• Journal of Life Science
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• v.18 no.1
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• pp.1-8
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• 2008

The purpose of this study was to determine the possible additive effects of endurance exercise training (EXER) and selenium (SELE) on the improvements of glucose and lactate transport capacities in diabetic Goto-kakizaki rats. Animals either remained sedentary control (SED) or performed EXER or received SELE [$5{\mu}mol$ kg body wt (-1) day (-1)], or underwent both EXER and SELE (COMBI), which lasted for 6 wk. Compared with sedentary control, EXER alone or the SELE alone group, or the combined treatment group had significant reduction in glucose response measured at 90 min and 120 min during an intraperitoneal glucose tolerance test (IPGTT) and body weight after 6week treatment. EXER alone, or combined group individually had significantly higher glycogen contents in liver compared with SED or SELE groups. EXER alone increased glycogen content in soleus and plantaris compared with SED, and this parameter was increased to greatest extent in the combined treatment groups compared with SED or SELE groups. EXER alone, SELE alone or COMBI, caused significant decreases in the plasma lactates, serum glucose, insulin, total cholesterol and HOMA-IR along with a significant increase in high-density lipoprotein cholesterol compared with SED. In addition, EXER or COMBI individually had significantly lower serum triacylglycerol compared with SED or SELE. With respect to protein expression related to glucose and lactate transport capacities, EXER alone, SELE alone, or COMBI increased in MCT1 and MCT4 protein level in soleus and plantaris. Furthermore, EXER alone, SELE alone or COMBI caused significant increases in mt MCT1 protein level in soleus and plantaris. The findings of the current study suggest that endurance exercise training and selenium treatment may provide therapeutic values to type II diabetic patients with peripheral insulin resistance and hyperlactatecemia by improving glucose and lactate transport capacities, leading to improvements in plasma lactate, serum glucose, insulin and lipid profiles (TC, TG, HDL).

• 한국체육학회지인문사회과학편
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• v.55 no.6
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• pp.691-700
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• 2016

The purpose of this study was to investigate the effects of long-term endurance exercise or resistance exercise training on muscle anabolic/catabolic pathway. 50wks-old male Wistar rats(n=30) were randomly assigned for 3 groups (sedentary, endurance exercise, resistance exercise group). After 12-week of training, plantaris muscles were dissect to measure protein level. Akt/mTOR signal-related proteins were significantly increased only after resistance exercise training, but catabolic signal-related proteins, FoxO1 and MuRF1, were significantly decreased after resistance and endurance exercise training. After endurance exercise training, AMPK and PGC-1α protein levels were significantly increased. Therefore, the endurance exercise training has been shown to affect the protein balance of aging muscle through inhibition of muscle protein catabolism. The present results suggest the possibility that not only resistance exercise but also endurance exercise will be affectable to keep or increase muscle volume and capacity of middle-aged people.

• Proceedings of the Korea Contents Association Conference
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• 2012.05a
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• pp.407-408
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• 2012

요약은 이 연구는 다양한 식이 섭취와 일회 지구성 운동으로 야기되는 근육(백색 비복근) 내 AMP-activated protein kinase(AMPK), Extracellular signal-regulated kinase(ERK 1/2)와 p38 mitogen-activated protein kinase(MAPK)의 신호전달체계를 구명해 보고자 실시되었다. 실험에 사용된 쥐(Sprague-Dawley)는 총 160마리로 크게 일반 탄수화물 식이(CHO; 40마리), 포화지방 식이(SAFA; 40마리), 단일불포화 식이(MUFA; 40마리)와 다불포화 식이(PUFA; 40마리)로 나누어 연구를 진행하였다. 운동 프로그램은 일회 지구성 운동으로 30분 운동 후 5분 휴식의 사이클을 지속적으로 6번 반복하여 총 3시간의 지구성 수영 운동을 실시하였고, 분석을 위한 조직 샘플링은 운동 전, 운동 후 0시간, 1시간, 4시간, 24시간에 걸쳐서 이루어졌다. 연구의 결과는 서로 다른 식이 섭취와 운동에 따른 AMPK의 신호전달 단백질의 발현은 유의한 치이가 나타나지 않았다. 그러나 서로 다른 식이를 섭취한 쥐의 근육에서 ERK 1/2(p<.01)와 p38 MAPK(p<.001)의 신호전달 단백질의 발현은 유의한 차이를 보였다(p<.05). 흥미로운 결과는 운동에 대한 유의한 차이는 AMPK, ERK1/2와 p38 MAPK 모두 유의한 차이를 보이지 않았다는 것이다. 결론적으로 일회 지구성 운동보다 서로 다른 식이의 섭취가 근육 내(백색 비복근)의 대사적 변화를 일으키는데 주도적인 영향을 미칠 수 있음을 시사할 수 있다.

• Journal of Life Science
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• v.27 no.3
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• pp.361-369
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• 2017

Mitochondrial homeostasis is tightly regulated by two major processes: mitochondrial biogenesis and mitochondrial degradation by autophagy (mitophagy). Research in mitochondrial biogenesis in skeletal muscle in response to endurance exercise training has been well established, while the mechanisms regulating mitophagy and the relationship between mitochondrial biogenesis and degradation following endurance exercise training are not yet well defined. Studies have demonstrated that endurance exercise training increases the expression levels of mitochondrial biogenesis-, dynamics-, mitophagy-related genes in skeletal muscle. However, the increased levels of mitochondrial biogenesis marker proteins such as Cox IV and citrate synthase, by endurance exercise training were abolished when autophagy/mitophagy was inhibited in skeletal muscle. This suggests that both autophagy/mitophagy plays an important role in mitochondrial biogenesis/homeostasis and the coordination between the opposing processes may be important for skeletal muscle adaptation to endurance exercise training to improve metabolic function and endurance exercise performance. It is considered that endurance exercise training regulates each of these processes, mitochondrial biogenesis, fusion and fission events and autophagy/mitophagy, ensuring a relatively constant mitochondrial population. Exercise training may also have contributed to mitochondrial quality control which replaces old and/or unhealthy mitochondria with new and/or healthy ones in skeletal muscle. In this review paper, the molecular mechanisms regulating mitochondrial biogenesis and mitophagy and the coordination between the opposing processes is involved in the cellular adaptation to endurance exercise training in skeletal muscle will be discussed.

• Journal of the Korean Applied Science and Technology
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• v.37 no.3
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• pp.571-581
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• 2020

The purpose of this study was to investigate the effect of endurance and resistance exercise by using different intensity on diabetic-related blood profiles in impaired glucose tolerance mice. 54 C57BL/6 mice were divided into (1) Control group (CO, n=9), (2) impaired glucose tolerance group (IGT, n=9), (3) IGT + 50% of VO_2max endurance exercise group (IGT50A, n=9), (4) IGT + 75% of VO_2max endurance exercise group (IGT75A, n=9), (5) IGT +50% of 1RM resistance exercise group (IGT50R, n=9), 그리고 (6) IGT + 75% of 1RM resistance exercise group (IGT75R, n=9). Endurance exercise program was performed 40 min/day, 5 days a week for 8 weeks on treadmill. Resistance exercise program was consisted in ladder-climbing 8 set/day, 5 days a week for 8 weeks. After completed the exercise program, there was no different insulin level in the groups. The fasting glucose was significantly lower in CO than in other groups, and it was not different among the exercised groups. However, IGT75R was statistically lower than IGT. HOMA-IR was only different between CO and IGT. HbA1c was higher in IGT than in other groups. As compared with exercised groups, IGT 75A was lower than IGT50R. TC was lower in CO than in other groups, but there was no different in TG. Endurance exercise groups showed higher than CO and IGT in HDL-C level. LDL-C was lower in CO than other groups. In addition, IGT75A was lower than IGT and IGT50R in LDL-C level. In conclusion, 75% of 1RM resistance exercise had more positive effect on fasting glucose, and 75% of VO_2max endurance exercise improved HbA1c and LDL-C level. In addition, endurance exercise had more effective in HDL-C improvement as compared with resistance exercise.

• 한국체육학회지인문사회과학편
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• v.55 no.4
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• pp.507-516
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• 2016

The purpose of this study is to identify the effects of PPARβ/δ over-expression on PGC-1α mRNA and protein stability after single bout of swimming exercise in mice skeletal muscle. Empty vector (EV) or PPARβ/δ was over-expressed in tibialis anterior(TA) using electroporation(EPO) technique to compare with non-treatment muscle(control; Con). TA muscles were dissected at 0h, 24h or 54h after termination of exercise. PGC-1α mRNA in Con, EV and PPARβ/δ over-expressed muscles were increased 6.8 fold (p<.001), 6.2 fold(p<.001) and 7.1 fold(p<.001), respectively, than sedentary(Sed) group at 0h after exercise and then reverted to Sed group levels at 24h and 54h after termination of exercise. PGC-1α and PGC-1α ubiquitination in EV treated muscles were increased 2.2 fold and 1.74 fold, respectively, than Sed group at 24h after termination of exercise, and then reverted to Sed group levels at 54h after termination of exercise. PGC-1α in PPARβ/δ over-expressed muscles at 24h and 54h after termination of exercise were increased 2.5 fold and 2.2 fold, respectively, than Sed group, but PGC-1α ubiquitination was not increased at 24h and 54h after termination of exercise. Our results indicate that PPARβ/δ over-expression does not increase PGC-1α mRNA stability, but increase PGC-1α protein stability through post-translation mechanism after termination of exercise.

• Journal of the Korean Applied Science and Technology
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• v.37 no.4
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• pp.744-754
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• 2020

We investigated the whether endurance exercise and MitoQ intake mediated neuroprotection are associated with mitochondrial function in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine(MPTP) -induced mice model of Parkinson's disease. C57BL/6 male mice were randomly assigned to five groups: Normal Conrol(NC, n=10), MPTP Control(MC, n=10), MPTP +MitoQ(MQ, n=10), MPTP + Exercise(ME, n=10) and MPTP + MitoQ + Exercise(MQE, n=10). Exercise intervention groups performed the treadmill exercise for 5days/week for 5 weeks with gradual increase of intensity. MitoQ intake groups consumed the MitoQ at a concentration of 250μmol by dissolving with water during experiment period. Our data demonstrated that ME and MQE group restored MPTP-induced motor dysfunction. In addition, treatment groups(MQ, ME and MQE) increased tyrosine hydroxylase levels, and suppressed the accumulation of α-synuclein levels. Futhermore, treatment groups modulated the mitochondrial function such as upregulated mitochondrial biogenesis, increased antioxidant enzyme, enhanced a anti-apoptotic protein(e.g., BCL2), and reduced a pro-apoptotic protein(e.g., BAX). Taken together, these results suggested that endurance exercise and MitoQ intake-mediated increase in mitochondrial function contributes to improvement of aggravated dopaminergic neuronal, resulting in attenuation of motor function of Parkinson's disease.

• Journal of Life Science
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• v.27 no.5
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• pp.591-599
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• 2017

It is well established that endurance performance is negatively affected by environmental heat stress. Numerous scientific investigations have attempted to improve performance in the heat with pre-cooling and per-cooling for endurance athletes. Some cooling strategies are more logistically challenging than others, and thus are often impractical for use in training or competition. The purpose of this study was to review the literature on the use of cooling interventions in the improvement of performance and recovery from exercise-induced heat stress. We undertook an examination that focused on the effects of pre-cooling and per-cooling on the improvement in endurance performance and the effects of post-exercise cooling on recovery. The benefits for pre-cooling and per-cooling strategies undertaken in the laboratory setting could be employed by athletes who compete in hot environmental conditions to improve performance. Most laboratory studies have shown improvements in endurance performance following pre-cooling and per-cooling, and in recovery following post-cooling. Cooling strategies such as cooling vest, neck cooling collar, menthol and ice slurry are practically relevant to sports field. Cooling interventions that can be applied frequently to reduce thermal strain prior to, during and directly after training appear to be the best effective strategy to improve performance and recovery. Future research is warranted to investigate the effectiveness of practical pre-cooling and per-cooling strategies in competition or field settings.

• Food Science and Preservation
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• v.24 no.5
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• pp.666-672
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• 2017

The purpose of this study was to examine the effects of long-term endurance exercise and salvia miltiorrhiza vinegar on body composition and insulin resistance of high-fat diet (30% carbohydrate, 50% fat and 20% protein) induced obese rats. After 8 weeks of high fat diet (50% of total calories), rats were divided into 4 groups (sedentary group, n=10; exercise group, n=10; Salvia miltiorrhiza vinegar group, n=10; exercise+Salvia miltiorrhiza vinegar group, n=10) for 8 weeks. Body weight, body composition, diet intake volume, oral glucose tolerance test, plasma total cholesterol were measured. The results showed that Salvia miltiorrhiza vinegar plus endurance exercise training for 8 weeks significantly improved body weight control, visceral fat weight, and insulin resistance. However, only Salvia miltiorrhiza vinegar treatment did not significantly improve body composition and insulin resistance. In addition, there was no additive by the combination of Salvia miltiorrhiza vinegar and endurance exercise in insulin, body fat, and total cholesterol. The reduction of body fat, glucose, insulin and cholesterol by combination was resulted from the exercise. These results suggest that Salvia miltiorrhiza vinegar has slight effect on anti-hyperglycemia and anti-obesity.

• 한국체육학회지인문사회과학편
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• v.51 no.3
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• pp.353-362
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• 2012

The purpose of this research was to find effects of high fat diet and endurance exercise on mitochondria biosynthesis and insulin resistance in male Wister rat. Th rats were randomly separated into 4 groups: A, Isocaloric high fat diet group (50% of calories from fat), B. Chow group, C. Isocaloric high fat diet with endurance exercise (treadmill running, slop 8%, 23 m/min, 120 min/day, 5 days per week), D. Chow group with endurance exercise. Both Isocaloric high fat diet group and chow group were given an equal caloric composition with 3.2kcal/g. equal amount of food were checked every day and given to both groups. 4 weeks of high fat diet did not show any change in body weight and amount of body fat. Further the level of glucose and insulin in blood, and insulin-stimuilated glucose transport rate in epitrochlearis muscle was not affected by Isocaloric high fat diet. However, the endurance exercise showed statistically significant change in the level of insulin in blood. Although either Isocaloric high fat diet or endurance exercise alone did not change on mitochondria biogenesis marker, Isocaloric high fat diet with endurance exercise could induce the increased level of marker (p<0.05). Also, plasma free fatty acids were increased in this group. From this investigation, Isocaloric high fat diet with moderate-intensity endurance exercise is effective way to induce mitochondrial biogenesis.