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김철현 ( Chul Hyun Kim ),이영익 ( Young Ik Lee ),김윤만 ( Yoon Man Kim ),조인호 ( In Ho Cho ),제임스전 ( James Jeon ),김지연 ( Ji Yeon Kim ),박재현 ( Jae Hyun Park ),김혜진 ( Hea Jin Kim ),신경아 ( Kyung A Shin ),이승주 ( Seong Ju 한국운동영양학회 2004 Physical Activity and Nutrition (Phys Act Nutr) Vol.8 No.3
The α-actinin is an actin-binding protein belonging to the spectrin protein superfamily. a-actinin-3(ACTN-3) expression is limited to skeletal muscle, especially Type Ⅱ muscle fiber. This gene has homozygosity for a premature stop codon resulting in a-actinin-3 deficiency. The deficiency in the type Ⅱ muscle is able to be compensated by a-actinin-2(ACTN-2). While that deficiency does not induce a disease phenotype, the ACTN-3 is highly conserved in evolutionary terms because of its functions independent of the ACTN2. Researchers have suggested that this trait is related to muscle function at the extremes of power performance. Therefore, we compared the relative frequencies of the ACTN-3 R577X polymorphism between anaerobic power athletes and control group. For this study, we recruited 158 sprint or power elite athletes and 414 healthy adults. The results of the current study showed significant differences in the genotype frequencies such that elite anaerobic power athletes have 4% higher of the RR genotype and 9% lower of the XX genotype than the healthy adults. With respect to the allele frequencies, the athletic group had significantly higher R allele frequency and significantly lower X allele frequency than the control group. In summary, these results suggest that the ACTN-3 R577X genotype may represent a genetic marker for anaerobic power performance.
지구성 운동 유발 전 처치에 따른 심장보호 효과 (iNOS knock-out mice 활용)
김철현 ( Chul Hyun Kim ),엄현섭 ( Hyun Sub Um ),이영익 ( Young Ik Lee ),김윤만 ( Yoon Man Kim ),조인호 ( In Ho Cho ),김명기 ( Myung Ki Kim ),이규성 ( Kyu Sung Lee ),양대승 ( Dea Seung Yang ),오윤선 ( Yoon Sun Oh ),오유성 ( Yoo Sun 한국운동영양학회 2005 Physical Activity and Nutrition (Phys Act Nutr) Vol.9 No.1
The goal of this study was to explore the role of inducible NOS (iNOS) and the delayed protection of exercise preconditioning from the relative myocardial ischemia reperfusion injury. Mice were randomly placed in one of five testing groups: wild-type mice group (n = 15), high-intensity wild-type mice acute exercised group (n = 6). low-intensity wild-type mice acute exercised group (n = 5), L-NAME + wild-type mice acute exercised group (11 = 5), and homozygous (-/-) iNOS gene knock-out mice acute exercised group (n = 5). All acute exercised groups ran on the treadmill (0% grade) at 65 m,`min as a high-intensity exercise and at 27-30 m/min as a low-intensity exercise. The results showed that all acute exercise significantly reduced magnitude of a myocardial infarction in biphasic manner. In accordance with these data, NFKB and HSP-70 protein expression was increased at 24 after exercise-induced preconditioning (PC) in both low-intensity wild-type mice acute exercised group and homozygous (-/-) iNOS gene knock-out mice acute exercised group compared with wild-type mice group. In contrast, neither endothelial nitric oxide synthase (eNOS) nor inducible nitric oxide synthase (iNOS) expression changed at both wild-type mice group and low-intensity wild-type mice acute exercised group. In conclusion, The strong evidence of this study indicates that HSP-70 is particulary cytoprotectiye against protein-damaging stress such as I-R. Also, this study demonstrate that the late phase of exercise-induced PC is not associated with up-regulation of eNOS and iNOS but infarct-sparing effect and mild up-regulation of NFKB and HSP-70 at the late phase of exercise-induced PC in wild-type mice and iNOS gene knock-out mice. Thus, this study identifies a specific protein that mediates late PC in vitro.
저 강도 운동에 따른 본태성고혈압 쥐의 병리학적 심근 비대 관련 분자적 표현형과 세포사멸 조절 단백질의 변화
이영익 ( Young Ik Lee ),김철현 ( Cheol Hyun Kim ),조인호 ( In Ho Cho ),엄현섭 ( Hyun Seob Um ),김윤만 ( Yoon Man Kim ),김명기 ( Myung Ki Kim ),오윤선 ( Yoon Sun Oh ),양춘호 ( Chun Ho Yang ),황대연 ( Dae Yun Hwang ),남기태 ( Ki Tae 한국운동생리학회(구-한국운동과학회) 2005 운동과학 Vol.14 No.4