Abstract

The aim of this study was to investigate the effects of resistance training (RT) on the redox status of skeletal muscle in older adults. Thirteen males aged 64 ± 9 years performed full-body RT 2x/week for 6 weeks. Muscle biopsies were obtained from the vastus lateralis prior to and following RT. The mRNA, protein, and enzymatic activity levels of various endogenous antioxidants were determined. In addition, skeletal muscle 4-hydroxynonenal and protein carbonyls were determined as markers of oxidative damage. Protein levels of heat shock proteins (HSPs) were also quantified. RT increased mRNA levels of all assayed antioxidant genes, albeit protein levels either did not change or decreased. RT increased total antioxidant capacity, catalase, and glutathione reductase activities, and decreased glutathione peroxidase activity. Lipid peroxidation also decreased and HSP60 protein increased following RT. In summary, 6 weeks of RT decreased oxidative damage and increased antioxidant enzyme activities. Our results suggest the older adult responses to RT involve multi-level (transcriptional, post-transcriptional, and post-translational) control of the redox status of skeletal muscle.

Highlights

  • Published: 26 February 2021Advancing age is characterized by a decline in skeletal muscle mass and function [1]and is associated with the development of several chronic diseases [2]

  • Resistance training significantly increased the mRNA expression of all assayed antioxidants

  • Despite reports that aged skeletal muscle fails to upregulate heat shock proteins (HSPs) following acute exercise, possibly due to heightened basal expression, we found increased HSP60 protein levels after 6 weeks of resistance training (RT)

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Summary

Introduction

Published: 26 February 2021Advancing age is characterized by a decline in skeletal muscle mass and function [1]and is associated with the development of several chronic diseases [2]. Reactive species are recognized as important regulators of several signaling pathways [11], their overproduction can cause damage to different cellular components Essential in preventing such damage and maintaining the redox homeostasis in skeletal muscle are the antioxidant enzymes superoxide dismutase 1 (SOD1) and 2 (SOD2), catalase (CAT), glutathione peroxidase (GPX), and glutathione reductase (GSR) [12]. Together, these endogenous antioxidants constitute a defense and repair system that works against the potentially harmful effects of reactive species. A family of stress-induced proteins called heat shock proteins (HSPs) have been shown to be responsive to oxidative stress and to have a role in the skeletal muscle defense system [13,14,15]

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