Exercise generates reactive oxygen and nitrogen species (RONS), which can contribute to fatigue and macromolecular damage when excessive but also serve as important signaling intermediates for mitochondrial biogenesis, endogenous antioxidant defense, and other components of training adaptation. This underlies a paradox in sports science—high-dose non-selective antioxidants (vitamins C and E) reduce oxidative stress but blunt training adaptations. Molecular hydrogen (H₂) is often proposed to resolve it, usually on an outdated premise: the 2007 framing of H₂ as a selective antioxidant that directly scavenges the hydroxyl radical is not quantitatively tenable in vivo, where H₂ is micromolar and reacts far too slowly to compete with endogenous reactants. Current evidence instead positions H₂ as a redox-active signaling and hormetic modulator acting through Nrf2/Keap1, mitochondrial, and inflammatory pathways, so its antioxidant effect is largely indirect. We reframe the mechanism beyond the scavenger misnomer, show that, in a controlled rat comparison, H₂—unlike vitamin C—did not suppress post-exercise mitochondrial-biogenesis signaling, and appraise human evidence, whose benefits are small and selective—that is, modest in magnitude and confined to specific outcomes (fatigue, perceived exertion, explosive power, and endogenous antioxidant capacity) rather than broad, across-the-board performance gains. We advance and operationalize the hypothesis that redox-selective signaling lets H₂ enhance recovery without compromising—and potentially while complementing—training adaptation, a property no conventional antioxidant possesses, and outline the trials and reporting standards needed to test it.