| Autor: |
No MH; Department of Kinesiology, Inha University, 100 Inha-ro, Michuhol-gu, Incheon, 22212, Republic of Korea., Heo JW; Department of Kinesiology, Inha University, 100 Inha-ro, Michuhol-gu, Incheon, 22212, Republic of Korea., Yoo SZ; Department of Kinesiology, Inha University, 100 Inha-ro, Michuhol-gu, Incheon, 22212, Republic of Korea., Kim CJ; Department of Physiology, Kyung Hee University, Seoul, South Korea., Park DH; Department of Kinesiology, Inha University, 100 Inha-ro, Michuhol-gu, Incheon, 22212, Republic of Korea., Kang JH; Department of Pharmacology and Medicinal Toxicology Research Center, Inha University School of Medicine, Incheon, South Korea., Seo DY; Department of Physiology and Cardiovascular and Metabolic Disease Center, Inje University School of Medicine, Busan, South Korea., Han J; Department of Physiology and Cardiovascular and Metabolic Disease Center, Inje University School of Medicine, Busan, South Korea., Kwak HB; Department of Kinesiology, Inha University, 100 Inha-ro, Michuhol-gu, Incheon, 22212, Republic of Korea. kwakhb@inha.ac.kr. |
| Abstrakt: |
Aging is associated with vulnerability to cardiovascular diseases, and mitochondrial dysfunction plays a critical role in cardiovascular disease pathogenesis. Exercise training is associated with benefits against chronic cardiac diseases. The purpose of this study was to determine the effects of aging and treadmill exercise training on mitochondrial function and apoptosis in the rat heart. Fischer 344 rats were divided into young sedentary (YS; n = 10, 4 months), young exercise (YE; n = 10, 4 months), old sedentary (OS; n = 10, 20 months), and old exercise (OE; n = 10, 20 months) groups. Exercise training groups ran on a treadmill at 15 m/min (young) or 10 m/min (old), 45 min/day, 5 days/week for 8 weeks. Morphological parameters, mitochondrial function, mitochondrial dynamics, mitophagy, and mitochondria-mediated apoptosis were analyzed in cardiac muscle. Mitochondrial O 2 respiratory capacity and Ca 2+ retention capacity gradually decreased, and mitochondrial H 2 O 2 emitting potential significantly increased with aging. Exercise training attenuated aging-induced mitochondrial H 2 O 2 emitting potential and mitochondrial O 2 respiratory capacity, while protecting Ca 2+ retention in the old groups. Aging triggered imbalanced mitochondrial dynamics and excess mitophagy, while exercise training ameliorated the aging-induced imbalance in mitochondrial dynamics and excess mitophagy. Aging induced increase in Bax and cleaved caspase-3 protein levels, while decreasing Bcl-2 levels. Exercise training protected against the elevation of apoptotic signaling markers by decreasing Bax and cleaved caspase-3 and increasing Bcl-2 protein levels, while decreasing the Bax/Bcl-2 ratio and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive myonuclei. These data demonstrate that regular exercise training prevents aging-induced impairment of mitochondrial function and mitochondria-mediated apoptosis in cardiac muscles. |
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