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Heat Acclimation Training Attenuates Oxidative Stress and Improves Mitochondrial Function to Protect the Heart from Exertional Heat Stroke in Mice.

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Τίτλος: Heat Acclimation Training Attenuates Oxidative Stress and Improves Mitochondrial Function to Protect the Heart from Exertional Heat Stroke in Mice.
Συγγραφείς: Huang P; Sports Medicine Key Laboratory of Sichuan Province, Chengdu Sport University, Chengdu, CHINA.; Exercise Biological Center, China Institute of Sport Science, Beijing, CHINA., Rao Z; Exercise Biological Center, China Institute of Sport Science, Beijing, CHINA.; College of Physical Education, Shanghai Normal University, Shanghai, CHINA., Liu S; Exercise Biological Center, China Institute of Sport Science, Beijing, CHINA., Qu C; Physical Education College, Hebei Normal University, Shijiazhuang, CHINA., Geng X; Exercise Biological Center, China Institute of Sport Science, Beijing, CHINA., Zhang J; Exercise Biological Center, China Institute of Sport Science, Beijing, CHINA., Gao D; Exercise Biological Center, China Institute of Sport Science, Beijing, CHINA., Wu D; Exercise Biological Center, China Institute of Sport Science, Beijing, CHINA., Wei Q; Exercise Biological Center, China Institute of Sport Science, Beijing, CHINA., Zhao J; Exercise Biological Center, China Institute of Sport Science, Beijing, CHINA.
Πηγή: Medicine and science in sports and exercise [Med Sci Sports Exerc] 2026 Jul 01; Vol. 58 (7), pp. 1449-1463. Date of Electronic Publication: 2026 Mar 12.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Lippincott Williams & Wilkins Country of Publication: United States NLM ID: 8005433 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1530-0315 (Electronic) Linking ISSN: 01959131 NLM ISO Abbreviation: Med Sci Sports Exerc Subsets: MEDLINE
Imprint Name(s): Publication: Hagerstown, Md : Lippincott Williams & Wilkins
Original Publication: Madison, Wis., American College of Sports Medicine.
Ιατρικοί όροι (MeSH): Oxidative Stress*/physiology , Heat Stroke*/prevention & control , Heat Stroke*/physiopathology , Heat Stroke*/complications , Physical Conditioning, Animal*/physiology , Mitochondria, Heart*/physiology , Mitochondria, Heart*/ultrastructure , Acclimatization*/physiology , Hot Temperature*, Myocardium/pathology ; Biomarkers/blood ; Physical Exertion/physiology ; Troponin I/blood ; Animals ; Mice, Inbred C57BL ; Male ; Mice ; Disease Models, Animal
Περίληψη: Introduction: Exertional heat stroke (EHS) leads to cardiac structural damage and functional impairment. Heat acclimation (HA) training may serve as an effective strategy to prevent and mitigate such damage, yet the underlying molecular and cellular alterations remain unclear.
Methods: A C57BL/6N mouse model was used to study EHS-induced myocardial injury and evaluate the cardioprotective effects and mechanisms of HA training. Cardiac injury was assessed via plasma biomarkers, echocardiography, and histopathology, and transcriptomic analysis revealed links among injury, oxidative stress, and mitochondrial alterations. Transmission electron microscopy, O2K respirometry, and redox measurements further elucidated the mechanisms underlying mitochondrial structural and functional changes.
Results: EHS was associated with structural damage to myocardial tissue, including myocardial fibrosis, pathological echocardiographic changes, and a substantial elevation of the myocardial injury biomarker (cardiac troponin I). Mitochondrial structural disruption, impaired respiratory capacity, decreased adenosine triphosphate production, and disrupted redox balance were identified as potential contributors to these pathological changes. HA training was associated with attenuated EHS-induced myocardial damage, as evidenced by the amelioration of cardiac dysfunction and histopathological alterations, mitigation of mitochondrial structural damage, restoration of mitochondrial function, and increase in antioxidant capacity. Furthermore, HA training enhanced the thermoregulatory capacity and aerobic endurance of mice under high-temperature conditions. Transcriptomic analysis revealed that biological processes and signaling pathways enriched in differentially expressed genes with mitochondrial dysfunction and oxidative stress.
Conclusions: This work identifies transcriptional alterations and signaling pathways associated with EHS-induced myocardial injury, suggesting pivotal roles for mitochondrial dysfunction and oxidative stress. Additionally, this research provides a theoretical basis and potential intervention targets for the prevention and mitigation of heat stress-induced cardiovascular damage through HA training.
(Copyright © 2026 by the American College of Sports Medicine.)
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Grant Information: 24-28 Fundamental Research Funds for the China Institute of Sport Science; 2019YFF0301600 National Key Technology R&D Program of China; 2025JT05 Sports Science and Technology Research Project of Hebei Sports Bureau; No.2025-A033 Sports Medicine Key Laboratory of Sichuan Province
Contributed Indexing: Keywords: EXERTIONAL HEAT STROKE; HEAT ACCLIMATION; MITOCHONDRIA; MYOCARDIAL INJURY; TRANSCRIPTOMICS
Substance Nomenclature: 0 (Biomarkers)
0 (Troponin I)
Entry Date(s): Date Created: 20260316 Date Completed: 20260616 Latest Revision: 20260622
Update Code: 20260622
DOI: 10.1249/MSS.0000000000003971
PMID: 41839179
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1530-0315
DOI:10.1249/MSS.0000000000003971