The purpose of this study was to examine the effect of D-ribose supplementation on the changes of blood fatigue substances (lactate, ammonia, phosphate and hypoxanthine) after maximal exercise performance in college male students. The experimental trials of each subject were divided into the following conditions: placebo supplement trial and D-ribose supplement trial. The subjects exercised using a Concept Ⅱ Indoor rowing ergometer for 2,000 m Single Skull event. The subjects ingested 200 mg/kg of D-ribose after breakfast, lunch, dinner, as well as thirty minutes before exercising, for six days. Blood fatigue substances were continuously measured before exercise, immediately after exercise, and thirty minutes after exercise. The results indicated a significant difference in blood phosphate and hypoxanthine levels between the two experimental trials in the 30 minute recovery period (p<0.05). However, there were no significant differences in blood lactate and phosphate levels between the two experimental trials. The results of our study suggest that D-ribose supplementation during maximal rowing exercise for 7~8 minutes may contribute to the improvement of metabolic responses as a beneficial ergogenic aid accelerating fatigue clearance.
The purpose of this study was to investigate the biological effect of obesity-induced oxidative damage on neurogenesis and early protein expression. Obesity was induced I thirty 4-week old male Sprague-Dawley rats through a high fat diet for 15 weeks. After one week of environmental adaptation, the rats were divided into 2 groups: high fat diet sedentary group (HDS, n=15) and high fat diet training group (HDT, n=15). Exercise training was performed 5 times a week for 8 weeks, with mild-intensity treadmill running for weeks 1-4 and moderate-intensity treadmill running for weeks 5-8. After the 8 week training period, we analyzed lipid profiles, serum 8-hydroxyguanosine (8-OHdG), liver tissue malondialdehyde (MDA) related to oxidative damage factors, nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), c-fos, c-jun, and extracellular signal regulated kinase (Erk) in the hippocampus. The results of this study are as follows. There were differences between HDS and HDT in triglyceride (TG) and total cholesterol (TC) (p<0.05). In high density lipoprotein (HDL-c), the HDT was higher than HDS after treadmill training (p<0.05). In 8-OHdG, the HDT was lower than HDS after treadmill training (p<0.05). Genetic expressions of c-jun, BDNF and MDA in the HDT were higher than in the HDS after treadmill training in hippocampus (p<0.05). Therefore, we conclude that 8 weeks of treadmill training can improve imbalanced lipid profiles, reduce oxidative damage, and activate neurogenesis in obese rats.
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