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Effects of intermittent exposure to hypobaric hypoxia and cold on skeletal muscle regeneration: Mitochondrial dynamics, protein oxidation and turnover

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Title: Effects of intermittent exposure to hypobaric hypoxia and cold on skeletal muscle regeneration: Mitochondrial dynamics, protein oxidation and turnover
Authors: Sergio Sánchez-Nuño, Garoa Santocildes, Josep Rebull, Raquel G. Bardallo, Montserrat Girabent-Farrés, Ginés Viscor, Teresa Carbonell, Joan Ramon Torrella
Source: Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)
Dipòsit Digital de la UB
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Publisher Information: Elsevier BV, 2024.
Publication Year: 2024
Subject Terms: Anoxemia, Male, 0301 basic medicine, Proteasome Endopeptidase Complex, 0303 health sciences, Oxidation-reduction reaction, Nitric Oxide Synthase Type III, Electron transport, Anoxèmia, Transport d'electrons, Mitochondrial Dynamics, Rats, Mitochondria, Muscle, Cold Temperature, 03 medical and health sciences, Reacció d'oxidació-reducció, Animals, Regeneration, Rats, Wistar, Muscle, Skeletal, Hypoxia, Oxidation-Reduction
Description: Muscle injuries and the subsequent regeneration events compromise muscle homeostasis at morphological, functional and molecular levels. Among the molecular alterations, those derived from the mitochondrial function are especially relevant. We analysed the mitochondrial dynamics, the redox balance, the protein oxidation and the main protein repairing mechanisms after 9 days of injury in the rat gastrocnemius muscle. During the recovery rats were exposed to intermittent cold exposure (ICE), intermittent hypobaric hypoxia (IHH), and both simultaneous combined stimuli. Non-injured contralateral legs were also analysed to evaluate the specific effects of the three environmental exposures. Our results showed that ICE enhanced mitochondrial adaptation by improving the electron transport chain efficiency during muscle recovery, decreased the expression of regulatory subunit of proteasome and accumulated oxidized proteins. Exposure to IHH did not show mitochondrial compensation or increased protein turnover mechanisms; however, no accumulation of oxidized proteins was observed. Both ICE and IHH, when applied separately, elicited an increased expression of eNOS, which could have played an important role in accelerating muscle recovery. The combined effect of ICE and IHH led to a complex response that could potentially impede optimal mitochondrial function and enhanced the accumulation of protein oxidation. These findings underscore the nuanced role of environmental stressors in the muscle healing process and their implications for optimizing recovery strategies.
Document Type: Article
File Description: application/pdf
Language: English
ISSN: 0891-5849
DOI: 10.1016/j.freeradbiomed.2024.09.032
Access URL: https://pubmed.ncbi.nlm.nih.gov/39313011
https://hdl.handle.net/2445/215752
http://hdl.handle.net/2445/215788
Rights: CC BY NC ND
Accession Number: edsair.doi.dedup.....c66c26c47cd1e56478f3afd45455c443
Database: OpenAIRE
Description
Abstract:Muscle injuries and the subsequent regeneration events compromise muscle homeostasis at morphological, functional and molecular levels. Among the molecular alterations, those derived from the mitochondrial function are especially relevant. We analysed the mitochondrial dynamics, the redox balance, the protein oxidation and the main protein repairing mechanisms after 9 days of injury in the rat gastrocnemius muscle. During the recovery rats were exposed to intermittent cold exposure (ICE), intermittent hypobaric hypoxia (IHH), and both simultaneous combined stimuli. Non-injured contralateral legs were also analysed to evaluate the specific effects of the three environmental exposures. Our results showed that ICE enhanced mitochondrial adaptation by improving the electron transport chain efficiency during muscle recovery, decreased the expression of regulatory subunit of proteasome and accumulated oxidized proteins. Exposure to IHH did not show mitochondrial compensation or increased protein turnover mechanisms; however, no accumulation of oxidized proteins was observed. Both ICE and IHH, when applied separately, elicited an increased expression of eNOS, which could have played an important role in accelerating muscle recovery. The combined effect of ICE and IHH led to a complex response that could potentially impede optimal mitochondrial function and enhanced the accumulation of protein oxidation. These findings underscore the nuanced role of environmental stressors in the muscle healing process and their implications for optimizing recovery strategies.
ISSN:08915849
DOI:10.1016/j.freeradbiomed.2024.09.032