2000). In a seminal study, Goodpaster and colleagues (2000) demonstrated that intramuscular fat was similar to visceral fat in its risk for insulin resistance. An increase in insulin resistance is important not only for the increased risk of developing diabetes but also for the increased risk of muscle and mobility dysfunction associated with insulin resistance. Far from being an isolated blood sugar problem, insulin resistance has been associated with a decline in muscle mass, decreased muscle strength, and accelerated aging (Barzilai et al., 2012). Further compounding the problem of age-related insulin resistance, aging also leads to impaired beta cell function and production of insulin in the pancreas. The beta cells are the producers of insulin, and impaired function only compounds the systemic problems associated with insulin resistance (Apostolopoulou et al., 2012). Many of the changes in the endocrine system, which sends chemical messengers throughout the body, have direct implications for changes in the musculoskeletal system. both an increased death in the type II fibers and a loss of type II muscle fiber satellite cells (Koopman & van Loon, 2009). Satellite cells are the muscle precursor cells that are responsible for the repair and regeneration of muscle fiber. An increase in the death of satellite cells leads to an inability to repair damaged muscle fibers and eventual death of those fibers. A loss of the alpha- motor neurons to type II motor units also results in a 50% loss of the type II motor units. With aging, these changes produce a gradual shift toward a muscle with increased type I, or slow twitch, muscle fibers (Koopman & van Loon, 2009). Though it may seem intuitive that the loss of muscle mass leads to an equal loss of strength, it is now known that the loss of muscle strength actually exceeds the loss of muscle mass. Aging results in a loss of both muscle strength (how much force a muscle can produce) and muscle power (the ability of a muscle to rapidly produce force) (Goodpaster et al., 2006; Young & Skelton, 1994). In a study of more than 1,800 healthy older adults followed over 3 years, Goodpaster and colleagues (2006) demonstrated that while rates of muscle mass loss were ~1% per year, strength may decrease by up to 4% per year. Remarkably, this study demonstrated that even those older individuals who gained muscle mass lost strength and that the loss of muscle mass was able to explain only 5% of the decrease in strength. This disparity suggests that aging leads not only to a decrease in muscle mass but also to a loss in the muscle’s ability to efficiently produce strength. Similar to the loss of strength, a decrease in the ability of a muscle to rapidly produce force occurs at greater than 3% a year (Young & Skelton, 1994). The loss of both muscle strength and power at rates greater than the loss of muscle mass has been termed muscle quality (Barbat-Artigas, Rolland, Zamboni, & Aubertin-Leheudre, 2012; Russ, Gregg-Cornell, Conaway, & Clark, 2012). Muscle quality is the relationship of the muscle’s ability to produce strength or power relative to the muscle size (Russ et al., 2012). If the loss of strength and power exceeds the loss of muscle mass, then muscle quality has decreased. Even more importantly, while lean mass may decrease at 1% per year, muscle quality may be lost by as much as 2.5% per year in healthy individuals (Goodpaster et al., 2006). This is more than double the loss of lean muscle mass. These findings indicate that neurological changes or some change in the intrinsic force-generating capacity of the muscle are responsible for the decrease in muscle quality. One reason for the decrease in muscle quality seen with aging may be the increase in fatty infiltration found in the muscle. As mentioned previously, aging is associated with a change in the body fat distribution away from subcutaneous tissue and toward storage in the more harmful ectopic locations, including the muscle. It is currently unknown whether increases in intramuscular fat are a product of aging, inactivity, or both, but it is known that increased levels of intramuscular fat are associated with decreased muscle strength, muscle quality, and mobility function in older adults (Addison et al., 2014). Even older adults
and muscle strength and are more likely to experience mobility limitations and disability than those who have lower rates of chronic inflammation (Addison et al., 2011). Increased levels of inflammation are also associated with an increase in insulin resistance in older adults. The incidence of type 2 diabetes rises with age and may affect up to 30% of older adults (Gunasekaran & Gannon, 2011). The underlying mechanism behind the increased rate of type 2 diabetes in older adults is not currently known, but it is theorized that increased inflammation combined with changes in body fat distribution, as well as decreased physical activity, may result in increased insulin resistance and ultimately increased rates of type 2 diabetes. As body fat in ectopic storage locations increases, so does insulin resistance (Goodpaster, Thaete, & Kelley, 2000). In fact, increased levels of both visceral adipose tissue in the abdomen and intramuscular fat are independently associated with increased levels of insulin resistance (Goodpaster et al., Musculoskeletal system changes As seen in the other body systems, aging also brings about numerous significant changes in the musculoskeletal system. While changes in all body systems may potentially impair mobility and function in older adults, declines in the function of the musculoskeletal system may be especially harmful. All parts of the musculoskeletal system are affected by aging, including the connective tissues, muscles, and bones. Ligaments, tendons, and joint capsules become stiffer with age as elastic fibers decrease and cross-links between collagen fibers increase (Ahmed et al., 2005). The combined decrease in elastic fibers and increase in the cross-links between collagen fibers leads to a decrease in the range of motion and an increased stiffness in most major joints (Ahmed et al., 2005). Not only does the connective tissue surrounding a joint change, but the amount and quality of synovial fluid within a joint also decreases. Decreases in the quality and amount of synovial fluid make movement more difficult by increasing the friction within the joint. The combination of changes in connective tissue and the synovial fluid results in impaired and slower joint movements in older adults (Ahmed et al., 2005). Similar to changes in the joints, changes in the muscles result in impaired muscle function with aging. Sarcopenia, literally meaning a “poverty of flesh,” refers to the combined loss of muscle mass and strength that occurs with aging (Roubenoff & Hughes, 2000). Sarcopenia is believed to play a major role in functional decline in older adults (Roubenoff & Hughes, 2000). The loss of muscle mass and strength that accompanies aging creates a harmful cycle whereby a loss of muscle function leads to decreases in movement ability and a consequent increase in sedentary behavior, resulting in further declines in both the cardiovascular and the musculoskeletal system. Aging results in a decrease in muscle mass, even in healthy older individuals. While muscle mass accounts for 50% of the total body weight in young adults, by the age of 75, it accounts for less than 25% of total body weight (Koopman & van Loon, 2009). The loss of muscle mass may begin as early as the fourth decade of life and by the age of 70 may occur at a rate of 1% per year in healthy individuals (Goodpaster et al., 2006). Hospitalization, chronic illness, and sedentary behavior all result in increased rates of muscle loss. Healthy older adults placed on bed rest for just 10 days experienced an average loss of 1 kg of muscle mass in their legs alone (Kortebein, Ferrando, Lombeida, Wolfe, & Evans, 2007). As little as 5 to 7 days of bed rest in healthy older adults results in a decrease of lean mass in the leg by 3% to 4% (Drummond et al., 2012; Reidy et al., 2017). If older healthy adults suffer such a rapid loss of muscle mass with decreased physical activity, it is reasonable to suspect that in older, frail, or hospitalized patients the loss of muscle mass may actually be much greater than 1% per year. At a cellular level, the loss of muscle mass is predominantly due to the loss of type II, or fast twitch, muscle fibers (Koopman & van Loon, 2009). The loss of type II muscle fibers results from
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