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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Molecular hydrogen downregulates acute exhaustive exercise-induced skeletal muscle damage

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Author(s):
Nogueira, Jonatas E. [1] ; Amorim, Mateus R. [2] ; Pinto, Ana P. [3] ; da Rocha, Alisson L. [4, 3] ; da Silva, Adelino S. R. [1, 3] ; Branco, Luiz G. S. [4, 2, 3]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Sch Phys Educ & Sports Ribeirao Preto, Ribeirao Preto, SP - Brazil
[2] Univ Sao Paulo, Dent Sch Ribeirao Preto, Dept Basic & Oral Biol, Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Sch Med Ribeirao Preto, Postgrad Program Rehabil & Funct Performance, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, Ribeirao Preto, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Canadian Journal of Physiology and Pharmacology; v. 99, n. 8, p. 812-820, AUG 2021.
Web of Science Citations: 0
Abstract

Physical exercise-induced skeletal muscle damage may be characterized by increased oxidative stress, inflammation, and apoptosis which may be beneficial when exercise is regular, but it is rather harmful when exercise is exhaustive and performed acutely by unaccustomed individuals. Molecular hydrogen (H-2) has emerged as a potent antioxidant, anti-inflammatory, and anti-apoptotic agent, but its action on the deleterious effects of acute exhaustive exercise in muscle damage remain unknown. Therefore, we tested the hypothesis that H-2 decreases acute exhaustive exercise-induced skeletal muscle damage of sedentary rats. Rats ran to exhaustion on a sealed treadmill inhaling an H-2-containing mixture or the control gas. We measured oxidative stress (SOD, GSH, and TBARS), inflammatory (TNF-alpha, IL-1 beta, IL-6, IL-10, and NF-kappa B phosphorylation), and apoptotic (expression of caspase-3, Bcl-2, and HSP70) markers. Exercise caused no changes in SOD activity but increased TBARS levels. H-2 caused increases in exercise-induced SOD activity and blunted exercise-induced increased TBARS levels. We observed exercise-induced TNF-alpha and IL-6 surges as well as NF-kappa B phosphorylation, which were blunted by H-2. Exercise increased cleaved caspase-3 expression, and H-2 reduced this response. In conclusion, H-2 effectively downregulates muscle damage, reducing oxidative stress, inflammation, and apoptosis after acute exhaustive exercise performed by an unaccustomed organism. (AU)

FAPESP's process: 17/09878-0 - Effect of vagal stimulation during LPS immune challenge in normotensive and spontaneously hypertensive rats
Grantee:Mateus Ramos Amorim
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 16/17681-9 - Pathophysiological changes during systemic inflammation
Grantee:Luiz Guilherme de Siqueira Branco
Support type: Research Projects - Thematic Grants
FAPESP's process: 17/19869-8 - Molecular mechanisms related to increased hepatic fat content in response to excessive physical exercise
Grantee:Ana Paula Pinto
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 17/12765-2 - Emerging role of rev-erb-alpha in molecular adaptations to different physical exercise models
Grantee:Alisson Luiz da Rocha
Support type: Scholarships in Brazil - Doctorate