scholarly journals Exploring the Impact of Obesity on Skeletal Muscle Function in Older Age

2020 ◽  
Vol 7 ◽  
Author(s):  
Paul T. Morgan ◽  
Benoit Smeuninx ◽  
Leigh Breen
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Weight Bearing ◽  
Research Field ◽  
Older Age ◽  
Older Individuals ◽  
And Function ◽  
The Impact

Sarcopenia is of important clinical relevance for loss of independence in older adults. The prevalence of obesity in combination with sarcopenia (“sarcopenic-obesity”) is increasing at a rapid rate. However, whilst the development of sarcopenia is understood to be multi-factorial and harmful to health, the role of obesity from a protective and damaging perspective on skeletal muscle in aging, is poorly understood. Specifically, the presence of obesity in older age may be accompanied by a greater volume of skeletal muscle mass in weight-bearing muscles compared with lean older individuals, despite impaired physical function and resistance to anabolic stimuli. Collectively, these findings support a potential paradox in which obesity may protect skeletal muscle mass in older age. One explanation for these paradoxical findings may be that the anabolic response to weight-bearing activity could be greater in obese vs. lean older individuals due to a larger mechanical stimulus, compensating for the heightened muscle anabolic resistance. However, it is likely that there is a complex interplay between muscle, adipose, and external influences in the aging process that are ultimately harmful to health in the long-term. This narrative briefly explores some of the potential mechanisms regulating changes in skeletal muscle mass and function in aging combined with obesity and the interplay with sarcopenia, with a particular focus on muscle morphology and the regulation of muscle proteostasis. In addition, whilst highly complex, we attempt to provide an updated summary for the role of obesity from a protective and damaging perspective on muscle mass and function in older age. We conclude with a brief discussion on treatment of sarcopenia and obesity and a summary of future directions for this research field.

scholarly journals FRI0384 BODY COMPOSITION AS A MEDIATOR IN THE RELATIONSHIP BETWEEN PHYSICAL ACTIVITY AND PHYSICAL FUNCTION IN LOWER-LIMB OSTEOARTHRITIS: RESULTS FROM THE KHOALA COHORT

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 789.1-790 ◽  
Author(s):  
M. Wieczorek ◽  
C. Rotonda ◽  
J. Sellam ◽  
F. Guillemin ◽  
A. C. Rat
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Muscle Mass ◽  
Fat Mass ◽  
Skeletal Muscle Mass ◽  
Weight Bearing ◽  
Fat Mass Index ◽  
Mediating Role ◽  
Skeletal Muscle Mass Index

Background:Many trials investigated the beneficial effect of physical activity (PA) on physical function (PF) in people with osteoarthritis (OA), but factors involved in this relationship are poorly understood. Considering the link between OA and obesity and obesity-related disorders, body composition (BC) could be one of these factors.Objectives:To examine the relationships between baseline components of PA and 5-year PF scores, considering BC variables measured at 3 years as potential mediators in theses associations (Figure).Methods:We used data from the KHOALA cohort, a French population-based multicenter cohort of 878 patients with symptomatic knee and/or hip OA, aged between 40 and 75 years old. Baseline PA intensity (Metabolic Equivalent of Task, MET), frequency (times/week), duration (hours/week) and type (weight-bearing or not) were assessed by the Modifiable Activity Questionnaire. PF was measured with the WOMAC questionnaire at 5 years (higher scores = greater functional limitations).Skeletal muscle mass (grams) and fat mass (grams) were measured by dual X-ray absorptiometry (DXA) in 358 patients at 3 years. Fat mass index (kg/m2), appendicular fat mass (kg), % of fat mass, lean mass index (kg/m2), appendicular muscle mass (kg), skeletal muscle mass index (kg/m2or %) were calculated based on DXA data. Sarcopenia was defined according to the FNIH Sarcopenia Project recommendations.A causal mediation analysis was used to highlight the mediating role of BC variables. Bivariate analyses (multiple linear and logistic regressions) were performed to select the variables of interest. Separate generalized linear models were used to describe the relationships between PA components, PF and selected BC variables. Unadjusted and adjusted for baseline confounders (age, gender, number of comorbidities, disease duration, mental health and vitality scores) models were ran.Results:A 1-MET increase in baseline PA intensity was significantly associated with an improvement in PF at 5 years (-3 points). Weight-bearing PA was also significantly associated with better PF scores (-5 points).A 1-MET-increase in PA intensity at baseline was associated with a subsequent decrease at 3 years in fat mass index (-0.86 k/m2), an increase in skeletal muscle mass index (≥ 6%), and a decrease in % of fat mass (-2%). Non-weight-bearing PA was significantly associated with a decrease in fat mass index (-2.5 kg/m2).A 1-point increase in PF score was associated with a reduction in skeletal muscle mass index (calculated from body mass index, -0.3%) and an increase in skeletal muscle mass index (calculated from height, +3 kg/m2). The presence of sarcopenia was significantly associated with a degradation of PF (+7 points).Crude analyses indicated that 20.4% of the effect of baseline PA intensity on PF scores at 5 years was mediated by skeletal muscle mass index (calculated from height), 23.2% by fat mass index and 26.6% by % of fat mass. Similarly, 19.3% of the effect of baseline PA type on PF scores at 5 years was mediated by fat mass index and 15.1% by % of fat mass. After adjustment, we found no longer evidence of a mediating role of BC variables in these associations.Conclusion:We found significant associations between a 1-MET increase in PA intensity, weight-bearing PA at baseline and improvement in PF at 5 years, without any mediating role of BC variables. Further studies are needed to better understand the factors involved in these associations, especially psychosocial variables.Disclosure of Interests:Maud Wieczorek: None declared, Christine Rotonda: None declared, Jérémie SELLAM: None declared, Francis Guillemin Grant/research support from: Francis Guillemin received a grant from Expanscience paid to his institution., Anne-Christine Rat: None declared

Activation of the CRF 2 receptor modulates skeletal muscle mass under physiological and pathological conditions

2003 ◽  
Vol 285 (4) ◽  
pp. E889-E898 ◽  
Author(s):  
Richard T. Hinkle ◽  
Elizabeth Donnelly ◽  
David B. Cody ◽  
Steven Samuelsson ◽  
Jana S. Lange ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Nerve Damage ◽  
Skeletal Muscle Atrophy ◽  
Function Loss ◽  
Selective Agonists ◽  
And Function ◽  
First Time

Two receptors activated by the corticotropin-releasing factor (CRF) family of peptides have been identified, the CRF 1 receptor (CRF1R) and the CRF 2 receptor (CRF2R). Of these, the CRF2R is expressed in skeletal muscle. To understand the role of the CRF2R in skeletal muscle, we utilized CRFR knockout mice and CRF2R-selective agonists to modulate nerve damage and corticosteroid- and disuse-induced skeletal muscle atrophy in mice. These analyses demonstrated that activation of the CRF2R decreased nerve damage and corticosteroid- and disuse-induced skeletal muscle mass and function loss. In addition, selective activation of the CRF2R increased nonatrophy skeletal muscle mass. Thus we describe for the first time a novel activity of the CRF2R, modulation of skeletal muscle mass.

scholarly journals Recent advances and future avenues in understanding the role of adipose tissue cross talk in mediating skeletal muscle mass and function with ageing

GeroScience ◽  
2021 ◽  
Author(s):  
Andrew Wilhelmsen ◽  
Kostas Tsintzas ◽  
Simon W. Jones
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Muscle Mass ◽  
Extracellular Vesicles ◽  
Cross Talk ◽  
Skeletal Muscle Mass ◽  
Activity Level ◽  
Age Related ◽  
And Function

AbstractSarcopenia, broadly defined as the age-related decline in skeletal muscle mass, quality, and function, is associated with chronic low-grade inflammation and an increased likelihood of adverse health outcomes. The regulation of skeletal muscle mass with ageing is complex and necessitates a delicate balance between muscle protein synthesis and degradation. The secretion and transfer of cytokines, long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), both discretely and within extracellular vesicles, have emerged as important communication channels between tissues. Some of these factors have been implicated in regulating skeletal muscle mass, function, and pathologies and may be perturbed by excessive adiposity. Indeed, adipose tissue participates in a broad spectrum of inter-organ communication and obesity promotes the accumulation of macrophages, cellular senescence, and the production and secretion of pro-inflammatory factors. Pertinently, age-related sarcopenia has been reported to be more prevalent in obesity; however, such effects are confounded by comorbidities and physical activity level. In this review, we provide evidence that adiposity may exacerbate age-related sarcopenia and outline some emerging concepts of adipose-skeletal muscle communication including the secretion and processing of novel myokines and adipokines and the role of extracellular vesicles in mediating inter-tissue cross talk via lncRNAs and miRNAs in the context of sarcopenia, ageing, and obesity. Further research using advances in proteomics, transcriptomics, and techniques to investigate extracellular vesicles, with an emphasis on translational, longitudinal human studies, is required to better understand the physiological significance of these factors, the impact of obesity upon them, and their potential as therapeutic targets in combating muscle wasting.

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.

scholarly journals Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass

2020 ◽  
Vol 21 (5) ◽  
pp. 1628 ◽  
Author(s):  
Keisuke Hitachi ◽  
Masashi Nakatani ◽  
Shiori Funasaki ◽  
Ikumi Hijikata ◽  
Mizuki Maekawa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Skeletal Muscle Mass ◽  
Muscle Size ◽  
Skeletal Muscle Atrophy ◽  
Myostatin Gene ◽  
Expression Levels ◽  
Non Coding Rnas

Skeletal muscle is a highly plastic organ that is necessary for homeostasis and health of the human body. The size of skeletal muscle changes in response to intrinsic and extrinsic stimuli. Although protein-coding RNAs including myostatin, NF-κβ, and insulin-like growth factor-1 (IGF-1), have pivotal roles in determining the skeletal muscle mass, the role of long non-coding RNAs (lncRNAs) in the regulation of skeletal muscle mass remains to be elucidated. Here, we performed expression profiling of nine skeletal muscle differentiation-related lncRNAs (DRR, DUM1, linc-MD1, linc-YY1, LncMyod, Neat1, Myoparr, Malat1, and SRA) and three genomic imprinting-related lncRNAs (Gtl2, H19, and IG-DMR) in mouse skeletal muscle. The expression levels of these lncRNAs were examined by quantitative RT-PCR in six skeletal muscle atrophy models (denervation, casting, tail suspension, dexamethasone-administration, cancer cachexia, and fasting) and two skeletal muscle hypertrophy models (mechanical overload and deficiency of the myostatin gene). Cluster analyses of these lncRNA expression levels were successfully used to categorize the muscle atrophy models into two sub-groups. In addition, the expression of Gtl2, IG-DMR, and DUM1 was altered along with changes in the skeletal muscle size. The overview of the expression levels of lncRNAs in multiple muscle atrophy and hypertrophy models provides a novel insight into the role of lncRNAs in determining the skeletal muscle mass.

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