急性運動誘発性炎症および酸化ストレスに対する分子状水素吸入の影響
Sedentary rats exercised on a treadmill at 80% of maximum running speed while inhaling either 2% H2 gas or a control gas mixture. Animals were sacrificed immediately or 3 hours post-exercise. Plasma concentrations of TNF-α, IL-1β, and IL-6 were measured alongside oxidative stress markers including superoxide dismutase (SOD) activity, thiobarbituric acid reactive species (TBARS), and nitrite/nitrate (NOx). Intracellular signaling via GSK3α/β and CREB phosphorylation was also evaluated. Exercise elevated all measured parameters. H2 inhalation suppressed the exercise-induced rises in TNF-α and IL-6, enhanced SOD activity, and reduced TBARS levels at the 3-hour time point. CREB phosphorylation, which increased with exercise, was attenuated by H2, whereas GSK3α/β phosphorylation was unaffected by either exercise or H2. These findings indicate that H2 inhalation modulates multiple stress-response pathways activated during acute exercise.
H2 inhalation suppresses exercise-induced TNF-α and IL-6 surges, enhances SOD-mediated antioxidant capacity, reduces lipid peroxidation (TBARS), and attenuates CREB phosphorylation, collectively dampening inflammatory and oxidative stress cascades in skeletal muscle.
For inhalation applications of molecular hydrogen, the lower flammability limit (LFL) deserves careful handling. The classical 4% figure applies to closed-system mixtures; the practical inhalation-environment threshold is 10%. Even pure-hydrogen output (the UFL 75% paradox) passes through the flammable range at the air–gas boundary. High-concentration (66% / 100%) inhalers are documented in the Japanese Consumer Affairs Agency accident-information database and are not recommended.
See also:
https://h2-papers.org/en/papers/30243702