Endurance training without weight loss lowers systemic, but not muscle, oxidative stress with no effect on inflammation in lean and obese women

Devries, Michaela C.; Hamadeh, Mazen J.; Glover, Alexander W.; Raha, Sandeep; Samjoo, Imtiaz A.; Tarnopolsky, Mark A.

doi:10.1016/j.freeradbiomed.2008.04.039

Cited by 94 publications

(86 citation statements)

References 74 publications

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“…These authors suggested that the amount of exercise was more important in relation to lipid and lipoprotein responses than the intensity of exercise [37]. Also, nutritional status in our study was compatible with the findings of Devries et al who demonstrated no change in body weight and body fat percentage in women after endurance training for 12 weeks [38]. They suggested that high-intensity exercise could change body composition [39].…”

Section: Discussionsupporting

confidence: 91%

Effect of Low-Intensity Exercise on Oxidative Stress, Inflammatory and Nutritional Responsiveness in Sedentary People

Burtscher¹

2017

JNHFS

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Section: Discussionsupporting

confidence: 91%

Effect of Low-Intensity Exercise on Oxidative Stress, Inflammatory and Nutritional Responsiveness in Sedentary People

Burtscher¹

2017

JNHFS

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“…Vergleichbare Resultate werden auch aus mehreren nicht-kontrollierten Interventionsstudien berichtet, bei denen um 25 bis 34% erniedrigte F2-Isoprostankonzentrationen nach einem körperlichen Training über zwölf bis 15 Wochen gemessen wurden [53,54]. In einer randomisierten achtwöchigen Studie bei älte-ren Patienten mit Typ-2-Diabetes wurden hingegen keine signifikanten Effekte beobachtet [55].…”

Section: Wirkung Auf Den Oxidativen Stress Und Auf Dna-reparatur-mechunclassified

Physiologische und molekulare Mechanismen der Wirkung von körperlicher Aktivität auf das Krebsrisiko und den Verlauf einer Krebserkrankung

Ulrich

Wiskemann

Steindorf

2011

Bundesgesundheitsbl.

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Physical activity is associated with a reduced risk of colon, breast, endometrial, lung, and pancreatic cancer. Evidence for mediating molecular mechanisms from experimental studies substantially strengthens the causal inference for this relationship. Randomized controlled trials indicate that exercise affects metabolic profiles, including hormone levels (estrogen, insulin signaling), inflammation (e.g., C-reactive protein), and adipokine concentrations (e.g., leptin). The size of the effect depends frequently on concurrent changes in body composition. There is also initial evidence for effects on immune function, oxidative stress, and possibly DNA repair capacity. Finally, outdoor physical activity can directly increase 25(OH)-vitamin D levels, providing another potential mechanism for linking physical activity to cancer risk. Randomized controlled studies with biomarker measurements are essential to increase evidence for causality and to identify the most effective intervention strategies and pharmacologic targets.

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“…For example ROS are involved in the activation of transcription factors that regulate cellular antioxidative responses to ROS. These transcription factors include Nrf2 [147,148], hypoxia-inducible factor [149,150,151], nuclear factor kappa B [152] and p53 [153,154]. High levels of ROS, however, can result in damages to the mitochondrial DNA, in the unspecific overoxidation of proteins and lipids as well as in the initiation of mitophagy and apoptosis, consequently leading to a decrease of consequence of a misbalance between ROS-detoxifying pathways and ROS production and ROS interconversion.…”

Section: Introductionmentioning

confidence: 99%

Axonal Transport and Mitochondrial Dysfunction in Alzheimer's Disease

Riemer

Kins²

2012

Neurodegener Dis

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Alzheimer's disease (AD) is the most common form of dementia. It is characterized by pathological hallmarks such as extracellular deposits of amyloid plaques as well as intracellular neurofibrillary tangles and a progressive loss of neurons. Additional early pathological features of AD also include a decline in synapse number, axonal dystrophies, mitochondrial hypometabolism and increased oxidative stress. It is assumed that the aggregates of amyloid-β and tau are not the major pathogenic players in AD, but that nonaggregated oligomeric forms of amyloid-β and specific phosphorylated forms of tau cause neurodegeneration. It is tempting to speculate that oligomeric amyloid-β and phosphorylated tau might trigger mitochondrial dysfunction associated with oxidative stress as well as dysfunctions of axonal transport, leading to the loss of spines and neurodegeneration. Here, we summarize the actual data supporting this hypothesis and provide a model how these different mechanisms might be intertwined with each other.

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Endurance training without weight loss lowers systemic, but not muscle, oxidative stress with no effect on inflammation in lean and obese women

Cited by 94 publications

References 74 publications

Effect of Low-Intensity Exercise on Oxidative Stress, Inflammatory and Nutritional Responsiveness in Sedentary People

Effect of Low-Intensity Exercise on Oxidative Stress, Inflammatory and Nutritional Responsiveness in Sedentary People

Physiologische und molekulare Mechanismen der Wirkung von körperlicher Aktivität auf das Krebsrisiko und den Verlauf einer Krebserkrankung

Axonal Transport and Mitochondrial Dysfunction in Alzheimer's Disease

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