scholarly journals Exercise Training Protects against Atorvastatin-Induced Skeletal Muscle Dysfunction and Mitochondrial Dysfunction in the Skeletal Muscle of Rats

2020 ◽  
Vol 9 (7) ◽  
pp. 2292
Author(s):  
Dae Yun Seo ◽  
Jun-Won Heo ◽  
Mi-Hyun No ◽  
Su-Zi Yoo ◽  
Jeong Rim Ko ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Mitochondrial Dysfunction ◽  
Skeletal Muscles ◽  
The Other ◽  
Aerobic Exercise Training ◽  
Atherosclerotic Cardiovascular Disease ◽  
Ampk Phosphorylation ◽  
Gastrocnemius Muscles ◽  
White Gastrocnemius

Statins are used to prevent and treat atherosclerotic cardiovascular disease, but they also induce myopathy and mitochondrial dysfunction. Here, we investigated whether exercise training prevents glucose intolerance, muscle impairment, and mitochondrial dysfunction in the skeletal muscles of Wistar rats treated with atorvastatin (5 mg kg−1 day−1) for 12 weeks. The rats were assigned to the following three groups: the control (CON), atorvastatin-treated (ATO), and ATO plus aerobic exercise training groups (ATO+EXE). The ATO+EXE group exhibited higher glucose tolerance and forelimb strength and lower creatine kinase levels than the other groups. Mitochondrial respiratory and Ca2+ retention capacity was significantly lower in the ATO group than in the other groups, but exercise training protected against atorvastatin-induced impairment in both the soleus and white gastrocnemius muscles. The mitochondrial H2O2 emission rate was relatively higher in the ATO group and lower in the ATO+EXE group, in both the soleus and white gastrocnemius muscles, than in the CON group. In the soleus muscle, the Bcl-2, SOD1, SOD2, Akt, and AMPK phosphorylation levels were significantly higher in the ATO+EXE group than in the ATO group. In the white gastrocnemius muscle, the SOD2, Akt, and AMPK phosphorylation levels were significantly higher in the ATO+EXE group than in the ATO group. Therefore, exercise training might regulate atorvastatin-induced muscle damage, muscle fatigue, and mitochondrial dysfunction in the skeletal muscles.

scholarly journals Role of estrogen on skeletal muscle mitochondrial function in ovariectomized rats: a time course study in different fiber types

2014 ◽  
Vol 116 (7) ◽  
pp. 779-789 ◽  
Author(s):  
J. P. A. Cavalcanti-de-Albuquerque ◽  
I. C. Salvador ◽  
Eduarda Lopes Martins ◽  
D. Jardim-Messeder ◽  
J. P. S. Werneck-de-Castro ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Atp Synthesis ◽  
Ovariectomized Rats ◽  
Proton Leak ◽  
Fiber Types ◽  
Estrogen Replacement ◽  
Gastrocnemius Muscles ◽  
White Gastrocnemius

Postmenopausal women are prone to develop obesity and insulin resistance, which might be related to skeletal muscle mitochondrial dysfunction. In a rat model of ovariectomy (OVX), skeletal muscle mitochondrial function was examined at short- and long-term periods after castration. Mitochondrial parameters in the soleus and white gastrocnemius muscle fibers were analyzed. Three weeks after surgery, there were no differences in coupled mitochondrial respiration (ATP synthesis) with pyruvate, malate, and succinate; proton leak respiration; or mitochondrial reactive oxygen species production. However, after 3 wk of OVX, the soleus and white gastrocnemius muscles of the OVX animals showed a lower use of palmitoyl-carnitine and glycerol-phosphate substrates, respectively, and decreased peroxisome proliferator-activated receptor-γ coactivator-1α expression. Estrogen replacement reverted all of these phenotypes. Eight weeks after OVX, ATP synthesis was lower in the soleus and white gastrocnemius muscles of the OVX animals than in the sham-operated and estrogen-treated animals; however, when normalized by citrate synthase activity, these differences disappeared, indicating a lower muscle mitochondria content. No differences were observed in the proton leak parameter. Mitochondrial alterations did not impair the treadmill exercise capacity of the OVX animals. However, blood lactate levels in the OVX animals were higher after the physical test, indicating a compensatory extramitochondrial ATP synthesis system, but this phenotype was reverted by estrogen replacement. These results suggest early mitochondrial dysfunction related to lipid substrate use, which could be associated with the development of the overweight phenotype of ovariectomized animals.

Exercise training alleviates MCT1 and MCT4 reductions in heart and skeletal muscles of STZ-induced diabetic rats

2003 ◽  
Vol 94 (6) ◽  
pp. 2433-2438 ◽  
Author(s):  
Taisuke Enoki ◽  
Yuko Yoshida ◽  
Hideo Hatta ◽  
Arend Bonen
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Skeletal Muscles ◽  
Diabetic Rats ◽  
Monocarboxylate Transporter ◽  
Sedentary Control ◽  
Monocarboxylate Transporter 1

We compared the changes in monocarboxylate transporter 1 (MCT1) and 4 (MCT4) proteins in heart and skeletal muscles in sedentary control and streptozotocin (STZ)-induced diabetic rats (3 wk) and in trained (3 wk) control and STZ-induced diabetic animals. In nondiabetic animals, training increased MCT1 in the plantaris (+51%; P < 0.01) but not in the soleus (+9%) or the heart (+14%). MCT4 was increased in the plantaris (+48%; P < 0.01) but not in the soleus muscles of trained nondiabetic animals. In sedentary diabetic animals, MCT1 was reduced in the heart (−30%), and in the plantaris (−31%; P < 0.01) and soleus (−26%) muscles. MCT4 content was also reduced in sedentary diabetic animals in the plantaris (−52%; P < 0.01) and soleus (−25%) muscles. In contrast, in trained diabetic animals, MCT1 and MCT4 in heart and/or muscle were similar to those of sedentary, nondiabetic animals ( P > 0.05) but were markedly greater than in the sedentary diabetic animals [MCT1: plantaris +63%, soleus +51%, heart +51% ( P > 0.05); MCT4: plantaris +107%, soleus +17% ( P > 0.05)]. These studies have shown that 1) with STZ-induced diabetes, MCT1 and MCT4 are reduced in skeletal muscle and/or the heart and 2) exercise training alleviated these diabetes-induced reductions.

scholarly journals Cellular and Animal Models of Striated Muscle Laminopathies

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 291 ◽  
Author(s):  
Hannah A. Nicolas ◽  
Marie-Andrée Akimenko ◽  
Frédérique Tesson
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Molecular Mechanisms ◽  
Striated Muscle ◽  
Nuclear Lamina ◽  
The Other ◽  
Lamin A ◽  
Lmna Gene ◽  
Future Directions ◽  
Exon 10

The lamin A/C (LMNA) gene codes for nuclear intermediate filaments constitutive of the nuclear lamina. LMNA has 12 exons and alternative splicing of exon 10 results in two major isoforms—lamins A and C. Mutations found throughout the LMNA gene cause a group of diseases collectively known as laminopathies, of which the type, diversity, penetrance and severity of phenotypes can vary from one individual to the other, even between individuals carrying the same mutation. The majority of the laminopathies affect cardiac and/or skeletal muscles. The underlying molecular mechanisms contributing to such tissue-specific phenotypes caused by mutations in a ubiquitously expressed gene are not yet well elucidated. This review will explore the different phenotypes observed in established models of striated muscle laminopathies and their respective contributions to advancing our understanding of cardiac and skeletal muscle-related laminopathies. Potential future directions for developing effective treatments for patients with lamin A/C mutation-associated cardiac and/or skeletal muscle conditions will be discussed.

scholarly journals Home-based aerobic exercise training improves skeletal muscle oxidative metabolism in patients with metabolic myopathies

2016 ◽  
Vol 121 (3) ◽  
pp. 699-708 ◽  
Author(s):  
Simone Porcelli ◽  
Mauro Marzorati ◽  
Lucia Morandi ◽  
Bruno Grassi
Keyword(s):  
Skeletal Muscle ◽  
Infrared Spectroscopy ◽  
Exercise Training ◽  
Near Infrared Spectroscopy ◽  
Oxidative Metabolism ◽  
Near Infrared ◽  
Aerobic Training ◽  
Aerobic Exercise Training ◽  
Low Intensity ◽  
Home Based

Aerobic training can be effective in patients with mitochondrial myopathies (MM) and McArdle's disease (McA). The aim of the study was to use noninvasive functional evaluation methods, specifically aimed at skeletal muscle oxidative metabolism, to evaluate the effects of an aerobic exercise training (cycle ergometer, 12 wk, 4 days/wk, ∼65-70% of maximal heart rate) in 6 MM and 7 McA. Oxygen uptake and skeletal muscle vastus lateralis fractional O2 extraction by near-infrared spectroscopy were assessed during incremental and low-intensity constant work rate (CWR) exercises before (BEFORE) and at the end (AFTER) of training. Peak O2 uptake increased significantly with training both in MM [14.7 ± 1.2 vs. 17.6 ± 1.4 ml·kg−1·min−1 (mean ± SD)] and in McA (18.5 ± 1.8 ml·kg−1·min−1 vs. 21.6 ± 1.9). Peak skeletal muscle fractional O2 extraction increased with training both in MM (22.0 ± 6.7 vs. 32.6 ± 5.9%) and in McA (18.5 ± 6.2 vs. 37.2 ± 7.2%). During low-intensity CWR in both MM and McA: V̇o2 kinetics became faster in AFTER, but only in the patients with slow V̇o2 kinetics in BEFORE; the transient overshoot in fractional O2 extraction kinetics disappeared. The level of habitual physical activity was not higher 3 mo after training (FOLLOW-UP vs. PRE). In MM and McA patients a home-based aerobic training program significantly attenuated the impairment of skeletal muscle oxidative metabolism and improved variables associated with exercise tolerance. Our findings indicate that in MM and McA patients near-infrared spectroscopy and V̇o2 kinetics can effectively detect the functional improvements obtained by training.

scholarly journals Two Weeks of Smoking Cessation Reverse Cigarette Smoke-Induced Skeletal Muscle Atrophy and Mitochondrial Dysfunction in Mice

2020 ◽  
Author(s):  
Tom Tanjeko Ajime ◽  
Jef Serré ◽  
Rob C I Wüst ◽  
Guy Anselme Mpaka Messa ◽  
Chiel Poffé ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Smoking Cessation ◽  
Mitochondrial Dysfunction ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Skeletal Muscles ◽  
Skeletal Muscle Atrophy ◽  
Limb Muscle ◽  
Male Mice ◽  
And Function

Abstract Introduction Apart from its adverse effects on the respiratory system, cigarette smoking also induces skeletal muscle atrophy and dysfunction. Whether short-term smoking cessation can restore muscle mass and function is unknown. We, therefore, studied the impact of 1- and 2-week smoking cessation on skeletal muscles in a mouse model. Methods Male mice were divided into four groups: Air-exposed (14 weeks); cigarette smoke (CS)-exposed (14 weeks); CS-exposed (13 weeks) followed by 1-week cessation; CS-exposed (12 weeks) followed by 2 weeks cessation to examine exercise capacity, physical activity levels, body composition, muscle function, capillarization, mitochondrial function and protein expression in the soleus, plantaris, and diaphragm muscles. Results CS-induced loss of body and muscle mass was significantly improved within 1 week of cessation due to increased lean and fat mass. Mitochondrial respiration and protein levels of the respiratory complexes in the soleus were lower in CS-exposed mice, but similar to control values after 2 weeks of cessation. Exposing isolated soleus muscles to CS extracts reduced mitochondrial respiration that was reversed after removing the extract. While physical activity was reduced in all groups, exercise capacity, limb muscle force, fatigue resistance, fiber size and capillarization, and diaphragm cytoplasmic HIF-1α were unaltered by CS-exposure. However, CS-induced diaphragm atrophy and increased capillary density were not seen after 2 weeks of smoking cessation. Conclusion In male mice, 2 weeks of smoking cessation reversed smoking-induced mitochondrial dysfunction, limb muscle mass loss, and diaphragm muscle atrophy, highlighting immediate benefits of cessation on skeletal muscles. Implications Our study demonstrates that CS-induced skeletal muscle mitochondrial dysfunction and atrophy are significantly improved by 2 weeks of cessation in male mice. We show for the first time that smoking cessation as short as 1 to 2 weeks is associated with immediate beneficial effects on skeletal muscle structure and function with the diaphragm being particularly sensitive to CS-exposure and cessation. This could help motivate smokers to quit smoking as early as possible. The knowledge that smoking cessation has potential positive extrapulmonary effects is particularly relevant for patients referred to rehabilitation programs and those admitted to hospitals suffering from acute or chronic muscle deterioration yet struggling with smoking cessation.

scholarly journals Molecular Adaptations to Aerobic Exercise Training in Skeletal Muscle of Older Women

2010 ◽  
Vol 65A (11) ◽  
pp. 1201-1207 ◽  
Author(s):  
A. R. Konopka ◽  
M. D. Douglass ◽  
L. A. Kaminsky ◽  
B. Jemiolo ◽  
T. A. Trappe ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Older Women ◽  
Aerobic Exercise Training

The responsiveness of skeletal muscle mRNAs to aerobic exercise training is not blunted in COPD

2019 ◽  
Author(s):  
Lorna Latimer ◽  
Despina Constantin ◽  
Bhavesh Popat ◽  
Linzy Houchen-Wolloff ◽  
Dumitru Constantin-Teodosiu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Aerobic Exercise Training
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