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1.
J Phys Act Health ; 17(9): 895-901, 2020 08 12.
Article in English | MEDLINE | ID: mdl-32788413

ABSTRACT

BACKGROUND: Endogenous antioxidants are critical to limiting cellular oxidative damage. METHODS: The authors determined if habitual physical activity (PA) and cardiorespiratory fitness were associated with skeletal muscle expression of endogenous antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) and circulating oxidative stress markers (serum 8-hydroxy-2'-deoxyguanosine [8-OHdG]; oxidized low-density lipoprotein [LDL]) in older adults. Moderate to vigorous PA (MVPA) was estimated using a validated PA questionnaire in 26 older adults (mean [SD]; M/F = 9/17, age = 68 [4] y, body mass index = 26 [3] kg·m-2). Maximal oxygen consumption was estimated using the YMCA submaximal cycle test. Skeletal muscle endogenous antioxidants and serum 8-OHdG and oxidized LDL were measured. Bivariate and partial correlations (controlling for body mass index) were utilized to determine associations among variables. RESULTS: MVPA (1640 [1176] kcal·wk-1) was correlated with superoxide dismutase 2 (r = .55), catalase (r = .55), glutathione peroxidase 1 (r = .48), and 8-OHdG (r = -.41) (all Ps < .05), but not oxidized LDL. MVPA and 8-OHdG were not significantly correlated when controlling for body mass index (r = -.29). Estimated maximal oxygen consumption was correlated with glutathione peroxidase 1 (r = .48; P < .05). CONCLUSIONS: These data show that skeletal muscle endogenous antioxidant expression and circulating oxidative damage are associated with habitual MVPA in older adults. Thus, MVPA in older adults may be protective against reactive oxygen species damage due to higher expression of endogenous antioxidants.


Subject(s)
Antioxidants , Exercise , Muscle, Skeletal/metabolism , Aged , Antioxidants/metabolism , Catalase/metabolism , Female , Humans , Male , Middle Aged , Oxidative Stress
2.
Appl Physiol Nutr Metab ; 41(4): 446-51, 2016 Apr.
Article in English | MEDLINE | ID: mdl-26988770

ABSTRACT

Elevated skeletal muscle expression of toll-like receptor 4 (TLR4) has been linked to increased inflammation in clinical populations. TNFα converting enzyme (TACE), which cleaves membrane-bound TNFα (mTNFα) to its soluble (sTNFα) and more bioactive form, has been linked to chronic disease. In contrast, higher physical activity level is associated with decreased chronic disease risk and inflammation. The purpose of the present study was to examine the relationship between physical activity and skeletal muscle TLR4, TACE, and TNFα in older adults. In 26 older adults (age = 68 ± 4 years, body mass index = 26 ± 3 kg·m(-2)), self-reported physical activity (kcal·week(-1)), estimated maximal oxygen consumption, and body composition (air plethysmography) were measured. TLR4, TACE, mTNFα, and sTNFα were measured in skeletal muscle biopsies (vastus lateralis) using western blot analyses. Pearson product-moment correlations were run between variables. Significance was set at p < 0.05. Skeletal muscle TACE was directly associated with sTNFα (r = 0.53, p < 0.01). Linear regression modeling showed that mTNFα and TACE expression were predictive of sTNFα expression. No correlations were observed between physical activity and TLR4, TACE, or sTNFα. Percent body fat was directly associated with skeletal muscle TLR4 (r = 0.52, p < 0.01) and TACE (r = 0.50, p < 0.01), whereas fasting blood glucose was directly associated with TACE and sTNFα. In conclusion, we found that percent body fat was directly associated with TLR4 and TACE expression in skeletal muscle of older adults. These findings suggest that elevated skeletal muscle expression of TLR4 and TACE may contribute to the augmented inflammation and chronic disease risk observed with increased adiposity.


Subject(s)
ADAM17 Protein/metabolism , Adiposity , Muscle, Skeletal/metabolism , Toll-Like Receptor 4/metabolism , ADAM17 Protein/genetics , Aged , Blood Glucose/metabolism , Body Mass Index , Exercise , Female , Humans , Linear Models , Male , Middle Aged , Oxygen Consumption , Self Report , Toll-Like Receptor 4/genetics , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/metabolism
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