High-dose antioxidant vitamin C supplementation does not prevent acute exercise-induced increases in markers of skeletal muscle mitochondrial biogenesis in rats

• Published in: Journal of applied physiology (1985) Vol. 108; no. 6; pp. 1719 - 1726
• Main Authors: WADLEY, G. D, MCCONELLL, G. K
• Format: Journal Article
• Language: English
• Published: Bethesda, MD American Physiological Society 01.06.2010
• Subjects: Animals; Antioxidants; Ascorbic Acid - administration & dosage; Biological and medical sciences; Biomarkers; Biomarkers - metabolism; Biosynthesis; Cell Proliferation - drug effects; Dietary Supplements; Dose-Response Relationship, Drug; Fundamental and applied biological sciences. Psychology; Male; Mitochondria; Mitochondria - drug effects; Mitochondria - physiology; Mitochondrial Proteins - metabolism; Muscle Proteins - metabolism; Muscle, Skeletal - drug effects; Muscle, Skeletal - physiology; Muscle, Skeletal - ultrastructure; Musculoskeletal system; Phosphorylation; Physical Conditioning, Animal - methods; Physical Exertion - physiology; Physiology; Rats; Rats, Sprague-Dawley; Rodents; Vitamin C; Physical exercise; Reactive oxygen species; Ascorbic acid; Rat; Acute; Rodentia; Vitamin; peroxisome proliferator-activated receptor-γ coactivator-1α; Antioxidant; Striated muscle; PPAR-γ receptor; Muscle contraction; Vertebrata; Mitochondria; Mammalia; contraction; Supplementation
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00127.2010

High doses of the antioxidant vitamin C prevent the increases in skeletal muscle mitochondrial biogenesis after exercise training. Since exercise training effects rely on the acute stimulus of each exercise bout, we examined whether vitamin C supplementation also attenuates the increases in skeletal muscle metabolic signaling and mitochondrial biogenesis in response to an acute exercise bout. Male Sprague-Dawley rats performed 60 min of treadmill running (27 m/min, 5% grade) or remained sedentary. For 7 days before this, one-half of the rats received water containing 500 mg/kg body wt vitamin C. Acute exercise significantly (P<0.05) increased the phosphorylation of p38 MAPK, AMP-activated kinase-alpha, and activating transcription factor (ATF)-2 and the ratio of oxidized to total glutathione (GSSG/TGSH) in the gastrocnemius. However, vitamin C had no effect on these increases. Similarly, vitamin C did not prevent the exercise-induced increases in peroxisome proliferator-activated receptor-gamma coactivator-1alpha, nuclear respiratory factor (NRF)-1, NRF-2, mitochondrial transcription factor A, glutathione peroxidase-1, MnSOD, extracellular SOD, or glucose transporter 4 (P<0.05) mRNA after exercise. Surprisingly, vitamin C supplementation significantly increased the basal levels of GSSG/TGSH, NRF-1, and NRF-2 mRNA and basal ATF-2 phosphorylation. In summary, despite other studies in rats showing that vitamin C supplementation prevents increases in skeletal muscle mitochondrial biogenesis and antioxidant enzymes with exercise training, vitamin C had no affect on the acute exercise-induced increases of these markers.