title: Vitamin E-enriched diet reduces adaptive responses to training determining respiratory capacity and redox homeostasis in rat heart.
abstract: We investigated whether reactive oxygen species (ROS) are involved in heart adaptive responses administering a vitamin E-enriched diet to trained rats. Using the homogenates and/or mitochondria from rat hearts we determined the aerobic capacity, tissue level of mitochondrial proteins, and expression of cytochrome c and factors (PGC-1, NRF-1, and NRF-2) involved in mitochondrial biogenesis. We also determined the oxidative damage, glutathione peroxidase (GPX) and reductase activities, glutathione content, mitochondrial ROS release rate, and susceptibility to in vitro oxidative challenge. Glutathione (GSH) content was not affected by both training and antioxidant supplementation. Conversely, antioxidant supplementation prevented metabolic adaptations to training, such as the increases in oxidative capacity, tissue content of mitochondrial proteins, and cytochrome c expression, attenuated some protective adaptations, such as the increase in antioxidant enzyme activities, and did not modify the decrease in ROS release by succinate supplemented mitochondria. Moreover, vitamin E prevented the training-linked increase in tissue capacity to oppose an oxidative attach. The antioxidant effects were associated with decreased levels of PGC-1, NRF-1, and NRF-2 expression. Our results support the idea that some heart adaptive responses to training depend on ROS produced during the exercise sessions and are mediated by the increase in PGC-1 expression which is involved in both the regulation of respiratory capacity and antioxidant protection. However, vitamin inability to prevent some adaptations suggests that other signaling pathways impinging on PGC-1 can modify the response to the antioxidant integration.
authors.affiliation: a Dipartimento di Biologia , Università di Napoli , Napoli , Italy.
authors.forename: Paola
authors.initials: P
authors.lastname: Venditti
authors.affiliation: a Dipartimento di Biologia , Università di Napoli , Napoli , Italy.
authors.forename: Gaetana
authors.initials: G
authors.lastname: Napolitano
authors.affiliation: a Dipartimento di Biologia , Università di Napoli , Napoli , Italy.
authors.forename: Daniela
authors.initials: D
authors.lastname: Barone
authors.affiliation: a Dipartimento di Biologia , Università di Napoli , Napoli , Italy.
authors.forename: Emanuela
authors.initials: E
authors.lastname: Pervito
authors.affiliation: a Dipartimento di Biologia , Università di Napoli , Napoli , Italy.
authors.forename: Sergio
authors.initials: S
authors.lastname: Di Meo
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects*; D000818:Animals; D019587:Dietary Supplements; D015870:Gene Expression; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000187:drug effects / Q000235:genetics; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010805:Physical Conditioning, Animal; D051381:Rats; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D024101:Mitochondrial Proteins; D014810:Vitamin E
keywords: H2O2 release; mitochondria; oxidative damage; rat heart; training; vitamin E