scholarly journals Preserved Skeletal Muscle Mitochondrial Function, Redox State, Inflammation and Mass in Obese Mice with Chronic Heart Failure

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3393
Author(s):  
Gianluca Gortan Cappellari ◽  
Aneta Aleksova ◽  
Matteo Dal Ferro ◽  
Antonio Cannatà ◽  
Annamaria Semolic ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Insulin Signaling ◽  
Redox State ◽  
Excess Body Weight ◽  
Ros Production ◽  
Atp Production ◽  
Mitochondrial Ros ◽  
Per Se ◽  
Muscle Mass Loss

Background: Skeletal muscle (SM) mitochondrial dysfunction, oxidative stress, inflammation and muscle mass loss may worsen prognosis in chronic heart failure (CHF). Diet-induced obesity may also cause SM mitochondrial dysfunction as well as oxidative stress and inflammation, but obesity per se may be paradoxically associated with high SM mass and mitochondrial adenosine triphosphate (ATP) production, as well as with enhanced survival in CHF. Methods: We investigated interactions between myocardial infarction(MI)-induced CHF and diet-induced obesity (12-wk 60% vs. standard 10% fat) in modulating gastrocnemius muscle (GM) mitochondrial ATP and tissue superoxide generation, oxidized glutathione (GSSG), cytokines and insulin signalling activation in 10-wk-old mice in the following groups: lean sham-operated, lean CHF (LCHF), obese CHF (ObCHF; all n = 8). The metabolic impact of obesity per se was investigated by pair-feeding ObCHF to standard diet with stabilized excess body weight until sacrifice at wk 8 post-MI. Results: Compared to sham, LCHF had low GM mass, paralleled by low mitochondrial ATP production and high mitochondrial reative oxygen species (ROS) production, pro-oxidative redox state, pro-inflammatory cytokine changes and low insulin signaling (p < 0.05). In contrast, excess body weight in pair-fed ObCHF was associated with high GM mass, preserved mitochondrial ATP and mitochondrial ROS production, unaltered redox state, tissue cytokines and insulin signaling (p = non significant vs. Sham, p < 0.05 vs. LCHF) despite higher superoxide generation from non-mitochondrial sources. Conclusions: CHF disrupts skeletal muscle mitochondrial function in lean rodents with low ATP and high mitochondrial ROS production, associated with tissue pro-inflammatory cytokine profile, low insulin signaling and muscle mass loss. Following CHF onset, obesity per se is associated with high skeletal muscle mass and preserved tissue ATP production, mitochondrial ROS production, redox state, cytokines and insulin signaling. These paradoxical and potentially favorable obesity-associated metabolic patterns could contribute to reported obesity-induced survival advantage in CHF.

scholarly journals Racial Differences in Relative Skeletal Muscle Mass Loss During Diet-Induced Weight Loss in Women

Obesity ◽  
2018 ◽  
Vol 26 (8) ◽  
pp. 1255-1260 ◽  
Author(s):  
Gary R. Hunter ◽  
David R. Bryan ◽  
Juliano H. Borges ◽  
M. David Diggs ◽  
Stephen J. Carter
Keyword(s):  
Skeletal Muscle ◽  
Weight Loss ◽  
Mass Loss ◽  
Racial Differences ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Mass Loss

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.

Denervation-induced skeletal muscle atrophy is associated with increased mitochondrial ROS production

2007 ◽  
Vol 293 (3) ◽  
pp. R1159-R1168 ◽  
Author(s):  
Florian L. Muller ◽  
Wook Song ◽  
Youngmok C. Jang ◽  
Yuhong Liu ◽  
Marian Sabia ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Muscle Atrophy ◽  
Common Factor ◽  
Skeletal Muscle Atrophy ◽  
Ros Generation ◽  
Ros Production ◽  
Muscle Mitochondria ◽  
Mitochondrial Ros ◽  
Hindlimb Muscle ◽  
Old Mice

Reactive oxygen species (ROS), especially mitochondrial ROS, are postulated to play a significant role in muscle atrophy. We report a dramatic increase in mitochondrial ROS generation in three conditions associated with muscle atrophy: in aging, in mice lacking CuZn-SOD ( Sod1−/−), and in the neurodegenerative disease, amyotrophic lateral sclerosis (ALS). ROS generation in muscle mitochondria is nearly threefold higher in 28- to 32-mo-old than in 10-mo-old mice and is associated with a 30% loss in gastrocnemius mass. In Sod1−/− mice, muscle mitochondrial ROS production is increased >100% in 20-mo compared with 5-mo-old mice along with a >50% loss in muscle mass. ALS G93A mutant mice show a 75% loss of muscle mass during disease progression and up to 12-fold higher muscle mitochondrial ROS generation. In a second ALS mutant model, H46RH48Q mice, ROS production is approximately fourfold higher than in control mice and is associated with a less dramatic loss (30%) in muscle mass. Thus ROS production is strongly correlated with the extent of muscle atrophy in these models. Because each of the models of muscle atrophy studied are associated to some degree with a loss of innervation, we were interested in determining whether denervation plays a role in ROS generation in muscle mitochondria isolated from hindlimb muscle following surgical sciatic nerve transection. Seven days postdenervation, muscle mitochondrial ROS production increased nearly 30-fold. We conclude that enhanced generation of mitochondrial ROS may be a common factor in the mechanism underlying denervation-induced atrophy.

scholarly journals Absence of Physiological Calcium Transients Triggers Mitochondrial ROS Production in Skeletal Muscle Following Denervation

2016 ◽  
Vol 110 (3) ◽  
pp. 311a
Author(s):  
Chehade Karam ◽  
Jianxun Yi ◽  
Carlos Manno ◽  
Heping Cheng ◽  
Jianjie Ma ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Calcium Transients ◽  
Ros Production ◽  
Mitochondrial Ros

scholarly journals Mitochondrial-targeted antioxidants protect skeletal muscle against immobilization-induced muscle atrophy

2011 ◽  
Vol 111 (5) ◽  
pp. 1459-1466 ◽  
Author(s):  
Kisuk Min ◽  
Ashley J. Smuder ◽  
Oh-sung Kwon ◽  
Andreas N. Kavazis ◽  
Hazel H. Szeto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Muscle Fibers ◽  
Skeletal Muscle Atrophy ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Protease Activation ◽  
Limb Immobilization

Prolonged periods of muscular inactivity (e.g., limb immobilization) result in skeletal muscle atrophy. Although it is established that reactive oxygen species (ROS) play a role in inactivity-induced skeletal muscle atrophy, the cellular pathway(s) responsible for inactivity-induced ROS production remain(s) unclear. To investigate this important issue, we tested the hypothesis that elevated mitochondrial ROS production contributes to immobilization-induced increases in oxidative stress, protease activation, and myofiber atrophy in skeletal muscle. Cause-and-effect was determined by administration of a novel mitochondrial-targeted antioxidant (SS-31) to prevent immobilization-induced mitochondrial ROS production in skeletal muscle fibers. Compared with ambulatory controls, 14 days of muscle immobilization resulted in significant muscle atrophy, along with increased mitochondrial ROS production, muscle oxidative damage, and protease activation. Importantly, treatment with a mitochondrial-targeted antioxidant attenuated the inactivity-induced increase in mitochondrial ROS production and prevented oxidative stress, protease activation, and myofiber atrophy. These results support the hypothesis that redox disturbances contribute to immobilization-induced skeletal muscle atrophy and that mitochondria are an important source of ROS production in muscle fibers during prolonged periods of inactivity.

scholarly journals Loss of Skeletal Muscle Mass Affects the Incidence of Minimal Hepatic Encephalopathy: A Case Control Study

2020 ◽  
Author(s):  
Masakuni Tateyama ◽  
Hideaki Naoe ◽  
Motohiko Tanaka ◽  
Kentaro Tanaka ◽  
Satoshi Narahara ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Mass Loss ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Lumbar Vertebra ◽  
Minimal Hepatic Encephalopathy ◽  
Skeletal Muscle Index ◽  
Muscle Mass Loss

Abstract Background: Sarcopenia is a syndrome characterized by progressive and systemic decreases in skeletal muscle mass and muscle strength. The influence or prognosis of various liver diseases in this condition have been widely investigated, but little is known about whether sarcopenia and/or muscle mass loss are related to minimal hepatic encephalopathy.Methods: To clarify the relationship between minimal hepatic encephalopathy and sarcopenia and/or muscle mass loss in patients with liver cirrhosis. Ninety-nine patients with liver cirrhosis were enrolled. Minimal hepatic encephalopathy was diagnosed by a neuropsychiatric test. Skeletal mass index was calculated by dividing muscle area at the third lumbar vertebra by the square of height in meters.Results: MHE was detected in 48 cases (48.5%) and sarcopenia in 6 cases (6.1%). Patients were divided into two groups, with or without MHE. Comparing groups, no significant differences were seen in serum ammonia concentration or rate of sarcopenia. Skeletal muscle index was smaller in patients with minimal hepatic encephalopathy (46.4 cm2/m2) than in those without (51.2 cm2/m2, P = 0.027). Skeletal muscle index represented a predictive factor related to minimal hepatic encephalopathy (<50 cm2/m2; odds ratio 0.300, P = 0.002).Conclusions: Muscle mass loss was related to minimal hepatic encephalopathy, although sarcopenia was not. Measurement of muscle mass loss might be useful to predict MHE.

scholarly journals Loss of skeletal muscle mass affects the incidence of minimal hepatic encephalopathy: A case control study

2020 ◽  
Author(s):  
Masakuni Tateyama ◽  
Hideaki Naoe ◽  
Motohiko Tanaka ◽  
Kentaro Tanaka ◽  
Satoshi Narahara ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Hepatic Encephalopathy ◽  
Mass Loss ◽  
Muscle Mass ◽  
Odds Ratio ◽  
Skeletal Muscle Mass ◽  
Psoas Muscle ◽  
Minimal Hepatic Encephalopathy ◽  
Muscle Area ◽  
Muscle Mass Loss

Abstract Background: Sarcopenia is a syndrome characterized by progressive and systemic decreases in skeletal muscle mass and muscle strength. The influence or prognosis of various liver diseases in this condition have been widely investigated, but little is known about whether sarcopenia and/or muscle mass loss are related to minimal hepatic encephalopathy (MHE).Methods: To clarify the relationship between MHE and sarcopenia and/or muscle mass loss in patients with liver cirrhosis.Methods: Ninety-nine patients with liver cirrhosis were enrolled. MHE was diagnosed by a neuropsychiatric test. Skeletal mass index (SMI) and Psoas muscle index (PMI) were calculated by dividing skeletal muscle area and psoas muscle area at the third lumbar vertebra by the square of height in meters, respectively, to evaluate muscle volume.Results: This study enrolled 99 patients (61 males, 38 females). MHE was detected in 48 cases (48.5%) and sarcopenia in 6 cases (6.1%). Patients were divided into two groups, with or without MHE. Comparing groups, no significant differences were seen in serum ammonia concentration or rate of sarcopenia. SMI was smaller in patients with MHE (46.4 cm2/m2) than in those without (51.2 cm2/m2, P = 0.027). Similarly, PMI was smaller in patients with MHE (4.24 cm2/m2) than in those without (5.53 cm2/m2, P = 0.003). Skeletal muscle volume, which is represented by SMI or PMI was a predictive factor related to MHE (SMI ≥ 50 cm2/m2; odds ratio 0.300, P = 0.002, PMI ≥ 4.3 cm2/m2; odds ratio 0.192, P = 0.001).Conclusions: Muscle mass loss was related to minimal hepatic encephalopathy, although sarcopenia was not. Measurement of muscle mass loss might be useful to predict MHE.

scholarly journals Skeletal muscle mass loss and dose‐limiting toxicities in metastatic colorectal cancer patients

2019 ◽  
Vol 10 (4) ◽  
pp. 803-813 ◽  
Author(s):  
Sophie Kurk ◽  
Petra Peeters ◽  
Rebecca Stellato ◽  
B. Dorresteijn ◽  
Pim Jong ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Skeletal Muscle ◽  
Mass Loss ◽  
Metastatic Colorectal Cancer ◽  
Cancer Patients ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Mass Loss ◽  
Colorectal Cancer Patients
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