scholarly journals Nutrition and microRNAs: Novel Insights to Fight Sarcopenia

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 951
Author(s):  
Alessandra Barbiera ◽  
Laura Pelosi ◽  
Gigliola Sica ◽  
Bianca Maria Scicchitano
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Molecular Mechanisms ◽  
Muscle Protein ◽  
Low Grade ◽  
Protein Homeostasis ◽  
Dietary Interventions ◽  
Physiological Processes ◽  
Age Related ◽  
And Function

Sarcopenia is a progressive age-related loss of skeletal muscle mass and strength, which may result in increased physical frailty and a higher risk of adverse events. Low-grade systemic inflammation, loss of muscle protein homeostasis, mitochondrial dysfunction, and reduced number and function of satellite cells seem to be the key points for the induction of muscle wasting, contributing to the pathophysiological mechanisms of sarcopenia. While a range of genetic, hormonal, and environmental factors has been reported to contribute to the onset of sarcopenia, dietary interventions targeting protein or antioxidant intake may have a positive effect in increasing muscle mass and strength, regulating protein homeostasis, oxidative reaction, and cell autophagy, thus providing a cellular lifespan extension. MicroRNAs (miRNAs) are endogenous small non-coding RNAs, which control gene expression in different tissues. In skeletal muscle, a range of miRNAs, named myomiRNAs, are involved in many physiological processes, such as growth, development, and maintenance of muscle mass and function. This review aims to present and to discuss some of the most relevant molecular mechanisms related to the pathophysiological effect of sarcopenia. Besides, we explored the role of nutrition as a possible way to counteract the loss of muscle mass and function associated with ageing, with special attention paid to nutrient-dependent miRNAs regulation. This review will provide important information to better understand sarcopenia and, thus, to facilitate research and therapeutic strategies to counteract the pathophysiological effect of ageing.

scholarly journals Molecular regulation of human skeletal muscle protein synthesis in response to exercise and nutrients: a compass for overcoming age-related anabolic resistance

2019 ◽  
Vol 317 (6) ◽  
pp. C1061-C1078 ◽  
Author(s):  
Nathan Hodson ◽  
Daniel W. D. West ◽  
Andrew Philp ◽  
Nicholas A. Burd ◽  
Daniel R. Moore
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Mass ◽  
Human Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Negative Impact ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Anabolic Resistance ◽  
Age Related

Skeletal muscle mass, a strong predictor of longevity and health in humans, is determined by the balance of two cellular processes, muscle protein synthesis (MPS) and muscle protein breakdown. MPS seems to be particularly sensitive to changes in mechanical load and/or nutritional status; therefore, much research has focused on understanding the molecular mechanisms that underpin this cellular process. Furthermore, older individuals display an attenuated MPS response to anabolic stimuli, termed anabolic resistance, which has a negative impact on muscle mass and function, as well as quality of life. Therefore, an understanding of which, if any, molecular mechanisms contribute to anabolic resistance of MPS is of vital importance in formulation of therapeutic interventions for such populations. This review summarizes the current knowledge of the mechanisms that underpin MPS, which are broadly divided into mechanistic target of rapamycin complex 1 (mTORC1)-dependent, mTORC1-independent, and ribosomal biogenesis-related, and describes the evidence that shows how they are regulated by anabolic stimuli (exercise and/or nutrition) in healthy human skeletal muscle. This review also summarizes evidence regarding which of these mechanisms may be implicated in age-related skeletal muscle anabolic resistance and provides recommendations for future avenues of research that can expand our knowledge of this area.

scholarly journals Sarcopenia: Monitoring, Molecular Mechanisms, and Physical Intervention

2014 ◽  
pp. 683-691 ◽  
Author(s):  
A. ZEMBROŃ-ŁACNY ◽  
W. DZIUBEK ◽  
Ł. ROGOWSKI ◽  
E. SKORUPKA ◽  
G. DĄBROWSKA
Keyword(s):  
Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Muscle Protein ◽  
Interval Training ◽  
The Elderly ◽  
Low Grade ◽  
Protein Mass ◽  
Age Related ◽  
Increased Risk ◽  
European Working

According to European Working Group on Sarcopenia in Older People (EWGSOP) sarcopenia includes both a loss of muscle strength and a decline in functional quality in addition to the loss of muscle protein mass. In order to develop strategies to prevent and treat sarcopenia, the risk factors and causes of sarcopenia must be identified. Age-related muscle loss is characterized by the contribution of multiple factors, and there is growing evidence for a prominent role of low-grade chronic inflammation in sarcopenia. The elderly who are less physically active are more likely to have lower skeletal muscle mass and strength and are at increased risk of developing sarcopenia. Resistance training added to aerobic exercise or high-intensity interval training promote numerous changes in skeletal muscle, many of which may help to prevent or reverse sarcopenia. In this review, we provided current information on definition and monitoring, molecular mechanisms, and physical intervention to counteract sarcopenia.

scholarly journals NEUROMUSCULAR CHANGES WITH AGING AND SARCOPENIA

2018 ◽  
pp. 1-3
Author(s):  
B.C. Clark
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Function ◽  
Skeletal Muscle Mass ◽  
The Past ◽  
Conceptual Definition ◽  
Age Related ◽  
Per Se ◽  
Definition Of ◽  
And Function

Sarcopenia was originally conceptualized as the age-related loss of skeletal muscle mass. Over the ensuing decades, the conceptual definition of sarcopenia has changed to represent a condition in older adults that is characterized by declining muscle mass and function, with “function” most commonly conceived as muscle weakness and/or impaired physical performance (e.g., slow gait speed). Findings over the past 15-years, however, have demonstrated that changes in grip and leg extensor strength are not primarily due to muscle atrophy per se, and that to a large extent, are reflective of declines in the integrity of the nervous system. This article briefly summarizes findings relating to the complex neuromuscular mechanisms that contribute to reductions in muscle function associated with advancing age, and the implications of these findings on the development of effective therapies.

Skeletal Muscle Mass Regulation in Critical Illness

2014 ◽  
Author(s):  
Zudin Puthucheary ◽  
Hugh Montgomery ◽  
Nicholas Hart ◽  
Stephen Harridge
Keyword(s):  
Skeletal Muscle ◽  
Critical Illness ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Bed Rest ◽  
Protein Homeostasis ◽  
Highly Sensitive ◽  
And Function ◽  
Inadequate Nutrition

Muscle is a dynamic, plastic, and malleable tissue that is highly sensitive to mechanical and metabolic signals. Muscle mass is regulated by protein homeostasis, with protein being continually turned over, reflecting a balance between synthesis and breakdown. This chapter discusses the effect of critical illness on skeletal muscle mass, protein homeostasis, and the intracellular signalling driving anabolism and catabolism. The focus will be on the unique challenges to which the skeletal muscle are exposed, such as inflammation, sepsis, sedation, and inadequate nutrition, which, in combination with the disuse signals of immobilization and bed rest, engender dramatic changes in muscle structure and function. The mechanisms regulating muscle loss during critical illness are being unravelled, but many questions remain unanswered. Detailed understanding of these mechanisms will help drive strategies to minimize or prevent intensive care-acquired muscle weakness and the long-term consequences experienced by ICU survivors.

Diminished overload-induced hypertrophy in aged fast-twitch skeletal muscle is associated with AMPK hyperphosphorylation

2005 ◽  
Vol 98 (2) ◽  
pp. 557-564 ◽  
Author(s):  
David M. Thomson ◽  
Scott E. Gordon
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Protein ◽  
Male Rats ◽  
Brown Norway ◽  
Ampk Phosphorylation ◽  
Age Related ◽  
Ampk Activity ◽  
Slow Twitch ◽  
Fast Twitch

Skeletal muscle mass declines with age, as does the potential for overload-induced fast-twitch skeletal muscle hypertrophy. Because 5′-AMP-activated protein kinase (AMPK) activity is thought to inhibit skeletal muscle protein synthesis and may therefore modulate muscle mass and hypertrophy, the purpose of this investigation was to examine AMPK phosphorylation status (a marker of AMPK activity) and its potential association with the attenuated overload-induced hypertrophy observed in aged skeletal muscle. One-week overload of fast-twitch plantaris and slow-twitch soleus muscles was achieved in young adult (8 mo; n = 7) and old (30 mo; n = 7) Fischer344 × Brown Norway male rats via unilateral gastrocnemius ablation. Significant ( P ≤ 0.05) age-related atrophy (as measured by total protein content) was noted in plantaris and soleus control (sham-operated) muscles. In fast-twitch plantaris muscles, percent hypertrophy with overload was significantly attenuated with age, whereas AMPK phosphorylation status as determined by Western blotting [phospho-AMPK (Thr172)/total AMPK] was significantly elevated with age (regardless of loading status). There was also a main effect of loading on AMPK phosphorylation status in plantaris muscles (overload > control). Moreover, a strong and significant negative correlation ( r = −0.82) was observed between AMPK phosphorylation status and percent hypertrophy in the overloaded plantaris muscles of all animals. In contrast to the plantaris, overload-induced hypertrophy of the slow-twitch soleus muscle was similar between ages, and AMPK phosphorylation in this muscle was also unaffected by age or overload. These data support the possibility that an age-related elevation in AMPK phosphorylation may partly contribute to the attenuated hypertrophic response observed with age in overloaded fast-twitch plantaris muscle.

Aging, exercise, and muscle protein metabolism

2009 ◽  
Vol 106 (6) ◽  
pp. 2040-2048 ◽  
Author(s):  
René Koopman ◽  
Luc J. C. van Loon
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Food Intake ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
The Elderly ◽  
Age Related

Aging is accompanied by a progressive loss of skeletal muscle mass and strength, leading to the loss of functional capacity and an increased risk of developing chronic metabolic disease. The age-related loss of skeletal muscle mass is attributed to a disruption in the regulation of skeletal muscle protein turnover, resulting in an imbalance between muscle protein synthesis and degradation. As basal (fasting) muscle protein synthesis rates do not seem to differ substantially between the young and elderly, many research groups have started to focus on the muscle protein synthetic response to the main anabolic stimuli, i.e., food intake and physical activity. Recent studies suggest that the muscle protein synthetic response to food intake is blunted in the elderly. The latter is now believed to represent a key factor responsible for the age-related decline in skeletal muscle mass. Physical activity and/or exercise stimulate postexercise muscle protein accretion in both the young and elderly. However, the latter largely depends on the timed administration of amino acids and/or protein before, during, and/or after exercise. Prolonged resistance type exercise training represents an effective therapeutic strategy to augment skeletal muscle mass and improve functional performance in the elderly. The latter shows that the ability of the muscle protein synthetic machinery to respond to anabolic stimuli is preserved up to very old age. Research is warranted to elucidate the interaction between nutrition, exercise, and the skeletal muscle adaptive response. The latter is needed to define more effective strategies that will maximize the therapeutic benefits of lifestyle intervention in the elderly.

scholarly journals Effects of long-term exposures to low iron and branched-chain amino acid containing diets on aging skeletal muscle of Fisher 344 × Brown Norway rats

2018 ◽  
Vol 43 (2) ◽  
pp. 165-173 ◽  
Author(s):  
Yuho Kim ◽  
Sok Sambo Men ◽  
Chen Liang ◽  
Candace N. Receno ◽  
Tom D. Brutsaert ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Citrate Synthase ◽  
Muscle Protein ◽  
Iron Status ◽  
Protein Carbonyls ◽  
Brown Norway ◽  
Age Related ◽  
Branched Chain ◽  
Norway Rats

Aging skeletal muscle displays an altered iron status that may promote oxidative stress and sarcopenia. A diet containing low iron (LI) could reduce muscle iron status and attenuate age-related muscle atrophy. Supplemental branched-chain amino acids (BCAA) may also alleviate sarcopenia by promoting muscle protein synthesis and iron status improvement. This study examined individual and combined effects of LI and BCAA diets on anabolic signaling and iron status in skeletal muscle of aging rats. Twenty-nine-month-old male Fisher 344 × Brown Norway rats consumed the following control-base diets: control + regular iron (35 mg iron/kg) (CR; n = 11); control + LI (∼6 mg iron/kg) (CL; n = 11); 2×BCAA + regular iron (BR; n = 10); and 2×BCAA + LI (BL; n = 12) for 12 weeks. Although LI and/or 2×BCAA did not affect plantaris muscle mass, 2×BCAA groups showed lower muscle iron content than did CR and CL groups (P < 0.05). p70 ribosomal protein S6 kinase phosphorylation was greater in 2×BCAA and LI animals compared with CR animals (P < 0.05). Interactions between IRON and BCAA were observed for proteins indicative of mitochondrial biogenesis (peroxisome proliferator-activated receptor gamma coactivator 1 alpha) and oxidative capacity (cytochrome c oxidase subunit 2 and citrate synthase) (P < 0.05) wherein the combined diet (BL) negated potential benefits of individual diets. Antioxidant capacity, superoxide dismutase activity, and oxidative injury (3-nitrotyrosine, protein carbonyls, and 4-hydroxynonenal) were similar between groups. In conclusion, 12 weeks of LI and 2×BCAA diets showed significant impacts on increasing anabolic signaling as well as ameliorating iron status; however, these interventions did not affect muscle mass.

DIETARY PROTEIN TO MAINTAIN MUSCLE MASS IN AGING: A CASE FOR PER-MEAL PROTEIN RECOMMENDATIONS

2016 ◽  
pp. 1-10
Author(s):  
C.H. MURPHY ◽  
S.Y. OIKAWA ◽  
S.M. PHILLIPS
Keyword(s):  
Muscle Mass ◽  
Dietary Protein ◽  
Protein Intake ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Dietary Advice ◽  
Age Related ◽  
Meal Protein ◽  
Single Meal ◽  
And Function

It is well accepted that daily protein intake is an important dietary consideration to limit and treat age-related declines in muscle mass, strength, and function. Furthermore, we propose that there is a growing appreciation for the need to consider protein intake on a per-meal basis rather than simply focusing on the total daily protein intake. The existence of a saturable dose-response relationship between muscle protein synthesis (MPS) and the quantity of protein consumed in a single meal/bolus provides the rationale for promoting an even/balanced pattern of daily protein intake. We hypothesize that a balanced/even protein intake pattern with the ingestion a quantity of protein shown to optimally stimulate MPS at each meal may be an effective strategy to alleviate sarcopenic muscle loss. In this review we examine the available evidence supporting the influence of dietary protein intake pattern on muscle protein turnover, muscle mass, and muscle function. We present several practical considerations that, it is proposed, should be taken into account when translating a per-meal protein recommendation into dietary advice for older adults.

scholarly journals Accumulation of intramuscular toxic lipids, a link between fat mass accumulation and sarcopenia

OCL ◽  
2019 ◽  
Vol 26 ◽  
pp. 24 ◽  
Author(s):  
Frederic Capel ◽  
Alexandre Pinel ◽  
Stéphane Walrand
Keyword(s):  
Muscle Mass ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Intramyocellular Lipids ◽  
Age Related ◽  
Degradation Rates ◽  
Lipid Species ◽  
Risk Of Falls ◽  
Muscle Protein Metabolism ◽  
And Function

Aging is characterized by a loss in muscle mass and function, which is defined as sarcopenia. It weakens individuals by increasing the risk of falls and altering their quality of life. The loss of muscle mass results from the age-related impairment of the anabolic effect of nutrients and insulin, which normally increase and decrease muscle protein synthesis and degradation rates respectively. Alterations in muscle protein metabolism have been related to the accumulation of body fat and intramyocellular lipids. In particular, some lipid species such as ceramides or diacylglycerols have been described as inhibitors of the insulin signaling pathway in different models. Accumulation of these molecules in skeletal muscle could result from a lowered buffering capacity of circulating fatty acids by adipose tissue in response to the meal, a reduction of mitochondrial oxidative capacities or chronic inflammation. However, some nutritional strategies have been identified to limit or prevent the accumulation of lipotoxic metabolites and to improve the sensitivity of muscle to nutrients or insulin.

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