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Updated: May 14, 2026

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Published on: February 7, 2018
Update: Is exercise-induced oxidative stress a friend or foe?
Scott K Powers1, Mari Carmen Gomez-Cabrera2
1Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, 32608, USA.
Exercise increases reactive oxygen species (ROS), which can cause oxidative damage but also promote beneficial adaptations. This review analyzes the dual role of exercise-induced ROS as friend or foe.
Area of Science:
- Exercise Physiology
- Cellular Biology
- Biochemistry
Background:
- Muscular exercise elevates the production of free radicals and reactive oxygen species (ROS).
- Early research identified exercise-induced ROS as a cause of tissue oxidative damage.
- Recent findings highlight ROS's role as signaling molecules in exercise adaptations.
Purpose of the Study:
- To review the dual effects of exercise-induced ROS on cellular macromolecules.
- To analyze the adaptive responses mediated by ROS signaling in skeletal muscle.
- To conduct a risk/benefit analysis of exercise-induced ROS production.
Main Methods:
- Literature review of studies on exercise, oxidative stress, and redox signaling.
- Examination of damage to cellular macromolecules caused by exercise-induced ROS.
- Analysis of adaptive signaling pathways activated by ROS in contracting muscles.
Main Results:
- Exercise-induced ROS can lead to oxidative damage in muscles and other tissues.
- ROS produced during exercise also act as crucial signaling molecules.
- These signaling pathways promote beneficial adaptations like increased mitochondrial volume and antioxidant capacity.
Conclusions:
- Exercise-induced ROS present a dichotomy: potential damage versus beneficial signaling.
- Understanding this duality is key to optimizing exercise benefits and mitigating risks.
- A balanced perspective on ROS is essential for exercise science and health.
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