地西泮与运动训练对大鼠骨骼肌部分生化和组织化学特性的影响。

J Padilla, W C Fielding, A N Belcastro, P F Gardiner, A W Taylor
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引用次数: 0

摘要

在50只雄性白化大鼠胫骨前肌(TA)、比目鱼肌(Sol)和跖肌(Plt)中,研究了慢性地西泮(D)治疗和运动训练对总体重(TBM)、微粒体蛋白产量(MPY)、碎片化肌浆网(SR)钙摄取、肌纤维截面积以及PFK和SDH活性的影响。将大鼠随机分为对照组(C)、短跑训练组(S)和耐力训练组(E)。培训为期12周。每组一半的小鼠每天腹腔注射5 mg kg-1的TBM。运动降低TBM (p < 0.05);增加了TA的相对BM (E = 2.02 +/- 0.02, p < 0.01)和Plt (E = 1.15 +/- 0.02, p < 0.01);S = 1.13 +/- 0.03, p < 0.01),以及Sol SR对Ca++的吸收(C = 0.08 +/- 0.02, E = 0.16 +/- 01, p < 0.05)。S- sol组MPY升高(C = 1.12 +/- 0.6, S = 1.52 +/- 0.1, p < 0.01)。D升高Sol MPY和TA PFK。s训练的动物的平均纤维面积比e训练(d治疗和未治疗)的动物低。TA和Plt的相对质量升高是由于运动减少了TBM。钙离子对Sol吸收的增加表明E增强了这一功能,而MPY的增加可能意味着sr的增加。D可能是D升高的Sol MPY和TA PFK的原因。El D并没有将神经肌肉活动降低到对氧化酶活性产生不利影响的程度,但在TA肌肉中PFK活性的情况下,这种降低是明显的。
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The effect of diazepan and exercise training on selected biochemical and histochemical properties of rat skeletal muscle.

The effects of chronic diazepam (D) treatment and exercise training on total body mass (TBM), microsomal protein yield (MPY), calcium uptake by fragmented sarcoplasmic reticulum (SR), muscle fibre cross-sectional area, and both PFK and SDH activities were investigated in the tibialis anterior (TA), soleus (Sol), and plantaris (Plt) muscles of 50 male albino Sprague-Dawley rats. Rats were assigned randomly to control (C), sprint-trained (S), or endurance-trained (E) groups. Training was of 12 weeks duration. One-half of each group received daily intraperitoneally D doses of 5 mg kg-1 of TBM. Exercise reduced TBM (p < 0.05); increased the relative BM of the TA (E = 2.02 +/- 0.02, p < 0.01) and Plt (E = 1.15 +/- 0.02, p < 0.01; S = 1.13 +/- 0.03, p < 0.01), as well as the Ca++ uptake of the Sol SR (C = 0.08 +/- 0.02, E = 0.16 +/- 01, p < 0.05). MPY was elevated in S-Sol (C = 1.12 +/- 0.6, S = 1.52 +/- 0.1, p < 0.01). D elevated Sol MPY as well as TA PFK. S-trained animals had lower mean fibre areas than the E-trained (D-treated and untreated) animals. The elevated relative masses of TA and Plt are explained by a decreased TBM with exercise. The increased Ca++ uptake of the Sol indicates that E enhances this function, and the increased MPY probably implies an increased SR. The D could be responsible for the D-elevated Sol MPY as well as the TA PFK. El D did not reduce neuromuscular activity to a level adversely affecting oxidative enzyme activity, but in the case of PFK activity in the TA muscle, such a reduction was evident.

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