Membrane Estrogen Receptors Regulate Voluntary Wheel Running and Contractile Function in Skeletal Muscle in Mice

2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 781
Author(s):  
Jacqueline M. Crissey ◽  
J. Andries Ferreira ◽  
Dennis B. Lubahn ◽  
Marybeth Brown
2012 ◽  
Vol 19 (8) ◽  
pp. 729-738 ◽  
Author(s):  
Catherine R. Mikus ◽  
Bruno T. Roseguini ◽  
Grace M. Uptergrove ◽  
E. Matthew Morris ◽  
Randy Scott Rector ◽  
...  

2019 ◽  
Vol 317 (6) ◽  
pp. C1313-C1323 ◽  
Author(s):  
Matthew A. Romero ◽  
Petey W. Mumford ◽  
Paul A. Roberson ◽  
Shelby C. Osburn ◽  
Hailey A. Parry ◽  
...  

Transposable elements (TEs) are mobile DNA and constitute approximately half of the human genome. LINE-1 (L1) is the only active autonomous TE in the mammalian genome and has been implicated in a number of diseases as well as aging. We have previously reported that skeletal muscle L1 expression is lower following acute and chronic exercise training in humans. Herein, we used a rodent model of voluntary wheel running to determine whether long-term exercise training affects markers of skeletal muscle L1 regulation. Selectively bred high-running female Wistar rats ( n = 11 per group) were either given access to a running wheel (EX) or not (SED) at 5 wk of age, and these conditions were maintained until 27 wk of age. Thereafter, mixed gastrocnemius tissue was harvested and analyzed for L1 mRNA expression and DNA content along with other L1 regulation markers. We observed significantly ( P < 0.05) lower L1 mRNA expression, higher L1 DNA methylation, and less L1 DNA in accessible chromatin regions in EX versus SED rats. We followed these experiments with 3-h in vitro drug treatments in L6 myotubes to mimic transient exercise-specific signaling events. The AMP-activated protein kinase (AMPK) agonist 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR; 4 mM) significantly decreased L1 mRNA expression in L6 myotubes. However, this effect was not facilitated through increased L1 DNA methylation. Collectively, these data suggest that long-term voluntary wheel running downregulates skeletal muscle L1 mRNA, and this may occur through chromatin modifications. Enhanced AMPK signaling with repetitive exercise bouts may also decrease L1 mRNA expression, although the mechanism of action remains unknown.


2004 ◽  
Vol 93 (5-6) ◽  
pp. 655-664 ◽  
Author(s):  
Maria Antonietta Pellegrino ◽  
Lorenza Brocca ◽  
Francesco Saverio Dioguardi ◽  
Roberto Bottinelli ◽  
Giuseppe D’Antona

2020 ◽  
Vol 8 (20) ◽  
Author(s):  
Angelika Schmitt ◽  
Pascal Herzog ◽  
Franziska Röchner ◽  
Anne‐Lena Brändle ◽  
Annunziata Fragasso ◽  
...  

2013 ◽  
pp. 361-369 ◽  
Author(s):  
R. L. SCHULTZ ◽  
E. L. KULLMAN ◽  
R. P. WATERS ◽  
H. HUANG ◽  
J. P. KIRWAN ◽  
...  

The Spontaneously Hypertensive Heart Failure (SHHF) rat mimics the human progression of hypertension from hypertrophy to heart failure. However, it is unknown whether SHHF animals can exercise at sufficient levels to observe beneficial biochemical adaptations in skeletal muscle. Thirty-seven female SHHF and Wistar-Furth (WF) rats were randomized to sedentary (SHHFsed and WFsed) and exercise groups (SHHFex and WFex). The exercise groups had access to running wheels from 6-22 months of age. Hindlimb muscles were obtained for metabolic measures that included mitochondrial enzyme function and expression, and glycogen utilization. The SHHFex rats ran a greater distance and duration as compared to the WFex rats (P<0.05), but the WFex rats ran at a faster speed (P<0.05). Skeletal muscle citrate synthase and β-hydroxyacyl-CoA dehydrogenase enzyme activity was not altered in the SHHFex group, but was increased (P<0.05) in the WFex animals. Citrate synthase protein and gene expression were unchanged in SHHFex animals, but were increased in WFex rats (P<0.05). In the WFex animals muscle glycogen was significantly depleted after exercise (P<0.05), but not in the SHHFex group. We conclude that despite robust amounts of aerobic activity, voluntary wheel running exercise was not sufficiently intense to improve the oxidative capacity of skeletal muscle in adult SHHF animals, indicating an inability to compensate for declining heart function by improving peripheral oxidative adaptations in the skeletal muscle.


2011 ◽  
Vol 300 (2) ◽  
pp. E327-E340 ◽  
Author(s):  
Chikwendu Ibebunjo ◽  
John K. Eash ◽  
Christine Li ◽  
QiCheng Ma ◽  
David J. Glass

Declines in skeletal muscle size and strength, often seen with chronic wasting diseases, prolonged or high-dose glucocorticoid therapy, and the natural aging process in mammals, are usually associated with reduced physical activity and testosterone levels. However, it is not clear whether the decline in testosterone and activity are causally related. Using a mouse model, we found that removal of endogenous testosterone by orchidectomy results in an almost complete cessation in voluntary wheel running but only a small decline in muscle mass. Testosterone replacement restored running behavior and muscle mass to normal levels. Orchidectomy also suppressed the IGF-I/Akt pathway, activated the atrophy-inducing E3 ligases MuRF1 and MAFBx, and suppressed several energy metabolism pathways, and all of these effects were reversed by testosterone replacement. The study also delineated a distinct, previously unidentified set of genes that is inversely regulated by orchidectomy and testosterone treatment. These data demonstrate the necessity of testosterone for both speed and endurance of voluntary wheel running in mice and suggest a potential mechanism for declined activity in humans where androgens are deficient.


Sign in / Sign up

Export Citation Format

Share Document