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Recent Advances in Molecular Hydrogen Research Reducing Exercise-Induced Oxidative Stress and Inflammation.

運動誘発性酸化ストレスおよび炎症に対する分子状水素研究の最新動向

review mixed routes not assessed

Abstract

Regular physical exercise generates moderate levels of oxidative stress and inflammation that are generally beneficial to the organism; however, exhaustive or unaccustomed exercise can produce harmful levels of these responses. Molecular hydrogen (H2) has attracted attention as a potent antioxidant and anti-inflammatory agent across various pathological contexts, yet its role under physiological conditions such as exercise remains poorly characterized. This review consolidates findings from both animal and human studies to provide an overview of how H2 modulates exercise-induced oxidative stress and inflammatory pathways, highlighting the current state of knowledge and identifying gaps that warrant further investigation.

Mechanism

H2 is proposed to selectively neutralize excess reactive oxygen species generated during exercise and to suppress pro-inflammatory signaling cascades, thereby reducing both oxidative damage and inflammatory responses in exercising organisms.

Bibliographic

Authors
Nogueira JE, Branco LGS
Journal
Curr Pharm Des
Year
2021
PMID
33185152
DOI
10.2174/1381612826666201113100245

Tags

Disease:運動・疲労回復 Mechanism:抗酸化酵素 ヒドロキシルラジカル消去 炎症抑制 脂質過酸化 酸化ストレス 活性酸素種

Delivery context

This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).

Safety notes

This study combines multiple delivery routes. As a general principle, the most efficient route for routine hydrogen intake is inhalation. Inhalation carries explosion risk (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).

See also:

Other papers on the same disease / condition

Cite as: H2 Papers — PMID 33185152. https://h2-papers.org/en/papers/33185152
Source: PubMed PMID 33185152