Sarcopenia is the progressive loss of skeletal muscle mass and function with age. It often is a result of or leads to decrease in physical activity which leads to functional impairement or disability and increases vulnerability towards other chronic ailments such as cardiovascular disease, insulin resistance, type 2 diabetes etc (Roubenoff & Hughes 2000). With age there is a decline in mitochondrial biogenesis as well as reduction in the ability to promote muscle protein synthesis which has substantial impact on the age-associated loss of muscle mass and strength, both of which are the two most recognized risk phenotypes associated with sarcopenia. Previous work has reported enormous inter-individual variability in these phenotypes arising
The study used Duchenne Muscular Dystrophy patients age-matched with healthy volunteers to take serum sample and test for metabolic biomarkers. Fourteen metabolites were found using a coupled system of liquid chromatography and mass spectroscopy. Of the fourteen found, the researchers found a ratio of creatine to creatinine that increases with age in Duchenne Muscular Dystrophy patients and decreases with healthy volunteers.1
It is a known fact that all measures of physiological function decline in human aging. While genetics certainly play a role in the declining of physiological function with age, it can be argued that a fundamental part of aging can be reflected by chemical processes resulting in the appearance of harmful side products of the normal metabolism over time. When enzymes speed up reactions it is harder to slow them down. At the same time side reactions are constantly occurring and more and more unwanted side products are continuously being formed.
The European Working Group on Sarcopenia in Older People (EWGSOP) developed a clinical definition and consensus diagnostic criteria for age-related sarcopenia (Cruz-Jentoft et al., 2010).
Blood circulation is vital to the body and may also contribute to the pathology. Aging associated with changes in microcirculation and structure of the vascular endothelium (Tommy et al., 2011) decrease in vascular endothelial functions (Burton et al., 2011), and a decrease in exercise-induced blood flow which is partly resulted from an age-related reduction in vasodilation capacity. (Degens, 1998).
As humans age, a progressive loss of neural function leads to a decrease of skeletal muscle mass and strength. This is called sarcopenia. A 10% loss of muscle mass occurs between 25-50 years and an additional 40% loss between 50-80 years. Not only is there a loss of muscle, but a transition of fast to slow muscle fibers (Howley et al, 2009). There are ways to counter balance this loss by adopting an active lifestyle and adding nutritional supplements. With the loss of type II muscle fibers, a loss of strength, power, and rate limiting substrates occur. One of the rate limiting substrates, carnosine, is found primarily in type II muscle fibers and contribute to buffering hydrogen ions and thus preventing a drop of pH. Carnosine is found in food,
As we get older, cell turnover decreases and leads to the decrease of the normal functioning of the organs. A prevalent condition in otherwise healthy old adults is sarcopenia results from the natural decrease in skeletal muscle mass, which directly affects the independence of old adult to conduct daily activities such as walking, cooking and exercising. Therefore, Sarcopenia is one of the reasons for malnutrition in the elderly since it interferes with their ability to obtain and prepare their meal. Sarcopenia should receive attention and thus more research on its treatment should be conducted because, without it, otherwise healthy old adult adults could enjoy their daily activities away from costly nursing homes and hospitals. This literature review shows that
In the article, "Exercise Really Can Keep You Young” written by Reynolds, Gretchen expresses the concept of immune systems and muscle tissue being related to exercise, in which they are intertwined and help reduce the aging process. The major idea discussed in the article is about looking and staying young, working out can keep muscle tissues healthy and strong which delays the aging process. A study was conducted on cyclists in the age group of 55-79, the results showed that they seemly had reflexes, memories, balance and metabolic profiles nearing the ages of 30 year olds. Recently they decided to see the aging process had been delayed by looking at their muscle tissues as well as T cells in their legs, the results showed that the muscle
The synthesis conducted by Ogan and Pritchett (2013) presents several findings from other studies that support the inclusion of vitamin D as an important component for muscular activity. The synthesis includes a review of studies that discuss the possible effects of vitamin D on muscles, factors involved with vitamin D insufficiency, the required amount of vitamin D and the possible effects of vitamin D with athletic performance.
AGEs normally form at slow but constant rates in the cells and may accumulate with time. The accumulation of AGEs occurs when there is an increase in their production and/or a decrease in their elimination. With aging, low protein turnover, for example, results in the accumulation of extracellular AGEs on collagen, resulting in wrinkles. In diabetics, high plasma levels of glycosylated hemoglobin (HbA1c) increase as a result of high blood glucose levels. Studies show
A study done by Gurd et al, 2010 looked at the effects of a six week HIIT workout on the SIRT1 levels in human skeletal muscle. SIRT1 is the silent mating-type information regulator 2 homolog1; which signifies increases in gene expression of mitochondrial (mitochondrial biogenesis) and fatty
H19 is highly expressed in skeletal muscle (Fig. 1A), confirming previous reports (Gabory et al., 2010). We also observed that its expression is the highest in the oxidative fiber-enriched soleus muscle (Fig. 1B). As siRNA-mediated H19 knockdown impaired insulin-stimulated glucose uptake in cultured C2C12 mouse myotubes (Gao et al., 2014), we wanted to test whether H19 regulates muscle insulin sensitivity in vivo. To this end, we used a whole-body H19 knockout mouse model (H19KO) that carries a targeted deletion of the entire H19 transcription unit (Ripoche et al., 1997). The H19KO mice exhibited an overgrowth phenotype (Fig. 1C), consistent with previous observations (Martinet et al., 2016; Ripoche et al., 1997). Overgrowth could be attributed to an increase in the lean mass (Fig. 1D-F, E), which was not surprising because the H19KO mice exhibit skeletal muscle hyperplasia and hypertrophy (Martinet et al., 2016). InsulinYet, insulin tolerance tests (ITT) unexpectedly revealed a decreased whole-body insulin sensitivity in the H19KO mice (Fig. 1F, G). Taken together with the notion that H19 is highly and almost exclusively expressed in muscle (Fig. 1A) and that
Skeletal muscle is the major type of muscle tissue and its main functions are controlling body movement and generating body heat. Skeletal muscle atrophy, also known as wasting or cachexia, is a condition characterized by the loss of muscle mass that is often associated with an underlying primary illness such as AIDS, cancer, and sepsis (Argiles, Moore-Carrasco, Fuster, Busquets, & Lopez-Soriano, 2003; Tisdale, 1997) . It is also associated with normal physiological changes like aging, referred to as sarcopenia (Evans, 2010). The consequences of skeletal muscle atrophy range from poor quality of life to increased mortality rate (Fanzani, Conraads, Penna, & Martinet, 2012) . In cancer, it is estimated that cachexia is the cause of death in
The recovery from illness or injury often requires otherwise healthy humans to undergo a period of muscle disuse (e.g. bed rest or limb immobilization). A major consequence of disuse is skeletal muscle atrophy. The ensuing impairments in muscle function, metabolic rate and insulin sensitivity, and accrual of body fat mass following two or more weeks of muscle disuse have been well documented. Studies investigating muscle disuse atrophy generally employ relatively long experimental periods, ranging from two to as long as 17 weeks of bed rest or limb immobilization. However, over the last decade, efforts have been made within healthcare systems to reduce the duration of bed rest/immobilization that patients endure due to illness or injury. At
Q has reached maximum body growth and biological aging or senescence has begun. Biological ageing is “genetically influenced declines in the functioning of organs and systems that are universal in all members of our species” (Berk, 2010, p. 432). Q exercises daily but he admits that he doesn’t eat a healthy diet all the time. “Regular moderate to
Aging of the population is a worldwide phenomenon that is accompanied by a series of modifications to several physiological parameters, such as a progressive increase in fat mass and a decrease in lean body mass. However, these alterations are not linear and must be constantly monitored.In elderly individuals, changes in body composition result in the prevalence of overweight and obesity combined with a loss of muscle mass and strength; this has recently been defined as sarcopenic obesity.Sarcopenic obesity is associated with functional limitations and increased mortality.The aim of the present study was to investigate the prevalence of sarcopenic obesity and its association with obesity and sarcopenia in elderly Brazilian women. Two hundred