Redox Water Consumption Attenuates Exercise-Induced Inflammation and Oxidative Stress in Physically Active Adults: A...

Acute high-intensity exercise induces transient inflammatory and oxidative stress responses, mediated by redox-sensitive signaling pathways and reflected by elevations in interleukin-6 (IL-6) and lipid peroxidation products. Modulation of these responses through hydration-based redox interventions remains insufficiently characterized at the biochemical level.

This randomized controlled trial investigated whether regular consumption of redox (alkaline) water influences exercise-induced inflammatory and oxidative stress markers in physically active adults.

Forty physically active adults were randomized into an experimental group (EG; n = 20) and consumed redox water subjected to molecular-level modification, yielding alkaline hydrogen-enriched water (pH 9.2-9.4), or a control group (CG; n = 20) that consumed standard water. After eight weeks of intervention, participants performed a standardized maximal aerobic exercise test. Plasma IL-6 and malondialdehyde (MDA) concentrations were measured at baseline and immediately post-exercise. Statistical analyses included two-way repeated measures ANOVA and ANCOVA.

A pronounced group × time interaction was observed for IL-6 (F(1,38) = 36.89, p < 0.001). The EG exhibited a significant post-exercise reduction in IL-6, whereas the CG demonstrated a robust increase. A significant group × time interaction was also detected for MDA (F(1,38) = 4.98, p = 0.029), reflecting stable lipid peroxidation levels in the EG and increased levels in the CG; however, baseline-adjusted analyses indicated that post-exercise MDA differences were largely attributable to initial variability. Hematological and coagulation parameters remained within physiological ranges in both groups.

Redox water intake was associated with lower immediate post-exercise IL-6 compared with controls after baseline adjustment; however, pronounced baseline imbalance limits causal interpretation and warrants confirmation in larger trials with balanced inflammatory profiles. These findings highlight a potential biochemical mechanism linking hydration redox properties with inflammatory regulation during physical stress.