Low intensity training decreases markers of oxidative stress in skeletal muscle of mdx mice

2007 ◽  
Vol 43 (1) ◽  
pp. 145-154 ◽  
Author(s):  
Jan J. Kaczor ◽  
Julie E. Hall ◽  
Eric Payne ◽  
Mark A. Tarnopolsky
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Mdx Mice ◽  
Low Intensity ◽  
Markers Of Oxidative Stress ◽  
Intensity Training

scholarly journals Role of miR-200c in Myogenic Differentiation Impairment via p66Shc: Implication in Skeletal Muscle Regeneration of Dystrophic mdx Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Marco D’Agostino ◽  
Alessio Torcinaro ◽  
Luca Madaro ◽  
Lorenza Marchetti ◽  
Sara Sileno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Myogenic Differentiation ◽  
Dystrophin Gene ◽  
Muscle Differentiation ◽  
Skeletal Muscle Regeneration ◽  
Mdx Mice ◽  
Pathological Disease ◽  
Dependent Mechanism

Duchenne muscular dystrophy (DMD) is a genetic disease associated with mutations of Dystrophin gene that regulate myofiber integrity and muscle degeneration, characterized by oxidative stress increase. We previously published that reactive oxygen species (ROS) induce miR-200c that is responsible for apoptosis and senescence. Moreover, we demonstrated that miR-200c increases ROS production and phosphorylates p66Shc in Ser-36. p66Shc plays an important role in muscle differentiation; we previously showed that p66Shc−/− muscle satellite cells display lower oxidative stress levels and higher proliferation rate and differentiated faster than wild-type (wt) cells. Moreover, myogenic conversion, induced by MyoD overexpression, is more efficient in p66Shc−/− fibroblasts compared to wt cells. Herein, we report that miR-200c overexpression in cultured myoblasts impairs skeletal muscle differentiation. Further, its overexpression in differentiated myotubes decreases differentiation indexes. Moreover, anti-miR-200c treatment ameliorates myogenic differentiation. In keeping, we found that miR-200c and p66Shc Ser-36 phosphorylation increase in mdx muscles. In conclusion, miR-200c inhibits muscle differentiation, whereas its inhibition ameliorates differentiation and its expression levels are increased in mdx mice and in differentiated human myoblasts of DMD. Therefore, miR-200c might be responsible for muscle wasting and myotube loss, most probably via a p66Shc-dependent mechanism in a pathological disease such as DMD.

scholarly journals Markers of oxidative stress in the skeletal muscle of patients on haemodialysis

2007 ◽  
Vol 22 (4) ◽  
pp. 1177-1183 ◽  
Author(s):  
A. V. Crowe ◽  
A. McArdle ◽  
F. McArdle ◽  
D. M. Pattwell ◽  
G. M. Bell ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Markers Of Oxidative Stress

The effects of 3 weeks of oral glutathione supplementation on whole body insulin sensitivity in obese males with and without type 2 diabetes: A randomized trial

2021 ◽  
Author(s):  
Stine D. Søndergård ◽  
Ida Cintin ◽  
Anja Birk Kuhlman ◽  
Thomas Morville ◽  
Marie Louise Bergmann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Oxidation Product ◽  
Emission Rate ◽  
Whole Body ◽  
Markers Of Oxidative Stress ◽  
Obese Subjects

The effect of oral glutathione (GSH) supplementation was studied in obese subjects with and without type 2 diabetes (T2DM) on measures of glucose homeostasis and markers of oxidative stress. Twenty subjects (10 patients with T2DM and 10 obese subjects) were recruited for the study, and randomized in a double-blinded placebo-controlled manner to consume either 1000mg GSH per day or placebo for three weeks. Before and after the 3 weeks insulin sensitivity was measured with the hyperinsulinemic-euglycemic clamp and a muscle biopsy was obtained to measure GSH and skeletal muscle mitochondrial hydrogen peroxide (H2O2) emission rate. Whole body insulin sensitivity increased significantly in the GSH group. Skeletal muscle GSH was numerically increased (app. 19%) in the GSH group, no change was seen in GSH to glutathione disulfide (GSSG) ratio. Skeletal muscle mitochondrial H2O2 emission rate did not change in response to the intervention and neither did the urinary excretion of the RNA oxidation product 8-oxo-7,8-dihydroguanosine (8-oxoGuo) or the DNA oxidation product 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG ), although 8-oxodG decreased as a main effect of time. Oral GSH supplementation improves insulin sensitivity in obese subjects with and without T2DM, although it does not alter markers of oxidative stress. The study has been registered in clinicaltrials.gov (NCT02948673). Novelty bullets: • Reduced glutathione supplementation increases insulin sensitivity in obese subjects with and without type 2 diabetes • H2O2 emission rate from skeletal muscle mitochondria was not affected by glutathione supplementation

scholarly journals Impact of Modality and Intensity of Early Exercise Training on Ventricular Remodeling after Myocardial Infarction

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Diego Fernando Batista ◽  
Bertha Furlan Polegato ◽  
Renata Candido da Silva ◽  
Renan Turini Claro ◽  
Paula Shmidt Azevedo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Exercise Training ◽  
High Intensity ◽  
Interval Training ◽  
High Intensity Interval Training ◽  
Energetic Metabolism ◽  
Low Intensity ◽  
High Intensity Interval ◽  
Intensity Training

The objective of this study was to analyze the impact of different modalities and intensities of exercise training on cardiac remodeling started early after experimental myocardial infarction (MI). Male Wistar rats, weighing 200–250 g, were subjected to experimental MI. After 5 days, the animals were allocated into three experimental groups and observed for three months: S (sedentary control animals), C (animals subjected to continuous low-intensity training), and HIT (animals subjected to high-intensity interval training). Low-intensity exercise training was performed at a treadmill speed corresponding to 40% VO2 max, which was kept unchanged throughout the entire session (i.e., continuous low-intensity training). High-intensity interval training was performed in such a way that rats run during 3 min at 60% VO2 max, followed by 4-minute intervals at 85% VO2 max (i.e., high-intensity interval training). After the follow-up period, we studied hypertrophy and ventricular geometry, functional alterations in vivo and in vitro, oxidative stress, apoptosis, and cardiac energetic metabolism. Our data showed that both high-intensity interval and continuous low-intensity modalities improved cardiac energetic metabolism variables in comparison with sedentary infarcted animals. In addition, high-intensity interval training decreased cardiac oxidative stress, associated with improved diastolic function. On the other hand, the continuous low-intensity group showed impairment of cardiac function. Therefore, altogether, our data suggest that high-intensity interval training could be the best modality for early physical exercise after MI and should be better studied in this clinical scenario.

Recovery of Damaged Skeletal Muscle in mdx Mice through Low-intensity Endurance Exercise

2013 ◽  
Vol 35 (01) ◽  
pp. 19-27 ◽  
Author(s):  
M. Frinchi ◽  
F. Macaluso ◽  
A. Licciardi ◽  
V. Perciavalle ◽  
M. Coco ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Mdx Mice ◽  
Low Intensity

Melatonin: a novel strategy for prevention of obesity and fat accumulation in peripheral organs through the improvements of circadian rhythms and antioxidative capacity

2020 ◽  
Vol 3 (1) ◽  
pp. 58-76 ◽  
Author(s):  
Bohan Rong ◽  
Qiong Wu ◽  
Chao Sun
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Circadian Rhythms ◽  
Regulatory Mechanisms ◽  
Antioxidative Capacity ◽  
Unicellular Alga ◽  
Peripheral Tissues ◽  
Peripheral Organs ◽  
Regulatory Effects ◽  
Novel Strategy

Melatonin is a well-known molecule for its involvement in circadian rhythm regulation and its contribution to protection against oxidative stress in organisms including unicellular alga, animals and plants. Currently, the bio-regulatory effects of melatonin on the physiology of various peripheral tissues have drawn a great attention of scientists. Although melatonin was previously defined as a neurohormone secreted from pineal gland, recently it has been identified that virtually, every cell has the capacity to synthesize melatonin and the locally generated melatonin has multiple pathophysiological functions, including regulations of obesity and metabolic syndromes. Herein, we focus on the effects of melatonin on fat deposition in various peripheral organs/tissues. The two important regulatory mechanisms related to the topic, i.e., the improvements of circadian rhythms and antioxidative capacity will be thoroughly discussed since they are linked to several biomarkers involved in obesity and energy imbalance, including metabolism and immunity. Furthermore, several other functions of melatonin which may serve to prevent or promote obesity and energy dysmetabolism-induced pathological states are also addressed. The organs of special interest include liver, pancreas, skeletal muscle, adipose tissue and the gut microbiota.

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