The continuing education (CE) article (page 175) provides a synthesis of nutritional guidelines. The article focuses on clinical nutrition assessments, analysis, and the link of nutrition to sarcopenia.
Various definitions of “sarcopenia” are noted in the CE article; however, I’d like to advance the perspective that while adequate nutrients, including protein, are essential in the maintenance of muscle mass, size doesn’t always matter. Other factors exist in the causality, prevention, and treatment of sarcopenia, including the identification of functional deficits and increasing the strength of the muscles. Although a dearth of literature is available that focuses on muscle size or sarcopenia and its nutritional aspects, only a paucity of biomarkers exists by which to identify true sarcopenia from other phenotypes of regression of muscle mass. These include nervous system impairments, deficits in muscle activation, and impairment of the muscle systems that lead to functional limitations and physical disability.
The skeletal muscle is made up of a cell membrane—the sarcolemma—the sarcoplasm of the cell contains the contractile units called the myofibrils, which are the functional contractile unit of the striated muscle. The muscles are the engines of the body. The connective tissue encasing the muscle gives it shape for the efficient transmission of forces, from muscle to bone by the tendons. Beyond the prime mover function, the muscle mass (lean body mass) provides form, function, and protection. Biologically, the muscle tissue is also the effector (recipient) of adequate protein stores, glycogen, and neuromuscular activation through influences of the central and peripheral nervous system.
In 1989, Irwin Rosenberg coined the term sarcopenia (Greek “sarx” or flesh + “penia” or loss) to define loss of muscle mass that occurs with advancing age.1 Sarcopenia might affect up to half of people 80 years or older2; however, because of varying phenotypes, conflation of definitions, and research methodology in the literature, true estimates of prevalence and incidence are extremely challenging.2 Some estimates place the declination of muscle mass at approximately 1% per year after the age of 30 years. The prevalence of “severe muscle loss” is estimated at 5% to 13% for 60- to 70-year-olds and 11% to 50% for those 80 years or older.3 A new approach to defining sarcolemma proposed by Morley et al3 defines sarcopenia as “low muscle mass with limited mobility.” The definition uses sarcopenia as more than 2-SD loss in muscle mass compared with 20- to 30-year-olds but adds that individuals with a gait speed slower than 1.0 m/s are those who should be targeted for “clinical trials.”4 Although this definition adds functional mobility, “it does not include muscular strength as a component,” which according to Clark and Manini4 “stays true to the original definition of sarcopenia.”
To measure muscle size for research purposes, magnetic resonance imaging, computer axial tomography, ultrasonography, bioelectrical impedance analysis, and dual-energy x-ray absorptiometry are used. Sarcopenia is most often defined from measurements obtained using bioelectrical impedance or dual-energy X-ray absorptiometry. Although these tools measure muscle mass, they do not necessarily correlate to human functional performance and are mainly used for research and prognostication.3
To make a distinction between loss of muscle mass (sarcopenia), Clark and Manini4 proposed the term dynapenia4 (“dyna” = power, strength, or force and “penia” = poverty) to define the age-related loss of muscle strength and power. The model of dynapenia is an important adjunct, which allows for the assessment and treatment of decreased functional mobility and muscle power through resistance training and strength training.
Identifying muscle weakness in the older adult population is subject to the epidemiologic challenges of identifying the prevalence of sarcopenia and dynapenia. In the United States, data from the National Health and Nutrition Examination Survey, 2011–2012,5 estimate that 5% of adults older than 60 years had weak muscle strength; 13% had intermediate muscle strength, whereas 82% had normal muscle strength. In persons 80 years or older, women had a higher prevalence of weak muscle strength than did men.5 Several functional parameters indicate weak muscles and decreased strength, such as slow gait speed and difficulty in rising from an armless chair. A value for maximum hand-grip strength less than 26 kg for men and less than 16 kg for women is an additional functional parameter indicating weakness.5
Physical activity intervention is a key component of maintaining strength and functional mobility, including aged calibrated aerobic exercises, strength training, resistance training, flexibility, and balance training.6 The adjunctive use of antioxidants, angiotensin II–converting enzyme inhibitors, creatinine, and myostatin has appeared in recent literature.6 It is clear that an interprofessional approach to improving muscle strength and function in older adults is needed in the prevention of pressures ulcers.
1. Rosenberg IH. Sarcopenia: origins and clinical relevance. J Nutr 1997; 127 (5 Suppl): S990–1.
2. Kalyani RR, Corriere M, Ferrucci L. Age-related and disease-related muscle loss: the effect of diabetes, obesity, and other diseases. Lancet Diabetes Endocrinol 2014; 2: 819–29.
3. Morley JE, Abbatecola AM, Argiles JM, et al. Sarcopenia with limited mobility: an international consensus. J Am Med Dir Assoc 2011; 12: 403–9.
4. Clark BC, Manini TM. What is dynapenia? Nutrition 2012; 28: 495–503.
5. Looker AC, Wang CY. Prevalence of reduced muscle strength in older US Adults. United States, 2011-2012. NCHS Data Brief 2015; 179: 1–8.
6. Waters DL, Baumgartner RN, Garry PJ, Vellas B. Advantages of dietary, exercise-related, and therapeutic interventions to prevent and treat sarcopenia in adult patients: an update. Clin Interv Aging 2010; 5: 259–70.