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Academic literature on the topic 'Age-related decline in muscle mass'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Age-related decline in muscle mass"

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Goldspink, Geoffrey. "Age-Related Loss of Muscle Mass and Strength." Journal of Aging Research 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/158279.

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Age-related muscle wasting and increased frailty are major socioeconomic as well as medical problems. In the quest to extend quality of life it is important to increase the strength of elderly people sufficiently so they can carry out everyday tasks and to prevent them falling and breaking bones that are brittle due to osteoporosis. Muscles generate the mechanical strain that contributes to the maintenance of other musculoskeletal tissues, and a vicious circle is established as muscle loss results in bone loss and weakening of tendons. Molecular and proteomic approaches now provide strategies for preventing age-related muscle wasting. Here, attention is paid to the role of the GH/IGF-1 axis and the special role of the IGFI-Ec (mechano growth factor/MGF) which is derived from the IGF-I gene by alternative splicing. During aging MGF levels decline but when administered MGF activates the muscle satellite (stem) cells that “kick start” local muscle repair and induces hypertrophy.
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Proctor, D. N., J. R. Halliwill, D. P. Seamans, and M. J. Joyner. "ACTIVE MUSCLE MASS AND THE AGE-RELATED DECLINE IN ??VO2max203." Medicine &amp Science in Sports &amp Exercise 28, Supplement (May 1996): 34. http://dx.doi.org/10.1097/00005768-199605001-00203.

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Payne, Anthony M., Stephen L. Dodd, and Christiaan Leeuwenburgh. "Life-long calorie restriction in Fischer 344 rats attenuates age-related loss in skeletal muscle-specific force and reduces extracellular space." Journal of Applied Physiology 95, no. 6 (December 2003): 2554–62. http://dx.doi.org/10.1152/japplphysiol.00758.2003.

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The decline in muscle function is associated with an age-related decrease in muscle mass and an age-related decline in strength. However, decreased strength is not solely due to decreased muscle mass. The age-related decline in muscle-specific force (force/muscle cross-sectional area), a measure of intrinsic muscle function, also contributes to age-related strength decline, and the mechanisms by which this occurs are only partially known. Moreover, changes in the extracellular space could have a profound effect on skeletal muscle function. Life-long calorie restriction in rodents has shown to be a powerful anti-aging intervention. In this study, we examine whether calorie restriction is able to attenuate the loss of muscle function and elevations in extracellular space associated with aging. We hypothesize that calorie restriction attenuates the age-associated decline in specific force and increases in extracellular space. Measurements of in vitro contractile properties of the extensor digitorum longus (type II) and soleus (type I) muscles from 12-mo and 26- to 28-mo-old ad libitum-fed, as well as 27- to 28-mo-old life-long calorie-restricted male Fischer 344 rats, were performed. We found that calorie restriction attenuated the age-associated decline in muscle mass-to-body mass ratio (mg/g) and strength-to-body mass ratio (N/kg) in the extensor digitorum longus muscle ( P < 0.05) but not in the soleus muscle ( P > 0.05). Importantly, muscle-specific force (N/cm2) in the extensor digitorum longus, but not in the soleus muscle, of the old calorie-restricted rats was equal to that of the young 12-mo-old animals. Moreover, the age-associated increase in extracellular space was reduced in the fast-twitch extensor digitorum longus muscle ( P < 0.05) but not in the soleus muscle with calorie restriction. We also found a significant correlation between the extracellular space and the muscle-specific force in the extensor digitorum longus ( r = -0.58; P < 0.05) but not in the soleus muscle ( r = -0.38; P > 0.05). Hence, this study shows a loss of muscle function with age and suggests that long-term calorie restriction is an effective intervention against the loss of muscle function with age.
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Short, Kevin R., Janet L. Vittone, Maureen L. Bigelow, David N. Proctor, and K. Sreekumaran Nair. "Age and aerobic exercise training effects on whole body and muscle protein metabolism." American Journal of Physiology-Endocrinology and Metabolism 286, no. 1 (January 2004): E92—E101. http://dx.doi.org/10.1152/ajpendo.00366.2003.

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Aging in humans is associated with loss of lean body mass, but the causes are incompletely defined. Lean tissue mass and function depend on continuous rebuilding of proteins. We tested the hypotheses that whole body and mixed muscle protein metabolism declines with age in men and women and that aerobic exercise training would partly reverse this decline. Seventy-eight healthy, previously untrained men and women aged 19-87 yr were studied before and after 4 mo of bicycle training (up to 45 min at 80% peak heart rate, 3-4 days/wk) or control (flexibility) activity. At the whole body level, protein breakdown (measured as [13C]leucine and [15N]phenylalanine flux), Leu oxidation, and protein synthesis (nonoxidative Leu disposal) declined with age at a rate of 4-5% per decade ( P < 0.001). Fat-free mass was closely correlated with protein turnover and declined 3% per decade ( P < 0.001), but even after covariate adjustment for fat-free mass, the decline in protein turnover with age remained significant. There were no differences between men and women after adjustment for fat-free mass. Mixed muscle protein synthesis also declined with age 3.5% per decade ( P < 0.05). Exercise training improved aerobic capacity 9% overall ( P < 0.01), and mixed muscle protein synthesis increased 22% ( P < 0.05), with no effect of age on the training response for either variable. Fat-free mass, whole body protein turnover, and resting metabolic rate were unchanged by training. We conclude that rates of whole body and muscle protein metabolism decline with age in men and women, thus indicating that there is a progressive decline in the body's remodeling processes with aging. This study also demonstrates that aerobic exercise can enhance muscle protein synthesis irrespective of age.
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Lynch, N. A., E. J. Metter, R. S. Lindle, J. L. Fozard, J. D. Tobin, T. A. Roy, J. L. Fleg, and B. F. Hurley. "Muscle quality. I. Age-associated differences between arm and leg muscle groups." Journal of Applied Physiology 86, no. 1 (January 1, 1999): 188–94. http://dx.doi.org/10.1152/jappl.1999.86.1.188.

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To determine the differences between arm and leg muscle quality (MQ) across the adult life span in men and women, concentric (Con) and eccentric (Ecc) peak torque (PT) were measured in 703 subjects (364 men and 339 women, age range 19–93 yr) and appendicular skeletal muscle mass (MM) was determined in the arm and leg in a subgroup of 502 of these subjects (224 men and 278 women). Regression analysis showed that MQ, defined as PT per unit of MM, was significantly higher in the arm (∼30%) than in the leg across age in both genders ( P < 0.01). Arm and leg MQ declined at a similar rate with age in men, whereas leg MQ declined ∼20% more than arm MQ with increasing age in women ( P ≤ 0.01 and P < 0.05 for Con and Ecc PT, respectively). Moreover, the age-associated decrease in arm MQ was steeper in men than in women whether Con or Ecc PT was used (both P < 0.05). Arm MQ as determined by Con PT showed a linear age-related decline in men and women (28 and 20%, respectively, P < 0.001), whereas arm MQ as determined by Ecc PT showed a linear age-related decline in men (25%, P < 0.001) but not in women (not significant). In contrast, both genders exhibited an age-related quadratic decline in leg MQ as determined by Con PT (∼40%) and Ecc PT (∼25%; both P< 0.001), and the rate of decline was similar for men and women. Thus MQ is affected by age and gender, but the magnitude of this effect depends on the muscle group studied and the type of muscle action (Con vs. Ecc) used to assess strength.
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Lofaro, Francesco Demetrio, Barbara Cisterna, Maria Assunta Lacavalla, Federico Boschi, Manuela Malatesta, Daniela Quaglino, Carlo Zancanaro, and Federica Boraldi. "Age-Related Changes in the Matrisome of the Mouse Skeletal Muscle." International Journal of Molecular Sciences 22, no. 19 (September 29, 2021): 10564. http://dx.doi.org/10.3390/ijms221910564.

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Aging is characterized by a progressive decline of skeletal muscle (SM) mass and strength which may lead to sarcopenia in older persons. To date, a limited number of studies have been performed in the old SM looking at the whole, complex network of the extracellular matrix (i.e., matrisome) and its aging-associated changes. In this study, skeletal muscle proteins were isolated from whole gastrocnemius muscles of adult (12 mo.) and old (24 mo.) mice using three sequential extractions, each one analyzed by liquid chromatography with tandem mass spectrometry. Muscle sections were investigated using fluorescence- and transmission electron microscopy. This study provided the first characterization of the matrisome in the old SM demonstrating several statistically significantly increased matrisome proteins in the old vs. adult SM. Several proteomic findings were confirmed and expanded by morphological data. The current findings shed new light on the mutually cooperative interplay between cells and the extracellular environment in the aging SM. These data open the door for a better understanding of the mechanisms modulating myocellular behavior in aging (e.g., by altering mechano-sensing stimuli as well as signaling pathways) and their contribution to age-dependent muscle dysfunction.
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Garel, M., D. M. Forsyth, A. Loison, D. Dubray, J. M. Jullien, K. G. Tustin, D. Maillard, and J. M. Gaillard. "Age-related male reproductive effort in two mountain ungulates of contrasting sexual size dimorphism." Canadian Journal of Zoology 89, no. 10 (October 2011): 929–37. http://dx.doi.org/10.1139/z11-062.

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In polygynous ungulates, the reproductive effort of adult males peaks during a short period in which feeding activities are sacrificed for mating activities. Hence, both fat reserves and body mass are predicted to decline markedly during this period. The decline is also predicted to be greater in fat reserves than in body mass because fat is catabolized before muscle, and to increase with the intensity of sexual selection. In contrast, no specific patterns are expected in females for which late gestation and lactation rather than mating are the energetically most demanding periods. We tested these hypotheses in two mountain ungulates of contrasting sexual size dimorphism (SSD): Himalayan tahr ( Hemitragus jemlahicus (H. Smith, 1826)) (SSD = 123%) and alpine chamois ( Rupicapra rupicapra (L., 1758)) (SSD = 26%). As expected, kidney fat declined more rapidly than body mass in adult males of both species. Kidney fat declined faster in adult male tahr compared with adult male chamois. There was no consistent pattern of changes in body mass or kidney fat in female tahr or female chamois. Our results suggest that adult males of species with strong SSD allocate more energy to mating than males of less dimorphic species.
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Marzetti, Emanuele, Giuseppe Privitera, Vincenzo Simili, Stephanie E. Wohlgemuth, Lorenzo Aulisa, Marco Pahor, and Christiaan Leeuwenburgh. "Multiple Pathways to the Same End: Mechanisms of Myonuclear Apoptosis in Sarcopenia of Aging." Scientific World JOURNAL 10 (2010): 340–49. http://dx.doi.org/10.1100/tsw.2010.27.

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Sarcopenia, the age-related decline in muscle mass and function, represents a significant health issue due to the high prevalence of frailty and disability associated with this condition. Nevertheless, the cellular mechanisms responsible for the loss of muscle mass in old age are still largely unknown. An altered regulation of myocyte apoptosis has recently emerged as a possible contributor to the pathogenesis of sarcopenia. Studies in animal models have shown that the severity of skeletal muscle apoptosis increases over the course of aging and correlates with the degree of muscle mass and strength decline. Several apoptotic pathways are operative in aged muscles, with the mitochondria- and TNF-α-mediated pathways likely being the most relevant to sarcopenia. However, despite the growing number of studies on the subject, a definite mechanistic link between myocyte apoptosis and age-related muscle atrophy has not yet been established. Furthermore, the evidence on the role played by apoptosis in human sarcopenia is still sparse. Clearly, further research is required to better define the involvement of myocyte apoptosis in the pathogenesis of muscle loss at advanced age. This knowledge will likely help in the design of more effective therapeutic strategies to preserve muscle mass into old age, thus fostering independence of the elderly population and reducing the socioeconomic burden associated with sarcopenia.
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Seo, Hyeyeong, Seok-Hee Lee, Yooheon Park, Hee-Seok Lee, Jeong Sup Hong, Cho Young Lim, Dong Hyeon Kim, Sung-Soo Park, Hyung Joo Suh, and Ki-Bae Hong. "(−)-Epicatechin-Enriched Extract from Camellia sinensis Improves Regulation of Muscle Mass and Function: Results from a Randomized Controlled Trial." Antioxidants 10, no. 7 (June 25, 2021): 1026. http://dx.doi.org/10.3390/antiox10071026.

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Loss of skeletal muscle mass and function with age represents an important source of frailty and functional decline in the elderly. Antioxidants from botanical extracts have been shown to enhance the development, mass, and strength of skeletal muscle by influencing age-related cellular and molecular processes. Tannase-treated green tea extract contains high levels of the antioxidants (−)-epicatechin (EC) and gallic acid that may have therapeutic benefits for age-related muscle decline. The aim of this study was to investigate the effect of tannase-treated green tea extract on various muscle-related parameters, without concomitant exercise, in a single-center, randomized, double-blind, placebo-controlled study. Administration of tannase-treated green tea extract (600 mg/day) for 12 weeks significantly increased isokinetic flexor muscle and handgrip strength in the treatment group compared with those in the placebo (control) group. In addition, the control group showed a significant decrease in arm muscle mass after 12 weeks, whereas no significant change was observed in the treatment group. Blood serum levels of follistatin, myostatin, high-sensitivity C-reactive protein (hs-CRP), interleukin (IL)-6, IL-8, insulin-like growth factor-1 (IGF-1), and cortisol were analyzed, and the decrease in myostatin resulting from the administration of tannase-treated green tea extract was found to be related to the change in muscle mass and strength. In summary, oral administration of tannase-treated green tea extract containing antioxidants without concomitant exercise can improve muscle mass and strength and may have therapeutic benefits in age-related muscle function decline.
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Jung, Yeon Woo, Namki Hong, Joon Chae Na, Woong Kyu Han, and Yumie Rhee. "Computed Tomography-Derived Skeletal Muscle Radiodensity Is an Early, Sensitive Marker of Age-Related Musculoskeletal Changes in Healthy Adults." Endocrinology and Metabolism 36, no. 6 (December 31, 2021): 1201–10. http://dx.doi.org/10.3803/enm.2021.1206.

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Background: A decrease in computed tomography (CT)-derived skeletal muscle radiodensity (SMD) reflects age-related ectopic fat infiltration of muscle, compromising muscle function and metabolism. We investigated the age-related trajectory of SMD and its association with vertebral trabecular bone density in healthy adults.Methods: In a cohort of healthy adult kidney donors aged 19 to 69 years (n=583), skeletal muscle index (SMI, skeletal muscle area/height2), SMD, and visceral-to-subcutaneous fat (V/S) ratio were analyzed at the level of L3 from preoperative CT scans. Low bone mass was defined as an L1 trabecular Hounsfield unit (HU) <160 HU.Results: L3SMD showed constant decline from the second decade (annual change –0.38% and –0.43% in men and women), whereas the decline of L3SMI became evident only after the fourth decade of life (–0.37% and –0.18% in men and women). One HU decline in L3SMD was associated with elevated odds of low bone mass (adjusted odds ratio, 1.07; 95% confidence interval, 1.02 to 1.13; P=0.003), independent of L3SMI, age, sex, and V/S ratio, with better discriminatory ability compared to L3SMI (area under the receiver-operating characteristics curve 0.68 vs. 0.53, P<0.001). L3SMD improved the identification of low bone mass when added to age, sex, V/S ratio, and L3SMI (category-free net reclassification improvement 0.349, P<0.001; integrated discrimination improvement 0.015, P=0.0165).Conclusion: L3SMD can be an early marker for age-related musculoskeletal changes showing linear decline throughout life from the second decade in healthy adults, with potential diagnostic value for individuals with low bone mass.
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Dissertations / Theses on the topic "Age-related decline in muscle mass"

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Maden-Wilkinson, Thomas M. "Age related changes in skeletal muscle mass and function." Thesis, Manchester Metropolitan University, 2013. http://hdl.handle.net/2173/314011.

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The loss of muscle mass with age (Sarcopenia) has received growing attention over the past decade. Despite efforts to provide a universal definition with clinically meaningful cut-off points for diagnosis, there is no clear consensus on how to best quantify and assess the impact of loss of muscle mass and function on functional limitations. Whilst most previous studies have used dual energy x-ray absorptiometry (DXA) to quantify this loss, chapter 2 of this thesis shows that DXA underestimates the loss of muscle mass with age in comparison to the gold standard MRI. Muscle mass per se is not enough to determine whether a person has an exceptionally low muscle mass, as it can be readily seen that a healthy tall person will have a larger muscle mass than a small person. Clinicians and researchers thus need an index of muscle mass that takes differences in stature into account and also gives an objective cut off point to define low muscle mass. In Chapter3, we show that femur volume does not significantly differ between young and old. We used this observation to introduce a new index: thigh muscle mass normalised to femur volume, or the muscle to bone ratio. This index allows the examination of the true extent of muscle atrophy within an individual. In previous studies the appendicular lean mass (determined with DXA) divided by height squared appeared to be a relatively poor predictor of functional performance. In Chapter 4, the index introduced in Chapter 3, the muscle to bone ratio, proved to be a somewhat better predictor of functional performance in the overall cohort. This was, however, not true when examining the intra-group relationships. A similar situation applied to the maximal muscle strength. In older adults, the parameter which predicted functional performance best was muscle power per body mass, measured during a counter-movement jump. Chapter 5 shows that part of the larger loss power and force than muscle mass is attributable to a left-ward shift of the torque-frequency relationship, indicative of a slowing of the muscle, and reduction in maximal voluntary activation, as assessed using the interpolated twitch technique in older adults. Chapter 5 also shows that the fatigue resistance during a series of intermittent contractions was similar in young and older adults. However, older adults could sustain a 50% maximal voluntary contraction force longer than young people. Part of this discrepancy maybe due to an age-related slowing of the muscle.
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Book chapters on the topic "Age-related decline in muscle mass"

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Thompson, LaDora V. "Age-Related Decline in Actomyosin Structure and Function." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 75–111. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_5.

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Russell, Aaron P., and Bertrand Lèger. "Age-Related Changes in the Molecular Regulation of Skeletal Muscle Mass." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 207–21. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_10.

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McMahon, Chris D., Thea Shavlakadze, and Miranda D. Grounds. "Role of IGF-1 in Age-Related Loss of Skeletal Muscle Mass and Function." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 393–418. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_17.

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Tatebayashi, Daisuke, and Rei Ono. "Exercise Protocols for Counteracting Cancer Cachexia-Related Declines in Muscle Mass and Strength and the Clinical Assessment of Skeletal Muscle." In Physical Therapy and Research in Patients with Cancer, 215–51. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-6710-8_10.

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Kupisz-Urbańska, Malgorzata, Jacek Łukaszkiewicz, and Ewa Marcinowska-Suchowierska. "Vitamin D in Elderly." In Vitamin D. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97324.

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Vitamin D deficiency is common in elderly people, especially in patients with comorbidity and polypharmcy. In this group, low vitamin D plasma concentration is related to osteoporosis, osteomalacia, sarcopenia and myalgia. Vitamin D status in geriatric population is an effect of joint interaction of all vitamin D metabolic pathways, aging processes and multimorbidity. Therefore, all factors interfering with individual metabolic stages may affect 25-hydroxyvitamin D plasma concentration. The known factors affecting vitamin D metabolism interfere with cytochrome CYP3A4 activity. The phenomenon of drugs and vitamin D interactions is observed first and foremost in patients with comorbidity. This is a typical example of the situation where a lack of “hard evidence” is not synonymous with the possible lack of adverse effects. Geriatric giants, such as sarcopenia (progressive and generalized loss of skeletal muscle mass and strength) or cognitive decline, strongly influence elderly patients. Sarcopenia is one of the musculoskeletal consequences of hypovitaminosis D. These consequences are related to a higher risk of adverse outcomes, such as fracture, physical disability, a poor quality of life and death. This can lead not only to an increased risk of falls and fractures, but is also one of the main causes of frailty syndrome in the aging population. Generally, Vitamin D plasma concentration is significantly lower in participants with osteoporosis and muscle deterioration. In some observational and uncontrolled treatment studies, vitamin D supplementation led to a reduction of proximal myopathy and muscle pain. The most positive results were found in subjects with severe vitamin D deficiency and in patients avoiding high doses of vitamin D. However, the role of vitamin D in muscle pathologies is not clear and research has provided conflicting results. This is most likely due to the heterogeneity of the subjects, vitamin D doses and environmental factors.
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Bauer, Jürgen M., and Rebecca Diekmann. "Protein and energy requirements in health and illness." In Oxford Textbook of Geriatric Medicine, 455–62. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198701590.003.0060.

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The preservation of functionality in elders is closely associated with their nutritional status. In this context it is pivotal for them to meet their nutritional requirements, which vary according to their individual needs. The latter are influenced to a large degree by activity level and comorbidity. Most older individuals will cover their energy needs in the range 25–30 kcal/kg body weight (BW) per day, but in extreme states like hyperkinetic dementia, the daily energy requirement may amount to 40 kcal/kg BW per day. To achieve optimal protein intake, older persons will need more protein per kg BW than the World Health Organization (WHO) recommendation of 0.8 g/kg BW per day, which was not varied according to age. For slowing the associated decline in muscle mass and bone quality, 1.0–1.2 g protein/kg BW per day is recommended. In older individuals with relevant comorbidity, even higher protein intake is advisable.
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Benard, Townsend, and Roger A. Fielding. "Pathophysiology of sarcopenia." In Oxford Textbook of Geriatric Medicine, 415–20. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198701590.003.0055.

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A number of mechanisms have been proposed to contribute to the accelerated loss of muscle mass and/or function in sarcopenia. Ageing induces a loss of the anabolic nature of food and muscle contraction, failing to adequately stimulate muscle protein synthesis. Reductions in protein intake and/or blunting of vasodilation in muscle may contribute to this impairment, though conclusive evidence is still lacking. Increasing adiposity, particularly within muscle, has been associated with physical and functional declines in ageing. Short-term disuse, such as hospitalization or injury, appears to disproportionately accelerate muscle mass loss in older people. Age-induced, low-level, chronic elevations in NF-kβ‎-mediated pro-inflammatory cytokines (TNF-α‎, IL-6 & IL-1) have shown robust relationships with sarcopenia. Accelerated reactive oxygen species generation brought on by mitochondrial dysfunction may stimulate myocyte apoptosis, though this mechanism is still debated. Age-induced neuromuscular adaptations appear to contribute to sarcopenia, particularly for changes in muscular function.
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Altun, Mikael, Max Grnholdt-Klein, Lingzhan Wang, and Brun Ulfhake. "Cellular Degradation Machineries in Age-Related Loss of Muscle Mass (Sarcopenia)." In Senescence. InTech, 2012. http://dx.doi.org/10.5772/34274.

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Fukase, Naomasa, Ingrid K. Stake, Yoichi Murata, William S. Hambright, Sudheer Ravuri, Marc J. Philippon, and Johnny Huard. "Interventional Strategies to Delay Aging-Related Dysfunctions of the Musculoskeletal System." In Muscle Cell and Tissue - Novel Molecular Targets and Current Advances [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97311.

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Aging affects bones, cartilage, muscles, and other connective tissue in the musculoskeletal system, leading to numerous age-related pathologies including osteoporosis, osteoarthritis, and sarcopenia. Understanding healthy aging may therefore open new therapeutic targets, thereby leading to the development of novel approaches to prevent several age-related orthopaedic diseases. It is well recognized that aging-related stem cell depletion and dysfunction leads to reduced regenerative capacity in various musculoskeletal tissues. However, more recent evidence suggests that dysregulated autophagy and cellular senescence might be fundamental mechanisms associated with aging-related musculoskeletal decline. The mammalian/mechanical target of Rapamycin (mTOR) is known to be an essential negative regulator of autophagy, and its inhibition has been demonstrated to promote longevity in numerous species. Besides, several reports demonstrate that selective elimination of senescent cells and their cognate Senescence-Associated Secretory Phenotype (SASP) can mitigate musculoskeletal tissue decline. Therefore, senolytic drugs/agents that can specifically target senescent cells, may offer a novel therapeutic strategy to treat a litany of age-related orthopaedic conditions. This chapter focuses on osteoarthritis and osteoporosis, very common debilitating orthopaedic conditions, and reviews current concepts highlighting new therapeutic strategies, including the mTOR inhibitors, senolytic agents, and mesenchymal stem cell (MSC)-based therapies.
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Won Won, Chang, and Sunyoung Kim. "Age-associated breathlessness." In Oxford Textbook of Geriatric Medicine, 1129–32. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198701590.003.0146.

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Breathlessness in older adults is a common symptom of cardiovascular, respiratory diseases, psychological disorders such as panic disorder, and respiratory muscle weakness, but this symptom is also prevalent during daily activities as a result of age-related changes. With ageing, physical fitness, the strength of respiratory muscles and elastic recoil of the small airways all decline, and, as a result, breathing becomes more difficult and gas exchange less efficient. Differentiation between cardiac and pulmonary cause of dyspneoa is very important and sometimes difficult. In acutely breathless elderly patients, an elevated level of brain natriuretic peptide is a sensitive and specific marker for the presence of ventricular failure. Once a diagnosis is made, the reversible factors contributing to the breathlessness should be corrected as far as possible, and the initial focus should be on optimizing treatment of the patient’s underlying disease, followed by reducing the impact of breathless on everyday activities and quality of life.
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Conference papers on the topic "Age-related decline in muscle mass"

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Anderson, Dennis E., Alexander G. Bruno, Brett T. Allaire, and Mary L. Bouxsein. "CT-Based Muscle Attenuation May be Able to Account for Age- and Muscle-Specific Differences in Maximum Muscle Stress." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80330.

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In musculoskeletal modeling, isometric muscle strength has been primarily determined based on muscle size. Specifically, the maximum force a muscle can produce may be calculated as: (1)FMAX=MMS×PCSA where FMAX is maximum isometric muscle force, MMS is maximum muscle stress, and PCSA is muscle physiological cross-sectional area. In general, modeling studies have selected a constant value of MMS, and applied it to all muscles in the model. However, the values reported in the literature for MMS vary widely [1, 2], from as little as 23 N/cm2 up to 137 N/cm2. Furthermore, MMS is likely lower in older adults than young adults, as age-related declines in muscle strength are significantly greater than declines in muscle mass [3], and the specific tension of gastrocnemius fascicles is 30% lower in elderly men than young men [4]. In addition, MMS is not constant between muscle groups. For example, the MMS of the elbow flexors is much greater than that of the elbow extensors [1], while the MMS of the ankle dorsiflexors is more than twice that of the ankle plantar flexors [5]. Thus, the use of a single constant for MMS in musculoskeletal models does not account for differences between individuals or muscle groups, and there is a need for a quantitative approach to assign different values of MMS to muscles in musculoskeletal models.
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Akkus, Ozan, Fran Adar, and Mitchell B. Schaffler. "Increased Collagen Mineralization Affects the Yield Stress But Not the Yield Strain in Cortical Bone of Rats: Implications for Age-Related Tissue Embrittlement." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32599.

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It has been well documented that the fracture susceptibility of cortical bone increases significantly with age [1]. Although the age-related decline in the fracture resistance of the cortical bone is attributed to reduced bone quantity; a substantial overlap in the bone mass of normal subjects and those sustaining fractures suggests that bone mass alone does not identify the fracture risk on an individual basis [2]. Therefore, the conceptual framework should be improved to include bone quality measures in addition to bone quantity to refine fracture risk assessment. In this study, Raman microspectroscopy was used to assess two key variables of bone tissue quality in aging rat cortical bone: the relative amount of mineral with respect to the amount of collagen (i.e. collagen mineralization) and the mineral crystallinity (i.e. size and stoichiometric perfection of mineral crystals). In this regard the first aim of this study was to investigate age-related changes in the extent of mineralization of collagen fibers and to test its relationship to elastic deformability of cortical bone tissue. The second aim of the study was to investigate age-related changes in the mineral crystallinity and to test its relationship to elastic deformability of cortical bone tissue. The first hypothesis of this study is that both collagen mineralization and mineral crystallinity will increase with age. The second hypothesis of this study was that age-related changes in compositional properties will compromise the elastic deformation capacity of cortical bone tissue.
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Dong, X. Neil, Daniel M. Sparkman, Huijie Leng, Harry R. Millwater, and Xiaodu Wang. "Probabilistic Prediction of Microdamage Progression in Bone." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192653.

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Age-related bone fractures are a major health concern to the elderly population. In addition to the loss of bone mass, the deterioration of bone quality is another major reason for such fractures. The decline of bone quality is manifested with the accumulation of microdamage in bone with age [1]. Two major types of microdamage have been observed in bone tissue: linear microcracks and diffuse damage [2]. Linear microcracks are individual cracks at a size of microns or larger and are usually visible under an optical microscope. On the other hand, diffuse damage is detectable only by staining and consists of an extensive network of fine, ultrastructural-level defects. The mechanisms for the formation of these two distinct types of microdamage in bone are still unclear. In this study, probabilistic finite element models of mineral-collagen composites were used to study the progression of microdamage in bone, thereby exploring the conditions under which linear microcracks and diffuse damage are produced in bone.
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Reports on the topic "Age-related decline in muscle mass"

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Geisler, Corinna, Mark Hübers, and Manfred Müller. Assessment of adult malnutrition with bioelectrical impedance analysis. Universitatsbibliothek Kiel, September 2018. http://dx.doi.org/10.21941/manueltask13.

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The two aims of this study were to evaluate (i) the prevalence of malnutrition based on age, sex and BMI specific PA and (ii) to determinate what specific body composition characteristics (skeletal muscle mass and adipose tissue) are related to a low PA.
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