Loss of skeletal muscle mass in aging adults is known as,low testosterone zoloft,muscle building workout everyday,fastest most effective weight loss pill youtube - Tips For You

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Aging is associated with a progressive loss of muscle mass and strength and a decline in neurophysiological functions. Regardless of the cause, when a motor neuron is lost, fibers previously innervated by that neuron, globally defined as a motor unit, are no longer controlled by the nervous system and fail to contribute to the force generated during a volitional muscle contraction. The reason for a progressive impairment of the re-innervation process with aging is unknown, but some lines of evidence point to changes that occur with aging in the neuromuscular junction (NMJ), which is the synaptic interface between a branch of a motor neuron and muscle cells. Mitochondria play a critical role in regulating energy production, metabolism, signal transduction, and apoptosis and are also the primary source of oxygen free radicals generated by the dislocation of electrons traveling across the respiratory chain (Peterson et al., 2012). Neuron loss (cell death) that occurs with aging is progressive and, as far as we know, irreversible.
Aging is characterized by high circulating levels of inflammatory markers such as interleukin 6 (IL-6), interleukin 1 (IL-1), tumor necrosis factor alpha (TNF-alpha), and C-reactive protein (CRP) in blood and tissues, often without a clear cause. The direct study of the NMJ in human beings presents challenges that are almost insurmountable. Neurotrophins are a family of proteins implicated in neural development, maintenance, and maturation that also play a role in neurotransmission.
There is evidence that short-term exercise increases levels of GDNF in the skeletal muscle and spinal cord of young and old rats (McCullough et al., 2013). Acetylcholine receptors clustering on the post-synaptic membrane is a main event in the differentiation of NMJ. Agrin is transported along the axons and finally released into synaptic basal lamina where it is inactivated by cleavage from neurotrypsin, a synaptic protease, which produces a soluble 22 kDa C-terminal agrin fragment (CAF). There is wide evidence, both in animals models and in humans, the Wnt signaling pathway is down regulated with aging and contributes to the progressive reduction in muscle regeneration and repair capacity (Conboy and Rando, 2012). Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is a transcription factor that promotes mitochondrial biogenesis.
The ubiquitin–proteasome and the autophagic-lysosomal pathways are activated during disease-related muscle atrophy and, perhaps, during the development of age-related sarcopenia.
The NMJ is the best model to study synaptogenesis, because, at least in animals, it is experimentally accessible in a living organism.
Muscle regulatory factor 4 (MRF4) is a member of the family of myogenic transcription factors (MyoD, myogenin, and myf-5) necessary for the differentiation of skeletal muscle (Weis et al., 2000). We carried out the first purpose of this study by examining the independent effect of age on DEXA-measured appendicular skeletal muscle mass (total, leg, and arm) in a cross-sectional cohort after controlling first for stature and body weight. Examination of TBK was intended to bridge the many earlier studies of skeletal muscle based on TBK to the present research effort. Total body fat, fat-free body mass, and TASM were measured with whole body DEXA (DPX, Lunar Radiation, Madison, WI). Leg skeletal muscle (LSM) mass and arm skeletal muscle (ASM) mass represent the sum of both right and left extremities, respectively. Earlier studies indicate that African-American subjects have significantly greater skeletal muscle mass (12) and longer appendicular bone lengths (1, 12, 21) compared with Caucasian subjects. There were significant negative correlations between most of the appendicular skeletal muscle components and age in all four groups (Table 2). In each of the following sections we develop appendicular skeletal muscle mass (TASM, LSM, and ASM) multiple-regression models.
Bioelectrical impedance (BIA) represents a simple, inexpensive and non-invasive method that is often used to assess fat-mass (FM) and fat-free mass (FFM) in large population-based cohorts.
The aim of this study was to describe the reference ranges and examine the influence of age and gender on FM, FFM and skeletal muscle mass (SMM) as well as height-adjusted estimates of FM [fat mass index (FMI)], FFM [fat-free mass index (FFMI)] and SMM [SMM index (SMI)] in a national, population-based cohort of Australian adults. The analytical sample included a total of 8,582 adults aged 25–91 years of Europid origin with complete data involved in the cross-sectional 1999–2000 Australian, Diabetes, Obesity and Lifestyle (AusDiab) Study. For both genders, FFM, SMM and SMI decreased linearly from the age of 25 years, with the exception that in men SMI was not related to age and FFM peaked at age 38 years before declining thereafter. In Australian adults there is heterogeneity in the age of onset, pattern and magnitude of changes in the different measures of muscle and fat mass derived from BIA, but overall the agerelated losses were similar between men and women. JavaScript is currently disabled, this site works much better if you enable JavaScript in your browser.
The most evident metabolic explanation for muscle decline is an imbalance between protein catabolism and anabolism. The important role of the FoxO transcription factors was underlined in a study by Liu et al. Studies investigating the age-related concentration of satellite cells have produced diverging results.
Caucasian and Asian women are most at risk for the disease, but African American and Hispanic women can get it too. Women who stop menstruating early because of heredity, surgery or lots of physical exercise may lose large amounts of bone tissue early in life. People who smoke or drink too much, or do not get enough exercise have an increased chance of osteoporosis. Research in Europe reported in 2003 that variations of a gene on chromosome 20 might make some postmenopausal women more likely to have osteoporosis. People often do not know they have the disease until a bone breaks, frequently in a minor fall that would not normally cause a fracture. Tell a friend about us, add a link to this page, or visit the webmaster's page for free fun content. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. Age-related neuromuscular junction (NMJ) plays a key role in musculoskeletal impairment that occurs with aging. The mechanism that leads to neuronal loss with aging is still unclear and may involve both impaired trophic signaling from the central nervous system (CNS), local degeneration, and feedback from dysfunctional muscle. In the attempt to counteract the functional consequence of this process, denervated orphan fibers express proteins and produce chemotactic signals that stimulate the sprouting of new dendrites from residual motor neurons. The NMJ is composed of three elements: pre-synaptic (motor nerve terminal), intrasynaptic (synaptic basal lamina), and post-synaptic part (muscle fiber and muscle membrane) (Punga and Ruegg, 2012). It has been proposed that such changes may be causally related to the decline in muscle mass and function that occurs in most aging individuals. There is strong evidence that changes in endplate morphology and NMJ remodeling occur with aging and precede loss of fast motor units. Loss of motor units in young adults results in re-innervation of denervated fibers by sprouting from other motor neurons and in death of fibers that are not successfully re-innervated. It has been hypothesized that age-related muscle uncoupling is due to a mismatch between DHPR and RyR.
The NMJ is seldom detected in muscle needle biopsies and requires open surgery biopsies that are only done for diagnostic purposes.
Changes in production and response to neurotrophins with aging may contribute to reduced axonal regeneration, and dysfunction at multiple levels, including motor axons, post-synaptic membrane, and Schwann cells. Many studies have found that circulating IGF-1 declines with aging and such decline may contribute to NMJ degeneration and motor unit denervation (Delbono, 2003; Messi and Delbono, 2003).
This process requires the presence of neural agrin, a basal lamina proteoglycan that activates a muscle-specific kinase (MuSK), which is essential for AChR clustering. Wnt proteins are a large family (19 members in humans) of secreted glycoproteins that are highly evolutionary conserved. Canonical and non-canonical Wnt pathways exert opposite effects on the formation of the vertebrate NMJ (Korkut and Budnik, 2009). Studies have consistently shown that PGC-1α decline with aging and in many age-related chronic diseases suggesting that such decline may explain the progressive mitochondrial dysfunction with aging. The ubiquitin–proteasome system is required to remove sarcomeric proteins, either because they are damaged or in response to decline in muscle activity. The mechanisms that lead to differentiation and maturation of the NMJ have been studied extensively while changes that occur with aging and lead to impairment of the NMJ are not fully understood.
This model is of great interest because the main function of SOD is to scavenge free oxygen radicals, being the oxidative stress, one of the landmarks of aging. However, the neuromuscular sarcopenic phenotypes exhibited by this mouse share several characteristics with age-related sarcopenia, namely shift from fast to slow fiber type, mitochondrial dysfunction, and increased mitochondrial ROS generation (Jang and Van Remmen, 2009, 2011). MRF4-null mice express genes encoding nAChR subunits and contractile proteins at normal levels, but express myogenin at dramatically increased levels. Our study supports the hypotheses that skeletal muscle is reduced in the elderly and that TBK provides a reasonable indirect assessment of skeletal muscle mass. Skeletal muscle atrophy and functional impairment with senescence in humans may be associated with osteoporotic fractures (28), the prolonged disability that accompanies hospitalizations for acute illness, falls with subsequent injury, and the frailty with inactivity often observed in geriatric populations (13).Although skeletal muscle loss with aging in humans is well documented, several unresolved questions remain that relate to the magnitude of loss and whether gender and ethnic differences exist in the age-associated muscle decline. We also explored the independent effects on appendicular skeletal muscle of gender and ethnicity (African-American and Caucasian) after controlling first for stature, body weight, and age. The possibility therefore exists that longer extremities in African-American subjects might explain their greater appendicular skeletal muscle mass after adjustment for covariates such as height, weight, age, and gender.
There were no significant differences between the two groups of men in body weight and BMI. After adjustment for the effects of age, TBK was positively correlated with TASM (P = 0.001) in all four subgroups.
A composite analysis section is then provided that summarizes the salient features of the three appendicular skeletal muscle multiple regression models.
These models explore the independent effects on TASM of height, weight, age, gender, and ethnicity. The relative loss from peak values to ?75 years in FFM (6–8%) and SMM (11–15%) was similar between men and women. From a histological point of view, sarcopenia is characterized by a decrease in the number and the size of the muscle fibers. Therefore, at least in sarcopenia, the UPS seems not to be the major pathway responsible for muscle loss.
Unfortunately, no correlation between muscle mass or protein synthesis rate was found [30], whereby the functional significance of the alterations are uncertain.
In animal studies, 3-NT was evaluated in muscles from young, adult and old rats [52–54]. Based on animal experiments, it even seems that MuRF1 is essential for TNF-α-induced loss of muscle function [63]. Induction of protein catabolism and the ubiquitin-proteasome pathway by mild oxidative stress. Apoptotic signaling induced by H2O2-mediated oxidative stress in differentiated C2C12 myotubes. Studies were continuing on how to identify the gene and use information from the research to prevent osteoporosis in carriers.
However, whether changes in the NMJ precede or follow the decline of muscle mass and strength remains unresolved. This process leads re-innervation by the expansion of pre-existing motor units and is aimed at returning to function previously denervated muscle fibers. When an action potential reaches the pre-synaptic element, voltage-dependent calcium channels open allowing calcium to enter the neuron and trigger the delivery of acetylcholine (ACh) in the synaptic cleft. Factors such as mitochondrial dysfunction, oxidative stress, inflammation, and changes in the innervation of muscle fiber and mechanical properties of the motor units could play an important role in the NMJ degeneration and development of sarcopenia. Structural changes together with functional alterations result in a NMJ impairment during aging.
Decline in number and function of mitochondria as well as frequent modification of their morphological structure with aging has been described in many tissues, including skeletal muscle. Newly emerging neurophysiological techniques may be used in the future to study the NMJ but they are still at an early stage of development. In accordance with this hypothesis, in mouse models, the overexpression of muscle-specific IGF-1 reverses sarcopenia (Musaro et al., 2001), prevents the age-dependent decrease in type IIB and increase in type IIA fibers (Messi and Delbono, 2003), and also leads to improved nerve regeneration by acting on axons, Schwann cells, and the NMJ.
Wnt signaling modulates the formation and the function of synapses and is involved in maintenance and function of many tissues including muscle and nerve.
In particular, the mitochondrial dysfunction might contribute to early motor terminal death in these mice (Muller et al., 2007).
These findings provide a foundation for investigating skeletal muscle mass in a wide range of health-related conditions. The first concern is that earlier investigations of skeletal muscle in humans were based largely on methods of questionable validity (14, 33). First, we examined the independent effect of age on TBK in the cross-sectional cohort after controlling first for stature and body weight. All parents and grandparents were required to be non-Hispanic African-American and non-Hispanic Caucasian, for African-American and Caucasian subjects, respectively. The calculation of appendicular skeletal muscle mass has been previously described in detail (15). We therefore also included in our multiple-regression models measurements of appendicular bone lengths. The40K raw counts accumulated over 9 min were adjusted for body size on the basis of a42K calibration equation (26).
Pearson’s correlation coefficients were used to establish the univariate relationships between total and regional skeletal muscle mass and age. There were no significant differences in height between African-American and Caucasian women. TASM and LSM were also positively correlated with height (P = 0.001) in African-American and Caucasian women and men. For FM and FMI, there was a curvilinear relationship with age in both genders, but peak values were detected 6–7 years later in women with a similar relative loss thereafter.
Even a sneeze or a sudden movement may be enough to break a bone in someone with severe osteoporosis.DescriptionOsteoporosis is a serious public health problem. While women commonly lose 30-50% of their bone mass over their lifetimes, men lose only 20-33%.
These can happen even after a seemingly normal activity, such as bending or twisting to pick up a light object. Many factors such as mitochondrial dysfunction, oxidative stress, inflammation, changes in the innervation of muscle fibers, and mechanical properties of the motor units probably perform an important role in NMJ degeneration and muscle mass and strength decline in late life.
This dynamic denervation–re-innervation cycle successfully compensates for neuronal loss, with little decline in global strength and only slightly reduced control. When the action potential reaches the motor nerve terminal the calcium channels open and the calcium enters in the neuron and delivers ACh in the synaptic cleft.
Understanding whether the primary event in the pathway to sarcopenia is muscle denervation, NMJ fragmentation or muscle fiber degeneration is important because the identification of the source of the primary event influences strategies to delay the onset of age-related muscle dysfunction. Mitochondria in the plaque region are numerically reduced and tend to show signs of degeneration. The excitation–contraction uncoupling leads to a loss of communication between the nervous and muscular system, causing a decline in skeletal muscle strength and muscle mass.
Dysfunctional mitochondria are often found with aging, characterized by increased levels of oxidation and nitrosylation products and decreased enzymatic activity.
One of the most promising areas of investigation and perhaps the one with the strongest translational potential is the study of circulating biomarkers, such as neurotrophic factors, muscle anabolic hormones, and growth factors that are known to have a role in NMJ dysfunction. Interestingly, there is some initial evidence that production of glia cell-derived neurotrophic factor (GDNF) declines with aging (Li et al., 1995). Different models of exercise type and intensity could have varying effects on GDNF protein content in slow- and fast-twitch muscle fibers.


Systemic administration of IGF-1 decreased motor neuron cell death and promoted muscle re-innervation after injury in young animals, suggesting that the decline in IGF-1 with aging may impair the ability of aging animals to repair and maintain the integrity of NMJ (Vergani et al., 1998). This is consistent with findings in experiments with transgenic mice overexpressing neurotrypsin in spinal motoneurons that shown the full sarcopenia phenotype (Butikofer et al., 2011).
In contrast, activation of the canonical Wnt pathway has a negative effect on NMJ formation. Two such methods, urinary creatinine excretion and total body potassium (TBK), assume that muscle is the sole or main source of intracellular creatine (30) and potassium (31), respectively. The independent effects on TBK of gender and ethnicity were also examined as they were for appendicular skeletal muscle mass. Recruitment of subjects occurred over a 3-yr period through advertisements in local newspapers, on radio stations, and in flyers posted in the local community. With the use of specific anatomic landmarks, the legs and arms are isolated on the skeletal X-ray planogram (anterior view).
The skeletal X-ray planogram generated by the DEXA scan was used specifically to measure tibia length, femur length, humerus length, and total subject skeletal lengths. Pearson’s correlation coefficients adjusted for age were used to establish the relationships between total and regional skeletal muscle mass and other body composition components, as well as subject demographic characteristics. Relative leg length was significantly (P = 0.0001) greater in African-American women compared with their Caucasian counterparts. Some 44 million people in the United States are at risk for this potentially debilitating disease, which is responsible for 1.5 million fractures (broken bones) annually. The fractures can cause severe back pain, but sometimes go unnoticed—either way, the vertebrae collapse down on themselves, and the person actually loses height. This review addresses the primary events that might lead to NMJ dysfunction with aging, including studies on biomarkers, signaling pathways, and animal models. In this report, we review our current understanding of the events that lead to NMJ dysfunction with aging, including studies on biomarkers, signaling pathways, and animal models.
In particular, some authors have described dramatic alterations in mitochondrial morphology in axon terminals, including cristae disruption, swelling, and formation of megamitochondria due to multiple fusions between adjacent mitochondria (Garcia et al., 2013).
It has been hypothesized that the diffusion of mitochondrial nitric oxide (NO) and hydrogen peroxide (H2O2) to the cytosol is decreased in the aged brain and may impair mitochondrial biogenesis (Navarro and Boveris, 2009). The mild pro-inflammatory state of aging may affect muscle performance and maintenance in many ways.
Although most of the biomarkers addressed in this section are known to change with aging, whether they modulate the causal pathway from aging to NMJ impairment with aging is not fully established. Denervation leads to an up regulation of GDNF in rat and human skeletal muscle (Lie and Weis, 1998). The authors concluded that GDNF may play a role in remodeling of the NMJ in slow and fast-twitch muscle fibers. IGF-1 sensitivity may not decrease with age, so that IGF-1 could promote regeneration after nerve injury even in older individuals. Thus, while the role of Wnt signaling on NMJ development and in muscle regeneration impairment with aging is well established, evidence for a direct effect of Wnt on NMJ plasticity, maintenance, and repair is lacking and requires further investigation.
Recent studies challenge these assumptions (14, 33) and raise concerns related to the use of these methods in estimating age-related muscle loss.An attempt was made to improve the use of TBK as a marker of skeletal muscle by devising a two-compartment method based on TBK and total body nitrogen (TBN) (5). In the second stage of analysis, we established in our cohort how much of the observed variation in TBK could be explained by total appendicular skeletal muscle (TASM) mass and other potential independent TBK determinants such as age, gender, and ethnicity.
Inclusion criteria required that subjects be ambulatory, nonvigorously exercising, with no orthopedic problems that could potentially affect any of the variables under investigation.
The arm encompasses all soft tissue extending from the center of the arm socket to the phalange tips, and contact with the ribs, pelvis, or greater trochanter is avoided. All dimensions were measured in millimeters by a single reader by using an engineering caliper (Staedtler, Frankfurt, Germany). The relationships between skeletal muscle measurements and height, weight, age, and ethnicity were investigated by using multiple-regression analysis. These fractures, which are often the first sign of the disease, can affect any bone, but the most common locations are the hip, spine, and wrist. Interventions such as caloric restriction and exercise may positively affect the NMJ through this mechanism and attenuate the age-related progressive impairment in motor function. Some denervated fibers are not successfully re-innervated, become apoptotic, and are not replaced by new fibers. Calcium released from the sarcoplasmic reticulum through the RyRs binds to troponin C and allows cross-bridge cycling and force production (Figure 1). Calcium released from the sarcoplasmic reticulum through the RyRs binds to troponin C and allows cross-bridge cycling and force production.
We propose that interventions aimed at preventing the deterioration of the NMJ should be aimed at reversing the mechanisms that lead to NMJ degeneration with aging. Studies of pre-synaptic plaque changes with aging have found high levels of oxidative damage, decreased number of synaptic vesicles, and lower quantities of neurotransmitter released during depolarization (Figure 2). These findings suggest that overexpression of IGF-1 may have a role in preventing muscle strength decline with aging.
For example, Schwann cell senescence has been associated with overexpression of IL-6, suggesting a role of inflammation in the age-related alterations in axonal regeneration (Saheb-Al-Zamani et al., 2013). Nevertheless, correlational studies may provide knowledge that in the future may help reconstructing a general model of the mechanism leading to NMJ degeneration with aging. Overexpression of muscle-specific IGF-1 in mice increases the size of NMJ without substantial changes in muscle fiber size suggesting that preservation of specific force in aged animals overexpressing IGF-1 in muscle is achieved, in part, by improved motor neurons-muscle coupling (Payne et al., 2006).
All together these data suggest that the impairment in neuromuscular transmission follows post-synaptic changes.
This method assumes that the TBK-to-TBN ratios in skeletal muscle and nonskeletal muscle lean tissues are known and constant (6).
Each subject completed a medical examination that included screening blood tests after an overnight fast. The leg consists of all soft tissue extending from an angled line drawn through the femoral neck to the phalange tips.
Total skeletal length was measured as the distance from the apex of the cranium to the plantar surface of the calcaneus bone.
TASM, LSM, and ASM were used as dependent variables and height, weight, age, ethnicity, and extremity lengths were used as independent variables in the multiple-regression models. Breaks in the hip and spine are of special concern because they almost always require hospitalization and major surgery, and may lead to other serious consequences, including permanent disability and even death.To understand osteoporosis, it is helpful to understand the basics of bone formation.
It is hypothesized that this phenomenon contributes to a progressive decline in muscle mass and strength with aging.
It is important to underline that our comprehension of the global mechanism that lead to NJM impairment with aging is still patchy. Indeed, it has been recently shown in sarcopenic rats with NMJ disruption that the expression of genes implicated in mitochondrial energy metabolism is down regulated (Ibebunjo et al., 2013). Chronic inflammation down regulates the production of IGF-1 and blunts its biological activity. Moreover, GDNF protein content in aged rat skeletal muscle might be controlled by stretching the muscle and the membrane depolarization of AChR acts to decrease GDNF protein content (McCullough et al., 2011). A recent study suggests, however, that skeletal muscle mass estimates derived from the TBK-TBN method are substantially lower than that observed by using whole body multislice computerized tomography (33).Much of the present understanding of skeletal muscle mass and aging is based on studies of urinary creatinine (33) and TBK (10, 22, 23) in adult populations.
Only healthy subjects, without any diagnosed medical conditions, were enrolled in the study. The system software provides the total mass, ratio of soft tissue attenuations, and bone mineral mass for the isolated regions.
In addition, potential interaction terms and nonlinear relationships were explored for selected variables.
Bone is living tissue that is constantly being renewed in a two-stage process (resorption and formation) that occurs throughout life. Some of the elements emerging in the literature will be described and their relationship with aging explored. These alterations in morphologic remodeling in the aged NMJ result in more dispersed AChR, with greater spatial uncoupling between ACh vesicle clusters and receptor clusters. Inflammation is associated with impaired amino acid (Aa) utilization and protein anabolism, especially in critical periods such as after a meal or after a bout of exercise. Questions surrounding the validity of these methods in accurately quantifying skeletal muscle mass raise concerns about the interpretation of earlier studies of skeletal muscle in relation to aging, gender, and ethnicity.A second limitation associated with earlier investigations of changes in skeletal muscle mass with aging is the inadequate control of factors known to influence muscle, such as body weight and stature. The ratio of soft tissue attenuation for each region was used to divide bone mineral-free tissue of the extremities into fat and fat-free components. These dimensions do not correspond precisely to anatomic bone lengths, although all measurements were consistent among subjects.
However, it is worth noticing that how these different parts participate and interact within a unique global mechanism and cause NMJ dysfunction with aging is not understood. In particular, Clark and Fielding (2012) suggest that the NMJ activation of muscle agonists is impaired in some older adults in whom weakness is more prominent than reduced muscle mass. Reduced ATP production and impaired calcium buffering in the subsarcolemmal mitochondria located near the NMJ may impair both neurotransmission and vesicular recycling (Deschenes, 2011). Older subjects in some studies were shorter and weighed more or less than their younger counterparts (7, 22, 23).
The fat and bone mineral-free portion of the extremities were assumed to represent appendicular skeletal muscle mass along with a small and relatively constant amount of skin and underlying connective tissues. The ratio of tibia plus femur length to total subject skeletal length was used as an index of relative leg length. It also can show how far the disease has progressed.Several diagnostic tools are available to measure bone density. The independent influence of these important factors on skeletal muscle mass is usually not considered, and the prevailing hypothesis is that skeletal muscle mass is relatively reduced in the elderly. The ratio of humerus length to total subject skeletal length was used as an index of relative arm length. During childhood and early adulthood, more bone is produced than removed, reaching its maximum mass and strength by the mid-30s. The ordinary x ray is one, though it is the least accurate for early detection of osteoporosis, because it does not reveal bone loss until the disease is advanced and most of the damage has already been done.
The hypothesis was evaluated by estimating appendicular skeletal muscle mass with dual-energy X-ray absorptiometry in a healthy adult cohort. A related concern is that little is known about how women and men compare across the age span with regard to loss in muscle mass. After that, bone is lost at a faster pace than it is formed, so the amount of bone in the skeleton begins to slowly decline. Two other tools that are more likely to catch osteoporosis at an early stage are computed tomography scans (CT scans) and machines called densitometers, which are designed specifically to measure bone density.The CT scan, which takes a large number of x rays of the same spot from different angles, is an accurate test, but uses higher levels of radiation than other methods. A second purpose was to test the hypothesis that whole body40K counting-derived total body potassium (TBK) is a reliable indirect measure of skeletal muscle mass. Women on average weigh less and are shorter than men (19), and, in most previous studies, between-gender comparisons of skeletal muscle did not adequately control for body weight, stature, and age differences (7).The third concern is that much of what is documented about skeletal muscle mass was derived from persons of Caucasian ethnicity, and there is relatively little information available on other ethnic groups. Most cases of osteoporosis occur as an acceleration of this normal aging process, which is referred to as primary osteoporosis. The most accurate and advanced of the densitometers uses a technique called DEXA (dual energy x-ray absorptiometry).
The independent effects on both appendicular skeletal muscle and TBK of gender (n = 148 women and 136 men) and ethnicity (n = 152 African-Americans and 132 Caucasians) were also explored. African-Americans may have different total amounts of skeletal muscle at any given age compared with Caucasian subjects (12, 21), and there may be ethnic differences in the relative loss of skeletal muscle with aging as there are with bone mineral (20).The recent introduction of dual-energy X-ray absorptiometry (DEXA) provides a new opportunity to study the appendicular portion of skeletal muscle mass in vivo. The condition also can be caused by other disease processes or prolonged use of certain medications that result in bone loss. Appendicular skeletal muscle accounts for >75% of total body skeletal muscle (31) and is the primary portion of skeletal muscle involved in ambulation and physical activities. If so, this is called secondary osteoporosis.Osteoporosis occurs most often in older people and in women after menopause. Earlier studies from our laboratory (15, 33) and from other research groups (17) support the validity of DEXA estimates of appendicular skeletal muscle.
Effects of body fatness and physical activity on cardiovascular risk: risk prediction using the bioelectrical impedance method. People should talk to their doctors about their risk factors for osteoporosis and if, and when, they should get the test. An important advantage of DEXA over previous skeletal muscle mass-measuring methods is its capability of providing separate estimates of lower and upper extremity appendicular muscle components (17).The primary purpose of this study was to test the hypothesis that skeletal muscle is reduced in the elderly after appropriate control for body weight and stature.
Ideally, women should have bone density measured at menopause, and periodically afterward, depending on the condition of their bones. A second study aim was to test the hypothesis that TBK reliably represents skeletal muscle mass. They have smaller, thinner bones than men to begin with, and they lose bone mass more rapidly after menopause (usually around age 50), when they stop producing a bone-protecting hormone called estrogen. In the five to seven years following menopause, women can lose about 20% of their bone mass. Men and women with additional risk factors, such as those who take certain medications, may need to be tested earlier.TreatmentThere are a number of good treatments for primary osteoporosis, most of them medications.
A prospective study of adiposity and postmenopausal breast cancer risk: the Malmo Diet and Cancer Study. Two medications, alendronate and calcitonin (in nose spray form), have been approved by the Food and Drug Administration (FDA). As an increasing number of men reach an older age, there is more awareness that osteoporosis is an important health issue for them as well. In fact, a 2003 report noted that one in every eight men over age 50 will suffer a hip fracture as a result of osteoporosis.Causes and symptomsA number of factors increase the risk of developing osteoporosis. For people with secondary osteoporosis, treatment may focus on curing the underlying disease.DrugsFor many women who have gone through menopause, the treatment of choice for osteoporosis has been hormone replacement therapy (HRT), also called estrogen replacement therapy. Many women choose HRT when they undergo menopause to alleviate symptoms such as hot flashes, but hormones increase a woman's supply of estrogen, which helps build new bone, while preventing further bone loss. Influence of sarcopenia on the development of physical disability: the Cardiovascular Health Study.
In fact, the trial was stopped early because the incidence of invasive breast cancer in women on HRT passed a threshold that was considered too risky for the benefits they were receiving.
Low relative skeletal muscle mass (sarcopenia) in older persons is associated with functional impairment and physical disability. The study also found that the women on combined hormone therapy were at increased risk for coronary heart disease and stroke.
Whether or not a woman takes hormones and for how long is a decision she should make carefully with her doctor. Women should talk to their doctors about personal risks for osteoporosis, as well as their risks for heart disease and breast cancer.Since estrogen may no longer be recommended for prevention of osteoporosis, selective use of alendronate and calcitonin are possible alternatives. Alendronate and calcitonin both stop bone loss, help build bone, and decrease fracture risk by as much as 50%. The loss of skeletal muscle strength, mass, and quality in older adults: the health, aging and body composition study. Alendronate (sold under the name Fosamax) is the first nonhormonal medication for osteoporosis ever approved by the FDA. It attaches itself to bone that has been targeted by bone-eating osteoclasts, protecting the bone from these cells.
Muscle mass, muscle strength, and muscle fat infiltration as predictors of incident mobility limitations in well-functioning older persons.


Osteoclasts help the body break down old bone tissue.Calcitonin is a hormone that has been used as an injection for many years. Glucose and insulin measurements from the oral glucose tolerance test and relationship to muscle mass. Fosamax has proven safe in large, multi-year studies, but not much is known about the effects of its long-term use. Anthropometric measurements of mid-upper arm as a mortality predictor for community-dwelling Japanese elderly: the Nagoya Longitudinal Study of Frail Elderly (NLS-FE). Several medications under study include other bisphosphonates that slow bone breakdown (like alendronate), sodium fluoride, vitamin D metabolites, and selective estrogen receptor modulators. Some of these treatments are already being used in other countries, but have not yet been approved by the FDA for use in the United States.In early 2003, a report announced that the FDA had recently approved the first drug that could form bone in osteoporosis patients.
Decreased muscle mass and increased central adiposity are independently related to mortality in older men.
Agreement of bioelectrical impedance with dual-energy X-ray absorptiometry and MRI to estimate changes in body fat, skeletal muscle and visceral fat during a 12-month weight loss intervention. There are some patients who cannot use the drug, so all considering the new treatment must check with their physician and may need to undergo bone densitometry scans or other testing.SurgeryUnfortunately, much of the treatment for osteoporosis is for fractures that result from advanced stages of the disease. For complicated fractures, such as broken hips, hospitalization and a surgical procedure are required. Accuracy of bioelectrical impedance consumer devices for measurement of body composition in comparison to whole body magnetic resonance imaging and dual X-ray absorptiometry.
In hip replacement surgery, the broken hip is removed and replaced with a new hip made of plastic, or metal and plastic. Though the surgery itself is usually successful, complications of the hip fracture can be serious. Those individuals have a 5-20% greater risk of dying within the first year following the injury than do others in their age group.
A large percentage of those who survive are unable to return to their previous level of activity, and many move self-care to a supervised living situation or nursing home. Age-related differences in fat-free mass, skeletal muscle, body cell mass and fat mass between 18 and 94 years.
That is why getting early treatment and taking steps to reduce bone loss are vital.Alternative treatmentAlternative treatments for osteoporosis focus on maintaining or building strong bones.
A healthy diet low in fats and animal products and containing whole grains, fresh fruits and vegetables, and calcium-rich foods (such as dairy products, dark-green leafy vegetables, sardines, salmon, and almonds), along with nutritional supplements (such as calcium, magnesium, and vitamin D), and weight-bearing exercises are important components of both conventional prevention and treatment strategies and alternative approaches to the disease. In addition, alternative practitioners recommend a variety of botanical medicines or herbal supplements. Herbal supplements designed to help slow bone loss emphasize the use of calcium-containing plants, such as horsetail (Equisetum arvense), oat straw (Avena sativa), alfalfa (Medicago sativa), licorice (Glycyrrhiza galbra), marsh mallow (Althaea officinalis), and yellow dock (Rumex crispus).
These remedies are likely to include such substances as Calcarea carbonica (calcium carbonate) or silica. Bioelectrical impedance analysis (BIA) using bipolar foot electrodes in the assessment of body composition in Type 2 diabetes mellitus.
In traditional Chinese medicine, practitioners recommend herbs thought to slow or prevent bone loss, including dong quai (Angelica sinensis) and Asian ginseng (Panax ginseng). Natural hormone therapy, using plant estrogens (from soybeans) or progesterone (from wild yams), may be recommended for women who cannot or choose not to take synthetic hormones.PrognosisThere is no cure for osteoporosis, but it can be controlled. The medicines available now build bone, protect against bone loss, and halt the progress of this disease.PreventionBuilding strong bones, especially before the age of 35, and maintaining a healthy lifestyle are the best ways to prevent osteoporosis. To build as much bone mass as early as possible in life, and to help slow the rate of bone loss later in life, doctors advise:Getting calcium from foodsExperts recommend 1,500 milligrams (mg) of calcium per day for adolescents, pregnant or breastfeeding women, older adults (over 65), and postmenopausal women not using hormone replacement therapy. Other foods that are high in calcium are green leafy vegetables, tofu, shellfish, Brazil nuts, sardines, and almonds.Taking calcium supplementsMany people, especially those who do not like or can not eat dairy foods, do not get enough calcium in their diets and may need calcium supplements. Dual energy X-ray absorptiometry body composition and aging in a population-based older cohort. Supplements should be taken with meals and accompanied by six to eight glasses of water a day.Getting vitamin dVitamin D helps the body absorb calcium. People can get vitamin D from sunshine with a quick (15-20 minute) walk each day or from foods such as liver, fish oil, and vitamin-D fortified milk. Age determines longitudinal changes in body composition better than menopausal and bone status: the OFELY study. Four hundred mg daily is usually the recommended amount.Avoiding smoking and alcoholSmoking reduces bone mass, as does heavy drinking.
Prevalence of Sarcopenia and Sarcopenic Obesity in the Korean Population Based on the Fourth Korean National Health and Nutritional Examination Surveys. An alcoholic drink is one-and-a-half ounces of hard liquor, 12 ounces of beer, or five ounces of wine.ExerciseExercising regularly builds and strengthens bones. These include aerobics, dancing, jogging, stair climbing, tennis, walking, and lifting weights.
People who have osteoporosis may want to attempt gentle exercise, such as walking, rather than jogging or fast-paced aerobics, which increase the chance of falling. Exercising three to four times per week for 20-30 minutes each time helps.ResourcesPeriodicalsDoering, Paul L. Reference values of fat-free and fat masses by bioelectrical impedance analysis in 3393 healthy subjects.
Women at risk for this disorder can reduce that risk by maintaining adequate calcium levels with dietary calcium or calcium supplements (see diet-related bone loss below), and taking estrogen in the perimenopausal period when indicated. Intestinal absorption of calcium becomes less efficient with age; hence older persons need more rather than less dietary calcium to maintain a positive calcium balance.
Although dairy products are the primary source of dietary calcium, supplementary calcium is needed by some women. Healthy premenopausal women over the age of 30 may need as much as 1000 mg of calcium a day, which is the amount supplied by a quart of milk. The use of bioelectrical impedance analysis for body composition in epidemiological studies. However, for pregnant women and those over the age of 50, the recommended daily intake increases to more than 1500 mg. The vitamin D metabolite 1,25-dihydroxycholecalciferol is the active hormone that helps maintain normal serum calcium and phosphate levels. Because of inadequate exposure to sunlight, decreased intestinal absorption of vitamin D, and limited intake of milk, elderly persons often are vitamin D–deficient. Vitamin D is a component of multivitamins, and health care providers often recommend supplemental multivitamins for the elderly.Disuse osteoporosis is related to the response of bone mass change to mechanical stress. Net bone mass does not change throughout much of adult life; however, living bone is never metabolically at rest and constantly remodels and reappropriates its mineral stores along lines of mechanical stress. As much as 30 to 40 per cent of initial bone mass may be lost after six months of total immobilization, as in paraplegia and quadriplegia due to spinal cord injury. Norm references of fatfree mass index and fat mass index and subtypes of obesity based on the combined FFMI-%BF indices in the Korean adults aged 18-89yr.
There must be weight-bearing activity and the use of antigravity muscles to maintain healthy bones.Heritable osteoporosis includes at least four types of congenital diseases grouped under the term osteogenesis imperfecta. Symptoms of varying severity that are characteristic of these disorders include skeletal fragility, multiple pathologic fractures, generalized osteoporosis, and scoliosis.
Ethnic and age-related fat free mass loss in older Americans: the Third National Health and Nutrition Examination Survey (NHANES III). All of the diseases included under osteogenesis imperfecta are thought to be associated with defective bone matrix formation.Endocrine-mediated bone loss can produce osteoporosis because numerous endocrine hormones affect skeletal remodeling and hence skeletal mass.
Examples of endocrine disorders that can produce associated osteopenia include hypogonadism, hyperthyroidism, hyperparathyroidism, and hyperadrenalism or chronic glucocorticoid hormone excess.Disease-related bone loss can occur with almost any kind of chronic disease that is associated with malnutrition and disuse. Leukemia, lymphoma, and the extremely rare mast cell tumor also may be associated with osteoporosis.Idiopathic osteoporosis, in both the adult and juvenile form, is extremely uncommon.
The variations of body mass index and body fat in adult Thai people across the age spectrum measured by bioelectrical impedance analysis.
Drug-induced bone loss may be associated with long-term use of heparin for anticoagulation therapy or with the administration of methotrexate, which has both cytotoxic and calciuric effects.Diagnosis. Osteoporosis is an insidious disease that silently robs the skeleton of its banked resources.
The most common sites for such bone loss and consequent fractures are the thoracic and lumbar vertebral bodies, ribs, proximal femur, and distal radius.
The earliest signs of osteoporosis are often associated with compression fracture of the spine characterized by an episode of acute pain in the middle to low thoracic or high lumbar region. Prevention of osteoporosis through diet, exercise, and the reduction of risk factors should be a priority.
Two other associated effects of vertebral compression are the result of a decrease in the size of the thoracic and abdominal cavities. The patient experiences diminished activity tolerance as a result of disease-related postural changes and often reports early satiety and a bloated feeling after eating only a small amount of food.Radiographs of the thoracic and lumbar spine show a visible loss of bone density. In general, as much as 30 to 50 per cent of the bone mass must be lost before the decrease can be seen on x-ray. Bone density measurement can help in evaluation of this disease and prediction of the likelihood of fracture.Treatment and Patient Care. The management of osteoporosis is concerned with treatment of symptomatic disease and its sequelae and with maintenance of skeletal mass and integrity. Treatment of acute symptoms is aimed at relieving pain, providing comfortable mechanical support for the spine, arranging assistance in activities of daily living, coordinating a rehabilitation program, and providing encouragement and reassurance to the patient and family. The rehabilitation process must include instruction in proper back care, and especially in how to avoid unnecessary spinal compression forces while lifting or bending.Estrogen replacement therapy is often prescribed for women at menopause. Because it increases the risk for breast and gynecologic malignancies, careful assessment of these patients is necessary.
They have also published clinical guidelines for the prevention and treatment of osteoporosis on their web site.Loss of bone mass due to osteoporosis produces characteristic changes in the curvature of the spine.
Figures to the right show the normal spine at age 40 and osteoporotic changes at 60 and 70 years of age. About 1.3 million fractures attributable to osteoporosis occur each year in people aged 45 and older, and this condition is responsible for 50% of fractures occurring in women older than age 50.
Although all bones are affected, compression fractures of the vertebrae and traumatic fractures of the wrist and femoral neck are most common.
Loss of body height and development of kyphosis may be the only signs of vertebral collapse.
Fractures in the elderly often lead to loss of mobility and independence, social alienation, fear of further falls and fractures, and depression. After hip fracture, most elderly patients fail to recover normal activity, and mortality within 1 year approaches 20%.
Bone constantly undergoes cycles of resorption and remodeling to maintain the concentration of calcium and phosphate in the extracellular fluid. When serum calcium concentration drops, increased secretion of parathyroid hormone stimulates bone resorption by osteoclasts to restore serum calcium levels to normal.
Bone mass declines with age and is influenced by sex, race, menopause, and weight-for-height. Dietary intake of calcium and vitamin D as well as intestinal and renal function affect calcium and phosphate homeostasis. Asian or white race, underweight, dietary calcium deficiency, sedentary lifestyle, alcohol use, and cigarette smoking appear to be independent risk factors.
The decline of vitamin D3 level with aging results in calcium malabsorption, which, in turn, stimulates bone resorption.
Estrogen deficiency exacerbates this problem by increasing the sensitivity of bone to resorbing agents.
Female athletes who become amenorrheic because of rigorous exercise and dietary restriction or eating disorders are at risk of osteoporosis. The formation and resorption of bone are also influenced by external physical factors such as body weight and exercise. Immobilization and prolonged bed rest produce rapid bone loss, whereas exercise involving weight-bearing, resistance, and high impact has been shown both to reduce bone loss and to increase bone mass.
Risk factors for osteoporosis in men include alcoholism, chronic lung disease, hypogonadism, and rheumatoid arthritis, and other disorders that restrict mobility. Osteoporosis is common in young adults with cystic fibrosis and in people receiving long-term thyroid hormone or glucocorticoid therapy.
The diagnosis of primary osteoporosis is established by documentation of reduced bone density after exclusion of known causes of excessive bone loss. Assessment of bone density is currently recommended for all women 65 and older and for younger women who are at increased risk of osteoporosis. Roentgenograms are insensitive indicators of bone loss, because bone density must have decreased by at least 20-30% before the reduction can be appreciated. Standard diagnostic procedures are determination of bone mineral density (BMD) at the ultradistal radius and midshaft radius by single-photon absorptiometry (SPA) and at the hip and lumbar spine by dual-energy x-ray absorptiometry (DEXA). A quantitative ultrasound procedure is comparable with bone density measurements by dual-energy x-ray absorptiometry in predicting fractures due to osteoporosis. The appropriate timing and proper use of agents such as calcium, vitamin D, estrogen, bisphosphonates, calcitonin, and raloxifene and the role of exercise have generated major research efforts and considerable controversy. Intake of adequate amounts of calcium and vitamin D, and continuing moderate weight-bearing exercise, are basic preventive measures for people of all ages. Those with demonstrated reduction of bone mineral density should take 1200-1500 mg of calcium and 400-800 IU of vitamin D daily. Administration of estrogen at and after menopause does not simply halt the loss of bone, but actually increases bone mass. However, to date there is no experimental proof that hormone replacement with estrogen reduces the risk of fractures in postmenopausal women. The possible benefits of estrogen therapy must be weighed against the increased risk of endometrial hyperplasia and endometrial carcinoma (which can be offset by concomitant administration of progestogen), myocardial infarction, stroke, invasive breast cancer, venous thromboembolism, and gallbladder disease. The selective estrogen receptor modulator raloxifene has been approved for prevention of osteoporosis. It does not cause endometrial hyperplasia but is less effective than estrogen in conserving bone mass.
The hormone calcitonin, administered by injection or nasal spray, inhibits bone resorption. Bisphosphonates such as alendronate and etidronate, which bind to bone crystals, rendering them resistant to enzymatic hydrolysis and inhibiting the action of osteoclasts, have been shown to increase bone mineral density. In contrast to other agents, teriparatide, a synthetic version of the biologically active segment of human parathyroid hormone, actually stimulates bone formation in osteoporosis. It occurs most frequently in postmenopausal women, sedentary or immobilized individuals, and patients on long-term steroid therapy. Osteoporosis may be without a known cause or secondary to other disorders, such as thyrotoxicosis or the bone demineralization caused by hyperparathyroidism. Bone density surveys should be encouraged every 1 to 3 years after age 49 for early detection. Instruction in fall and fracture prevention measures is important to help the individual decrease fracture risk and maintain independence in activities of daily living.
Generally osteoporosis starts with bone loss and this bone loss starts after the person crosses his mid 30`s.



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