No 2020 Pflugers Arch: Difference between revisions
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|keywords=Aging, Apoptosis, Exercise, Heart, Mitochondrial function | |keywords=Aging, Apoptosis, Exercise, Heart, Mitochondrial function | ||
|editor=[[Plangger M]], | |editor=[[Plangger M]], | ||
|mipnetlab=KR Busan Han J, KR Incheon Kwak HB | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, Exercise physiology;nutrition;life style | ||
|diseases=Aging;senescence | |||
|injuries=Cell death | |||
|organism=Rat | |||
|tissues=Heart | |||
|preparations=Permeabilized tissue | |||
|couplingstates=LEAK, OXPHOS | |||
|pathways=N, NS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=Labels, 2020-02, | |additional=Labels, 2020-02, | ||
}} | }} |
Revision as of 15:55, 19 February 2020
No MH, Heo JW, Yoo SZ, Kim CJ, Park DH, Kang JH, Seo DY, Han J, Kwak HB (2020) Effects of aging and exercise training on mitochondrial function and apoptosis in the rat heart. Pflugers Arch [Epub ahead of print]. |
No MH, Heo JW, Yoo SZ, Kim CJ, Park DH, Kang JH, Seo DY, Han J, Kwak HB (2020) Pflugers Arch
Abstract: 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; nโ=โ10, 4 months), young exercise (YE; nโ=โ10, 4 months), old sedentary (OS; nโ=โ10, 20 months), and old exercise (OE; nโ=โ10, 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 O2 respiratory capacity and Ca2+ retention capacity gradually decreased, and mitochondrial H2O2 emitting potential significantly increased with aging. Exercise training attenuated aging-induced mitochondrial H2O2 emitting potential and mitochondrial O2 respiratory capacity, while protecting Ca2+ 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. โข Keywords: Aging, Apoptosis, Exercise, Heart, Mitochondrial function โข Bioblast editor: Plangger M โข O2k-Network Lab: KR Busan Han J, KR Incheon Kwak HB
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Pathology: Aging;senescence
Stress:Cell death
Organism: Rat
Tissue;cell: Heart
Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS
Pathway: N, NS
HRR: Oxygraph-2k
Labels, 2020-02