title: Exercise at old age: does it increase or alleviate oxidative stress?
abstract: Aging is associated with increased free radical generation in the skeletal muscle that can cause oxidative modification of protein, lipid, and DNA. Physical activity has many well-established health benefits, but strenuous exercise increases muscle oxygen flux and elicits intracellular events that can lead to increased oxidative injury. The paradox arises as to whether exercise would be advisable to aged population. Research evidence indicates that senescent organisms are more susceptible to oxidative stress during exercise because of the age-related ultrastructural and biochemical changes that facilitate formation of reactive oxygen species (ROS). Aging also increases the incidence of muscle injury, and the inflammatory response can subject senescent muscle to further oxidative stress. Furthermore, muscle repair and regeneration capacity is reduced at old age that could potentially enhance the accrual of cellular oxidative damage. Predeposition of certain age-related pathologic conditions may exacerbate the risks. In spite of these risks, the elderly who are physically active benefit from exercise-induced adaptation in cellular antioxidant defense systems. Improved muscle mechanics, strength, and endurance make them less vulnerable to acute injury and chronic inflammation. Many critical questions remain regarding the relationship of aging and exercise as we enter a new millennium. For example, how does aging alter exercise-induced intracellular and intercellular mechanisms that generate ROS? Can acute and chronic exercise modulate the declined gene expression of metabolic and antioxidant enzymes seen at old age? Does exercise prevent age-dependent muscle loss (sarcopenia)? What kinds of antioxidant supplementation, if any, do aged people who are physically active need? Answers to these questions require highly specific research in both animals and humans.
authors.affiliation: Department of Kinesiology, Nutritional Science, and Institute on Aging, University of Wisconsin-Madison, 53706, USA. ji@soemadison.wisc.edu
authors.forename: L L
authors.initials: LL
authors.lastname: Ji
mesh_terms: D000368:Aged; D000375:Aging / Q000378:metabolism*; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use; D004198:Disease Susceptibility; D015444:Exercise; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D015227:Lipid Peroxidation; D008875:Middle Aged; D008928:Mitochondria / Q000378:metabolism; D008954:Models, Biological; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress; D010101:Oxygen Consumption; D005082:Physical Exertion / Q000502:physiology; D010809:Physical Fitness; D017382:Reactive Oxygen Species / Q000378:metabolism; D012306:Risk; D015398:Signal Transduction; D013482:Superoxide Dismutase / Q000378:metabolism; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000975:Antioxidants; D009124:Muscle Proteins; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; D013482:Superoxide Dismutase