Tissue-Specific Oxidative Stress Modulation by Exercise: A Comparison between MICT and HIIT in an Obese Rat Model.
Adipose Tissue
/ metabolism
Animals
Antioxidants
/ metabolism
Glutathione Peroxidase
/ metabolism
High-Intensity Interval Training
Lipoproteins, LDL
/ blood
Male
Malondialdehyde
/ blood
Muscle, Skeletal
/ metabolism
NADPH Oxidases
/ metabolism
Obesity
/ metabolism
Oxidants
/ metabolism
Oxidative Stress
Physical Conditioning, Animal
Rats
Rats, Zucker
Superoxide Dismutase
/ metabolism
Journal
Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826
Informations de publication
Date de publication:
2019
2019
Historique:
received:
18
02
2019
revised:
16
05
2019
accepted:
11
06
2019
entrez:
10
8
2019
pubmed:
10
8
2019
medline:
4
1
2020
Statut:
epublish
Résumé
Exercise is an effective strategy to reduce obesity-induced oxidative stress. The purpose of this study was to compare the effects of two training modalities (moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT)) on the pro/antioxidant status of different tissues in obese Zucker rats. Eight-week-old male Zucker rats ( Compared with the control, MICT increased GPx and catalase activities and the FRAP level in epididymal adipose tissue. HIIT increased the AOPP level in subcutaneous adipose tissue. In the muscle, HIIT increased both SOD and GPx activities and reduced the AOPP level, whereas MICT increased only SOD activity. Finally, plasma myeloperoxidase content was similarly decreased by both training modalities, whereas oxLDL was reduced only in the MICT group. Both HIIT and MICT improved the pro/antioxidant status. However, HIIT was more efficient than MICT in the skeletal muscle, whereas MICT was more efficient in epididymal adipose tissue. This suggests that oxidative stress responses to HIIT and MICT are tissue-specific. This could result in ROS generation via different pathways in these tissues. From a practical point of view, the two training modalities should be combined to obtain a global response in people with obesity.
Sections du résumé
BACKGROUND AND AIM
OBJECTIVE
Exercise is an effective strategy to reduce obesity-induced oxidative stress. The purpose of this study was to compare the effects of two training modalities (moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT)) on the pro/antioxidant status of different tissues in obese Zucker rats.
METHODS
METHODS
Eight-week-old male Zucker rats (
RESULTS
RESULTS
Compared with the control, MICT increased GPx and catalase activities and the FRAP level in epididymal adipose tissue. HIIT increased the AOPP level in subcutaneous adipose tissue. In the muscle, HIIT increased both SOD and GPx activities and reduced the AOPP level, whereas MICT increased only SOD activity. Finally, plasma myeloperoxidase content was similarly decreased by both training modalities, whereas oxLDL was reduced only in the MICT group.
CONCLUSION
CONCLUSIONS
Both HIIT and MICT improved the pro/antioxidant status. However, HIIT was more efficient than MICT in the skeletal muscle, whereas MICT was more efficient in epididymal adipose tissue. This suggests that oxidative stress responses to HIIT and MICT are tissue-specific. This could result in ROS generation via different pathways in these tissues. From a practical point of view, the two training modalities should be combined to obtain a global response in people with obesity.
Identifiants
pubmed: 31396298
doi: 10.1155/2019/1965364
pmc: PMC6664693
doi:
Substances chimiques
Antioxidants
0
Lipoproteins, LDL
0
Oxidants
0
oxidized low density lipoprotein
0
Malondialdehyde
4Y8F71G49Q
Glutathione Peroxidase
EC 1.11.1.9
Superoxide Dismutase
EC 1.15.1.1
NADPH Oxidases
EC 1.6.3.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1965364Déclaration de conflit d'intérêts
No conflicts of interest, financial or otherwise, are declared by the authors.
Références
Nature. 2000 Apr 6;404(6778):635-43
pubmed: 10766250
Endocr Rev. 2000 Dec;21(6):697-738
pubmed: 11133069
J Clin Endocrinol Metab. 2001 Dec;86(12):5755-61
pubmed: 11739435
Arterioscler Thromb Vasc Biol. 2003 Mar 1;23(3):365-7
pubmed: 12639823
Curr Opin Lipidol. 2003 Aug;14(4):353-9
pubmed: 12865732
Am J Physiol Endocrinol Metab. 2004 Sep;287(3):E558-65
pubmed: 15165998
J Clin Invest. 2004 Dec;114(12):1752-61
pubmed: 15599400
Arterioscler Thromb Vasc Biol. 2005 Jun;25(6):1102-11
pubmed: 15790935
Biochem Biophys Res Commun. 2005 Jun 17;331(4):1338-45
pubmed: 15883022
Am J Physiol Regul Integr Comp Physiol. 2006 Mar;290(3):R652-8
pubmed: 16223850
Int J Obes (Lond). 2006 Mar;30(3):400-18
pubmed: 16302012
Nature. 2006 Apr 13;440(7086):944-8
pubmed: 16612386
Free Radic Res. 2007 Feb;41(2):182-90
pubmed: 17364944
Cell Metab. 2007 May;5(5):323-5
pubmed: 17488634
Med Sci Sports Exerc. 2007 Aug;39(8):1423-34
pubmed: 17762377
Diabetes Obes Metab. 2007 Nov;9(6):813-39
pubmed: 17924865
Free Radic Biol Med. 2008 Jan 15;44(2):126-31
pubmed: 18191748
Cardiovasc Res. 2009 Mar 1;81(4):723-32
pubmed: 19047339
Nutrition. 2009 Mar;25(3):330-9
pubmed: 19062255
Biochem Biophys Res Commun. 2009 Feb 6;379(2):605-9
pubmed: 19121629
Med Sci Sports Exerc. 2009 Feb;41(2):459-71
pubmed: 19127177
J Hypertens. 2009 Apr;27(4):753-62
pubmed: 19300110
Circulation. 2010 Feb 16;121(6):759-67
pubmed: 20124122
Diabetes. 2010 May;59(5):1132-42
pubmed: 20150287
Med Sci Sports Exerc. 2010 Oct;42(10):1951-8
pubmed: 20195181
J Appl Physiol (1985). 2011 May;110(5):1311-8
pubmed: 21270351
J Sports Sci. 2011 Mar;29(6):547-53
pubmed: 21360405
J Appl Physiol (1985). 2011 Dec;111(6):1540-1
pubmed: 21979806
Endocr Regul. 2012 Jul;46(3):137-46
pubmed: 22808905
Horm Metab Res. 2013 Mar;45(3):190-6
pubmed: 22972182
Int J Sports Med. 2013 Mar;34(3):214-7
pubmed: 22972243
PLoS One. 2013 May 29;8(5):e65382
pubmed: 23734250
Int J Sports Med. 2014 Mar;35(3):199-202
pubmed: 23900899
Nutr Diabetes. 2013 Sep 16;3:e88
pubmed: 24042701
PLoS One. 2013 Nov 13;8(11):e80248
pubmed: 24236174
Sports Med. 2014 Jul;44(7):1005-17
pubmed: 24743927
Nutrients. 2014 Apr 21;6(4):1678-90
pubmed: 24763113
Pediatr Exerc Sci. 2015 Feb;27(1):67-76
pubmed: 25387489
J Exerc Nutrition Biochem. 2013 Dec;17(4):181-8
pubmed: 25566429
Oxid Med Cell Longev. 2015;2015:804794
pubmed: 25874024
J Phys Ther Sci. 2015 May;27(5):1435-9
pubmed: 26157235
Physiol Rep. 2015 Sep;3(9):null
pubmed: 26359238
Appl Physiol Nutr Metab. 2015 Dec;40(12):1242-52
pubmed: 26509584
Mol Cell Endocrinol. 2016 Jan 5;419:244-51
pubmed: 26522131
Sports Med. 2016 May;46(5):629-39
pubmed: 26666745
J Physiol. 2016 Sep 15;594(18):5081-92
pubmed: 26893258
Front Physiol. 2016 Apr 19;7:122
pubmed: 27148063
J Exerc Nutrition Biochem. 2016 Mar 31;20(1):29-35
pubmed: 27298810
PLoS One. 2016 Jul 01;11(7):e0158589
pubmed: 27368057
Med Sci Sports Exerc. 2017 Mar;49(3):403-412
pubmed: 27776003
Antioxidants (Basel). 2016 Dec 13;5(4):
pubmed: 27983587
Antioxid Redox Signal. 2017 Aug 10;27(5):276-310
pubmed: 28027662
Sleep. 2017 Aug 1;40(8):
pubmed: 28633495
Sports Med. 2018 Mar;48(3):733-746
pubmed: 28853029
Chronic Dis Transl Med. 2017 May 25;3(2):89-94
pubmed: 29063061
Sports Med. 2018 Feb;48(2):269-288
pubmed: 29127602
J Physiol Sci. 2018 Sep;68(5):699-706
pubmed: 29222739
Lipids Health Dis. 2018 Apr 16;17(1):81
pubmed: 29661202
Med Sci Sports Exerc. 2018 Oct;50(10):2058-2066
pubmed: 29762253
PLoS One. 2018 Jun 6;13(6):e0197124
pubmed: 29874256
Anal Biochem. 1988 Oct;174(1):331-6
pubmed: 3064653
PLoS One. 2019 Apr 9;14(4):e0214660
pubmed: 30964881
J Lab Clin Med. 1967 Jul;70(1):158-69
pubmed: 6066618
Methods Enzymol. 1984;105:457-64
pubmed: 6547201
Med Sci Sports Exerc. 1993 Oct;25(10):1135-40
pubmed: 8231758
Crit Rev Toxicol. 1993;23(1):21-48
pubmed: 8471159
Anal Biochem. 1996 Jul 15;239(1):70-6
pubmed: 8660627
Nat Genet. 1996 May;13(1):18-9
pubmed: 8673096
Kidney Int. 1996 May;49(5):1304-13
pubmed: 8731095