Effects of age and unaccustomed resistance exercise on mitochondrial transcript and protein abundance in skeletal muscle of men

Mitochondrial dysfunction may contribute to age-associated muscle atrophy. Previous data has shown that resistance exercise (RE) increases mitochondrial gene expression and enzyme activity in older adults; however, the acute response to RE has not been well characterized. To characterize the acute m...

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Bibliographic Details
Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2015-04, Vol.308 (8), p.R734-R741
Main Authors: Ogborn, Daniel I, McKay, Bryon R, Crane, Justin D, Safdar, Adeel, Akhtar, Mahmood, Parise, Gianni, Tarnopolsky, Mark A
Format: Article
Language:English
Subjects:
Adolescent
Age Factors
Aged
Aging - genetics
Aging - metabolism
Aging - pathology
Autophagy
Biopsy
DNA, Mitochondrial - metabolism
Gene expression
Gene Expression Regulation
Humans
Male
Mens health
Mitochondria, Muscle - metabolism
Mitochondria, Muscle - pathology
Mitochondrial DNA
Mitochondrial Proteins - genetics
Mitochondrial Proteins - metabolism
Muscle, Skeletal - metabolism
Muscle, Skeletal - pathology
Musculoskeletal system
Physiology
Resistance Training
RNA, Messenger - metabolism
RNA-protein interactions
Sports training
Time Factors
Transcription, Genetic
Young Adult
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Summary:Mitochondrial dysfunction may contribute to age-associated muscle atrophy. Previous data has shown that resistance exercise (RE) increases mitochondrial gene expression and enzyme activity in older adults; however, the acute response to RE has not been well characterized. To characterize the acute mitochondrial response to unaccustomed RE, healthy young (21 ± 3 yr) and older (70 ± 4 yr) men performed a unilateral RE bout for the knee extensors. Muscle biopsies were taken at rest and 3, 24, and 48 h following leg press and knee extension exercise. The expression of the mitochondrial transcriptional regulator proliferator-activated receptor γ coactivator 1-α (PGC-1α) mRNA was increased at 3 h postexercise; however, all other mitochondrial variables decreased over the postexercise period, irrespective of age. ND1, ND4, and citrate synthase (CS) mRNA were all lower at 48 h postexercise, along with specific protein subunits of complex II, III, IV, and ATP synthase. Mitochondrial DNA (mtDNA) copy number decreased by 48 h postexercise, and mtDNA deletions were higher in the older adults and remained unaffected by acute exercise. Elevated mitophagy could not explain the reduction in mitochondrial proteins and DNA, because there was no increase in ubiquitinated voltage-dependent anion channel (VDAC) or its association with PTEN-induced putative kinase 1 (Pink1) or Parkin, and elevated p62 content indicated an impairment or reduction in autophagocytic flux. In conclusion, age did not influence the response of specific mitochondrial transcripts, proteins, and DNA to a bout of RE.
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.00005.2014