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Physical exercise induces transient oxidative stress (hormesis) which triggers adaptive responses, including increased antioxidant enzyme activity (SOD, CAT, GPx) and mitochondrial biogenesis, ultimately reducing baseline oxidative stress in Type 2 Diabetes.

Engage in regular physical exercise, including moderate-intensity, resistance, or high-intensity interval training. While exercise temporarily increases oxidative stress, this triggers your body to produce more antioxidant enzymes and improve mitochondrial health, reducing overall oxidative stress.

ModerateSupportsMEDIUM confidence
The production of ROS during exercise is transient, with a peak of biomarker levels of oxidative damage between 24 and 48 h [97], inducing adaptation following the “hormesis” principle [93], thus enabling the activation of various signalling pathways that converge on the activation of transcription factors like Nrf2... The activation of Nrf2, NF-κB, and PGC-1α through exercise leads to an increase in the content and activity of enzymes such as SOD, CAT, and GPx [94,96,97,99].
Alfredo Caturano et al. · Current Issues in Molecular Biology · 2023

Why this rating

Review paper describing mechanisms and general effects; no specific human trial data provided.

Source

Oxidative Stress in Type 2 Diabetes: Impacts from Pathogenesis to Lifestyle Modifications

Alfredo Caturano et al. · Current Issues in Molecular Biology · 2023

DOI 10.3390/cimb45080420

narrative_reviewCited 490×
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DOI resolved against Crossref · corpus check 2026-06-10

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