Elevated mitochondrial oxidative stress impairs metabolic adaptations to exercise in skeletal muscle.
Summary of "Elevated mitochondrial oxidative stress impairs metabolic adaptations to exercise in skeletal muscle."
Mitochondrial oxidative stress is a complex phenomenon that is inherently tied to energy provision and is implicated in many metabolic disorders. Exercise training increases mitochondrial oxidative capacity in skeletal muscle yet it remains unclear if oxidative stress plays a role in regulating these adaptations. We demonstrate that the chronic elevation in mitochondrial oxidative stress present in Sod2 (+/-) mice impairs the functional and biochemical mitochondrial adaptations to exercise. Following exercise training Sod2 (+/-) mice fail to increase maximal work capacity, mitochondrial enzyme activity and mtDNA copy number, despite a normal augmentation of mitochondrial proteins. Additionally, exercised Sod2 (+/-) mice cannot compensate for their higher amount of basal mitochondrial oxidative damage and exhibit poor electron transport chain complex assembly that accounts for their compromised adaptation. Overall, these results demonstrate that chronic skeletal muscle mitochondrial oxidative stress does not impact exercise induced mitochondrial biogenesis, but impairs the resulting mitochondrial protein function and can limit metabolic plasticity.
Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada ; Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada.
This article was published in the following journal.
Name: PloS one
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/24324727
- DOI: http://dx.doi.org/10.1371/journal.pone.0081879
Reducing vascular endothelial growth factor (VEGF) in adipose tissue alters adipose vascularity and metabolic homeostasis. We hypothesized that this would also affect metabolic responses during exerci...
Mitochondrial respiration is a crucial component of cellular metabolism that can become dysregulated in cancer. Compared to normal hematopoietic cells, acute myeloid leukemia (AML) cells and patient s...
Excessive oxidative stress in the heart results in contractile dysfunction. While antioxidant therapies have been a disappointment clinically, exercise has shown beneficial results, in part by reducin...
Maximal exercise-associated oxidative capacity is strongly correlated with health and longevity in humans. Rats selectively bred for high running capacity (HCR) have improved metabolic health and are ...
Aerobic exercise can reduce postprandial lipemia, and possibly oxidative stress, when performed prior to a lipid-rich meal.
In Amyotrophic Lateral Sclerosis (ALS), malnutrition is frequent (16 to 50 % of the patients) and is an independent prognostic factor. One of the implicated factors is the increase of rest...
At the moment, most of efforts to prevent non-transmissible chronic diseases at population level have been centered in promoting healthful behaviors like physical activity, consumption of ...
The central aim of this study is to improve understanding of how metabolic pathways that contribute to adiposity also amplify risks of kidney disease progression and cardiovascular disease...
The purpose of this study is to compare oxidative stress markers and the immunologic characteristics of HIV-infected and non-HIV subjects during a bout of moderate aerobic exercise followe...
The purpose of the study is to examine whether Klacid® (Clarithromycin) will induce oxidative stress (stress from oxygen) in healthy subjects. This is done by measuring the content of a p...
Medical and Biotech [MESH] Definitions
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
A method of recording heart motion and internal structures by combining ultrasonic imaging with exercise testing (EXERCISE TEST) or pharmacologic stress.
A LIVER mitochondrial matrix flavoenzyme that catalyzes the oxidation of SARCOSINE to GLYCINE and FORMALDEHYDE. Mutation in the enzyme causes sarcosinemia, a rare autosomal metabolic defect characterized by elevated levels of SARCOSINE in BLOOD and URINE.
A toxic dye, chemically related to trinitrophenol (picric acid), used in biochemical studies of oxidative processes where it uncouples oxidative phosphorylation. It is also used as a metabolic stimulant. (Stedman, 26th ed)
Toxic substances isolated from various strains of Streptomyces. They are 20-membered macrolides that inhibit oxidative phosphorylation and mitochondrial ATPases. Venturicidins A and B are glycosides. Used mainly as tools in the study of mitochondrial function.