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Dr. Mona Maher Abd-Elsalam Allam :: Publications:

Title:
Resveratrol and/or exercise training counteract aging‑associated decline of physical endurance in aged mice; targeting mitochondrial biogenesis and function
Authors: Marwa Hassan Muhammad · Mona Maher Allam
Year: 2018
Keywords: Mitochondrial dysfunction · Resveratrol · PGC-1α · Citrate synthase
Journal: The Journal of Physiological Sciences
Volume: Not Available
Issue: Not Available
Pages: Not Available
Publisher: Tokyo Springer Japan
Local/International: International
Paper Link:
Full paper Not Available
Supplementary materials Not Available
Abstract:

Mitochondrial dysfunction and decreased mitochondrial content are hallmarks of aging that leads to decreased physical endurance. Our aim was to explore the anti-aging effect of resveratrol (RSVT) supplementation, a polyphenol, and/or exercise training, started at an older age, on improving physical activity, therefore, help in frailty avoidance and promotion of healthy aging in elderly. Eighteen-month-old aged mice received RSVT (15 mg/kg/day) and/or exercise trained for 4 weeks showed significant longer time to exhaustion with decreased blood lactate and free fatty acids levels associated with improved oxidative stress evidenced by decreased gastrocnemius muscle lipid peroxidation and increased antioxidant enzymes activities, catalase and superoxide dismutase, when compared to aged mice control group. These changes were accompanied by overexpression of skeletal muscle peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) mRNA, the master regulator of mitochondrial biogenesis, and increased muscle citrate synthase activity, a marker for mitochondrial function. These findings may provide evidence for improved physical endurance by RSVT supplementation or exercise training with better results of their combination, even at an older age, through increasing mitochondrial biogenesis and function. Increased muscle PGC-1α mRNA expression and citrate synthase enzyme activity in addition to improved aging-associated oxidative damage were among the mechanisms involved in this protection.

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