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Physiol Rep. 2016 Jul;4(13). pii: e12849. doi: 10.14814/phy2.12849.

Resistance exercise training and in vitro skeletal muscle oxidative capacity in older adults.

Author information

1
United Stated Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, North Dakota kdavy@vt.edu.
2
Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, Virginia Fralin Translational Obesity Research Center, Virginia Tech, Blacksburg, Virginia Center for Gerontology, Virginia Tech, Blacksburg, Virginia.
3
Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, Virginia.
4
Department of Internal Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut.
5
Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, Virginia Fralin Translational Obesity Research Center, Virginia Tech, Blacksburg, Virginia Metabolic Phenotyping Core, Virginia Tech, Blacksburg, Virginia.
6
Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, Virginia Fralin Translational Obesity Research Center, Virginia Tech, Blacksburg, Virginia Center for Gerontology, Virginia Tech, Blacksburg, Virginia Metabolic Phenotyping Core, Virginia Tech, Blacksburg, Virginia.
7
Department of Biology, Pikes Peak Community College, Colorado Springs, Colorado.
8
Fralin Translational Obesity Research Center, Virginia Tech, Blacksburg, Virginia Center for Gerontology, Virginia Tech, Blacksburg, Virginia Department of Human Development, Virginia Tech, Blacksburg, Virginia.

Abstract

Whether resistance exercise training (RET) improves skeletal muscle substrate oxidative capacity and reduces mitochondrial production of reactive oxygen species in older adults remains unclear. To address this, 19 older males (≥60 years) were randomized to a RET (n = 11) or to a waitlist control group (n = 8) that remained sedentary for 12 weeks. RET was comprised of three upper body and four lower body movements on resistance machines. One set of 8-12 repetitions to failure of each movement was performed on three nonconsecutive days/week. Improvements in chest press and leg press strength were assessed using a three-repetition maximum (3 RM). Body composition was assessed via dual energy X-ray absorptiometry. Muscle biopsies were obtained from the vastus lateralis muscle at baseline and at both 3 weeks and 12 weeks. Palmitate and pyruvate oxidation rates were measured from the (14)CO2 produced from [1-(14)C] palmitic acid and [U-(14)C] pyruvate, respectively, during incubation of muscle homogenates. PGC-1α, TFAM, and PPARδ levels were quantified using qRT-PCR Citrate synthase (CS) and β-HAD activities were determined spectrophotometrically. Mitochondrial production of reactive oxygen species (ROS) were assessed using the Amplex Red Hydrogen Peroxide/Peroxidase assay. There were no significant changes in body weight or body composition following the intervention. Chest press and leg press strength (3RM) increased ~34% (both P < 0.01) with RET There were no significant changes in pyruvate or fatty acid oxidation or in the expression of target genes with the intervention. There was a modest increase (P < 0.05) in βHAD activity with RET at 12 weeks but the change in CS enzyme activity was not significant. In addition, there were no significant changes in ROS production in either group following RET Taken together, the findings of this study suggest that 12 weeks of low volume RET does not increase skeletal muscle oxidative capacity or reduce ROS production in older adults.

KEYWORDS:

Metabolism; mitochondria; oxidative damage; strength

PMID:
27405968
PMCID:
PMC4945835
DOI:
10.14814/phy2.12849
[Indexed for MEDLINE]
Free PMC Article
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