Increased adipose storage in ectopic locations may be one reason for the increased systemic inflammation seen with aging (Apostolopoulou et al., 2012). Inflammation may contribute to the development of a host of age- related systemic diseases such as diabetes, cardiovascular disease, and dementia (Davan-Wetton et al., 2021). Aging is associated with an increase in numerous proinflammatory cytokines, or chemical messengers, that circulate, acting as hormones throughout the body. Chronic increases in proinflammatory cytokine levels in the blood are among the most important physiologic correlates of metabolic syndrome, and increased rates of inflammation are related to both aging and inactivity in older adults (Addison et al., 2011). It is currently unknown if the increase in inflammation seen with aging is a direct result of the aging process or if it is caused by increased levels of inactivity and comorbid conditions often seen with aging (Addison et al., 2011). What is known is that older adults who have higher rates of chronic inflammation compared to their peers experience a larger loss of lean tissue 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 increased insulin resistance in older adults. The incidence of type 2 diabetes mellitus 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 et al., 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., 2000). In a seminal study, Goodpaster et al. (2000) demonstrated that intramuscular fat is 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 interstitial system. out of the water, as fascia was only examined postmortem, where it acts completely different than in a living person (Myers, 2016). In a cadaver, fascia looks like webbing or papery-like material; in living tissue it is stretchy and surrounded by interstitial fluid. One common misconception about fascia throughout the literature is that fascia surrounds all tissue like plastic wrap; rather, fascia and cells are embedded in one another and create the interstitial spaces (Davis, 2017). Our understanding of the interstitial system
regulation of multiple hormones that result in changes in whole-body fat mass, increased inflammation, and increased risk for metabolic diseases such as diabetes (Davan-Wetton et al., 2021). The endocrine system also has complex interrelationships with the brain, immune system, and skeletal muscles (Clegg & Hassan-Smith, 2018). “The brain and endocrine system are intrinsically linked through the hypothalamic-pituitary axis, which controls metabolism and energy use via the signaling of several homeostatic hormones” (Clegg & Hassan-Smith, 2018, p. 744). In addition to the hypothalamic–pituitary axis, vitamin D and insulin resistance might have a potential role in the pathogenesis of frailty (Clegg & Hassan-Smith, 2018). The hypothalamus receives and integrates brain inputs to coordinate the body’s response to stress and inflammation, partly through the control of glucocorticoid secretion (Clegg & Hassan-Smith, 2018). While it is not clear if glucocorticoid secretion increases with age, age-related changes to the hypothalamic–pituitary–adrenal axis are evident in the blunting of the circadian rhythm, reduced suppression of cortisol secretion, and impaired recovery from stress (Clegg & Hassan-Smith, 2018). Glucocorticoids are involved in a range of metabolically active tissues, including skeletal muscle, bone, and the cardiovascular system (Clegg & Hassan-Smith, 2018). It has been shown that glucocorticoids relate proportionately to cortisol, and high cortisol is related to the catabolism of skeletal muscle and accumulation of fat. Total-body fat mass typically increases until age 65 and then either decreases or remains the same (Barzilai et al., 2012). As an individual ages, fat is no longer stored in the subcutaneous fat depot beneath the skin; rather, it is instead stored in other more harmful locations, such as in and around the abdominal organs and underneath the muscle fascia in and between muscle fibers. These alternate locations of fat storage, also known as ectopic fat deposits , result in increased release of proinflammatory cytokines from adipose tissue and increased whole-body inflammation (Barzilai et al., 2012; Davan-Wetton et al., 2021). Increased amounts of adipose tissue release a host of hormones and proinflammatory cytokines that have negative effects on mobility and function in older adults (Clegg & Hassan- Smith, 2018; Marcus et al., 2012). Uncontrolled inflammation has the potential to cause cellular damage, jeopardizing homeostatic regulation of the body at a local and a systemic level (Clegg & Hassan-Smith, 2018). Inflammation is typically a protective response triggered by infections and tissue damage. It is a glucocorticoid response intended to remove noxious stimuli and pathogens, restore physiological homeostasis, and help resolve infections and wound healing (Clegg & Hassan-Smith, 2018). If the mechanisms of inflammatory response are compromised, cellular damage occurs, accelerating the mechanisms of frailty (Clegg & Hassan-Smith, 2018). However, not all adipose tissue is equally harmful. Adipose tissue stored in the subcutaneous tissue poses less of a health risk than adipose tissue stored in the abdominal cavity, which is also known as visceral adipose tissue , or within the muscle, which is also known as intramuscular adipose tissue (Addison et al., 2014). Interstitial system changes The interstitial system comprises the fascial system, the lymphatic system, and adipose tissue. Therefore, for the purposes of this course, the interstitial system can be considered to be an extension of the endocrine system. The fascial system/interstitium is difficult to study because it is anatomically different in live tissue compared to what occupational and physical therapy practitioners learned in cadaver anatomy during their training. Until now, understanding the interstitium was like examining a jellyfish
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