Journal articles on the topic 'Age-related decline in muscle mass'
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1
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 & Science in Sports & 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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Visser, Marjolein. "Obesity, sarcopenia and their functional consequences in old age." Proceedings of the Nutrition Society 70, no. 1 (November 22, 2010): 114–18. http://dx.doi.org/10.1017/s0029665110003939.
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The prevalence of obesity is high in older persons and recent trends show a rapid increase in this prevalence. Results from observational and intervention studies (i.e. weight loss studies) show the strong negative impact of obesity on functional status in old age. There are different potential pathways through which obesity may lead to functional decline in older persons. Furthermore, the presence of overweight and obesity during the life course and trends in medical care are likely to influence the impact of obesity on disability. The concepts sarcopenia (age-related loss of muscle mass) and dynapenia (age-related loss of muscle strength) receive a lot of research attention as potential determinants of functional decline in old age. There is no consensus on the definitions of these concepts. Recent studies conducted in large cohort studies of mainly community-dwelling older persons show that poor muscle strength is strongly associated with functional decline compared to low muscle mass. In several studies, no association between muscle mass and functional status was observed. Current research on the combination of obesity with poor muscle strength (dynapenic-obesity) suggests a potential additive effect of both components on poor functional status in old age which seems independent of the level of physical activity.
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Sakuma, Kunihiro, and Akihiko Yamaguchi. "Sarcopenia and Age-Related Endocrine Function." International Journal of Endocrinology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/127362.
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Sarcopenia, the age-related loss of skeletal muscle, is characterized by a deterioration of muscle quantity and quality leading to a gradual slowing of movement, a decline in strength and power, and an increased risk of fall-related injuries. Since sarcopenia is largely attributed to various molecular mediators affecting fiber size, mitochondrial homeostasis, and apoptosis, numerous targets exist for drug discovery. In this paper, we summarize the current understanding of the endocrine contribution to sarcopenia and provide an update on hormonal intervention to try to improve endocrine defects. Myostatin inhibition seems to be the most interesting strategy for attenuating sarcopenia other than resistance training with amino acid supplementation. Testosterone supplementation in large amounts and at low frequency improves muscle defects with aging but has several side effects. Although IGF-I is a potent regulator of muscle mass, its therapeutic use has not had a positive effect probably due to local IGF-I resistance. Treatment with ghrelin may ameliorate the muscle atrophy elicited by age-dependent decreases in growth hormone. Ghrelin is an interesting candidate because it is orally active, avoiding the need for injections. A more comprehensive knowledge of vitamin-D-related mechanisms is needed to utilize this nutrient to prevent sarcopenia.
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Okabe, Takuhiro, Makoto Suzuki, Hiroshi Goto, Naoki Iso, Kilchoon Cho, Keisuke Hirata, and Junichi Shimizu. "Sex Differences in Age-Related Physical Changes among Community-Dwelling Adults." Journal of Clinical Medicine 10, no. 20 (October 19, 2021): 4800. http://dx.doi.org/10.3390/jcm10204800.
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The prevalence of physical functioning limitations is positively correlated with age in both men and women. However, whether the appearance of deterioration differs depending on physical function and sex remains unclear. This study aimed to clarify the modes of age-related changes in physical function and sex differences in middle-aged and older adults. This study comprised 124 (46 men and 78 women) healthy adults aged 30 years or older and examined gender differences in physical function. The results of this study showed that one-leg standing time had the highest rate of age-related decline in both men and women, followed by knee extension strength, skeletal muscle mass, the 5 m walking test, and the timed up and go test. The sex-specific points showed a high rate of decline in trunk forward bending in men and a high rate of decline in forced expiratory volume (1 s) and gradual rate of decline in the bone area ratio in women. After middle age, it is desirable to start monitoring and training balance, muscle function, and walking. Men require early intervention for flexibility, and women require early intervention for respiratory function and continued intervention for bone mineral density.
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Picca, Anna, and Riccardo Calvani. "Molecular Mechanism and Pathogenesis of Sarcopenia: An Overview." International Journal of Molecular Sciences 22, no. 6 (March 16, 2021): 3032. http://dx.doi.org/10.3390/ijms22063032.
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Alcazar, Julian, Per Aagaard, Bryan Haddock, Rikke S. Kamper, Sofie K. Hansen, Eva Prescott, Luis M. Alegre, Ulrik Frandsen, and Charlotte Suetta. "Age- and Sex-Specific Changes in Lower-Limb Muscle Power Throughout the Lifespan." Journals of Gerontology: Series A 75, no. 7 (January 16, 2020): 1369–78. http://dx.doi.org/10.1093/gerona/glaa013.
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Abstract Background Our main goal was to evaluate the pattern and time course of changes in relative muscle power and its constituting components throughout the life span. Methods A total of 1,305 subjects (729 women and 576 men; aged 20–93 years) participating in the Copenhagen Sarcopenia Study took part. Body mass index (BMI), leg lean mass assessed by dual-energy X-ray absorptiometry (DXA), and leg extension muscle power (LEP) assessed by the Nottingham power rig were recorded. Relative muscle power (normalized to body mass) and specific muscle power (normalized to leg lean mass) were calculated. Segmented regression analyses were used to identify the onset and pattern of age-related changes in the recorded variables. Results Relative muscle power began to decline above the age of 40 in both women and men, with women showing an attenuation of the decline above 75 years. Relative muscle power decreased with age due to (i) the loss of absolute LEP after the fourth decade of life and (ii) the increase in BMI up to the age of 75 years in women and 65 years in men. The decline in absolute LEP was caused by a decline in specific LEP up to the age of 75 in women and 65 in men, above which the loss in relative leg lean mass also contributed. Conclusions Relative power decreased (i) above 40 years by the loss in absolute power (specific power only) and the increase in body mass, and (ii) above ~70 years by the loss in absolute power (both specific power and leg lean mass).
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Scott, David. "Sarcopenia in Older Adults." Journal of Clinical Medicine 8, no. 11 (November 2, 2019): 1844. http://dx.doi.org/10.3390/jcm8111844.
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Tallis, Jason, Rob S. James, Alexander G. Little, Val M. Cox, Michael J. Duncan, and Frank Seebacher. "Early effects of ageing on the mechanical performance of isolated locomotory (EDL) and respiratory (diaphragm) skeletal muscle using the work-loop technique." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 6 (September 15, 2014): R670—R684. http://dx.doi.org/10.1152/ajpregu.00115.2014.
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Previous isolated muscle studies examining the effects of ageing on contractility have used isometric protocols, which have been shown to have poor relevance to dynamic muscle performance in vivo. The present study uniquely uses the work-loop technique for a more realistic estimation of in vivo muscle function to examine changes in mammalian skeletal muscle mechanical properties with age. Measurements of maximal isometric stress, activation and relaxation time, maximal power output, and sustained power output during repetitive activation and recovery are compared in locomotory extensor digitorum longus (EDL) and core diaphragm muscle isolated from 3-, 10-, 30-, and 50-wk-old female mice to examine the early onset of ageing. A progressive age-related reduction in maximal isometric stress that was of greater magnitude than the decrease in maximal power output occurred in both muscles. Maximal force and power developed earlier in diaphragm than EDL muscle but demonstrated a greater age-related decline. The present study indicates that ability to sustain skeletal muscle power output through repetitive contraction is age- and muscle-dependent, which may help rationalize previously reported equivocal results from examination of the effect of age on muscular endurance. The age-related decline in EDL muscle performance is prevalent without a significant reduction in muscle mass, and biochemical analysis of key marker enzymes suggests that although there is some evidence of a more oxidative fiber type, this is not the primary contributor to the early age-related reduction in muscle contractility.
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Kirkendall, Donald T., and William E. Garrett. "The Effects of Aging and Training on Skeletal Muscle." American Journal of Sports Medicine 26, no. 4 (July 1998): 598–602. http://dx.doi.org/10.1177/03635465980260042401.
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Aging results in a gradual loss of muscle function, and there are predictable age-related alterations in skeletal muscle function. The typical adult will lose muscle mass with age; the loss varies according to sex and the level of muscle activity. At the cellular level, muscles loose both cross-sectional area and fiber numbers, with type II muscle fibers being the most affected by aging. Some denervation of fibers may occur. The combination of these factors leads to an increased percentage of type I fibers in older adults. Metabolically, the glycolytic enzymes seem to be little affected by aging, but the aerobic enzymes appear to decline with age. Aged skeletal muscle produces less force and there is a general “slowing” of the mechanical characteristics of muscle. However, neither reduced muscle demand nor the subsequent loss of function is inevitable with aging. These losses can be minimized or even reversed with training. Endurance training can improve the aerobic capacity of muscle, and resistance training can improve central nervous system recruitment of muscle and increase muscle mass. Therefore, physical activity throughout life is encouraged to prevent much of the age-related impact on skeletal muscle.
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Proctor, D. N., P. C. O’Brien, E. J. Atkinson, and K. S. Nair. "Comparison of techniques to estimate total body skeletal muscle mass in people of different age groups." American Journal of Physiology-Endocrinology and Metabolism 277, no. 3 (September 1, 1999): E489—E495. http://dx.doi.org/10.1152/ajpendo.1999.277.3.e489.
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An estimate of total body muscle mass with dual-energy X-ray absorptiometry (DXA; appendicular muscle mass divided by 0.75) was compared with 24-h urinary creatinine excretion in 59 healthy men and women [20–30 yr (younger), 45–59 yr (middle age), and 60–79 yr (older)] who stayed in a clinical research center for 5 days. Total body water (2H2O dilution), fat (underwater weighing), bone mineral (DXA), and total body protein mass (based on a 4-compartment model) were also measured. Muscle mass estimates by DXA and creatinine were highly correlated ( r = 0.80). However, stepwise multiple regression indicated that a significant amount of additional between-subject variability in DXA-based muscle mass estimates could be explained by total body water. Creatinine excretion, knee extensor strength, and total body protein mass all decreased with age, suggesting a decline in muscle cell mass with aging. However, DXA-based muscle mass and measures of nonfat body mass (i.e., lean body mass by2H2O and fat-free body mass by underwater weighing) did not change with age. These results indicate that DXA and urinary creatinine excretion give different results regarding the decline in total body muscle mass with aging. The factor(s) responsible for the apparent underestimate of age-related sarcopenia by DXA remain to be fully defined, but changes in body water may be an important contributor.
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Kurosawa, Tamaki, Keitaro Minato, Madoka Ikemoto-Uezumi, Jun Hino, Kunihiro Tsuchida, and Akiyoshi Uezumi. "Transgenic Expression of Bmp3b in Mesenchymal Progenitors Mitigates Age-Related Muscle Mass Loss and Neuromuscular Junction Degeneration." International Journal of Molecular Sciences 22, no. 19 (September 23, 2021): 10246. http://dx.doi.org/10.3390/ijms221910246.
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Skeletal muscle is a vital organ for a healthy life, but its mass and function decline with aging, resulting in a condition termed sarcopenia. The etiology of sarcopenia remains unclear. We recently demonstrated that interstitial mesenchymal progenitors are essential for homeostatic muscle maintenance, and a diminished expression of the mesenchymal-specific gene Bmp3b is associated with sarcopenia. Here, we assessed the protective function of Bmp3b against sarcopenia by generating conditional transgenic (Tg) mice that enable a forced expression of Bmp3b specifically in mesenchymal progenitors. The mice were grown until they reached the geriatric stage, and the age-related muscle phenotypes were examined. The Tg mice had significantly heavier muscles compared to control mice, and the type IIB myofiber cross-sectional areas were preserved in Tg mice. The composition of the myofiber types did not differ between the genotypes. The Tg mice showed a decreasing trend of fibrosis, but the degree of fat infiltration was as low as that in the control mice. Finally, we observed the preservation of innervated neuromuscular junctions (NMJs) in the Tg muscle in contrast to the control muscle, where the NMJ degeneration was conspicuous. Thus, our results indicate that the transgenic expression of Bmp3b in mesenchymal progenitors alleviates age-related muscle deterioration. Collectively, this study strengthens the beneficial role of mesenchymal Bmp3b against sarcopenia and suggests that preserving the youthfulness of mesenchymal progenitors may be an effective means of combating sarcopenia.
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Balagopal, P., Olav E. Rooyackers, Deborah B. Adey, Philip A. Ades, and K. Sreekumaran Nair. "Effects of aging on in vivo synthesis of skeletal muscle myosin heavy-chain and sarcoplasmic protein in humans." American Journal of Physiology-Endocrinology and Metabolism 273, no. 4 (October 1, 1997): E790—E800. http://dx.doi.org/10.1152/ajpendo.1997.273.4.e790.
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A decline in muscle mass and contractile function are prominent features of the sarcopenia of old age. Because myosin heavy chain is an important contractile protein, it was hypothesized that synthesis of this protein decreases in sarcopenia. The fractional synthesis rate of myosin heavy chain was measured simultaneously with rates of mixed muscle and sarcoplasmic proteins from the increment of [13C]leucine in these proteins purified from serial needle biopsy samples taken from 24 subjects (age: from 20 to 92 yr) during a primed continuous infusion ofl-[1-13C]leucine. A decline in synthesis rate of mixed muscle protein ( P < 0.01) and whole body protein ( P < 0.01) was observed from young to middle age with no further change with advancing age. An age-related decline of myosin heavy-chain synthesis rate was also observed ( P < 0.01), with progressive decline occurring from young, through middle, to old age. However, sarcoplasmic protein synthesis did not decline with age. Myosin heavy-chain synthesis rate was correlated with measures of muscle strength ( P < 0.05), circulating insulin-like growth factor I ( P < 0.01), and dehydroepiandrosterone sulfate ( P < 0.05) in men and women and free testosterone levels in men ( P < 0.01). A decline in the synthesis rate of myosin heavy chain implies a decreased ability to remodel this important muscle contractile protein and likely contributes to the declining muscle mass and contractile function in the elderly.
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Traoré, Massiré, Christel Gentil, Chiara Benedetto, Jean-Yves Hogrel, Pierre De la Grange, Bruno Cadot, Sofia Benkhelifa-Ziyyat, et al. "An embryonic CaVβ1 isoform promotes muscle mass maintenance via GDF5 signaling in adult mouse." Science Translational Medicine 11, no. 517 (November 6, 2019): eaaw1131. http://dx.doi.org/10.1126/scitranslmed.aaw1131.
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Deciphering the mechanisms that govern skeletal muscle plasticity is essential to understand its pathophysiological processes, including age-related sarcopenia. The voltage-gated calcium channel CaV1.1 has a central role in excitation-contraction coupling (ECC), raising the possibility that it may also initiate the adaptive response to changes during muscle activity. Here, we revealed the existence of a gene transcription switch of the CaV1.1 β subunit (CaVβ1) that is dependent on the innervation state of the muscle in mice. In a mouse model of sciatic denervation, we showed increased expression of an embryonic isoform of the subunit that we called CaVβ1E. CaVβ1E boosts downstream growth differentiation factor 5 (GDF5) signaling to counteract muscle loss after denervation in mice. We further reported that aged mouse muscle expressed lower quantity of CaVβ1E compared with young muscle, displaying an altered GDF5-dependent response to denervation. Conversely, CaVβ1E overexpression improved mass wasting in aging muscle in mice by increasing GDF5 expression. We also identified the human CaVβ1E analogous and show a correlation between CaVβ1E expression in human muscles and age-related muscle mass decline. These results suggest that strategies targeting CaVβ1E or GDF5 might be effective in reducing muscle mass loss in aging.
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Shigehara, Kazuyoshi, Yuki Kato, Kouji Izumi, and Atsushi Mizokami. "Relationship between Testosterone and Sarcopenia in Older-Adult Men: A Narrative Review." Journal of Clinical Medicine 11, no. 20 (October 20, 2022): 6202. http://dx.doi.org/10.3390/jcm11206202.
Full textAbstract:
Age-related decline in testosterone is known to be associated with various clinical symptoms among older men and it is possible that the accompanying decline in muscle mass and strength might lead to a decline in motor and physical functions. Sarcopenia is an important pathophysiological factor associated with frailty in older adults and is diagnosed in older adults as a decrease in muscle strength, muscle mass, and walking speed, which can lead to a significant decline in the quality of life and shortened healthy life expectancy. Testosterone directly interacts with the androgen receptor expressed in myonuclei and satellite cells and is also indirectly associated with muscle metabolism through various cytokines and molecules. Currently, significant correlations between testosterone and frailty in men have been confirmed by numerous cross-sectional studies. Many randomized control studies have also supported the beneficial effect of testosterone replacement therapy (TRT) on muscle volume and strength among men with low to normal testosterone levels. In the world’s aging society, TRT can be a tool for preventing the onset of sarcopenia in older-adult men. This narrative review aims to show the relationship between the decline in testosterone with age, sarcopenia, and frailty, as well as the effects of testosterone replacement therapy on muscle mass and strength.
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Zampino, Marta, Richard D. Semba, Fatemeh Adelnia, Richard G. Spencer, Kenneth W. Fishbein, Jennifer A. Schrack, Eleanor M. Simonsick, and Luigi Ferrucci. "Greater Skeletal Muscle Oxidative Capacity Is Associated With Higher Resting Metabolic Rate: Results From the Baltimore Longitudinal Study of Aging." Journals of Gerontology: Series A 75, no. 12 (March 23, 2020): 2262–68. http://dx.doi.org/10.1093/gerona/glaa071.
Full textAbstract:
Abstract Resting metabolic rate (RMR) tends to decline with aging. The age-trajectory of decline in RMR is similar to changes that occur in muscle mass, muscle strength, and fitness, but while the decline in these phenotypes has been related to changes of mitochondrial function and oxidative capacity, whether lower RMR is associated with poorer mitochondrial oxidative capacity is unknown. In 619 participants of the Baltimore Longitudinal Study of Aging, we analyzed the cross-sectional association between RMR (kcal/day), assessed by indirect calorimetry, and skeletal muscle maximal oxidative phosphorylation capacity, assessed as postexercise phosphocreatine recovery time constant (τ PCr), by phosphorous magnetic resonance spectroscopy. Linear regression models were used to evaluate the relationship between τ PCr and RMR, adjusting for potential confounders. Independent of age, sex, lean body mass, muscle density, and fat mass, higher RMR was significantly associated with shorter τ PCr, indicating greater mitochondrial oxidative capacity. Higher RMR is associated with a higher mitochondrial oxidative capacity in skeletal muscle. This association may reflect a relationship between better muscle quality and greater mitochondrial health.
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Rosano, Caterina, Anne Newman, Xiaonan Zhu, Adam Santanasto, Bret Goodpaster, and Iva Miljkovic. "INTERMUSCULAR ADIPOSITY: A NOVEL RISK FACTOR FOR COGNITIVE DECLINE IN A BIRACIAL COHORT OF OLDER ADULTS." Innovation in Aging 6, Supplement_1 (November 1, 2022): 332. http://dx.doi.org/10.1093/geroni/igac059.1310.
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Abstract Skeletal muscle and brain health both decline with age. Poorer skeletal muscle characteristics may be early markers of cognitive decline. The Health ABC study obtained repeated measures of thigh intermuscular adiposity via CT (IMAT, Years 1 and 6) and Mini-Mental State Exam (MMSE, Years 1 through 10), in 1634 adults (69-79 years, 48% women, 35% black). Linear mixed effects models accounted for change (Years 1 and 6) in weight, muscle (strength, area), and adiposity characteristics (abdominal subcutaneous, visceral, total fat mass) and for dementia risk factors (education, APOE4, diabetes, hypertension, physical activity). IMAT increased by 0.97 cm2/year (SD:1.16), and MMSE declined by 0.4 points/year (0.02). Each SD of IMAT corresponded to a MMSE decline of 0.22 points/year (p<0.0001), similar in adjusted models and stratified by race or gender. Aging-related IMAT increase may be a novel predictor of cognitive decline beyond traditional risk factors, with potential implications for muscle-brain cross talk.
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Fleg, J. L., and E. G. Lakatta. "Role of muscle loss in the age-associated reduction in VO2 max." Journal of Applied Physiology 65, no. 3 (September 1, 1988): 1147–51. http://dx.doi.org/10.1152/jappl.1988.65.3.1147.
Full textAbstract:
A progressive decline in maximal O2 consumption (VO2max) expressed traditionally as per kilogram body weight generally occurs with advancing age. To investigate the extent to which this decline could be attributable to the age-associated loss of metabolically active tissue, i.e., muscle, we measured 24-h urinary creatinine excretion, an index of muscle mass, in 184 healthy nonobese volunteers, ages 22-87 yr, from the Baltimore Longitudinal Study of Aging who had achieved a true VO2max during graded treadmill exercise. A positive correlation was found between VO2max and creatinine excretion in both men (r = 0.64, P less than 0.001) and women (r = 0.47, P less than 0.001). As anticipated, VO2max showed a strong negative linear relationship with age in both men and women. Creatinine excretion also declined with age in men and women. When VO2max was normalized for creatinine excretion, the variance in the VO2max decline attributable to age declined from 60 to 14% in men and from 50 to 8% in women. Thus comparing the standard age regression of VO2max per kilogram body weight with that in which VO2max is normalized per milligram creatinine excretion, the decline in VO2max between a hypothetical 30 yr old and a 70 yr old was reduced from 39 to 18% in men and from 30 to 14% in women. We conclude that in both sexes, a large portion of the age-associated decline in VO2max in non-endurance-trained individuals is explicable by the loss of muscle mass, which is observed with advancing age.
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Song, Yiqi, Qian Zhang, Li Ni, Minmin Zhang, Mengjing Wang, Weichen Zhang, and Jing Chen. "Risk Factors Affecting Muscle Mass Decline in Maintenance Hemodialysis Patients." BioMed Research International 2022 (December 20, 2022): 1–8. http://dx.doi.org/10.1155/2022/2925216.
Full textAbstract:
Objective. There is a high prevalence of sarcopenia in maintenance hemodialysis (MHD) patients, which is known to be associated with increased mortality. This study is aimed at analyzing the risk factors affecting muscle mass decline in MHD patients. Methods. This retrospective study included MHD patients who underwent two body composition assessments in October 2013 and November 2017. Depending on whether there was muscle loss or not, the patients were divided into a normal muscle mass (NMM) group and a muscle mass decline (MMD) group. According to the muscle mass decline rate, patients in the MMD group were further classified into a low-rate group and a high-rate group. Biochemical variables, serum vitamin concentrations, anthropometric data, SGA, muscle mass, handgrip, and daily steps were assessed. Risk factors for muscle mass decline were screened by multivariate logistic analysis and linear regression analysis. Results. Of the 72 MHD patients included in this study, 33 were male and 39 were female with a mean age of 56.80 ± 10.86 years and a mean dialysis duration of 7.50 ± 5.20 years. Age ( P = .014 ) and serum 25(OH)D ( P = .040 ) were found to be associated with a higher risk of muscle mass decline after adjusting for gender, dialysis vintage, albumin, and hs-CRP ( P = .040 ). Further analysis found that dialysis vintage ( β = 0.285 , P = .030 ), 25(OH)D ( β = − 0.351 , P = .007 ), and log NT-proBNP ( β = 0.312 , P = .020 ) were risk factors associated with the muscle mass decline rate in MHD patients. Conclusion. Age and serum 25(OH)D were associated with a higher risk of muscle mass decline, while 25(OH)D, dialysis vintage, and NT-proBNP were associated with the muscle mass decline rate in MHD patients.
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Hill, Cameron, Rob S. James, Val M. Cox, Frank Seebacher, and Jason Tallis. "Age-related changes in isolated mouse skeletal muscle function are dependent on sex, muscle, and contractility mode." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 319, no. 3 (September 1, 2020): R296—R314. http://dx.doi.org/10.1152/ajpregu.00073.2020.
Full textAbstract:
The present study aimed to simultaneously examine the age-related, muscle-specific, sex-specific, and contractile mode-specific changes in isolated mouse skeletal muscle function and morphology across multiple ages. Measurements of mammalian muscle morphology, isometric force and stress (force/cross-sectional area), absolute and normalized (power/muscle mass) work-loop power across a range of contractile velocities, fatigue resistance, and myosin heavy chain (MHC) isoform concentration were measured in 232 isolated mouse (CD-1) soleus, extensor digitorum longus (EDL), and diaphragm from male and female animals aged 3, 10, 30, 52, and 78 wk. Aging resulted in increased body mass and increased soleus and EDL muscle mass, with atrophy only present for female EDL by 78 wk despite no change in MHC isoform concentration. Absolute force and power output increased up to 52 wk and to a higher level for males. A 23–36% loss of isometric stress exceeded the 14–27% loss of power normalized to muscle mass between 10 wk and 52 wk, although the loss of normalized power between 52 and 78 wk continued without further changes in stress ( P > 0.23). Males had lower power normalized to muscle mass than females by 78 wk, with the greatest decline observed for male soleus. Aging did not cause a shift toward slower contractile characteristics, with reduced fatigue resistance observed in male EDL and female diaphragm. Our findings show that the loss of muscle quality precedes the loss of absolute performance as CD-1 mice age, with the greatest effect seen in male soleus, and in most instances without muscle atrophy or an alteration in MHC isoforms.
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Zampino, Marta, Richard Semba, Fatemeh Adelnia, Jennifer Schrack, Richard Spencer, Kenneth Fishbein, Eleanor Simonsick, and Luigi Ferrucci. "Greater Skeletal Muscle Oxidative Capacity Is Associated With Higher Resting Metabolic Rate: Results From the BLSA." Innovation in Aging 4, Supplement_1 (December 1, 2020): 124. http://dx.doi.org/10.1093/geroni/igaa057.409.
Full textAbstract:
Abstract Resting metabolic rate (RMR) tends to decline with aging. The age-trajectory of decline in RMR is similar to changes that occur in muscle mass, muscle strength and fitness. However, while the decline in these phenotypes have been related to changes of mitochondrial function and oxidative capacity, whether lower RMR is associated with poorer mitochondrial oxidative capacity is unknown. In 619 participants of the Baltimore Longitudinal Study of Aging, we analyzed the cross-sectional association between RMR (kcal/day), assessed by indirect calorimetry, and skeletal muscle maximal oxidative phosphorylation capacity, assessed as post-exercise phosphocreatine recovery time constant (tau-PCr), by phosphorous magnetic resonance spectroscopy. Linear regression models were used to evaluate the relationship between tau-PCr and RMR, adjusting for potential confounders. We found that independent of age, sex, lean body mass, muscle density and fat mass, higher RMR was significantly associated with shorter tau-PCr, indicating greater mitochondrial oxidative capacity. In conclusion, higher RMR appears to be associated with a higher mitochondrial oxidative capacity in skeletal muscle. This association may reflect a relationship between better muscle quality and greater mitochondrial health.
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Damiano, Simona, Espedita Muscariello, Giuliana La Rosa, Martina Di Maro, Paolo Mondola, and Mariarosaria Santillo. "Dual Role of Reactive Oxygen Species in Muscle Function: Can Antioxidant Dietary Supplements Counteract Age-Related Sarcopenia?" International Journal of Molecular Sciences 20, no. 15 (August 5, 2019): 3815. http://dx.doi.org/10.3390/ijms20153815.
Full textAbstract:
Sarcopenia is characterized by the progressive loss of skeletal muscle mass and strength. In older people, malnutrition and physical inactivity are often associated with sarcopenia, and, therefore, dietary interventions and exercise must be considered to prevent, delay, or treat it. Among the pathophysiological mechanisms leading to sarcopenia, a key role is played by an increase in reactive oxygen and nitrogen species (ROS/RNS) levels and a decrease in enzymatic antioxidant protection leading to oxidative stress. Many studies have evaluated, in addition to the effects of exercise, the effects of antioxidant dietary supplements in limiting age-related muscle mass and performance, but the data which have been reported are conflicting. In skeletal muscle, ROS/RNS have a dual function: at low levels they increase muscle force and adaptation to exercise, while at high levels they lead to a decline of muscle performance. Controversial results obtained with antioxidant supplementation in older persons could in part reflect the lack of univocal effects of ROS on muscle mass and function. The purpose of this review is to examine the molecular mechanisms underlying the dual effects of ROS in skeletal muscle function and the analysis of literature data on dietary antioxidant supplementation associated with exercise in normal and sarcopenic subjects.
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McBride, Marin Jane, Kevin P. Foley, Donna M. D’Souza, Yujin E. Li, Trevor C. Lau, Thomas J. Hawke, and Jonathan D. Schertzer. "The NLRP3 inflammasome contributes to sarcopenia and lower muscle glycolytic potential in old mice." American Journal of Physiology-Endocrinology and Metabolism 313, no. 2 (August 1, 2017): E222—E232. http://dx.doi.org/10.1152/ajpendo.00060.2017.
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The mechanisms underpinning decreased skeletal muscle strength and slowing of movement during aging are ill-defined. “Inflammaging,” increased inflammation with advancing age, may contribute to aspects of sarcopenia, but little is known about the participatory immune components. We discovered that aging was associated with increased caspase-1 activity in mouse skeletal muscle. We hypothesized that the caspase-1-containing NLRP3 inflammasome contributes to sarcopenia in mice. Male C57BL/6J wild-type (WT) and NLRP3−/− mice were aged to 10 (adult) and 24 mo (old). NLRP3−/− mice were protected from decreased muscle mass (relative to body mass) and decreased size of type IIB and IIA myofibers, which occurred between 10 and 24 mo of age in WT mice. Old NLRP3−/− mice also had increased relative muscle strength and endurance and were protected from age-related increases in the number of myopathic fibers. We found no evidence of age-related or NLRP3-dependent changes in markers of systemic inflammation. Increased caspase-1 activity was associated with GAPDH proteolysis and reduced GAPDH enzymatic activity in skeletal muscles from old WT mice. Aging did not alter caspase-1 activity, GAPDH proteolysis, or GAPDH activity in skeletal muscles of NLRP3−/− mice. Our results show that the NLRP3 inflammasome participates in age-related loss of muscle glycolytic potential. Deletion of NLRP3 mitigates both the decline in glycolytic myofiber size and the reduced activity of glycolytic enzymes in muscle during aging. We propose that the etiology of sarcopenia involves direct communication between immune responses and metabolic flux in skeletal muscle.
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Bondì, Michela, Elena Germinario, Marco Pirazzini, Giulia Zanetti, Francesca Cencetti, Chiara Donati, Luisa Gorza, Romeo Betto, Paola Bruni, and Daniela Danieli-Betto. "Ablation of S1P3 receptor protects mouse soleus from age-related drop in muscle mass, force, and regenerative capacity." American Journal of Physiology-Cell Physiology 313, no. 1 (July 1, 2017): C54—C67. http://dx.doi.org/10.1152/ajpcell.00027.2017.
Full textAbstract:
We investigated the effects of S1P3 deficiency on the age-related atrophy, decline in force, and regenerative capacity of soleus muscle from 23-mo-old male (old) mice. Compared with muscle from 5-mo-old (adult) mice, soleus mass and muscle fiber cross-sectional area (CSA) in old wild-type mice were reduced by ~26% and 24%, respectively. By contrast, the mass and fiber CSA of soleus muscle in old S1P3-null mice were comparable to those of adult muscle. Moreover, in soleus muscle of wild-type mice, twitch and tetanic tensions diminished from adulthood to old age. A slowing of contractile properties was also observed in soleus from old wild-type mice. In S1P3-null mice, neither force nor the contractile properties of soleus changed during aging. We also evaluated the regenerative capacity of soleus in old S1P3-null mice by stimulating muscle regeneration through myotoxic injury. After 10 days of regeneration, the mean fiber CSA of soleus in old wild-type mice was significantly smaller (−28%) compared with that of regenerated muscle in adult mice. On the contrary, the mean fiber CSA of regenerated soleus in old S1P3-null mice was similar to that of muscle in adult mice. We conclude that in the absence of S1P3, soleus muscle is protected from the decrease in muscle mass and force, and the attenuation of regenerative capacity, all of which are typical characteristics of aging.
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Aytekin, N., K. N. Mileva, and A. D. Cunliffe. "Selected B vitamins and their possible link to the aetiology of age-related sarcopenia: relevance of UK dietary recommendations." Nutrition Research Reviews 31, no. 2 (March 9, 2018): 204–24. http://dx.doi.org/10.1017/s0954422418000045.
Full textAbstract:
AbstractThe possible roles of selected B vitamins in the development and progression of sarcopenia are reviewed. Age-related declines in muscle mass and function are associated with huge and increasing costs to healthcare providers. Falls and loss of mobility and independence due to declining muscle mass/function are associated with poor clinical outcomes and their prevention and management are attractive research targets. Nutritional status appears a key modifiable and affordable intervention. There is emerging evidence of sarcopenia being the result not only of diminished anabolic activity but also of declining neurological integrity in older age, which is emerging as an important aspect of the development of age-related decline in muscle mass/function. In this connection, several B vitamins can be viewed as not only cofactors in muscle synthetic processes, but also as neurotrophic agents with involvements in both bioenergetic and trophic pathways. The B vitamins thus selected are examined with respect to their relevance to multiple aspects of neuromuscular function and evidence is considered that requirements, intakes or absorption may be altered in the elderly. In addition, the evidence base for recommended intakes (UK recommended daily allowance) is examined with particular reference to original datasets and their relevance to older individuals. It is possible that inconsistencies in the literature with respect to the nutritional management of sarcopenia may, in part at least, be the result of compromised micronutrient status in some study participants. It is suggested that in order, for example, for intervention with amino acids to be successful, underlying micronutrient deficiencies must first be addressed/eliminated.
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Rezuş, Elena, Alexandra Burlui, Anca Cardoneanu, Ciprian Rezuş, Cătălin Codreanu, Mirela Pârvu, Gabriela Rusu Zota, and Bogdan Ionel Tamba. "Inactivity and Skeletal Muscle Metabolism: A Vicious Cycle in Old Age." International Journal of Molecular Sciences 21, no. 2 (January 16, 2020): 592. http://dx.doi.org/10.3390/ijms21020592.
Full textAbstract:
Aging is an inevitable and gradually progressive process affecting all organs and systems. The musculoskeletal system makes no exception, elderly exhibit an increased risk of sarcopenia (low muscle mass),dynapenia (declining muscle strength), and subsequent disability. Whereas in recent years the subject of skeletal muscle metabolic decline in the elderly has been gathering interest amongst researchers, as well as medical professionals, there are many challenges yet to be solved in order to counteract the effects of aging on muscle function efficiently. Noteworthy, it has been shown that aging individuals exhibit a decline in skeletal muscle metabolism, a phenomenon which may be linked to a number of predisposing (risk) factors such as telomere attrition, epigenetic changes, mitochondrial dysfunction, sedentary behavior (leading to body composition alterations), age-related low-grade systemic inflammation (inflammaging), hormonal imbalance, as well as a hypoproteic diet (unable to counterbalance the repercussions of the age-related increase in skeletal muscle catabolism). The present review aims to discuss the relationship between old age and muscle wasting in an effort to highlight the modifications in skeletal muscle metabolism associated with aging and physical activity.
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Dobrowolny, Gabriella, Alessandra Barbiera, Gigliola Sica, and Bianca Maria Scicchitano. "Age-Related Alterations at Neuromuscular Junction: Role of Oxidative Stress and Epigenetic Modifications." Cells 10, no. 6 (May 24, 2021): 1307. http://dx.doi.org/10.3390/cells10061307.
Full textAbstract:
With advancing aging, a decline in physical abilities occurs, leading to reduced mobility and loss of independence. Although many factors contribute to the physio-pathological effects of aging, an important event seems to be related to the compromised integrity of the neuromuscular system, which connects the brain and skeletal muscles via motoneurons and the neuromuscular junctions (NMJs). NMJs undergo severe functional, morphological, and molecular alterations during aging and ultimately degenerate. The effect of this decline is an inexorable decrease in skeletal muscle mass and strength, a condition generally known as sarcopenia. Moreover, several studies have highlighted how the age-related alteration of reactive oxygen species (ROS) homeostasis can contribute to changes in the neuromuscular junction morphology and stability, leading to the reduction in fiber number and innervation. Increasing evidence supports the involvement of epigenetic modifications in age-dependent alterations of the NMJ. In particular, DNA methylation, histone modifications, and miRNA-dependent gene expression represent the major epigenetic mechanisms that play a crucial role in NMJ remodeling. It is established that environmental and lifestyle factors, such as physical exercise and nutrition that are susceptible to change during aging, can modulate epigenetic phenomena and attenuate the age-related NMJs changes. This review aims to highlight the recent epigenetic findings related to the NMJ dysregulation during aging and the role of physical activity and nutrition as possible interventions to attenuate or delay the age-related decline in the neuromuscular system.
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Koopman, René. "Dietary protein and exercise training in ageing." Proceedings of the Nutrition Society 70, no. 1 (November 22, 2010): 104–13. http://dx.doi.org/10.1017/s0029665110003927.
Full textAbstract:
Ageing is accompanied by a progressive loss of skeletal muscle mass and strength, leading to the loss of functional capacity and an increased risk for developing chronic metabolic diseases such as diabetes. The age-related loss of skeletal muscle mass results from a chronic disruption in the balance between muscle protein synthesis and degradation. As basal muscle protein synthesis rates are likely not different between healthy young and elderly human subjects, it was proposed that muscles from older adults lack the ability to regulate the protein synthetic response to anabolic stimuli, such as food intake and physical activity. Indeed, the dose–response relationship between myofibrillar protein synthesis and the availability of essential amino acids and/or resistance exercise intensity is shifted down and to the right in elderly human subjects. This so-called ‘anabolic resistance’ represents a key factor responsible for the age-related decline in skeletal muscle mass. Interestingly, long-term resistance exercise training is effective as a therapeutic intervention to augment skeletal muscle mass, and improves functional performance in the elderly. The consumption of different types of proteins, i.e. protein hydrolysates, can have different stimulatory effects on muscle protein synthesis in the elderly, which may be due to their higher rate of digestion and absorption. Current research aims to elucidate the interactions between nutrition, exercise and the skeletal muscle adaptive response that will define more effective strategies to maximise the therapeutic benefits of lifestyle interventions in the elderly.
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FLOREZ-DUQUET, MARIA, and ROGER B. McDONALD. "Cold-Induced Thermoregulation and Biological Aging." Physiological Reviews 78, no. 2 (April 1, 1998): 339–58. http://dx.doi.org/10.1152/physrev.1998.78.2.339.
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Florez-Duquet, Maria, and Roger B. McDonald. Cold-Induced Thermoregulation and Biological Aging. Physiol. Rev. 78: 339–358, 1998. — Aging is associated with diminished cold-induced thermoregulation (CIT). The mechanisms accounting for this phenomenon have yet to be clearly elucidated but most likely reflect a combination of increased heat loss and decreased metabolic heat production. The inability of the aged subject to reduce heat loss during cold exposure is associated with diminished reactive tone of the cutaneous vasculature and, to a lesser degree, alterations in the insulative properties of body fat. Cold-induced metabolic heat production via skeletal muscle shivering thermogenesis and brown adipose tissue nonshivering thermogenesis appears to decline with age. Few investigations have directly linked diminished skeletal muscle shivering thermogenesis with the age-related reduction in cold-induced thermoregulatory capacity. Rather, age-related declines in skeletal muscle mass and metabolic activity are cited as evidence for decreased heat production via shivering. Reduced mass, GDP binding to brown fat mitochondria, and uncoupling protein (UCP) levels are cited as evidence for attenuated brown adipose tissue cold-induced nonshivering thermogenic capacity during aging. The age-related reduction in brown fat nonshivering thermogenic capacity most likely reflects altered cellular signal transduction rather than changes in neural and hormonal signaling. The discussion in this review focuses on how alterations in CIT during the life span may offer insight into possible mechanisms of biological aging. Although the preponderance of evidence presented here demonstrates that CIT declines with chronological time, the mechanism reflecting this attenuated function remains to be elucidated. The inability to draw definitive conclusions regarding biological aging and CIT reflects the lack of a clear definition of aging. It is unlikely that the mechanisms accounting for the decline in cold-induced thermoregulation during aging will be determined until biological aging is more precisely defined.
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Meltzer, D. E. "Body-mass dependence of age-related deterioration in human muscular function." Journal of Applied Physiology 80, no. 4 (April 1, 1996): 1149–55. http://dx.doi.org/10.1152/jappl.1996.80.4.1149.
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Maximal anaerobic power of human muscles declines with increasing chronological age and is correlated with body mass. This study investigated whether the rate of deterioration in human muscular function among trained weight lifters is also correlated with body mass. Cross-sectional analysis of performance data of over 1,100 Masters competitors in Olympic-style weight lifting was carried out; eight body-weight classes and six age groups were represented. Two-lift total data (sum of snatch and clean and jerk lifts) were analyzed. Mean deterioration rates in the performance of athletes of widely diverse body masses were compared over the following age ranges: 42-57, 42-62, and 42-67 yr. No statistically significant correlation (P < 0.05) was found between rate of performance decline and body mass. The relationship between body mass and the magnitude of age-related variation of deterioration rate was also studied; no significant correlation was found. Previous studies have demonstrated that performance in Olympic-style weight lifting is correlated with maximal anaerobic muscular power. This leads us to suggest that the age-related deterioration rate of anaerobic power in trained subjects may not be correlated with the body mass of the individual.
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Kanova, Marcela, and Pavel Kohout. "Molecular Mechanisms Underlying Intensive Care Unit-Acquired Weakness and Sarcopenia." International Journal of Molecular Sciences 23, no. 15 (July 29, 2022): 8396. http://dx.doi.org/10.3390/ijms23158396.
Full textAbstract:
Skeletal muscle is a highly adaptable organ, and its amount declines under catabolic conditions such as critical illness. Aging is accompanied by a gradual loss of muscle, especially when physical activity decreases. Intensive care unit-acquired weakness is a common and highly serious neuromuscular complication in critically ill patients. It is a consequence of critical illness and is characterized by a systemic inflammatory response, leading to metabolic stress, that causes the development of multiple organ dysfunction. Muscle dysfunction is an important component of this syndrome, and the degree of catabolism corresponds to the severity of the condition. The population of critically ill is aging; thus, we face another negative effect—sarcopenia—the age-related decline of skeletal muscle mass and function. Low-grade inflammation gradually accumulates over time, inhibits proteosynthesis, worsens anabolic resistance, and increases insulin resistance. The cumulative consequence is a gradual decline in muscle recovery and muscle mass. The clinical manifestation for both of the above conditions is skeletal muscle weakness, with macromolecular damage, and a common mechanism—mitochondrial dysfunction. In this review, we compare the molecular mechanisms underlying the two types of muscle atrophy, and address questions regarding possible shared molecular mechanisms, and whether critical illness accelerates the aging process.
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McArdle, Anne, and Malcolm J. Jackson. "The role of attenuated redox and heat shock protein responses in the age-related decline in skeletal muscle mass and function." Essays in Biochemistry 61, no. 3 (July 11, 2017): 339–48. http://dx.doi.org/10.1042/ebc20160088.
Full textAbstract:
The loss of muscle mass and weakness that accompanies ageing is a major contributor to physical frailty and loss of independence in older people. A failure of muscle to adapt to physiological stresses such as exercise is seen with ageing and disruption of redox regulated processes and stress responses are recognized to play important roles in theses deficits. The role of redox regulation in control of specific stress responses, including the generation of heat shock proteins (HSPs) by muscle appears to be particularly important and affected by ageing. Transgenic and knockout studies in experimental models in which redox and HSP responses were modified have demonstrated the importance of these processes in maintenance of muscle mass and function during ageing. New data also indicate the potential of these processes to interact with and influence ageing in other tissues. In particular the roles of redox signalling and HSPs in regulation of inflammatory pathways appears important in their impact on organismal ageing. This review will briefly indicate the importance of this area and demonstrate how an understanding of the manner in which redox and stress responses interact and how they may be controlled offers considerable promise as an approach to ameliorate the major functional consequences of ageing of skeletal muscle (and potentially other tissues) in man.
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Wåhlin-Larsson, Britta, Daniel J. Wilkinson, Emelie Strandberg, Adrian Hosford-Donovan, Philip J. Atherton, and Fawzi Kadi. "Mechanistic Links Underlying the Impact of C-Reactive Protein on Muscle Mass in Elderly." Cellular Physiology and Biochemistry 44, no. 1 (2017): 267–78. http://dx.doi.org/10.1159/000484679.
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Background/Aims: Mechanisms underlying the relationship between systemic inflammation and age-related decline in muscle mass are poorly defined. The purpose of this work was to investigate the relationship between the systemic inflammatory marker CRP and muscle mass in elderly and to identify mechanisms by which CRP mediates its effects on skeletal muscle, in-vitro. Methods: Muscle mass and serum CRP level were determined in a cohort of 118 older women (67±1.7 years). Human muscle cells were differentiated into myotubes and were exposed to CRP. The size of myotubes was determined after immunofluorescent staining using troponin. Muscle protein synthesis was assessed using stable isotope tracers and key signalling pathways controlling protein synthesis were determined using western-blotting. Results: We observed an inverse relationship between circulating CRP level and muscle mass (β= -0.646 (95% CI: -0.888, -0.405) p<0.05) and demonstrated a reduction (p < 0.05) in the size of human myotubes exposed to CRP for 72 h. We next showed that this morphological change was accompanied by a CRP-mediated reduction (p < 0.05) in muscle protein fractional synthetic rate of human myotubes exposed to CRP for 24 h. We also identified a CRP-mediated increased phosphorylation (p<0.05) of regulators of cellular energy stress including AMPK and downstream targets, raptor and ACC-β, together with decreased phosphorylation of Akt and rpS6, which are important factors controlling protein synthesis. Conclusion: This work established for the first time mechanistic links by which chronic elevation of CRP can contribute to age-related decline in muscle function.
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Cvecka, Jan, Veronika Tirpakova, Milan Sedliak, Helmut Kern, Winfried Mayr, and Dušan Hamar. "Physical activity in elderly." European Journal of Translational Myology 25, no. 4 (August 25, 2015): 249. http://dx.doi.org/10.4081/ejtm.2015.5280.
Full textAbstract:
Aging is a multifactorial irreversible process associated with significant decline in muscle mass and neuromuscular functions. One of the most efficient methods to counteract age-related changes in muscle mass and function is physical exercise. An alternative effective intervention to improve muscle structure and performance is electrical stimulation. In the present work we present the positive effects of physical activity in elderly and a study where the effects of a 8-week period of functional electrical stimulation and strength training with proprioceptive stimulation in elderly are compared.
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Ungvari, Zoltan, Nazar Labinskyy, Sachin Gupte, Praveen N. Chander, John G. Edwards, and Anna Csiszar. "Dysregulation of mitochondrial biogenesis in vascular endothelial and smooth muscle cells of aged rats." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (May 2008): H2121—H2128. http://dx.doi.org/10.1152/ajpheart.00012.2008.
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Mitochondrial biogenesis is involved in the control of cell metabolism, signal transduction, and regulation of mitochondrial reactive oxygen species (ROS) production. Despite the central role of mitochondria in cellular aging and endothelial physiology, there are no studies extant investigating age-related alterations in mitochondrial biogenesis in blood vessels. Electronmicroscopy and confocal microscopy (en face Mitotracker staining) revealed that in aortas of F344 rats, a decline in mitochondrial biogenesis occurs with aging. In aged vessels, the expression of the mitochondrial biogenesis factors (including mitochondrial transcription factor A and peroxisome proliferator-activated receptor-γ coactivator-1) was decreased. The vascular expression of complex I, III, and IV significantly declined with age, whereas aging did not alter the expression of complex II and V. Cytochrome c oxidase (COX) expression/activity exhibited the greatest age-related decline, which was associated with increased mitochondrial ROS production in the aged vessels. In cultured coronary arterial endothelial cells, a partial knockdown of COX significantly increased mitochondrial ROS production. In conclusion, vascular aging is characterized by a decline in mitochondrial mass in the endothelial cells and an altered expression of components of the mitochondrial electron transport chain likely due to a dysregulation of mitochondrial biogenesis factors. We posit that impaired mitochondrial biogenesis and downregulation of COX may contribute to the increased mitochondrial oxidative stress in aged endothelial cells.
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Marcell, Taylor J., S. Mitchell Harman, Randall J. Urban, Daniel D. Metz, Buel D. Rodgers, and Marc R. Blackman. "Comparison of GH, IGF-I, and testosterone with mRNA of receptors and myostatin in skeletal muscle in older men." American Journal of Physiology-Endocrinology and Metabolism 281, no. 6 (December 1, 2001): E1159—E1164. http://dx.doi.org/10.1152/ajpendo.2001.281.6.e1159.
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Growth hormone (GH), insulin-like growth factor I (IGF-I), and testosterone (T) are important mediators of muscle protein synthesis, and thus muscle mass, all of which decline with age. We hypothesized that circulating hormones would be related to the transcriptional levels of their respective receptors and that this expression would be negatively related to expression of the myostatin gene. We therefore determined content of mRNA transcripts (by RT-PCR) for GH receptor (GHR), IGF-I, androgen receptor (AR), and myostatin in skeletal muscle biopsy samples from 27 healthy men >65 yr of age. There were no significant relationships between age, lean body mass, or percent body fat and transcript levels of GHR, IGF-I, AR, or myostatin. Moreover, there were no significant correlations of serum GH, IGF-I, or T with their corresponding target mRNA levels (GHR, intramuscular IGF-I, or AR) in skeletal muscle. However, GHR was negatively correlated ( r = −0.60, P = 0.001) with myostatin mRNA levels. The lack of apparent relationships of muscle transcripts with their respective ligands in healthy older adults suggests that age-related deficits in both GH and T may lead to an increase in myostatin expression and a disassociation in autocrine IGF-I effects on muscle protein synthesis, both of which could contribute to age-related sarcopenia.
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Zembron-Lacny, Agnieszka, Wioletta Dziubek, Edyta Wolny-Rokicka, Grazyna Dabrowska, and Marek Wozniewski. "The Relation of Inflammaging With Skeletal Muscle Properties in Elderly Men." American Journal of Men's Health 13, no. 2 (March 2019): 155798831984193. http://dx.doi.org/10.1177/1557988319841934.
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Aging is associated with a progressive decline of muscle mass and/or the qualitative impairment of the muscle tissue. There is growing evidence of the prominent role of low-grade chronic inflammation in age-related changes in the neuromuscular system. The purpose of the study was to identify the inflammatory mediators responsible for deficit in functional fitness and to explain whether inflammation is related to changes in body composition and the decline of muscle strength in older men. Thirty-three old-aged males (73.5 ± 6.3 years) and twenty young-aged males (21.2 ± 1.3 years) participated in the study. The body composition (bioelectrical impedance analysis), functional capacity (6-min walking test) and knee extension strength (isokinetic test) were estimated. In serum, circulating inflammatory markers H2O2, IL-1β, TNFα, and hsCRP as well as growth factors IGF-I and PDGFBB concentrations were determined (immunoenzymatic methods). The concentrations of H2O2, IL-1β, TNFα, and hsCRP were significantly higher in older than young men. The growth factors IGF-I and PDGFBB were twofold lower and related to high levels of IL-1β and TNFα in the elderly. The changes in cytokines and growth factors levels were correlated with age and peak torque (TQ at 60°/s and 180°/s) in the knee extension. The result of the 6-min walking test was inversely correlated with fat mass index (FMI, r = −.983; p < .001). The generation of inflammatory mediators in older men was related to changes in body composition, maximum strength muscle, and age-related changes in skeletal muscle properties responsible for deficit in functional fitness.
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Paez, Hector G., Christopher R. Pitzer, and Stephen E. Alway. "Age-Related Dysfunction in Proteostasis and Cellular Quality Control in the Development of Sarcopenia." Cells 12, no. 2 (January 7, 2023): 249. http://dx.doi.org/10.3390/cells12020249.
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Sarcopenia is a debilitating skeletal muscle disease that accelerates in the last decades of life and is characterized by marked deficits in muscle strength, mass, quality, and metabolic health. The multifactorial causes of sarcopenia have proven difficult to treat and involve a complex interplay between environmental factors and intrinsic age-associated changes. It is generally accepted that sarcopenia results in a progressive loss of skeletal muscle function that exceeds the loss of mass, indicating that while loss of muscle mass is important, loss of muscle quality is the primary defect with advanced age. Furthermore, preclinical models have suggested that aged skeletal muscle exhibits defects in cellular quality control such as the degradation of damaged mitochondria. Recent evidence suggests that a dysregulation of proteostasis, an important regulator of cellular quality control, is a significant contributor to the aging-associated declines in muscle quality, function, and mass. Although skeletal muscle mammalian target of rapamycin complex 1 (mTORC1) plays a critical role in cellular control, including skeletal muscle hypertrophy, paradoxically, sustained activation of mTORC1 recapitulates several characteristics of sarcopenia. Pharmaceutical inhibition of mTORC1 as well as caloric restriction significantly improves muscle quality in aged animals, however, the mechanisms controlling cellular proteostasis are not fully known. This information is important for developing effective therapeutic strategies that mitigate or prevent sarcopenia and associated disability. This review identifies recent and historical understanding of the molecular mechanisms of proteostasis driving age-associated muscle loss and suggests potential therapeutic interventions to slow or prevent sarcopenia.
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Perrini, Sebastio, Luigi Laviola, Marcos C. Carreira, Angelo Cignarelli, Annalisa Natalicchio, and Francesco Giorgino. "The GH/IGF1 axis and signaling pathways in the muscle and bone: mechanisms underlying age-related skeletal muscle wasting and osteoporosis." Journal of Endocrinology 205, no. 3 (March 2, 2010): 201–10. http://dx.doi.org/10.1677/joe-09-0431.
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The widespread increase in life expectancy is accompanied by an increased prevalence of features of physical frailty. Signs and symptoms may include sarcopenia and osteopenia, reduced exercise capacity, and diminished sense of well-being. The pathogenesis of age-associated sarcopenia and osteopenia is multifactorial, and hormonal decline may be a contributing factor. Aging is associated with a progressive decrease in GH secretion, and more than 30% of elderly people have circulating IGF1 levels below the normal range found in the young. GH acts directly on target tissues, including skeletal muscle and bone among many others, but many effects are mediated indirectly by circulating (liver-derived) or locally produced IGF1. Aging is also associated with reduced insulin sensitivity which, in turn, may contribute to the impairment of IGF1 action. Recent experimental evidence suggests that besides the age-dependent decline in GH and IGF1 serum levels, the dysregulation of GH and IGF1 actions due to impairment of the post-receptor signaling machinery may contribute to the loss of muscle mass and osteopenia. This article will focus on the molecular mechanisms of impaired GH and IGF1 signaling and action in aging, and their role in the pathogenesis of sarcopenia and osteoporosis.
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Ruan, Ling, Bharati Mendhe, Carlos Isales, William Hill, Meghan McGee-Lawrence, Sadanand Fulzele, and Mark Hamrick. "Depletion of the miR-34a “sponge” MALAT1 in aging skeletal muscle: Implications for age-related muscle loss." Innovation in Aging 5, Supplement_1 (December 1, 2021): 684–85. http://dx.doi.org/10.1093/geroni/igab046.2573.
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Abstract We have recently shown that increased levels of reactive oxygen species (ROS) in aging skeletal muscle are associated with increased expression of the senescence-associated microRNA miR-34a-5p (miR-34a). The histone deacetylase Sirt1 is a validated target of miR-34a, and miR-34a expression is induced by the tumor suppressor p53 which is itself stimulated by ROS. Long noncoding RNAs (lncRNAs) are known to function as “sponges” for microRNAs, but the role of such competing endogenous RNAs (ceRNA) in muscle aging is not well understood. We therefore examined in skeletal muscles of young (4-6 mos) and aged (22-24) male and female mice the expression of several lncRNAs that are predicted to bind miR-34a-5p in silico and whose predicted binding has been validated experimentally. Results indicate a significant decrease in lncRNA MALAT1 expression with aging. MALAT1 is known to be highly expressed during the later stages of myoblast differentiation and myotube maturation. We therefore treated C2C12 cells at 48 hrs with hydrogen peroxide (10 uM) and examined changes in MALAT1 expression. MALAT1 was significantly decreased with H2O2 treatment, whereas miR-34a is increased in C2C12 cells after hydrogen peroxide exposure. Age-related muscle atrophy mediated by ROS may therefore result in part from related mechanisms involving miR-34a activity: an increase in miR-34a targeting Sirt1 resulting from p53 activation and an increase in miR-34a bioavailability resulting from a decline in miR-34a “sponging” due to ceRNA MALAT1 depletion. These findings suggest that therapeutic interventions increasing MALAT1 expression in muscle may potentially enhance the preservation of muscle mass with aging.
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Namiki, Chizuru, Koji Hara, Ryosuke Yanagida, Kazuharu Nakagawa, Kohei Yamaguchi, Takuma Okumura, Tomoe Tamai, Yukiko Kurosawa, Tomoko Komatsu, and Haruka Tohara. "Association between Tongue Pressure and Jaw-Opening Force in Older Adults." International Journal of Environmental Research and Public Health 19, no. 16 (August 9, 2022): 9825. http://dx.doi.org/10.3390/ijerph19169825.
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Tongue pressure (TP) is used to assess tongue muscle strength and is related to function and frailty. While performing TP, it is necessary to elevate the tongue and oral floor by contracting the suprahyoid muscles. However, the association between TP and suprahyoid muscle strength remains unclear. Accordingly, this study investigated the relationship between TP and jaw-opening force (JOF), an indicator of suprahyoid muscle strength. This cross-sectional study included 88 independent community-dwelling participants aged ≥65 years. Age, sex, and the number of remaining teeth were recorded. Ultrasonography was used to evaluate the cross-sectional area of the tongue and geniohyoid muscle, as representatives of the suprahyoid muscles. Sarcopenia was diagnosed based on appendicular skeletal muscle mass index, handgrip strength, and gait speed. Multiple regression analysis was performed with TP as the dependent variable. TP was significantly associated with JOF (β = 0.371, p = 0.003). This study revealed that decreased TP was associated with a decline in JOF and suprahyoid muscle mass in older adults. Thus, low TP may be associated with decreased JOF. Prevention of the weakness of the suprahyoid muscles and maintaining TP may also contribute to the prevention of frailty associated with TP.
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Brown, Marybeth. "Skeletal muscle and bone: effect of sex steroids and aging." Advances in Physiology Education 32, no. 2 (June 2008): 120–26. http://dx.doi.org/10.1152/advan.90111.2008.
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Both estrogen and testosterone are present in males and females. Both hormones contribute to the well being of skeletal muscle and bone in men and women, and there is evidence that the loss of sex hormones is associated with the age-related decline in bone and skeletal muscle mass. Hormonal supplementation of older adults to restore estrogen and testosterone levels to those of young men and women is not without penalty.