Exercise activation of muscle peroxisome proliferator-activated receptor-γ coactivator-1α signaling is redox sensitive

Kang, Chounghun; OʼMoore, K M.; Dickman, Jonathan R.; Ji, Li Li

doi:10.1016/j.freeradbiomed.2009.08.007

Cited by 189 publications

(176 citation statements)

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“…Recently, it has been demonstrated that ROS can induce an increase in PGC1-α transcription via both AMP kinase-dependent and independent pathways [47]. The increase in PGC1-α also causes an increase in NRF-1 and TFAM levels [51]. This directly links ROS production to mitochondrial biogenesis, that is, links the exerciseinduced production of ROS in muscle cells to the cell's shift towards a more oxidative metabolism.…”

Section: Exercise and Generation Of Reactive Oxygen Andmentioning

confidence: 99%

The exercised skeletal muscle: a review

Marini

Veicsteinas

2010

Eur J Transl Myol

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The skeletal muscle is the second more plastic tissue of the body -second to the nervous tissue only. In fact, both physical activity and inactivity contribute to modify the skeletal muscle, by continuous signaling through nerve impulses, mechanical stimuli and humoral clues. In turn, the skeletal muscle sends signals to the body, thus contributing to its homeostasis. We'll review here the contribute of physical exercise to the shaping of skeletal muscle, to the adaptation of its mass and function to the different needs imposed by different physical activities and to the attainment of the health benefits associated with active skeletal muscles. Focus will primarily be on the molecular pathways and on gene regulation that result in skeletal muscle adaptation to exercise.

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Section: Exercise and Generation Of Reactive Oxygen Andmentioning

confidence: 99%

The exercised skeletal muscle: a review

Marini

Veicsteinas

2010

Eur J Transl Myol

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“…On the other hand, an elevated level of ROS activates AMPK, thus leading to an increase in PGC-1α promoter activity and mRNA level 36) . ROS are also suggested to regulate PGC-1α expression via the p38 MAPK and NFκB pathways 37) .…”

Section: Intracellular Signaling Involved In Endurance Traininginducementioning

confidence: 99%

Reactive oxygen species and endurance training-induced adaptations

Matsui

2013

JPFSM

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Endurance training induces mitochondrial biogenesis and angiogenesis in skeletal muscle. Endurance training also improves insulin sensitivity at both the skeletal muscle and whole body level. Recently, ROS have been suggested to play an important role in endurance training-induced adaptations. However, this hypothesis is not yet fully supported. To advance understanding of the role of ROS and antioxidants in endurance training-induced adaptations, efforts should be made in future studies to clarify the sites of ROS production and the influence of antioxidants on the redox status under each training condition. Effort should also be directed to identifying the signaling pathways involved. In this situation, it should be recognized that in vivo cellular signaling is redundant. Therefore, efforts to evaluate the relative importance and interactions among the multiple cellular signaling pathways involved in each training condition are required. Without elucidating the role of ROS and antioxidants in endurance traininginduced adaptations, then evidence-based sound advice regarding antioxidant supplementation cannot be made.

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“…However, aside from these positive adaptive responses, oxidative stress due to reactive oxygen species (ROS) also increases within skeletal muscles during muscle contractions (13-15). Increased oxidative stress, or increased ROS, is known to play a harmful role in the human body, but recent studies have reported its positive effects, such as being involved in mitochondrial biogenesis (13,(16)(17)(18) as well. Because of this, there have been reports from recent studies that have examined the effects of AO supplementation, such as with vitamins, on adaptive responses from endurance training in skeletal muscles.…”

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confidence: 99%

“…Such adaptive responses occur owing to increased expression or activation of peroxisome proliferator-activated receptor g (PPAR-g) coactivator-1a (PGC-1a) through Ca 21 -dependent pathways, AMP-activated protein kinase (AMPK), and p38 mitogen-activated protein kinases (MAPK) (11,12). However, aside from these positive adaptive responses, oxidative stress due to reactive oxygen species (ROS) also increases within skeletal muscles during muscle contractions (13)(14)(15). Increased oxidative stress, or increased ROS, is known to play a harmful role in the human body, but recent studies have reported its positive effects, such as being involved in mitochondrial biogenesis (13,(16)(17)(18) as well.…”

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confidence: 99%

“…Elevation of ROS by H2O2 treatment decreases the cellular ATP level, and as a result, activated AMPK increases PPARGC1A mRNA expression (16). Moreover, pharmacological inhibition of ROS regulates PGC-1a expression by inhibiting exercise-mediated activation of p38 MAPK (13). Therefore, in order for mitochondrial biogenesis from endurance training to be inhibited by AO supplementation, activation of AMPK and p38 MAPK must be inhibited, leading to regulation of PGC-1a.…”

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confidence: 99%

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Inhibition of Oxidative Stress by Antioxidant Supplementation Does Not Limit Muscle Mitochondrial Biogenesis or Endurance Capacity in Rats

Kim

Park

Kim

2017

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryThe objective of the present study was to analyze the activation and expression patterns of upstream and downstream factors of PGC-1a to determine whether antioxidant (AO) supplementation inhibits mitochondrial biogenesis in skeletal muscles as an adaptation to endurance training, as well as to analyze changes in endurance capacity based on such findings. For this objective, 24 male Sprague-Dawley (SD) rats were allocated into 4 groups (vehicle-sedentary, V-Sed; vehicle-exercise, V-EX; antioxidant-sedentary, AOSed; antioxidant-exercise, AO-EX) of 6 rats each. The rats were then treated with vitamin C (500 mg•kg 21 body weight•d 21) or a placebo for 8 wk, and a swimming program was implemented in some rats during the last 4 wk of this period. Immediately after the last training session, blood was collected from the tail of each rat, and TBARS was measured to test the effect of vitamin C as an AO. As a result, increased oxidative stress from exercise was inhibited by vitamin C supplementation. Analysis of whether reduced oxidative stress by vitamin C supplementation also inhibited mitochondrial biogenesis within skeletal muscles showed that phosphorylation of p38 MAPK and AMPK, along with levels of PGC-1a, NRF-1, mtTFA, and mitochondrial electron transport enzymes, increased after endurance training in spite of vitamin C supplementation. Moreover, running time, distance, and total work increased significantly in the exercise group as compared to those in the sedentary group, regardless of vitamin C supplementation. These results indicate that mitochondrial biogenesis and endurance capacity increase as a result of endurance training, regardless of AO supplementation. Key Words exercise, antioxidants, mitochondria, oxidative stress Endurance training promotes not only mitochondrial biogenesis (1-3), but also various adaptive responses within skeletal muscles, such as improved insulin sensitivity (4-6), fatty acid oxidation (7,8), and antioxidant (AO) defense system efficiency (9, 10). Such adaptive responses occur owing to increased expression or activation of peroxisome proliferator-activated receptor g (PPAR-g) coactivator-1a (PGC-1a) through Ca 21 -dependent pathways, AMP-activated protein kinase (AMPK), and p38 mitogen-activated protein kinases (MAPK) (11,12). However, aside from these positive adaptive responses, oxidative stress due to reactive oxygen species (ROS) also increases within skeletal muscles during muscle contractions (13-15). Increased oxidative stress, or increased ROS, is known to play a harmful role in the human body, but recent studies have reported its positive effects, such as being involved in mitochondrial biogenesis (13,(16)(17)(18) as well. Because of this, there have been reports from recent studies that have examined the effects of AO supplementation, such as with vitamins, on adaptive responses from endurance training in skeletal muscles. However, these study results conflict with claims that skeletal muscle adaptations from endurance training are decreased by AO supplementatio...

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Exercise activation of muscle peroxisome proliferator-activated receptor-γ coactivator-1α signaling is redox sensitive

Cited by 189 publications

References 42 publications

The exercised skeletal muscle: a review

The exercised skeletal muscle: a review

Reactive oxygen species and endurance training-induced adaptations

Inhibition of Oxidative Stress by Antioxidant Supplementation Does Not Limit Muscle Mitochondrial Biogenesis or Endurance Capacity in Rats

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