Role of Ultrasonography in Estimating Muscle Mass in Sarcopenic Obesity

2020 ◽  
Vol 44 (8) ◽  
pp. 1398-1406 ◽  
Author(s):  
Olgun Deniz ◽  
Alfonso Cruz‐Jentoft ◽  
Gozde Sengul Aycicek ◽  
Pelin Unsal ◽  
Mert Esme ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Sarcopenic Obesity

scholarly journals The Critical Role of Oxidative Stress in Sarcopenic Obesity

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Andrea Gonzalez ◽  
Felipe Simon ◽  
Oscar Achiardi ◽  
Cristian Vilos ◽  
Daniel Cabrera ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Muscle Mass ◽  
Critical Role ◽  
Critical Factor ◽  
Sarcopenic Obesity ◽  
Hormonal Changes ◽  
Cell Functions ◽  
Increased Risk ◽  
Metabolic Dysfunctions

Sarcopenic obesity (SO) is a combination of obesity and sarcopenia that primarily develops in older people. Patients with SO have high fat mass, low muscle mass, low muscle strength, and low physical function. SO relates to metabolic syndrome and an increased risk of morbimortality. The prevalence of SO varies because of lacking consensus criteria regarding its definition and the methodological difficulty in diagnosing sarcopenia and obesity. SO includes systemic alterations such as insulin resistance, increased proinflammatory cytokines, age-associated hormonal changes, and decreased physical activity at pathophysiological levels. Interestingly, these alterations are influenced by oxidative stress, which is a critical factor in altering muscle function and the generation of metabolic dysfunctions. Thus, oxidative stress in SO alters muscle mass, the signaling pathways that control it, satellite cell functions, and mitochondrial and endoplasmic reticulum activities. Considering this background, our objectives in this review are to describe SO as a highly prevalent condition and look at the role of oxidative stress in SO pathophysiology.

MOLECULAR ASPECTS OF SARCOPENIA PATHOGENESIS IN CHRONOC KIDNEY DISEASE: INTEGRATED ROLE OF mTOR

2018 ◽  
Vol 22 (5) ◽  
pp. 9-16 ◽  
Author(s):  
M. Z. Gasanov
Keyword(s):  
Kidney Disease ◽  
Muscle Mass ◽  
Protein Metabolism ◽  
Mammalian Target Of Rapamycin ◽  
Healthy Person ◽  
Scientific Review ◽  
Cytoskeleton Organization ◽  
Molecular Aspects ◽  
End Stage

In recent decades, the main pathogenetic mechanisms for maintaining muscle mass and strength have been discovered. Most of the scientific papers on the molecular aspects of the  pathogenesis of sarcopenia were focused on the Akt-signaling  pathway. The subject of the study were people of elderly and senile  age, immobilized patients, patients with CKD 1-4 stages, animals. However, recently more attention has been paid to the role  of protein – the mammalian target of rapamycin mTOR. It seems to be a key link in the control of muscle mass and is a promising  marker in understanding the mechanisms of the pathogenesis of  sarcopenia. Its importance in protein metabolism in patients with  end stage kidney disease is not studied and requires further research. The presented scientific review contains  information on the role of mTOR and its components – mTORC1 and mTORC2 in maintaining muscle mass and strength in a healthy  person and in the formation of sarcopenia in patients with CKD. The  general aid of mTORC1 complex is regulation of protein production  which is necessary for cell growth and differentiation. mTORC2  complex functions are not enough studied. It is established that it  plays important role in such biological processes as cytoskeleton  organization, intracellular homeostasis maintaining, so it provides  cell resistance and cell survivability in negative external and internal  impulses. mTOR protein can be considered as promising molecular  marker in diagnostics of protein metabolism early disturbances in  patients with CKD and also as additory factor of sarcopenia severity assessment.

MO612THE ROLE OF MECHANICAL MUSCLE POWER IN PHYSICAL DYSFUNCTION: A MODEL FOR TAILORING RESISTANCE-BASED REHABILITATION IN CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Thomas Wilkinson ◽  
Eleanor Gore ◽  
Jared Palmer ◽  
Luke Baker ◽  
Emma Watson ◽  
...  
Keyword(s):  
Activities Of Daily Living ◽  
Strength Training ◽  
Physical Function ◽  
Muscle Mass ◽  
Gait Speed ◽  
Daily Living ◽  
Muscle Power ◽  
Mechanical Power ◽  
Relative Power

Abstract Background and Aims Individuals living with CKD are characterised by adverse changes in physical function. Knowledge of the factors that mediate impairments in physical functioning is crucial for developing effective interventions that preserve mobility and future independence. Mechanical muscle power describes the rate of performing work and is the product of muscular force and velocity of contraction. Muscle power has been shown to have stronger associations with functional limitations and mortality than sarcopenia in older adults. In CKD, the role of mechanical muscle power is poorly understood and is overlooked as a target in many rehabilitation programmes, often at the expense of muscle mass or strength. The aims of this study were to 1) explore the prevalence of low absolute mechanical power, low relative mechanical power, and low specific mechanical power in CKD; and 2) investigate the association of mechanical power with the ability to complete activities of daily living and physical performance. Method Mechanical muscle power (relative, allometric, specific) was calculated using the sit-to-stand-5 (STS5) test as per previously validated equations. Legs lean mass was derived from regional analyses conducted using bioelectrical impedance analysis (BIA). Physical performance was assessed using two objective tests: usual gait speed and the ‘time-up-and-go’ (TUAG) test. Self-reported activities of daily living (ADLs) were assessed via the Duke Activity Status Index (DASI). Balance and postural stability (postural sway and velocity) was assessed using a FysioMeter. Sex-specific tertiles were used to determine low, medium and high levels of relative STS power and its main components. Results 102 participants with non-dialysis CKD were included (mean age: 62.0 (±14.1) years, n=49 males (48%), mean eGFR: 38.0 (±21.5) ml.min.1.73m2). The mean estimated relative power was 3.1 (±1.5) W.kg in females and 3.3 (±1.3) W.kg in males. Low relative power was found in 35/102 (34%) patients. Relative power was a significant independent predictor of self-reported ADLs (via the DASI) (B=.413, P=.004), and performance on the TUAG (B=-.719, P<.001) and gait speed (B=.404, P=.003) tests. Skeletal muscle mass was not associated with the DASI or any of the objective function tests Conclusion Patients presenting with low muscle power would benefit from participation in appropriate interventions designed to improve the physiological components accounting for low relative muscle power. Assessment of power can be used to tailor renal rehabilitation programmes as shown in Figure 1. Incorporation of power-based training, a novel type of strength training, designed by manipulating traditional strength training variables and primarily movement velocity and training intensity may present the best strategy for improving physical function in CKD.

Abstract 791: A Critical Role for Bmper (BMP-binding Endothelial cell precursor-derived Regulator) in Cardiac Muscle Mass Regulation during Development and Pressure Overload Induced Hypertrophy

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Monte Willis ◽  
Rongqin Ren ◽  
Cam Patterson
Keyword(s):  
Cardiac Function ◽  
Cardiac Muscle ◽  
Muscle Mass ◽  
Cardiac Development ◽  
Critical Role ◽  
Pressure Overload ◽  
Posterior Wall ◽  
Fractional Shortening

Bone morphogenetic proteins (BMPs) of the TGF-beta superfamily, have been implicated in multiple processes during cardiac development. Our laboratory recently described an unprecedented role for Bmper in antagonizing BMP-2, BMP-4, and BMP-6. To determine the role of Bmper on cardiac development in vivo, we created Bmper null (Bmper −/−) mice by replacing exons 1 and 2 with GFP. Since Bmper −/− mice are perinatally lethal, we determined pre-natal cardiac function of Bmper −/− mice in utero just before birth. By echocardiography, E18.5 Bmper −/− embryos had decreased cardiac function (24.2 +/− 8.1% fractional shortening) compared to Bmper +/− and Bmper +/+ siblings (52.2 +/− 1.6% fractional shortening) (N=4/group). To further characterize the role of Bmper on cardiac function in adult mice, we performed echocardiography on 8-week old male and female Bmper +/− and littermate control Bmper +/+. Bmper +/− mice had an approximately 15% decrease in anterior and posterior wall thickness compared to sibling Bmper +/+ mice at baseline (n=10/group). Cross-sectional areas of Bmper +/− cardiomyocytes were approximately 20% less than wild type controls, indicating cardiomyocyte hypoplasia in adult Bmper +/− mice at baseline. Histologically, no significant differences were identified in representative H&E and trichrome stained adult Bmper +/− and Bmper +/+ cardiac sections at baseline. To determine the effects of Bmper expression on the development of cardiac hypertrophy, both Bmper +/− and Bmper +/+ sibling controls underwent transaortic constriction (TAC), followed by weekly echocardiography. While a deficit was identified in Bmper +/− mice at baseline, both anterior and posterior wall thicknesses increased after TAC, such that identical wall thicknesses were identified in Bmper +/− and Bmper +/+ mice 1–4 weeks after TAC. Notably, cardiac function (fractional shortening %) and histological evaluation revealed no differences between Bmper +/− and Bmper +/+ any time after TAC. These studies identify for the first time that Bmper expression plays a critical role in regulating cardiac muscle mass during development, and that Bmper regulates the development of hypertrophy in response to pressure overload in vivo.

scholarly journals Factors associated with skeletal muscle mass, sarcopenia, and sarcopenic obesity in older adults: a multi-continent study

2015 ◽  
Vol 7 (3) ◽  
pp. 312-321 ◽  
Author(s):  
Stefanos Tyrovolas ◽  
Ai Koyanagi ◽  
Beatriz Olaya ◽  
Jose Luis Ayuso-Mateos ◽  
Marta Miret ◽  
...  
Keyword(s):  
Older Adults ◽  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Sarcopenic Obesity ◽  
Factors Associated

The COX-2 pathway regulates growth of atrophied muscle via multiple mechanisms

2006 ◽  
Vol 290 (6) ◽  
pp. C1651-C1659 ◽  
Author(s):  
Brenda A. Bondesen ◽  
Stephen T. Mills ◽  
Grace K. Pavlath
Keyword(s):  
Muscle Mass ◽  
Muscle Regeneration ◽  
Muscle Growth ◽  
Cell Activity ◽  
Hindlimb Suspension ◽  
Normal Muscle ◽  
Cox 2 ◽  
Proliferation In Vitro

Loss of muscle mass occurs with disease, injury, aging, and inactivity. Restoration of normal muscle mass depends on myofiber growth, the regulation of which is incompletely understood. Cyclooxygenase (COX)-2 is one of two isoforms of COX that catalyzes the synthesis of prostaglandins, paracrine hormones that regulate diverse physiological and pathophysiological processes. Previously, we demonstrated that the COX-2 pathway regulates early stages of myofiber growth during muscle regeneration. However, whether the COX-2 pathway plays a common role in adult myofiber growth or functions specifically during muscle regeneration is unknown. Therefore, we examined the role of COX-2 during myofiber growth following atrophy in mice. Muscle atrophy was induced by hindlimb suspension (HS) for 2 wk, followed by a reloading period, during which mice were treated with either the COX-2-selective inhibitor SC-236 (6 mg·kg−1·day−1) or vehicle. COX-2 protein was expressed and SC-236 attenuated myofiber growth during reloading in both soleus and plantaris muscles. Attenuated myofiber growth in the soleus was associated with both decreased myonuclear addition and decreased inflammation, whereas neither of these processes mediated the effects of SC-236 on plantaris growth. In addition, COX-2−/− satellite cells exhibited impaired activation/proliferation in vitro, suggesting direct regulation of muscle cell activity by COX-2. Together, these data suggest that the COX-2 pathway plays a common regulatory role during various types of muscle growth via multiple mechanisms.

scholarly journals Inflammation and metabolism: the role of adiposity in sarcopenic obesity

2020 ◽  
Vol 79 (4) ◽  
pp. 435-447
Author(s):  
G. M. Lynch ◽  
C. H. Murphy ◽  
E. de Marco Castro ◽  
H. M. Roche
Keyword(s):  
Nutritional Status ◽  
Sarcopenic Obesity ◽  
Obesity Risk ◽  
Dietary Interventions ◽  
Double Burden ◽  
Metabolic Inflammation ◽  
Fat Composition ◽  
Dietary Components ◽  
Potential Impact

Sarcopenic obesity is characterised by the double burden of diminished skeletal muscle mass and the presence of excess adiposity. From a mechanistic perspective, both obesity and sarcopenia are associated with sub-acute, chronic pro-inflammatory states that impede metabolic processes, disrupting adipose and skeletal functionality, which may potentiate disease. Recent evidence suggests that there is an important cross-talk between metabolism and inflammation, which has shifted focus upon metabolic-inflammation as a key emerging biological interaction. Dietary intake, physical activity and nutritional status are important environmental factors that may modulate metabolic-inflammation. This paradigm will be discussed within the context of sarcopenic obesity risk. There is a paucity of data in relation to the nature and the extent to which nutritional status affects metabolic-inflammation in sarcopenic obesity. Research suggests that there may be scope for the modulation of sarcopenic obesity with alterations in diet. The potential impact of increasing protein consumption and reconfiguration of dietary fat composition in human dietary interventions are evaluated. This review will explore emerging data with respect to if and how different dietary components may modulate metabolic-inflammation, particularly with respect to adiposity, within the context of sarcopenic obesity.

scholarly journals Role of Muscle Mass and Muscle Quality in the Association Between Diabetes and Gait Speed

Diabetes Care ◽  
2012 ◽  
Vol 35 (8) ◽  
pp. 1672-1679 ◽  
Author(s):  
S. Volpato ◽  
L. Bianchi ◽  
F. Lauretani ◽  
F. Lauretani ◽  
S. Bandinelli ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Gait Speed ◽  
Muscle Quality
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