
Evans, W. 1997. Functional and Metabolic Consequences of Sarcopenia. The Journal of Nutrition 127(5S):998S-1003S.
Hasten, D.L. et al. 2000. Resistance Exercise Acutely Increases MHC and Mixed Muscle Protein Synthesis Rates in 78-84 and 23-32 yr olds. American Journal of Physiology 278:620-626.
Nair, K.S. 1995. Muscle Protein Turnover: Methodological Issues and the Effect of Aging. The Journals of Gerontology 50A:107-114.
Pollock, M. L., Gaesser, G. A., Butcher, J. D., Despres, J-P, Dishman, R. K., Franklin, B. A., and Garber, C. E. 1998. The Recommended Quantity and Quality of Exercise for Developing and Maintaining Cardiorespiratory and Muscular Fitness and Flexibility in Health Adults. Medicine & Science in Sports & Exercise 30(6): 975-991.
Porter, M.M. 2001. The Effects of Strength Training on Sarcopenia. Canadian Journal of Applied Physiology 26(1): 123-141.
Porter, M. M. 2000. Resistance Training Recommendations for Older Adults. Topics in Geriatric Rehabilitation 15(3): 60-69.
Roth, S.M., R.E. Ferrel, & B.F. Hurley. 2000. Strength Training for the Prevention and Treatment of Sarcopenia. The Journal of Nutrition, Health & Aging 4(3):143-155.
Roubenoff, R. 2001. Origins and Clinical Relevance of Sarcopenia. Canadian Journal of Applied Physiology 26(1):78-89.
Roubenoff, R. & V.A. Hughes. 2000. Sarcopenia: Current Concepts. The Journals of Gerontology 55A(12):M716-24.
Vandervoort, A.A. & T.B. Symons. 2001. Functional and Metabolic Consequences of Sarcopenia. Canadian Journal of Applied Physiology 26(1):90-101.
Waters, D.L., R.N. Baumgartner & P.J. Garry. 2000. Sarcopenia: Current Perspectives. The Journal of Nutrition, Health & Aging 4(3):133-139.
Yarasheski, K.E. et al. 1999. Resistance Exercise Training Increases Mixed Muscle Protein Synthesis Rate in Frail Women and Men &Mac179;76 yr old. American Journal of Physiology 277: 118-125.
Yarasheski, K.E. et al. 1993. Acute effects of resistance exercise on muscle protein synthesis rate in young and elderly men and women. American Journal of Physiology 265: E210-E214.
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