scholarly journals Effect of long‐term caloric restriction on mitochondrial function in skeletal muscle and non‐exercise activity in aged rats

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Jill M Schimke ◽  
Stephane Walrand ◽  
Katherine A Klaus ◽  
Dawn Morse ◽  
Kevin R Short ◽  
...  
2005 ◽  
Vol 19 (10) ◽  
pp. 1320-1322 ◽  
Author(s):  
Russell T. Hepple ◽  
David J. Baker ◽  
Jan J. Kaczor ◽  
Daniel J. Krause

2005 ◽  
Vol 40 (1-2) ◽  
pp. 27-35 ◽  
Author(s):  
Danila Paula Argentino ◽  
Fernando Pablo Dominici ◽  
Marina Cecilia Muñoz ◽  
Khalid Al-Regaiey ◽  
Andrzej Bartke ◽  
...  

2002 ◽  
Vol 283 (1) ◽  
pp. E38-E43 ◽  
Author(s):  
R. Sreekumar ◽  
J. Unnikrishnan ◽  
A. Fu ◽  
J. Nygren ◽  
K. R. Short ◽  
...  

Rodent skeletal muscle mitochondrial DNA has been shown to be a potential site of oxidative damage during aging. Caloric restriction (CR) is reported to reduce oxidative stress and prolong life expectancy in rodents. Gene expression profiling and measurement of mitochondrial ATP production capacity were performed in skeletal muscle of male rats after feeding them either a control diet or calorie-restricted diet (60% of control diet) for 36 wk to determine the potential mechanism of the beneficial effects of CR. CR enhanced the transcripts of genes involved in reactive oxygen free radical scavenging function, tissue development, and energy metabolism while decreasing expression of those genes involved in signal transduction, stress response, and structural and contractile proteins. Real-time PCR measurments confirmed the changes in transcript levels of cytochrome- c oxidase III, superoxide dismutase (SOD)1, and SOD2 that were noted by the microarray approach. Mitochondrial ATP production and citrate synthase were unaltered by the dietary changes. We conclude that CR alters transcript levels of several genes in skeletal muscle and that mitochondrial function in skeletal muscle remains unaltered by the dietary intervention. Alterations in transcripts of many genes involved in reactive oxygen scavenging function may contribute to the increase in longevity reported with CR.


2005 ◽  
Vol 60 (1) ◽  
pp. 28-34 ◽  
Author(s):  
D. P. Argentino ◽  
F. P. Dominici ◽  
K. Al-Regaiey ◽  
M. S. Bonkowski ◽  
A. Bartke ◽  
...  

Oncotarget ◽  
2015 ◽  
Vol 6 (37) ◽  
pp. 39469-39481 ◽  
Author(s):  
Sabzali Javadov ◽  
Sehwan Jang ◽  
Natividad Rodriguez-Reyes ◽  
Ana E. Rodriguez-Zayas ◽  
Jessica Soto Hernandez ◽  
...  

2012 ◽  
Vol 15 (04) ◽  
pp. 1250019
Author(s):  
Laura L. Pauwels ◽  
Brittany Dowling ◽  
Nkeonye Okafor ◽  
Ryan Breighner ◽  
Zachary J. Domire

It has been shown that elderly skeletal muscle does not respond as effectively to exercise as young muscle. This impairment not only limits the effectiveness of interventions in an elderly population but may also be a cause of sarcopenia. One possible explanation for diminished response to exercise is that stiffening of muscle tissue, as a result of glycation, changes the mechanical environment around the muscle cells and that the cells therefore experience less force for any given stimulus. To examine this possibility, it is necessary to manipulate muscle material properties. The purpose of this study is to examine the possibility of using caloric restriction to accomplish this. It was found that calorie-restricted rats were less sarcopenic than ad libitum (AL) fed rats and that there was a significant negative relationship between muscle stiffness and muscle size in all rats. While the caloric-restricted rats' muscles were not statistically less stiff than the AL-fed rats, the majority of them were less stiff and the use of this group broadened the range of muscle stiffness. In conclusion, caloric restriction appears to be a promising method to manipulate muscle stiffness to study the effects of stiffness on diminished response to exercise.


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