Mitochondrial DNA rejuvenescence: Why Resist?
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abstract
We previously reported that satellite cells from older adults do not accumulate aging‐associated mitochondrial DNA (mtDNA) deletions (Safdar et al, 2007). Resistance (RES) training induces satellite cell activation and skeletal muscle hypertrophy, and is recommended as an effective countermeasure to sarcopenia in the elderly. We aimed to delineate the protective mechanism underlying this effect. Muscle biopsies were taken from the vastus lateralis of 16 older subjects (70 ± 5 y; 8 women) before and after 6 months of RES training and analyzed for protein content of electron transport chain (complex I ND6, complex III core protein 2, complex IV COX subunits –II and –IV, and complex V alpha subunit), antioxidant enzymes (Mn‐SOD, Cu/Zn‐SOD, and catalase), markers of mitochondrial abundance (citrate synthase CS) and oxidative damage (protein carbonyl PC, 4‐hydroxynonenal 4HNE, and total DNA 8‐hydroxy‐2‐deoxyguanosine 8‐OHdG), mtDNA deletions, as well as CS, COX, and catalase enzyme activity. RES training increased protein content of ND6, core protein 2, COX‐II, COX‐IV, complex V alpha subunit and catalase by 25%, 41%, 62%, 69%, 31%, and 95% respectively (P < 0.042), and COX and catalase enzyme activity by 79% and 89%, respectively (P < 0.028). RES training decreased mtDNA deletions (63%), PC (45%), 4‐HNE (29%), and total DNA 8‐OHdG (45%) content (P < 0.01). We conclude that the improvements in mitochondrial function occurred through RES training‐induced recruitment of satellite cells resulting in mitochondrial gene shifting and rejuvenescence in the skeletal muscle of older adults. We propose that RES training is a viable therapy to attenuate and/or “reverse” mitochondrial abnormalities associated with sarcopenia. (Funded by CIHR Institute of Aging, and Warren Lammert and Kathy Corkins).
