The combination of oral quercetin supplementation and exercise prevents brain mitochondrial biogenesis

The purpose of this study was to investigate whether the combination of oral quercetin (Q) supplementation and exercise prevents mitochondrial biogenesis. Four groups of Wistar rats were tested: quercetin-sedentary (Q-sedentary); quercetin-exercised (Q-exercised); no-quercetin-sedentary (NQ-sedentar...

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Bibliographic Details
Authors: Casuso Pérez, Rafael, Martínez-López, Emilio J, Camiletti-Moirón, Daniel, Martínez-Romero, Rubén, Cañuelo, Ana, Martínez-Amat, Antonio
Format: article
Publication Date:2014
Country:España
Institution:Universidad Loyola Andalucía
Repository:Brújula
OAI Identifier:oai:repositorio.uloyola.es:20.500.12412/6265
Online Access:https://hdl.handle.net/20.500.12412/6265
Access Level:Open access
Keyword:Quercetin
Exercise
Brain
Mitochondria
Redox status
Description
Summary:The purpose of this study was to investigate whether the combination of oral quercetin (Q) supplementation and exercise prevents mitochondrial biogenesis. Four groups of Wistar rats were tested: quercetin-sedentary (Q-sedentary); quercetin-exercised (Q-exercised); no-quercetin-sedentary (NQ-sedentary); and no-quercetin-exercised (NQ-exercised). Treadmill exercise training took place 5 days a week for 6 weeks. Quercetin groups were supplemented with 25 mg/kg of quercetin throughout the experimental period. Sirtuin 1 (SIRT1), peroxisome-proliferator-activated receptor γ coactivator-1α (PGC-1α) mRNA levels and the activity of citrate synthase (CS) were measured in the brain. Redox status was also quantified by measuring the enzymatic activity of catalase (CAT) and superoxide dismutase (SOD) and protein carbonyls content (PCC). Q-Exercised (P < 0.001) and Q-sedentary (P = 0.042) groups increased PCC. In the Q-sedentary, there was an antioxidant enzymatic activity modulation for CAT (P < 0.001) and SOD (P < 0.01) but not in the Q-exercised. Q-sedentary showed a similar response to exercise in the brain by increasing CS activity in the brain (P < 0.01) and by activating the transcription of SIRT1 (P < 0.001) and PGC-1α (P = 0.03). These effects were hampered in the Q-exercised group. Quercetin is a pro-oxidant agent in the brain, but it modulates antioxidant activity in a sedentary condition. Quercetin supplementation during exercise compromises mitochondrial biogenesis induced separately by quercetin and exercise.