Project/Area Number |
12480012
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
体育学
|
Research Institution | Tokai University |
Principal Investigator |
TAMAKI Tetsuro Tokai University, School of Medicine, Assistant Professor, 医学部, 講師 (10217177)
|
Co-Investigator(Kenkyū-buntansha) |
UCHIYAMA Shuichi Tokai University, School of Physical, Associate Professor, 体育学部, 助教授 (80256164)
YOSHIMURA Shinichi Tokai University, School of Medicine, Assistant Professor, 医学部, 講師 (30230808)
|
Project Period (FY) |
2000 – 2002
|
Project Status |
Completed (Fiscal Year 2002)
|
Budget Amount *help |
¥14,400,000 (Direct Cost: ¥14,400,000)
Fiscal Year 2002: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2001: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2000: ¥9,000,000 (Direct Cost: ¥9,000,000)
|
Keywords | weight-lifting exercise / fatigue resistance capacity / amino acid uptake / muscle damage / norepinephrine / serotonin / c-fos / H-Thymidine / 代償性筋肥大 / 蛋白代謝 / 筋芽細胞 / 培養細胞 / 細胞増殖 / 細胞周期 / Anabolic steroid / 中枢神経系 / 視床下部 / 筋力トレーニング / Creatine Kinase / ^<14>C-Leucine / Fatigue Resistance / Muscle Damage |
Research Abstract |
The influence of an anabolic androgenic steroid (AAS) on thymidine and amino acid uptake in rat hindlimb skeletal muscles after a single exhaustive bout of weight-lifting was determined. Nandrolone decanoate or oil vehicle was administered to the Steroid group one week prior to the experiments. Serum creatine kinase (CK) activity, used as a measure of muscle damage, increased 30 and 60 min after exercise in both groups. The total amount of weight lifted was higher, whereas CK levels were lower in Steroid than Control rats. Thymidine uptake (cellular mitotic activity) peaked two days after exercise in both groups and was 90% higher in Control than Steroid rats, reflecting a higher level of muscle damage. Leucine uptake (amino-acid metabolism) was ~80% higher at rest and recovered 33% faster post-exercise in Steroid than Control rats. The in situ isometric mechanical properties of the plantaris muscle were determined. The only significant difference was a higher fatigue resistance in the
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Steroid compared to the Control group. These results indicate that AAS treatment 1) ameliorates CK efflux and muscle fiber damages and enhances the rate of protein synthesis and 2) enhances in vivo work capacity and the in situ fatigue resistance of a primary plantarflexor muscle. To identify possible mechanisms for AAS induced increase in aggressive behavior and work capacity, the levels of some biogenic amines were measured in selected regions of the brain. The levels of norepinephrine and its metabolite MHPG (4-hydroxy-3- methoxyphenylglycol) were increased by -2- and -7-fold in the hypothalamus of the Steroid compared to the Control and Vehicle groups. The levels of serotonin and its metabolite 5-HIAA (5-hydroxy-indole-3-acetic acid) were -40 and -50% higher in the Steroid compared to the Control and Vehicle groups. A significantly higher number of c-fos expressing neurons were observed in the periventricular region of the Steroid than the Control and Vehicle groups, indicating enhanced neuronal activity following nandrolone decanoate treatment Combined, the physical performance enhancement following anabolic-androgenic steroid treatment, are consistent with the interpretation that elevated levels of adrenergic and serotonergic amines in the hypothalamus could contribute to aggressive behaviors as well as improved physical performance. Less
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