scholarly journals Exercise training for a time-poor generation: enhanced skeletal muscle mitochondrial biogenesis

2010 ◽  
Vol 588 (11) ◽  
pp. 1817-1818 ◽  
Author(s):  
Helen S. Palmer
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Mitochondrial Biogenesis

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 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.

High-dose antioxidant vitamin C supplementation does not prevent acute exercise-induced increases in markers of skeletal muscle mitochondrial biogenesis in rats

2010 ◽  
Vol 108 (6) ◽  
pp. 1719-1726 ◽  
Author(s):  
G. D. Wadley ◽  
G. K. McConell
Keyword(s):  
Skeletal Muscle ◽  
Transcription Factor ◽  
Exercise Training ◽  
Vitamin C ◽  
Mitochondrial Biogenesis ◽  
Acute Exercise ◽  
Exercise Bout ◽  
Antioxidant Vitamin ◽  
Vitamin C Supplementation ◽  
Exercise Induced

High doses of the antioxidant vitamin C prevent the increases in skeletal muscle mitochondrial biogenesis after exercise training. Since exercise training effects rely on the acute stimulus of each exercise bout, we examined whether vitamin C supplementation also attenuates the increases in skeletal muscle metabolic signaling and mitochondrial biogenesis in response to an acute exercise bout. Male Sprague-Dawley rats performed 60 min of treadmill running (27 m/min, 5% grade) or remained sedentary. For 7 days before this, one-half of the rats received water containing 500 mg/kg body wt vitamin C. Acute exercise significantly ( P < 0.05) increased the phosphorylation of p38 MAPK, AMP-activated kinase-α, and activating transcription factor (ATF)-2 and the ratio of oxidized to total glutathione (GSSG/TGSH) in the gastrocnemius. However, vitamin C had no effect on these increases. Similarly, vitamin C did not prevent the exercise-induced increases in peroxisome proliferator-activated receptor-γ coactivator-1α, nuclear respiratory factor (NRF)-1, NRF-2, mitochondrial transcription factor A, glutathione peroxidase-1, MnSOD, extracellular SOD, or glucose transporter 4 ( P < 0.05) mRNA after exercise. Surprisingly, vitamin C supplementation significantly increased the basal levels of GSSG/TGSH, NRF-1, and NRF-2 mRNA and basal ATF-2 phosphorylation. In summary, despite other studies in rats showing that vitamin C supplementation prevents increases in skeletal muscle mitochondrial biogenesis and antioxidant enzymes with exercise training, vitamin C had no affect on the acute exercise-induced increases of these markers.

scholarly journals Exercise training‐induced mitochondrial biogenesis is impaired in skeletal muscle‐specific LKB1 knockout mice

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
David M. Hallowell ◽  
Colby B. Tanner ◽  
Megan R. Nuttall ◽  
Stephen K. Anderson ◽  
Jared M. Bradshaw ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Mitochondrial Biogenesis ◽  
Knockout Mice

Exercise early in life in rats born small does not normalize reductions in skeletal muscle PGC-1α in adulthood

2012 ◽  
Vol 302 (10) ◽  
pp. E1221-E1230 ◽  
Author(s):  
Rhianna C. Laker ◽  
Mary E. Wlodek ◽  
Glenn D. Wadley ◽  
Linda A. Gallo ◽  
Peter J. Meikle ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Mitochondrial Biogenesis ◽  
Cell Mass ◽  
Treadmill Running ◽  
Male Rats ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Adult Skeletal Muscle ◽  
Early Exercise

We have previously shown that 4 wk of exercise training early in life normalizes the otherwise greatly reduced pancreatic β-cell mass in adult male rats born small. The aim of the current study was to determine whether a similar normalization in adulthood of reduced skeletal muscle mitochondrial biogenesis markers and alterations in skeletal muscle lipids of growth-restricted male rats occurs following early exercise training. Bilateral uterine vessel ligation performed on day 18 of gestation resulted in Restricted offspring born small ( P < 0.05) compared with both sham-operated Controls and a sham-operated Reduced litter group. Offspring remained sedentary or underwent treadmill running from 5–9 (early exercise) or 20–24 (later exercise) wk of age. At 24 wk of age, Restricted and Reduced litter offspring had lower ( P < 0.05) skeletal muscle peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) protein expression compared with Control offspring. Early exercise training had the expected effect of increasing skeletal muscle markers of mitochondrial biogenesis, but, at this early age (9 wk), there was no deficit in Restricted and Reduced litter skeletal muscle mitochondrial biogenesis. Unlike our previous observations in pancreatic β-cell mass, there was no “reprogramming” effect of early exercise on adult skeletal muscle such that PGC-1α was lower in adult Restricted and Reduced litter offspring irrespective of exercise training. Later exercise training increased mitochondrial biogenesis in all groups. In conclusion, although the response to exercise training remains intact, early exercise training in rats born small does not have a reprogramming effect to prevent deficits in skeletal muscle markers of mitochondrial biogenesis in adulthood.

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.  

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