TY - JOUR
T1 - Inhibition of oxidative stress by antioxidant supplementation does not limit muscle mitochondrial biogenesis or endurance capacity in rats
AU - Kim, Jae Cheol
AU - Park, Gi Duck
AU - Kim, Sang Hyun
N1 - Publisher Copyright:
© 2017, Center for Academic Publications Japan. All rights reserved.
PY - 2017
Y1 - 2017
N2 - The 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-1 body weight·d-1) 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.
AB - The 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-1 body weight·d-1) 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.
KW - Antioxidants
KW - Exercise
KW - Mitochondria
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=85037849406&partnerID=8YFLogxK
U2 - 10.3177/jnsv.63.277
DO - 10.3177/jnsv.63.277
M3 - Article
C2 - 29225311
AN - SCOPUS:85037849406
SN - 0301-4800
VL - 63
SP - 277
EP - 283
JO - Journal of Nutritional Science and Vitaminology
JF - Journal of Nutritional Science and Vitaminology
IS - 5
ER -