Training and acute exercise modulates mitochondrial dynamics in football players’ blood mononuclear cells

Busquets-Cortés, Carla; Capó, Xavier; Martorell, Miquel; Tur, Josep A.; Sureda, Antoni; Pons, Antoni

doi:10.1007/s00421-017-3684-z

Cited by 28 publications

(33 citation statements)

References 54 publications

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“…In addition, both effects could be rescued by ectopic overexpression of IKKα. Curiously, PGC-1α-dependent mitochondrial biogenesis and ROS production, as well as improved mitochondrial function and antioxidant capacity, were noted in peripheral blood mononuclear cells obtained from professional football players who underwent an eight week period of active training, all of which was attributed to NF-κB activation [ 164 ].…”

Section: Signaling Pathways Controlling Mitochondrial Dynamicsmentioning

confidence: 99%

Reactive Oxygen Species and Mitochondrial Dynamics: The Yin and Yang of Mitochondrial Dysfunction and Cancer Progression

2018

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Mitochondria are organelles with a highly dynamic ultrastructure maintained by a delicate equilibrium between its fission and fusion rates. Understanding the factors influencing this balance is important as perturbations to mitochondrial dynamics can result in pathological states. As a terminal site of nutrient oxidation for the cell, mitochondrial powerhouses harness energy in the form of ATP in a process driven by the electron transport chain. Contemporaneously, electrons translocated within the electron transport chain undergo spontaneous side reactions with oxygen, giving rise to superoxide and a variety of other downstream reactive oxygen species (ROS). Mitochondrially-derived ROS can mediate redox signaling or, in excess, cause cell injury and even cell death. Recent evidence suggests that mitochondrial ultrastructure is tightly coupled to ROS generation depending on the physiological status of the cell. Yet, the mechanism by which changes in mitochondrial shape modulate mitochondrial function and redox homeostasis is less clear. Aberrant mitochondrial morphology may lead to enhanced ROS formation, which, in turn, may deteriorate mitochondrial health and further exacerbate oxidative stress in a self-perpetuating vicious cycle. Here, we review the latest findings on the intricate relationship between mitochondrial dynamics and ROS production, focusing mainly on its role in malignant disease.

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Section: Signaling Pathways Controlling Mitochondrial Dynamicsmentioning

confidence: 99%

Reactive Oxygen Species and Mitochondrial Dynamics: The Yin and Yang of Mitochondrial Dysfunction and Cancer Progression

2018

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“…In skeletal muscle, exercise can demethylate the CONTACT PPARGC1A −260 CpG site which has been shown to concurrently upregulate PPARGC1A mRNA expression [8,10,21]. Although well characterised in skeletal muscle, the regulation of PPARGC1A expression in other cells and tissues, including immune cells is poorly understood [22].…”

Section: Introductionmentioning

confidence: 99%

Impact of aerobic exercise and fatty acid supplementation on global and gene-specific DNA methylation

et al. 2019

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Lifestyle interventions, including exercise and dietary supplementation, can modify DNA methylation and exert health benefits; however, the underlying mechanisms are poorly understood. Here we investigated the impact of acute aerobic exercise and the supplementation of omega-3 polyunsaturated fatty acids (n-3 PUFA) and extra virgin olive oil (EVOO) on global and gene-specific (PPARGC1A, IL6 and TNF) DNA methylation, and DNMT mRNA expression in leukocytes of diseasefree individuals. Eight trained male cyclists completed an exercise test before and after a four-week supplementation of n-3 PUFA and EVOO in a double-blind, randomised, repeated measures design. Exercise triggered global hypomethylation (Pre 79.2%; Post 78.7%; p = 0.008), alongside, hypomethylation (Pre 6.9%; Post 6.3%; p < 0.001) and increased mRNA expression of PPARGC1A (p < 0.001). Associations between PPARGC1A methylation and exercise performance were also detected. An interaction between supplement and trial was detected for a single CpG of IL6 indicating increased DNA methylation following n-3 PUFA and decreased methylation following EVOO (p = 0.038). Global and gene-specific DNA methylation associated with markers of inflammation and oxidative stress. The supplementation of EVOO reduced DNMT1 mRNA expression compared to n-3 PUFA supplementation (p = 0.048), whereas, DNMT3a (p = 0.018) and DNMT3b (p = 0.046) mRNA expression were decreased following exercise. In conclusion, we demonstrate that acute exercise and dietary supplementation of n-3 PUFAs and EVOO induce DNA methylation changes in leukocytes, potentially via the modulation of DNMT mRNA expression. Future studies are required to further elucidate the impact of lifestyle interventions on DNA methylation. ARTICLE HISTORY

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“…Maximal respiration and spare respiratory capacity of PBMCs mitochondria correlated with gait speed in older adults (Tyrrell et al, 2015). Training increased the mitochondrial biogenesis and improved the antioxidant capacity of mitochondria in well-trained individual PBMCs (Busquets-Cortes et al, 2017). In a recent study, the mitochondrial function of PBMCs did not reflect interval training-induced changes in muscle mitochondria of young healthy men (Hedges et al, 2019).…”

Section: Introductionmentioning

confidence: 95%

Low‐intensity exercise stimulates bioenergetics and increases fat oxidation in mitochondria of blood mononuclear cells from sedentary adults

et al. 2020

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Training and acute exercise modulates mitochondrial dynamics in football players’ blood mononuclear cells

Cited by 28 publications

References 54 publications

Reactive Oxygen Species and Mitochondrial Dynamics: The Yin and Yang of Mitochondrial Dysfunction and Cancer Progression

Reactive Oxygen Species and Mitochondrial Dynamics: The Yin and Yang of Mitochondrial Dysfunction and Cancer Progression

Impact of aerobic exercise and fatty acid supplementation on global and gene-specific DNA methylation

Low‐intensity exercise stimulates bioenergetics and increases fat oxidation in mitochondria of blood mononuclear cells from sedentary adults

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