scholarly journals Srf KO and wild-type mice similarly adapt to endurance exercise

2019 ◽  
Vol 29 (2) ◽  
Author(s):  
Haidar Djemai ◽  
Medhi Hassani ◽  
Nissrine Daou ◽  
Zhenlin Li ◽  
Athanassia Sotiropoulos ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Serum Response Factor ◽  
Wheel Running ◽  
Voluntary Exercise ◽  
Muscle Performance ◽  
Adaptive Responses ◽  
Aerobic Activity ◽  
Exercise Adaptation ◽  
Muscle Homeostasis

Physical exercise has important effects as secondary prevention or intervention against several diseases. Endurance exercise induces local and global effects, resulting in skeletal muscle adaptations to aerobic activity and contributes to an amelioration of muscle performance. Furthermore, it prevents muscle loss. Serum response factor (Srf) is a transcription factor of pivotal importance for muscle tissues and animal models of Srf genetic deletion/over-expression are widely used to study Srf role in muscle homeostasis, physiology and pathology. A global characterisation of exercise adaptation in the absence of Srf has not been reported. We measured body composition, muscle force, running speed, energy expenditure and metabolism in WT and inducible skeletal muscle-specific Srf KO mice, following three weeks of voluntary exercise by wheel running. We found a major improvement in the aerobic capacity and muscle function in WT mice following exercise, as expected, and no major differences were observed in Srf KO mice as compared to WT mice, following exercise. Taken together, these observations suggest that Srf is not required for an early (within 3 weeks) adaptation to spontaneous exercise and that Srf KO mice behave similarly to the WT in terms of spontaneous physical activity and the resulting adaptive responses. Therefore, Srf KO mice can be used in functional muscle studies, without the results being affected by the lack of Srf. Since lack of Srf induces premature sarcopenia, our observations suggest that the modifications due to the absence of Srf take time to occur and that young, Srf KO mice behave similarly to WT in aerobic physical activities.

Cardiac and skeletal muscle adaptations to voluntary wheel running in the mouse

2001 ◽  
Vol 90 (5) ◽  
pp. 1900-1908 ◽  
Author(s):  
David L. Allen ◽  
Brooke C. Harrison ◽  
Alexander Maass ◽  
Matthew L. Bell ◽  
William C. Byrnes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Wheel Running ◽  
Average Distance ◽  
Histochemical Staining ◽  
Voluntary Exercise ◽  
Mrna Levels ◽  
Muscle Adaptations ◽  
Heart Mass ◽  
Running Wheels ◽  
Skeletal Muscle Adaptations

In this paper, we describe the effects of voluntary cage wheel exercise on mouse cardiac and skeletal muscle. Inbred male C57/Bl6 mice (age 8–10 wk; n = 12) ran an average of 4.3 h/24 h, for an average distance of 6.8 km/24 h, and at an average speed of 26.4 m/min. A significant increase in the ratio of heart mass to body mass (mg/g) was evident after 2 wk of voluntary exercise, and cardiac atrial natriuretic factor and brain natriuretic peptide mRNA levels were significantly increased in the ventricles after 4 wk of voluntary exercise. A significant increase in the percentage of fibers expressing myosin heavy chain (MHC) IIa was observed in both the gastrocnemius and the tibialis anterior (TA) by 2 wk, and a significant decrease in the percentage of fibers expressing IIb MHC was evident in both muscles after 4 wk of voluntary exercise. The TA muscle showed a greater increase in the percentage of IIa MHC-expressing fibers than did the gastrocnemius muscle (40 and 20%, respectively, compared with 10% for nonexercised). Finally, the number of oxidative fibers as revealed by NADH-tetrazolium reductase histochemical staining was increased in the TA but not the gastrocnemius after 4 wk of voluntary exercise. All results are relative to age-matched mice housed without access to running wheels. Together these data demonstrate that voluntary exercise in mice results in cardiac and skeletal muscle adaptations consistent with endurance exercise.

scholarly journals Voluntary exercise improves metabolic profile in high-fat fed glucocorticoid-treated rats

2015 ◽  
Vol 118 (11) ◽  
pp. 1331-1343 ◽  
Author(s):  
Jacqueline L. Beaudry ◽  
Emily C. Dunford ◽  
Erwan Leclair ◽  
Erin R. Mandel ◽  
Ashley J. Peckett ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Profile ◽  
Cell Function ◽  
Wheel Running ◽  
Insulin Response ◽  
Voluntary Exercise ◽  
Oral Glucose ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats

Diabetes is rapidly induced in young male Sprague-Dawley rats following treatment with exogenous corticosterone (CORT) and a high-fat diet (HFD). Regular exercise alleviates insulin insensitivity and improves pancreatic β-cell function in insulin-resistant/diabetic rodents, but its effect in an animal model of elevated glucocorticoids is unknown. We examined the effect of voluntary exercise (EX) on diabetes development in CORT-HFD-treated male Sprague-Dawley rats (∼6 wk old). Animals were acclimatized to running wheels for 2 wk, then given a HFD, either wax (placebo) or CORT pellets, and split into 4 groups: placebo-sedentary (SED) or -EX and CORT-SED or -EX. After 2 wk of running combined with treatment, CORT-EX animals had reduced visceral adiposity, and increased skeletal muscle type IIb/x fiber area, oxidative capacity, capillary-to-fiber ratio and insulin sensitivity compared with CORT-SED animals (all P < 0.05). Although CORT-EX animals still had fasting hyperglycemia, these values were significantly improved compared with CORT-SED animals (14.3 ± 1.6 vs. 18.8 ± 0.9 mM). In addition, acute in vivo insulin response to an oral glucose challenge was enhanced ∼2-fold in CORT-EX vs. CORT-SED ( P < 0.05) which was further demonstrated ex vivo in isolated islets. We conclude that voluntary wheel running in rats improves, but does not fully normalize, the metabolic profile and skeletal muscle composition of animals administered CORT and HFD.

scholarly journals Signals from the Circle: Tricarboxylic Acid Cycle Intermediates as Myometabokines

Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 474
Author(s):  
Jennifer Maurer ◽  
Miriam Hoene ◽  
Cora Weigert
Keyword(s):  
Skeletal Muscle ◽  
Tricarboxylic Acid Cycle ◽  
Cell Types ◽  
Tricarboxylic Acid ◽  
Muscle Performance ◽  
Whole Body ◽  
Small Proteins ◽  
Exercise Adaptation ◽  
Whole Body Metabolism ◽  
Adaptation Processes

Regular physical activity is an effective strategy to prevent and ameliorate aging-associated diseases. In particular, training increases muscle performance and improves whole-body metabolism. Since exercise affects the whole organism, it has countless health benefits. The systemic effects of exercise can, in part, be explained by communication between the contracting skeletal muscle and other organs and cell types. While small proteins and peptides known as myokines are the most prominent candidates to mediate this tissue cross-talk, recent investigations have paid increasing attention to metabolites. The purpose of this review is to highlight the potential role of tricarboxylic acid (TCA) metabolites as humoral mediators of exercise adaptation processes. We focus on TCA metabolites that are released from human skeletal muscle in response to exercise and provide an overview of their potential auto-, para- or endocrine health-promoting effects.

scholarly journals Calcineurin activates interleukin-6 transcription in mouse skeletal muscle in vivo and in C2C12 myotubes in vitro

2010 ◽  
Vol 298 (1) ◽  
pp. R198-R210 ◽  
Author(s):  
David L. Allen ◽  
Jill J. Uyenishi ◽  
Allison S. Cleary ◽  
Ryan S. Mehan ◽  
Sarah F. Lindsay ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Binding Sites ◽  
Promoter Activity ◽  
Wheel Running ◽  
Mrna Levels ◽  
Dna Binding Sites ◽  
Single Bout

Expression of the cytokine interleukin-6 (IL-6) by skeletal muscle is hugely increased in response to a single bout of endurance exercise, and this appears to be mediated by increases in intracellular calcium. We examined the effects of endurance exercise on IL-6 mRNA levels and promoter activity in skeletal muscle in vivo, and the role of the calcium-activated calcineurin signaling pathway on muscle IL-6 expression in vivo and in vitro. IL-6 mRNA levels in the mouse tibialis anterior (TA) were increased 2–10-fold by a single bout of treadmill exercise or by 3 days of voluntary wheel running. Moreover, an IL-6 promoter-driven luciferase transgene was activated in TA by both treadmill and wheel-running exercise and by injection with a calcineurin plasmid. Exercise also increased muscle mRNA expression of the calcineurin regulatory gene MCIP1, as did treatment of C2C12 myotubes with the calcium ionophore A23187. Cotransfection of C2C12 myotubes with a constitutively active calcineurin construct significantly increased while cotransfection with the calcineurin inhibitor CAIN inhibited activity of a mouse IL-6 promoter-reporter construct. Cotransfection with a myocyte enhancer-factor-2 (MEF-2) expression construct increased basal IL-6 promoter activity and augmented the effects of calcineurin cotransfection, while cotransfection with the MEF-2 antagonist MITR repressed calcineurin-activated IL-6 promoter activity in vitro. Surprisingly, cotransfection with a dominant-negative form of another calcineurin-activated transcription factor, nuclear factor activator of T cells (NFAT), greatly potentiated both basal and calcineurin-stimulated IL-6 promoter activity in C2C12 myotubes. Mutation of the MEF-2 DNA binding sites attenuated, while mutation of the NFAT DNA binding sites potentiated basal and calcineurin-activated IL-6 promoter activity. Finally, CREB and C/EBP were necessary for basal IL-6 promoter activity and sufficient to increase IL-6 promoter activity but had minimal roles in calcineurin-activated IL-6 promoter activity. Together, these results suggest that IL-6 transcription in skeletal muscle cells can be activated by a calcineurin-MEF-2 axis which is antagonized by NFAT.

scholarly journals An inducible knockout of Dicer in adult mice does not affect endurance exercise-induced muscle adaptation

2019 ◽  
Vol 316 (2) ◽  
pp. C285-C292 ◽  
Author(s):  
Satoshi Oikawa ◽  
Minjung Lee ◽  
Norio Motohashi ◽  
Seiji Maeda ◽  
Takayuki Akimoto
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Citrate Synthase ◽  
Wheel Running ◽  
Fiber Type ◽  
Tamoxifen Treatment ◽  
Muscle Adaptation ◽  
Adult Skeletal Muscle ◽  
Significant Difference ◽  
Exercise Induced

The contractile and metabolic properties of adult skeletal muscle change in response to endurance exercise. The mechanisms of transcriptional regulation in exercise-induced skeletal muscle adaptation, including fiber-type switching and mitochondrial biogenesis, have been investigated intensively, whereas the role of microRNA (miRNA)-mediated posttranscriptional gene regulation is less well understood. We used tamoxifen-inducible Dicer1 knockout (iDicer KO) mice to reduce the global expression of miRNAs in adult skeletal muscle and subjected these mice to 2 wk of voluntary wheel running. Dicer mRNA expression was completely depleted in fast-twitch plantaris muscle after tamoxifen injection. However, several muscle-enriched miRNAs, including miR-1 and miR-133a, were reduced by only 30–50% in both the slow and fast muscles. The endurance exercise-induced changes that occurred for many parameters (i.e., fast-to-slow fiber-type switch and increases in succinate dehydrogenase, respiratory chain complex II, and citrate synthase activity) in wild type (WT) also occurred in the iDicer KO mice. Protein expression of myosin heavy chain IIa, peroxisome proliferator-activated receptor-γ coactivator-1α, and cytochrome c complex IV was also increased in the iDicer KO mice by the voluntary running. Furthermore, there was no significant difference in oxygen consumption rate in the isolated mitochondria between the WT and iDicer KO mice. These data indicate that muscle-enriched miRNAs were detectable even after 4 wk of tamoxifen treatment and there was no apparent specific endurance-exercise-induced muscle phenotype in the iDicer KO mice.

Wheel-running exercise alters rat diaphragm action potentials and their regulation by K+ channels

2003 ◽  
Vol 95 (2) ◽  
pp. 602-610 ◽  
Author(s):  
Erik van Lunteren ◽  
Michelle Moyer
Keyword(s):  
Skeletal Muscle ◽  
Ion Channels ◽  
Action Potential ◽  
Endurance Exercise ◽  
Wheel Running ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Free Access ◽  
Diaphragm Action ◽  
Action Potential Repolarization

Endurance exercise modifies regulatory systems that control skeletal muscle Na+ and K+ fluxes, in particular Na+-K+-ATPase-mediated transport of these ions. Na+ and K+ ion channels also play important roles in the regulation of ionic movements, specifically mediating Na+ influx and K+ efflux that occur during contractions resulting from action potential depolarization and repolarization. Whether exercise alters skeletal muscle electrophysiological properties controlled by these ion channels is unclear. The present study tested the hypothesis that endurance exercise modifies diaphragm action potential properties. Exercised rats spent 8 wk with free access to running wheels, and they were compared with sedentary rats living in conventional rodent housing. Diaphragm muscle was subsequently removed under anesthesia and studied in vitro. Resting membrane potential was not affected by endurance exercise. Muscle from exercised rats had a slower rate of action potential repolarization than that of sedentary animals ( P = 0.0098), whereas rate of depolarization was similar in the two groups. The K+ channel blocker 3,4-diaminopyridine slowed action potential repolarization and increased action potential area of both exercised and sedentary muscle. However, these effects were significantly smaller in diaphragm from exercised than sedentary rats. These data indicate that voluntary running slows diaphragm action potential repolarization, most likely by modulating K+ channel number or function.

Methylglyoxal reduces molecular responsiveness to 4 weeks of endurance exercise in mouse plantaris muscle

2022 ◽  
Author(s):  
Tatsuro Egawa ◽  
Takeshi Ogawa ◽  
Takumi Yokokawa ◽  
Kohei Kido ◽  
Katsumasa Goto ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Mitochondrial Biogenesis ◽  
Insulin Signaling ◽  
Exercise Group ◽  
Voluntary Exercise ◽  
Plantaris Muscle ◽  
Muscle Adaptations ◽  
Exercise Induced ◽  
Skeletal Muscle Adaptations

Endurance exercise triggers skeletal muscle adaptations, including enhanced insulin signaling, glucose metabolism, and mitochondrial biogenesis. However, exercise-induced skeletal muscle adaptations may not occur in some cases, a condition known as exercise-resistance. Methylglyoxal (MG) is a highly reactive dicarbonyl metabolite and has detrimental effects on the body such as causing diabetic complications, mitochondrial dysfunction, and inflammation. This study aimed to clarify the effect of methylglyoxal on skeletal muscle molecular adaptations following endurance exercise. Mice were randomly divided into 4 groups (n = 12 per group): sedentary control group, voluntary exercise group, MG-treated group, and MG-treated with voluntary exercise group. Mice in the voluntary exercise group were housed in a cage with a running wheel, while mice in the MG-treated groups received drinking water containing 1% MG. Four weeks of voluntary exercise induced several molecular adaptations in the plantaris muscle, including increased expression of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α), mitochondria complex proteins, toll-like receptor 4 (TLR4), 72-kDa heat shock protein (HSP72), hexokinase II, and glyoxalase 1; this also enhanced insulin-stimulated Akt Ser473 phosphorylation and citrate synthase activity. However, these adaptations were suppressed with MG treatment. In the soleus muscle, the exercise-induced increases in the expression of TLR4, HSP72, and advanced glycation end products receptor 1 were inhibited with MG treatment. These findings suggest that MG is a factor that inhibits endurance exercise-induced molecular responses including mitochondrial adaptations, insulin signaling activation, and the upregulation of several proteins related to mitochondrial biogenesis, glucose handling, and glycation in primarily fast-twitch skeletal muscle.

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