Exercise training and taurine supplementation reduce oxidative stress and prevent endothelium dysfunction in rats fed a highly palatable diet

Life Sciences ◽  
2015 ◽  
Vol 139 ◽  
pp. 91-96 ◽  
Author(s):  
Leandro Kansuke Oharomari ◽  
Nádia Fagundes Garcia ◽  
Ellen Cristini de Freitas ◽  
Alceu Afonso Jordão Júnior ◽  
Paula Payão Ovídio ◽  
...  
2016 ◽  
Vol 22 (1) ◽  
pp. 12-17 ◽  
Author(s):  
Nádia F. Garcia ◽  
Carmem P. Valgas da Silva ◽  
Maycon Jr. Ferreira ◽  
Leandro K. Oharomari ◽  
Thalita Rocha ◽  
...  

2020 ◽  
Vol 16 (S10) ◽  
Author(s):  
Sarah Wehle Gehres ◽  
Andreia Silva da Rocha ◽  
Yuri Elias Rodrigues ◽  
Guilherme G Schu Peixoto ◽  
Afonso Kopczynski Carvalho ◽  
...  

2017 ◽  
Vol 68 (5) ◽  
pp. 699-706 ◽  
Author(s):  
Daniela Delwing-de Lima ◽  
Ariene Sampaio Souza Farias Ulbricht ◽  
Carla Werlang-Coelho ◽  
Débora Delwing-Dal Magro ◽  
Victor Hugo Antonio Joaquim ◽  
...  

Author(s):  
Nanna Skytt Pilmark ◽  
Laura Oberholzer ◽  
Jens Frey Halling ◽  
Jonas M. Kristensen ◽  
Christina Pedersen Bønding ◽  
...  

Metformin and exercise both improve glycemic control, but in vitro studies have indicated that an interaction between metformin and exercise occurs in skeletal muscle, suggesting a blunting effect of metformin on exercise training adaptations. Two studies (a double-blind, parallel-group, randomized clinical trial conducted in 29 glucose-intolerant individuals and a double-blind, cross-over trial conducted in 15 healthy lean males) were included in this paper. In both studies, the effect of acute exercise +/- metformin treatment on different skeletal muscle variables, previously suggested to be involved in a pharmaco-physiological interaction between metformin and exercise, was assessed. Furthermore, in the parallel-group trial, the effect of 12 weeks of exercise training was assessed. Skeletal muscle biopsies were obtained before and after acute exercise and 12 weeks of exercise training, and mitochondrial respiration, oxidative stress and AMPK activation was determined. Metformin did not significantly affect the effects of acute exercise or exercise training on mitochondrial respiration, oxidative stress or AMPK activation, indicating that the response to acute exercise and exercise training adaptations in skeletal muscle is not affected by metformin treatment. Further studies are needed to investigate whether an interaction between metformin and exercise is present in other tissues, e.g. the gut. Trial registration: ClinicalTrials.gov (NCT03316690 and NCT02951260). Novelty bullets • Metformin does not affect exercise-induced alterations in mitochondrial respiratory capacity in human skeletal muscle • Metformin does not affect exercise-induced alterations in systemic levels of oxidative stress nor emission of reactive oxygen species from human skeletal muscle • Metformin does not affect exercise-induced AMPK activation in human skeletal muscle


1995 ◽  
Vol 79 (3) ◽  
pp. 675-686 ◽  
Author(s):  
C. K. Sen

There is consistent evidence from human and animal studies that strenuous physical exercise may induce a state wherein the antioxidant defenses of several tissues are overwhelmed by excess reactive oxygen. A wide variety of physiological and dietary antioxidants act in concert to evade such a stress. Submaximal long-duration exercise training may augment the physiological antioxidant defenses in several tissues; however, this enhanced protection may not be sufficient to completely protect highly fit individuals from exhaustive exercise-induced oxidative stress. Regular physical activity in association with dietary habits that ensure adequate supply of a combination of appropriate antioxidants may be expected to yield desirable results. The significance of this area of research, current state of information, and possibilities of further investigation are briefly reviewed.


2021 ◽  
Vol 8 ◽  
Author(s):  
Yan Wang ◽  
Yuhong Jia ◽  
Molin Li ◽  
Sirui Jiao ◽  
Henan Zhao

Background: Exercise training has been extensively studied in heart failure (HF) and psychological disorders, which has been shown to worsen each other. However, our understanding of how exercise simultaneously protect heart and brain of HF patients is still in its infancy. The purpose of this study was to take advantage of big data techniques to explore hotspots and frontiers of mechanisms that protect the heart and brain simultaneously through exercise training.Methods: We studied the scientific publications on related research between January 1, 2003 to December 31, 2020 from the WoS Core Collection. Research hotspots were assessed through open-source software, CiteSpace, Pajek, and VOSviewer. Big data analysis and visualization were carried out using R, Cytoscape and Origin.Results: From 2003 to 2020, the study on HF, depression, and exercise simultaneously was the lowest of all research sequences (two-way ANOVAs, p < 0.0001). Its linear regression coefficient r was 0.7641. The result of hotspot analysis of related keyword-driven research showed that inflammation and stress (including oxidative stress) were the common mechanisms. Through the further analyses, we noted that inflammation, stress, oxidative stress, apoptosis, reactive oxygen species, cell death, and the mechanisms related to mitochondrial biogenesis/homeostasis, could be regarded as the primary mechanism targets to study the simultaneous intervention of exercise on the heart and brain of HF patients with depression.Conclusions: Our findings demonstrate the potential mechanism targets by which exercise interferes with both the heart and brain for HF patients with depression. We hope that they can boost the attention of other researchers and clinicians, and open up new avenues for designing more novel potential drugs to block heart-brain axis vicious circle.


2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Tatiana Sousa Cunha ◽  
Roberta Hack Mendes ◽  
Mariane Bertagnolli ◽  
Vinícius Viegas ◽  
Cristiano Teixeira Mostarda ◽  
...  

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