Redox modulation of mitochondriogenesis in exercise. Does antioxidant supplementation blunt the benefits of exercise training?
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic pathways and literature without systematic review methodology.
PubMed 25889822 · doi:10.1016/j.freeradbiomed.2015.04.006
What was done
This narrative review synthesizes research on exercise-induced reactive oxygen species (ROS) production, extramitochondrial ROS sources (such as NADPH oxidase and xanthine oxidase), and redox-sensitive signaling pathways (including MAP kinases, NF-κB, PGC-1α, p53, and heat shock factor) that drive mitochondrial biogenesis and endogenous antioxidant enzyme expression.
What was found
The abstract reports no quantitative values, sample sizes, or effect estimates. It outlines the qualitative concept that ROS generated during exercise serve as necessary signals for muscular adaptation and mitochondriogenesis, and argues that exogenous antioxidant supplementation may attenuate the expression of endogenous antioxidant enzymes (such as superoxide dismutase and glutathione peroxidase) and blunt training benefits.
Why it matters
It emphasizes a biological rationale against the indiscriminate use of antioxidant supplements during athletic training, framing exercise-induced ROS as physiological signals rather than solely damaging agents.
Limits
As a narrative review, the paper provides theoretical and mechanistic reasoning rather than new empirical data or a systematic review of clinical trials. The abstract includes no statistical data, study counts, or formal risk-of-bias assessments.
Cited by
- supports Supplemental antioxidants taken after exercise blunt the exercise-induced reactive oxygen species needed to stimulate mitochondrial biogenesis.