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Cardiac calcium pump inactivation and nitrosylation in senescent rat myocardium are not attenuated by long-term treadmill training.

https://arctichealth.org/en/permalink/ahliterature101470
Source
Exp Gerontol. 2011 Jul 8;
Publication Type
Article
Date
Jul-8-2011
Author
Melissa M Thomas
Chris Vigna
Andrew C Betik
A Russell Tupling
Russell T Hepple
Author Affiliation
Muscle and Aging Laboratory, Faculty of Kinesiology, 2500 University Dr, Calgary, Alberta, Canada, T2N 1N4.
Source
Exp Gerontol. 2011 Jul 8;
Date
Jul-8-2011
Language
English
Publication Type
Article
Abstract
The senescent heart has decreased systolic and diastolic functions, both of which could be related to alterations in cardiac sarcoplasmic reticulum (SR) calcium (Ca(2+)) handling. The purpose of this study was to determine if SR protein content and rates of Ca(2+) release and uptake and ATPase activity are lower in the senescent (34-36mo) Fisher 344×Brown-Norway F1 hybrid rat heart and if a long-term exercise training program could maintain SR function. Late middle aged (29mo) male rats underwent 5-7mo of treadmill training. Aging resulted in a decrease in SERCA activity and modest decrease in the rate of Ca(2+) uptake but no change in Ca(2+) release rate. SERCA2a content was not decreased with age but nitrotyrosine accumulation was increased and Ser16 phosphorylated phospholamban (PLN) was decreased. Ryanodine receptor content was not decreased with age but dihydropyridine receptor content was decreased in the senescent heart. Treadmill training had no significant effect on any of the SR properties or protein contents in the senescent rat heart. These results suggest that decreases in Ca(2+) uptake and SERCA activity in the senescent F344BN rat heart are due to increased SERCA2a damage from nitrotyrosine accumulation and inhibition by PLN and that exercise training initiated at late middle age is unable to prevent these age-related changes in cardiac SR function.
PubMed ID
21763413 View in PubMed
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Initiating exercise training in late middle age minimally protects muscle contractile function and increases myocyte oxidative damage in senescent rats.

https://arctichealth.org/en/permalink/ahliterature96298
Source
Exp Gerontol. 2010 Jul 17;
Publication Type
Article
Date
Jul-17-2010
Author
Melissa M Thomas
Warda Khan
Andrew C Betik
Kathryn J Wright
Russell T Hepple
Author Affiliation
Muscle and Aging Laboratory, Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada.
Source
Exp Gerontol. 2010 Jul 17;
Date
Jul-17-2010
Language
English
Publication Type
Article
Abstract
Age-related loss of muscle mass and function exhibits a marked acceleration from late middle age to senescence and exercise training is one method that has been proposed to slow this process. The purpose of this study was to determine if long-term treadmill exercise training initiated at late middle age could increase endogenous antioxidant enzyme activity and attenuate the loss of skeletal muscle contractile properties in the gastrocnemius/plantaris (GAS/Plan) and soleus (SOL) muscles of senescent rats (34-36mo) through a decrease in oxidative damage. Male Fisher 344 x Brown Norway F1-hybrid rats underwent 5-7mo of treadmill training beginning at late middle age (29mo). A 7mo sedentary adult group was used to investigate age-related changes. Aging caused an increase in antioxidant enzyme activities; however, only SOD activity was further increased with exercise training. Exercise training did not attenuate the decrease in twitch or tetanic tension of the GAS/Plan or SOL. It did, however, prevent the increase in twitch half relaxation time of the SOL muscle only. Oxidative damage, as reflected in carbonyl content, was increased with age and even further with exercise training in the GAS muscle. Muscle fibre cross sectional area was decreased with age and even further with exercise training. Interestingly, small muscle fibres showed the highest accumulation of carbonyls. Overall, despite an augmentation of select antioxidant enzyme activities, exercise training from late middle age through to senescence had minimal benefits for muscle contractile properties, perhaps in part due to exacerbated oxidation.
PubMed ID
20643203 View in PubMed
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Initiating treadmill training in late middle age offers modest adaptations in Ca2+ handling but enhances oxidative damage in senescent rat skeletal muscle.

https://arctichealth.org/en/permalink/ahliterature97827
Source
Am J Physiol Regul Integr Comp Physiol. 2010 Mar 3;
Publication Type
Article
Date
Mar-3-2010
Author
Melissa M Thomas
Chris Vigna
Andrew C Betik
Allan Russell Tupling
Russell T Hepple
Author Affiliation
University of Calgary.
Source
Am J Physiol Regul Integr Comp Physiol. 2010 Mar 3;
Date
Mar-3-2010
Language
English
Publication Type
Article
Abstract
Aging skeletal muscle shows an increased time to peak force and relaxation and a decreased specific force, all of which could relate to changes in muscle calcium (Ca(2+)) handling. The purpose of this study was to determine if Ca(2+) handling protein content and function is decreased in senescent gastrocnemius (GAS) muscle and if initiating a training program at late middle age (LMA; 29 mo old) could improve function in senescent (SEN; 34-36 mo old) muscle. LMA male Fisher 344 Brown-Norway rats underwent 5 to 7 mo of treadmill training. Aging resulted in a decrease in maximal SERCA activity and a decrease in Ca(2+) release rate, but no change in Ca(2+) uptake rate. Efficiency of the Ca(2+) pump was increased with age, as was the content of SERCA2a. Training caused a further increase in SERCA2a content. Aging also caused an increase in protein carbonyl and reactive nitrogen species (RNS) damage accumulation, and both further increased with training. Consistent with the increase in oxidative damage, there was increased Hsp70 content with age and a further increase with training. Together these results suggest that while initiating exercise training in LMA augments the age-related increase in expression of Hsp70 and the more efficient SERCA2a isoform, it did not prevent the decrease in SERCA activity and exacerbated oxidative damage in SEN GAS muscle. Key words: aging, sarcoplasmic reticulum, nitrotyrosine, carbonylation.
PubMed ID
20200131 View in PubMed
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