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1دورية أكاديمية
المؤلفون: Chen, Chiao Nan (Joyce), Liao, Yi Hung, Lin, Shang Ying, Yu, Jun Xian, Li, Zhen Jie, Lin, Yu Chieh, Chang, Gwo Jyh, Lin, Chung Hao, Wong, Alice May Kuen
المساهمون: 臺北護理健康大學運動保健系
مصطلحات موضوعية: blood lactate, lactate dehydrogenase, monocarboxylate transporter
الوقت: 10
الوصف: Blood lactate increases during incremental exercise at high-intensity workloads, and limited exercise capacity is a characteristic of obese animals. This study examined whether blood lactate changes in response to incremental exercise is disrupted in obese animals. Muscular and hepatic proteins that are critical in lactate metabolism were also investigated. Rats were randomized to either standard chow (control) or high-fat diet (HFD) groups. All animals underwent an incremental treadmill test after 14 wk of diet intervention. Blood lactate levels were measured before and after the treadmill test. Activities of mitochondrial oxidative phosphorylation and glycolysis were examined in muscle tissues. Proteins in the liver and skeletal muscles that participate in the turnover of blood lactate were determined by Western blot. Running time in the incremental treadmill test decreased in the HFD group, and blood lactate accumulated faster in these animals than in the control group. Animals with HFD had a decreased level of hepatic monocarboxylate transporter 2, the protein responsible for blood lactate uptake in the liver. Skeletal muscles of animals with HFD showed greater glycolytic activity and decreased content of lactate dehydrogenase B, which converts lactate to pyruvate. We conclude that blood lactate accumulated faster during incremental exercise in obese animals and was associated with their decreased exercise performance. Changes in the metabolic pattern of muscles and changes of liver and muscle proteins associated with lactate utilization likely contribute to the abnormal response of blood lactate to incremental exercise in obese animals.
وصف الملف: 207 bytes; text/html
العلاقة: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 313(5), R601-R607; http://140.131.94.7/handle/987654321/7182Test
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2دورية أكاديمية
المؤلفون: Chen, Chiao nan (Joyce), Lin, Shang Ying, Liao, Yi Hung, Li, Zhen jie, Wong, Alice May Kuen
المساهمون: 臺北護理健康大學運動保健系
مصطلحات موضوعية: dietary restriction, muscle, glycolysis, mitochondrial pyruvate carrier, lactate dehydrogenase
الوقت: 10
الوصف: Caloric restriction (CR) attenuates age-related muscle loss. However, the underlying mechanism responsible for this attenuation is not fully understood. This study evaluated the role of energy metabolism in the CR-induced attenuation of muscle loss. The aims of this study were twofold: 1) to evaluate the effect of CR on energy metabolism and determine its relationship with muscle mass, and 2) to determine whether the effects of CR are age dependent. Young and middle-aged rats were randomized into either 40% CR or ad libitum (AL) diet groups for 14 wk. Major energy-producing pathways in muscles, i.e., glycolysis and mitochondrial oxidative phosphorylation (OXPHOS), were examined. We found that the effects of CR were age dependent. CR improved muscle metabolism and normalized muscle mass in middle-aged animals but not young animals. CR decreased glycolysis and increased the cellular dependency for OXPHOS vs. glycolysis in muscles of middle-aged rats, which was associated with the improvement of normalized muscle mass. The metabolic reprogramming induced by CR was related to modulation of pyruvate metabolism and increased mitochondrial biogenesis. Compared with animals fed AL, middle-aged animals with CR had lower lactate dehydrogenase A content and greater mitochondrial pyruvate carrier content. Markers of mitochondrial biogenesis, including AMPK activation levels and SIRT1 and COX-IV content, also showed increased levels. In conclusion, 14 wk of CR improved muscle metabolism and preserved muscle mass in middle-aged animals but not in young developing animals. CR-attenuated age-related muscle loss is associated with reprogramming of the metabolic pathway from glycolysis to OXPHOS.
وصف الملف: 207 bytes; text/html
العلاقة: American Journal of Physiology-Endocrinology and Metabolism, 308(11), E942-E949; http://140.131.94.7/handle/987654321/7186Test
