scholarly journals PO-203 Across generations maternal exercise in hypoxic environment on mitochondrial biosynthetic factors in rat skeletal muscle

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Helong Quan ◽  
Yong Zhang ◽  
Zhouxiang Shan ◽  
Lei Ji ◽  
Changhyun Lim ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Mitochondrial Biogenesis ◽  
Skeletal Muscles ◽  
Related Protein ◽  
Three Generations ◽  
Hypoxic Environment ◽  
Protein Expressions ◽  
Maternal Exercise ◽  
Related Proteins

Objective Environmental and maternal exercise experienced even during the very earliest stages of life has the potential to cause developmental changes.The growing evidence demonstrated that diverse environmental stressors affect offspring in variousaspects in early stage of lifeand can be transmitted directly or indirectly by both parental lines.The purpose of the present study was to investigate the effect of across generations maternal exercise training under the hypoxic environment on mitochondrial biogenesis and angiogenesis related protein expressions of skeletal muscle in offspring ofmultiple generations. Methods The experimental groups were divided into four groups as NCON (control in normoxia), NEXE (exercise in normoxia), HCON (control under hypoxia), HEXE (exercise under hypoxia), and studied for three generations. Exercise groups were run on animal treadmill at 60%-75% VO2maxfor one hour per day, five times per week for 10 weeks (seven weeks before conception and during conception for three weeks). Animals were sacrificed at a given time table and assayed mitochondrial biogenesis and angiogenesis related protein expressions using western blotting. Results The major findings from the present study were firstly, maternal exercise training before and during conception under hypoxic environment increase in mitochondrial biogenesis and angiogenesis related proteins expressions in both maternal and offspring skeletal muscles, secondly, long term of exposure to hypoxic environment without exercise training increase in mitochondrial biogenesis and angiogenesis related proteins expressions in offspring skeletal muscles, and further increased when exercise training performed at hypoxic environment, lastly, there was no cumulative benefit by consecutively exposure for three generations under hypoxic environment, which is indicating world winning runners from high altitude dwellers may not relay on the duration of sojourn under hypoxic environment, but rather selection and training related factors. Conclusions In summary, maternal exercise training before and during conception under hypoxic environment increase in mitochondrial biogenesis(PGC-1α, COX-Ⅳ, NRF-1, mtTFA) and angiogenesis(HIF-1α, VEGFtotal) related proteins expressions in both maternal and offspring skeletal muscles, especially exercise training stimulated the protein expressions under hypoxic environment than normoxic condition. Therefore, exercise capacity may be endowed by both hypoxic environment and exercise training at hypoxic environment.  

Aerobic exercise training improves skeletal muscle function and Ca2+ handling-related protein expression in sympathetic hyperactivity-induced heart failure

2010 ◽  
Vol 109 (3) ◽  
pp. 702-709 ◽  
Author(s):  
C. R. Bueno ◽  
J. C. B. Ferreira ◽  
M. G. Pereira ◽  
A. V. N. Bacurau ◽  
P. C. Brum
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Protein Expression ◽  
Aerobic Exercise ◽  
Muscle Function ◽  
Exercise Tolerance ◽  
Aerobic Exercise Training ◽  
Related Protein ◽  
Skeletal Muscle Function ◽  
Related Proteins

The cellular mechanisms of positive effects associated with aerobic exercise training on overall intrinsic skeletal muscle changes in heart failure (HF) remain unclear. We investigated potential Ca2+ abnormalities in skeletal muscles comprising different fiber compositions and investigated whether aerobic exercise training would improve muscle function in a genetic model of sympathetic hyperactivity-induced HF. A cohort of male 5-mo-old wild-type (WT) and congenic α2A/α2C adrenoceptor knockout (ARKO) mice in a C57BL/6J genetic background were randomly assigned into untrained and trained groups. Exercise training consisted of a 8-wk running session of 60 min, 5 days/wk (from 5 to 7 mo of age). After completion of the exercise training protocol, exercise tolerance was determined by graded treadmill exercise test, muscle function test by Rotarod, ambulation and resistance to inclination tests, cardiac function by echocardiography, and Ca2+ handling-related protein expression by Western blot. α2A/α2CARKO mice displayed decreased ventricular function, exercise intolerance, and muscle weakness paralleled by decreased expression of sarcoplasmic Ca2+ release-related proteins [α1-, α2-, and β1-subunits of dihydropyridine receptor (DHPR) and ryanodine receptor (RyR)] and Ca2+ reuptake-related proteins [sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)1/2 and Na+/Ca2+ exchanger (NCX)] in soleus and plantaris. Aerobic exercise training significantly improved exercise tolerance and muscle function and reestablished the expression of proteins involved in sarcoplasmic Ca2+ handling toward WT levels. We provide evidence that Ca2+ handling-related protein expression is decreased in this HF model and that exercise training improves skeletal muscle function associated with changes in the net balance of skeletal muscle Ca2+ handling proteins.

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.

Beclin 1, LC3, and p62 expression in paraquat-induced pulmonary fibrosis

2019 ◽  
Vol 38 (7) ◽  
pp. 794-802 ◽  
Author(s):  
G Xu ◽  
X Wang ◽  
H Yu ◽  
C Wang ◽  
Y Liu ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Light Chain ◽  
Lung Fibrosis ◽  
Beclin 1 ◽  
Related Protein ◽  
Protein Expressions ◽  
Hematoxylin And Eosin ◽  
Hematoxylin And Eosin Staining ◽  
Related Proteins

Paraquat (PQ) is a highly toxic herbicide to humans. Pulmonary fibrosis is one of the most typical features of PQ poisoning, which develops from several days to weeks after ingestion. However, the mechanism of fibrosis is still unclear. In this study, we aimed to determine expressions of autophagy-related markers Beclin 1, microtubule-associated protein light chain 3 (LC3), and p62 in PQ-poisoned lungs and to explore the role of autophagy in pulmonary fibrosis induced by PQ. We detected markers of lung fibrosis and expressions of autophagy-related protein in the specimens from eight fatal cases of PQ poisoning by hematoxylin and eosin staining, Masson’s trichrome staining, and immunohistochemistry. Based on the staining results of lung fibrosis, these cases were divided into two groups, fibrosis and non-fibrosis groups. The correlation between autophagy protein expressions and pulmonary fibrosis was examined. The results demonstrated that the autophagy-related proteins were significantly expressed in fibrosis group compared with the non-fibrosis group. There was a significantly positive correlation between these protein expressions and severity of lung fibrosis. In conclusion, autophagy dysfunction may be involved in lung fibrogenesis caused by PQ poisoning. This may be a promising clue for understanding the molecular mechanism underlying PQ-induced lung fibrosis and provide evidence for treating fibrosis by regulating the level of autophagy.

scholarly journals Pterostilbene Enhances Endurance Capacity via Promoting Skeletal Muscle Adaptations to Exercise Training in Rats

Molecules ◽  
2020 ◽  
Vol 25 (1) ◽  
pp. 186 ◽  
Author(s):  
Jiawei Zheng ◽  
Wujian Liu ◽  
Xiaohui Zhu ◽  
Li Ran ◽  
Hedong Lang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Mitochondrial Biogenesis ◽  
C2c12 Myotubes ◽  
Endurance Capacity ◽  
Muscle Adaptations ◽  
Slow Twitch ◽  
Slow Twitch Fibers ◽  
Skeletal Muscle Adaptations

It has been demonstrated that skeletal muscle adaptions, including muscle fibers transition, angiogenesis, and mitochondrial biogenesis are involved in the regular exercise-induced improvement of endurance capacity and metabolic status. Herein, we investigated the effects of pterostilbene (PST) supplementation on skeletal muscle adaptations to exercise training in rats. Six-week-old male Sprague Dawley rats were randomly divided into a sedentary control group (Sed), an exercise training group (Ex), and exercise training combined with 50 mg/kg PST (Ex + PST) treatment group. After 4 weeks of intervention, an exhaustive running test was performed, and muscle fiber type transformation, angiogenesis, and mitochondrial content in the soleus muscle were measured. Additionally, the effects of PST on muscle fiber transformation, paracrine regulation of angiogenesis, and mitochondrial function were tested in vitro using C2C12 myotubes. In vivo study showed that exercise training resulted in significant increases in time-to-exhaustion, the proportion of slow-twitch fibers, muscular angiogenesis, and mitochondrial biogenesis in rats, and these effects induced by exercise training could be augmented by PST supplementation. Moreover, the in vitro study showed that PST treatment remarkably promoted slow-twitch fibers formation, angiogenic factor expression, and mitochondrial function in C2C12 myotubes. Collectively, our results suggest that PST promotes skeletal muscle adaptations to exercise training thereby enhancing the endurance capacity.

scholarly journals Exercise preconditioning diminishes skeletal muscle atrophy after hindlimb suspension in mice

2018 ◽  
Vol 125 (4) ◽  
pp. 999-1010 ◽  
Author(s):  
Nicholas T. Theilen ◽  
Nevena Jeremic ◽  
Gregory J. Weber ◽  
Suresh C. Tyagi
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Atrophy ◽  
Mitochondrial Biogenesis ◽  
Weight Ratio ◽  
Hindlimb Suspension ◽  
Skeletal Muscle Atrophy ◽  
Short Term ◽  
Concurrent Exercise ◽  
And Function

The aim of the present study was to investigate whether short-term, concurrent exercise training before hindlimb suspension (HLS) prevents or diminishes both soleus and gastrocnemius atrophy and to analyze whether changes in mitochondrial molecular markers were associated. Male C57BL/6 mice were assigned to control at 13 ± 1 wk of age, 7-day HLS at 12 ± 1 wk of age (HLS), 2 wk of exercise training before 7-day HLS at 10 ± 1 wk of age (Ex+HLS), and 2 wk of exercise training at 11 ± 1 wk of age (Ex) groups. HLS resulted in a 27.1% and 21.5% decrease in soleus and gastrocnemius muscle weight-to-body weight ratio, respectively. Exercise training before HLS resulted in a 5.6% and 8.1% decrease in soleus and gastrocnemius weight-to-body weight ratio, respectively. Exercise increased mitochondrial biogenesis- and function-associated markers and slow myosin heavy chain (SMHC) expression, and reduced fiber-type transitioning marker myosin heavy chain 4 (Myh4). Ex+HLS revealed decreased reactive oxygen species (ROS) and oxidative stress compared with HLS. Our data indicated the time before an atrophic setting, particularly caused by muscle unloading, may be a useful period to intervene short-term, progressive exercise training to prevent skeletal muscle atrophy and is associated with mitochondrial biogenesis, function, and redox balance. NEW & NOTEWORTHY Mitochondrial dysfunction is associated with disuse-induced skeletal muscle atrophy, whereas exercise is known to increase mitochondrial biogenesis and function. Here we provide evidence of short-term concurrent exercise training before an atrophic event protecting skeletal muscle from atrophy in two separate muscles with different, dominant fiber-types, and we reveal an association with the adaptive changes of mitochondrial molecular markers to exercise.

scholarly journals Supplementing the maternal diet of rats with butyrate enhances mitochondrial biogenesis in the skeletal muscles of weaned offspring

2017 ◽  
Vol 117 (1) ◽  
pp. 12-20 ◽  
Author(s):  
Yanping Huang ◽  
Shixing Gao ◽  
Guo Jun ◽  
Ruqian Zhao ◽  
Xiaojing Yang
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dna ◽  
Energy Metabolism ◽  
Mitochondrial Biogenesis ◽  
Uncoupling Protein ◽  
Virgin Female ◽  
Female Rats ◽  
Control Group ◽  
Mitochondrial Dna Copy Number ◽  
Protein Expressions

AbstractThe present study aimed to investigate the effects of maternal dietary butyrate supplementation on energy metabolism and mitochondrial biogenesis in offspring skeletal muscle and the possible mediating mechanisms. Virgin female rats were randomly assigned to either control or butyrate diets (1 % butyrate sodium) throughout gestation and lactation. At the end of lactation (21 d), the offspring were killed by exsanguination from the abdominal aorta under anaesthesia. The results showed that maternal butyrate supplementation throughout gestation and lactation did not affect offspring body weight. However, the protein expressions of G-protein-coupled receptors (GPR) 43 and 41 were significantly enhanced in offspring skeletal muscle of the maternal butyrate-supplemented group. The ATP content, most of mitochondrial DNA-encoded gene expressions, the cytochrome c oxidase subunit 1 and 4 protein contents and the mitochondrial DNA copy number were significantly higher in the butyrate group than in the control group. Meanwhile, the protein expressions of type 1 myosin heavy chain, mitochondrial transcription factor A, PPAR-coactivator-1α (PGC-1α) and uncoupling protein 3 were significantly increased in the gastrocnemius muscle of the treatment group compared with the control group. These results indicate for the first time that maternal butyrate supplementation during the gestation and lactation periods influenced energy metabolism and mitochondrial biogenesis through the GPR and PGC-1α pathways in offspring skeletal muscle at weaning.

scholarly journals Age-associated declines in mitochondrial biogenesis and protein quality control factors are minimized by exercise training

2012 ◽  
Vol 303 (2) ◽  
pp. R127-R134 ◽  
Author(s):  
Erika Koltai ◽  
Nikolett Hart ◽  
Albert W. Taylor ◽  
Sataro Goto ◽  
Jenny K. Ngo ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Quality Control ◽  
Exercise Training ◽  
Mitochondrial Biogenesis ◽  
Protein Quality ◽  
Mitochondrial Protein ◽  
Protein Quality Control ◽  
Treadmill Running ◽  
Common Finding ◽  
Moderate Intensity

A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate-intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats. Exercise training, consisting of treadmill running at 60% of the initial V̇o2max, reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (succinate dehydrogenase, citrate synthase, cytochrome- c oxidase-4, mtDNA), SIRT1 activity, AMPK, pAMPK, and peroxisome proliferator-activated receptor gamma coactivator 1-α, UCP3, and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters, including nuclear respiratory factor 1, mitochondrial transcription factor A, fission-1, mitofusin-1, and polynucleotide phosphorylase levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.

scholarly journals Exercise Training Attenuates Obesity-Induced Skeletal Muscle Remodeling and Mitochondria-Mediated Apoptosis in the Skeletal Muscle

2018 ◽  
Vol 15 (10) ◽  
pp. 2301 ◽  
Author(s):  
Jun-Won Heo ◽  
Su-Zi Yoo ◽  
Mi-Hyun No ◽  
Dong-Ho Park ◽  
Ju-Hee Kang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
High Fat Diet ◽  
Skeletal Muscles ◽  
Treadmill Exercise ◽  
Sectional Area ◽  
High Fat ◽  
Cross Sectional ◽  
Muscle Remodeling ◽  
Protective Intervention

Obesity is characterized by the induction of skeletal muscle remodeling and mitochondria-mediated apoptosis. Exercise has been reported as a positive regulator of skeletal muscle remodeling and apoptosis. However, the effects of exercise on skeletal muscle remodeling and mitochondria-mediated apoptosis in obese skeletal muscles have not been clearly elucidated. Four-week-old C57BL/6 mice were randomly assigned into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and HFD plus exercise groups (HFD + EX). After obesity was induced by 20 weeks of 60% HFD feeding, treadmill exercise was performed for 12 weeks. Exercise ameliorated the obesity-induced increase in extramyocyte space and a decrease in the cross-sectional area of the skeletal muscle. In addition, it protected against increases in mitochondria-mediated apoptosis in obese skeletal muscles. These results suggest that exercise as a protective intervention plays an important role in regulating skeletal muscle structure and apoptosis in obese skeletal muscles.

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.

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