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Molecular hydrogen (H) as a potential treatment for acute and chronic fatigue.

急性および慢性疲労に対する分子状水素(H₂)の潜在的効果に関するレビュー

review not specified not assessed

Abstract

Fatigue manifests in both acute forms—such as those following physical exertion or alcohol consumption—and chronic forms associated with conditions including Parkinson's disease, multiple sclerosis, influenza, and COVID-19. This review examines the mechanistic role of reactive oxygen and nitrogen species (ROS/RNS) in the pathogenesis of fatigue, with particular attention to downstream mitochondrial dysfunction as a shared pathological feature. The antioxidant properties of molecular hydrogen intake are evaluated in this context, and the authors propose that H2 may be well positioned to address oxidative stress-associated fatigue across both acute and chronic presentations. Evidence from prior antioxidant intervention studies is discussed to support this hypothesis.

Mechanism

ROS and reactive nitrogen species impair mitochondrial function, contributing to fatigue onset. Molecular hydrogen is proposed to selectively neutralize these reactive species, thereby restoring mitochondrial homeostasis and reducing fatigue symptoms.

Bibliographic

Authors
Lucas K, Rosch M, Langguth P
Journal
Arch Pharm (Weinheim)
Year
2021
PMID
33368699
DOI
10.1002/ardp.202000378

Tags

Disease:COVID-19 運動・疲労回復 パーキンソン病 Mechanism:炎症抑制 ミトコンドリア 酸化ストレス 活性酸素種

Delivery context

The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).

Safety notes

The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).

See also:

Other papers on the same disease / condition

Cite as: H2 Papers — PMID 33368699. https://h2-papers.org/en/papers/33368699
Source: PubMed PMID 33368699