2006 Fiscal Year Final Research Report Summary
Molecular biological studies of skeletal muscle adaptations to physical exercise
| Project/Area Number |
15200050
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Sports science
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| Research Institution | Fukuoka University |
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Principal Investigator |
TANAKA Hiroaki Fukuoka University, Faculty of Sports and Health Science, Professor, スポーツ科学部, 教授 (00078544)
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| Co-Investigator(Kenkyū-buntansha) |
KIYANAGA Akira Fukuoka University, Faculty of Sports and Health Science, Professor, スポーツ科学部, 教授 (70177955)
CHIBA Hitoshi Hokkaido University Hospital, Professor, 医学部附属病院, 教授 (70197622)
SHONO Naoko Saga University, Faculty of Medicine, adjunct professor, 医学部, 非常勤講師 (60223674)
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| Project Period (FY) |
2003 – 2006
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| Keywords | Lactate threshold / muscle / PGC1α / mitochondrial content / lipid metabolism / 遺伝子発現 / タンパク発現 / メタボリックシンドローム |
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| Research Abstract |
Exercise at lactate threshold (LT) is the minimum intensity that can promote health benefits. This mild-exercise training can be recommended to people with very limited range of exercise capacity, including the elderly and individuals with metabolic syndrome and coronary artery diseases (CAD). Indeed, supervised LT training improves physiological fitness, lipid profile, insulin sensitivity and cardio-pulmonary baroreflex in healthy adults. In this study we further investigated the mechanism to induce the above mentioned adaptation by the molecular biological approach. We developed rather noninvasive syringe biopsy to obtain the muscle sample for this purpose. We found that PGC-1α gene expression, which may play an important role for the mitochondrial biogenesis, lipid metabolism and insulin sensitivity, was activated by a single session of exercise at the LT but not by the exercise below the LT. Further the LT training has coordinately induced transcripts encoding enzymes in mitochondrial energy metabolism and fat oxidation as well as glucose and creatine metabolisms in young adult. Some of these changes, especially in mitochondrial function, are known to be inversely modulated in individuals with metabolic syndrome as well as atrophied muscle. Another molecular feature associated with LT training is the increases in transcripts encoding potent antioxidant enzymes and molecular chaperons, key genes involved in excitation-contraction coupling and electrolyte transport, and genes responsible for protein turnover. We also showed that CD36 in type I fiber increased with the LT training but did not change mitochondrial content.
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