Please use this identifier to cite or link to this item: http://hdl.handle.net/10773/40038
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dc.contributor.authorSilva, Mónica Garciapt_PT
dc.contributor.authorNunes, Paulopt_PT
dc.contributor.authorOliveira, Paulapt_PT
dc.contributor.authorFerreira, Ritapt_PT
dc.contributor.authorFardilha, Margaridapt_PT
dc.contributor.authorMoreira-Gonçalves, Danielpt_PT
dc.contributor.authorDuarte, José Albertopt_PT
dc.contributor.authorOliveira, Maria Manuelpt_PT
dc.contributor.authorPeixoto, Franciscopt_PT
dc.date.accessioned2024-01-10T11:22:46Z-
dc.date.available2024-01-10T11:22:46Z-
dc.date.issued2022-12-
dc.identifier.issn2079-7737pt_PT
dc.identifier.urihttp://hdl.handle.net/10773/40038-
dc.description.abstractMost studies on the effects of physical exercise have focused on its influence on muscle tissue, forgetting its interference in liver function. Ageing leads to the progressive impairment of hepatic functions. Several biochemical and bioenergetics parameters were determined to test the impact of a lifelong aerobic training program in the hepatic age-related and the development of an adaptative response. Liver samples were collected from 28 male Wistar rats (4-week-old, 159.4 ± 11.9 g at the beginning of the protocol), randomly distributed into two groups: non-exercised or exercised and submitted to a treadmill exercise program (60 min/day, 5 days/week, at 70% of maximal running speed), for 24 (n = 9) or 54 weeks (n = 10). A maximal running speed test was performed to determine the training speed. Antioxidant enzyme activity, cellular redox status, oxidative stress, mitochondrial respiratory chain enzymes and respiratory activity were performed in liver samples. Lifelong exercise decreased the age-associated decline in mitochondrial dysfunction, increasing the respiratory rate in state 2 (mitochondrial respiration stimulated by the substrate in the absence of added ADP) (p = 0.03) and citrate synthase enzymatic activity (p = 0.007). Complex II (p < 0.0001) and IV (p < 0.001) showed a decrease in enzymatic activity. Ageing-related oxidative stress was also attenuated by physical exercise, as showed by the increase in first-line defense antioxidant enzymes (superoxide dismutase (p = 0.07) and catalase (p = 0.03)), decreased lipid peroxidation levels (p = 0.864 for total fraction, p = 0,27 for mitochondrial fraction) and higher glutathione reduced/oxidized ratio (p = 0.02). According to our results, the regular practice of exercise can prevent the liver’s mitochondrial dysfunction and loss of antioxidant system efficacy that may arise from ageing, highlighting the benefit of lifelong aerobic exercise in preventing age-related hepatic impairment and associated diseases.pt_PT
dc.language.isoengpt_PT
dc.publisherMDPIpt_PT
dc.rightsopenAccesspt_PT
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectAerobic trainingpt_PT
dc.subjectAgeingpt_PT
dc.subjectAntioxidant enzymespt_PT
dc.subjectBiochemistrypt_PT
dc.subjectLiverpt_PT
dc.subjectOxidative stresspt_PT
dc.subjectMitochondriapt_PT
dc.titleLong-Term Aerobic Training Improves Mitochondrial and Antioxidant Function in the Liver of Wistar Rats Preventing Hepatic Age-Related Function Declinept_PT
dc.typearticlept_PT
dc.description.versionpublishedpt_PT
dc.peerreviewedyespt_PT
degois.publication.issue12pt_PT
degois.publication.titleBiologypt_PT
degois.publication.volume11pt_PT
dc.identifier.doi10.3390/biology11121750pt_PT
dc.identifier.essn2079-7737pt_PT
dc.identifier.articlenumber1750pt_PT
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