Metabolic mitochondrial alterations prevail in the female rat heart 8 weeks after exercise cessation.
cardiac remodelling
exercise cessation
female
high-fat high-sugar diet
metabolic dysfunction
mitochondria
Journal
European journal of clinical investigation
ISSN: 1365-2362
Titre abrégé: Eur J Clin Invest
Pays: England
ID NLM: 0245331
Informations de publication
Date de publication:
Nov 2023
Nov 2023
Historique:
revised:
15
06
2023
received:
26
03
2023
accepted:
30
06
2023
pubmed:
1
8
2023
medline:
1
8
2023
entrez:
1
8
2023
Statut:
ppublish
Résumé
The consumption of high-caloric diets strongly contributes to the development of non-communicable diseases (NCDs), including cardiovascular disease, the leading cause of mortality worldwide. Exercise (along with diet intervention) is one of the primary non-pharmacological approaches to promote a healthier lifestyle and counteract the rampant prevalence of NCDs. The present study evaluated the effects of exercise cessation after a short period training on the cardiac metabolic and mitochondrial function of female rats. Seven-week-old female Sprague-Dawley rats were fed a control or a high-fat, high-sugar (HFHS) diet and, after 7 weeks, the animals were kept on a sedentary lifestyle or submitted to endurance exercise for 3 weeks (6 days per week, 20-60 min/day). The cardiac samples were analysed 8 weeks after exercise cessation. The consumption of the HFHS diet triggered impaired glucose tolerance, whereas the HFHS diet and physical exercise resulted in different responses in plasma adiponectin and leptin levels. Cardiac mitochondrial respiration efficiency was decreased by the HFHS diet consumption, which led to reduced ATP and increased NAD(P)H mitochondrial levels, which remained prevented by exercise 8 weeks after cessation. Exercise training-induced cardiac adaptations in redox balance, namely increased relative expression of Nrf2 and downstream antioxidant enzymes persist after an eight-week exercise cessation period. Endurance exercise modulated cardiac redox balance and mitochondrial efficiency in female rats fed a HFHS diet. These findings suggest that exercise may elicit cardiac adaptations crucial for its role as a non-pharmacological intervention for individuals at risk of developing NCDs.
Sections du résumé
BACKGROUND
BACKGROUND
The consumption of high-caloric diets strongly contributes to the development of non-communicable diseases (NCDs), including cardiovascular disease, the leading cause of mortality worldwide. Exercise (along with diet intervention) is one of the primary non-pharmacological approaches to promote a healthier lifestyle and counteract the rampant prevalence of NCDs. The present study evaluated the effects of exercise cessation after a short period training on the cardiac metabolic and mitochondrial function of female rats.
METHODS
METHODS
Seven-week-old female Sprague-Dawley rats were fed a control or a high-fat, high-sugar (HFHS) diet and, after 7 weeks, the animals were kept on a sedentary lifestyle or submitted to endurance exercise for 3 weeks (6 days per week, 20-60 min/day). The cardiac samples were analysed 8 weeks after exercise cessation.
RESULTS
RESULTS
The consumption of the HFHS diet triggered impaired glucose tolerance, whereas the HFHS diet and physical exercise resulted in different responses in plasma adiponectin and leptin levels. Cardiac mitochondrial respiration efficiency was decreased by the HFHS diet consumption, which led to reduced ATP and increased NAD(P)H mitochondrial levels, which remained prevented by exercise 8 weeks after cessation. Exercise training-induced cardiac adaptations in redox balance, namely increased relative expression of Nrf2 and downstream antioxidant enzymes persist after an eight-week exercise cessation period.
CONCLUSIONS
CONCLUSIONS
Endurance exercise modulated cardiac redox balance and mitochondrial efficiency in female rats fed a HFHS diet. These findings suggest that exercise may elicit cardiac adaptations crucial for its role as a non-pharmacological intervention for individuals at risk of developing NCDs.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e14069Subventions
Organisme : European Regional Development Fund
ID : PTDC/DTP-DES/1082/2014 (POCI-01-0145-FEDER-016657)
Organisme : European Regional Development Fund
ID : CENTRO-01-0246-FEDER-000010
Organisme : European Regional Development Fund
ID : UIDB/04539/2020
Organisme : European Regional Development Fund
ID : UIDP/04539/2020
Organisme : European Regional Development Fund
ID : LA/P/0058/2020
Organisme : Fundação para a Ciência e a Tecnologia
ID : SFRH/BD/11924/2022
Organisme : Fundação para a Ciência e a Tecnologia
ID : SFRH/BD/11934/2022
Organisme : Fundação para a Ciência e a Tecnologia
ID : SFRH/BD/5539/2020
Organisme : Fundação para a Ciência e a Tecnologia
ID : SFRH/BPD/116061/2016
Organisme : H2020 Marie Skłodowska-Curie Actions
ID : 722619
Organisme : H2020 Marie Skłodowska-Curie Actions
ID : 734719
Organisme : European Union
ID : HORIZON-HLTH-2022-STAYHLTH-101080329
Informations de copyright
© 2023 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.
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