a higher bone density than inactive adults, thus decreasing their risk for osteoporosis (Booth et al., 2011; DeFina et al., 2016). Increased levels of proinflammatory cytokines, often associated with physical inactivity, stimulate osteoclasts and result in increased levels of bone resorption. Increased levels of adiposity, frequently attributed to a sedentary lifestyle, are also associated with low total bone mineral density. A study of more than 13,000 older adults demonstrated that percentage of body fat was positively associated with osteopenia, indicating that older adults with increased body fat were also more likely to have bone loss (Cao, 2011). While the exact mechanism behind the association between increased fat mass and bone loss is unknown, it is suspected that increased levels of inflammatory cytokines may be the reason (Cao, 2011). It is known, however, that increased physical activity can decrease inflammation as well as increase bone mineral density. A recent meta-analysis of 43 studies reported that physical exercise resulted in increased bone mineral density and a decreased risk of fracture in postmenopausal women. These findings suggest that exercise is important for both the prevention and treatment of osteoporosis (Howe et al., 2011). With aging, numerous changes take place throughout the body’s system, and a summary of the changes resulting from aging and inactivity can be found in Table 1. Table 1: A Summary of Changes in the Major Body Systems
without current mobility limitations are at an increased risk of future limitations if they have high amounts of intramuscular fat within their thigh muscles (Visser et al., 2005). It is also known that older adults with higher amounts of intramuscular fat may have a decreased ability to activate their muscles to produce a full contraction (Yoshida, Marcus, & Lastayo, 2012) and that they may experience a decreased ability to improve their muscle quality with exercise (Marcus, Addison, & Lastayo, 2012). This is an important finding because it suggests that increased intramuscular fat may not only impair the muscles’ ability to function, but it may also impair the ability to improve muscle function. Intramuscular fat may also impair bone function. Increased rates of intramuscular fat are associated with an increased risk of hip fracture, independent of bone density (Lang et al., 2010). Aging is known to result in a decrease in bone mass by 0.5% after the age of 40 and by as much as 2% to 3% in women after menopause (Concannon et al., 2012). Although osteoporosis is more common in women, it can also occur in men and is frequently underdiagnosed in men (Lambert, Zaidi, & Mechanick, 2011). Men are less likely to have osteoporosis but are more likely to experience complications and even death following a hip fracture. Lambert and colleagues (2011) found that men are more likely to experience subsequent fractures and are less likely to return to independent function than women who experience hip fracture. Therefore while osteoporosis may not occur as often in men, it is still a significant problem. Over a lifetime, the human skeleton continuously undergoes a regulated process of bone resorption and formation. This continuous process allows for the repair of microdamage in the bone, the removal of unneeded bone, and the release of calcium from the bones for the maintenance of calcium levels in the body (Schulman, Weiss, & Mechanick, 2011). Multiple types of cells are found within the bone, working together to regulate bone formation and resorption. Bone is composed of three distinct types of cells. Ninety percent of all bone cells are osteocytes – long-lived bone cells that participate in almost all major bone regulation activities (Atkins & Findlay, 2012). Osteocytes act as regulators of bone formation by detecting strain in the bone; to increase bone formation, the osteocytes transmit these signals to osteoblasts, which are the cells responsible for laying down the mineral matrix. Osteoblasts account for 4% to 6% of all bone cells (Atkins & Findlay, 2012). Layers of osteoblasts deposit successive layers of new bony matrix. As these layers are mineralized, new bone is formed. Equally as important as the formation of new bone is the resorption of older bone. Resorption of older or damaged bone allows for constant bone repair to occur, which ensures healthy bone turnover. Bone resorption is also important for the release of calcium stores from the bone in times of need. Calcium is critical for the propagation of nervous signals and for cellular transport. Cells called osteoclasts, working under the direction of osteocytes, are able to destroy the bony matrix, releasing calcium into the body for use by other cells (Schulman et al., 2011). Osteoclasts are large, multinucleated cells found on the surface of the bone; they account for only 1% to 2% of the cells in bone (Atkins & Findlay, 2012). In a younger adult, the resorption of bone by osteoclasts and the formation of new bone by osteoblasts is usually balanced and results in no net change in bone. In older adults, an uncoupling between bone resorption and formation occurs. With aging, osteoclasts typically increase their activity, while osteoblasts decrease the formation of new bone, resulting in a net bone loss in older adults (Schulman et al., 2011). This imbalance results in decreases in bone mass and an increased risk for fracture. While aging is associated with decreases in bone mass, inactivity accelerates this decline, and a sedentary lifestyle is a risk factor for the development of osteoporosis (Booth et al., 2011). Studies have shown that older adults who have been active throughout their lives and have a higher cardiovascular fitness also have
With Aging and Inactivity Cardiovascular Changes • Decreased number of cardiomyocytes.
• Increased size of cardiomyocytes. • Increased thickness of left ventricle. • Increased connective tissue in extracellular space. • Increased fatty infiltration. • Separation of sinoatrial node from heart tissue. • Decreased number of pacemaker cells. • Decreased maximal heart rate. • Decreased ability to alter heart rate. • Increased thickness of arterial walls. • Increased stiffness of arterial walls. • Increased systolic blood pressure. • Decreased diastolic blood pressure. • Decreased maximal cardiac output. • Decreased elastic tissue in lungs. • Decreased elastic recoil of lungs. • Premature closing of small airways. • Decreased ability to empty air from lungs. • Increased stiffness of intercostal muscles. • Calcification of costal cartilages. • Decreased ability of lungs to expand. • Increased kyphotic posture. • Decreased chest wall compliance. • Decreased strength of diaphragm. • Decreased efficiency of breathing. Endocrine Changes • Changes in body fat distribution: • Increased visceral fat. • Decreased VO 2 max. Respiratory Changes
• Increased intramuscular fat. • Decreased subcutaneous fat. • Decreased sex hormones. • Decreased growth hormone. • Increased systemic inflammation. • Increased insulin resistance.
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