Force deficit during the onset of muscle hypertrophy.

Force deficit during the onset of muscle hypertrophy.
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肌肉肥大开始时力量不足。

DOI:
10.1152/jappl.1989.67.6.2600
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发表时间:
1989
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
White,TP
White,TP
中科院分区:
--
文献类型:
--
作者:
Kandarian,SC;White,TP

文献摘要

被引文献

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目的是研究与骨骼肌肥大早期发展过程中最大比力(N/cm2)不足相关的特定结构变化。在35d龄大鼠(n=41)行双侧腓肠肌和足底肌切开术,术后第1~30d观察比目鱼肌的变化。与年龄匹配的未手术大鼠(n=48)的对照肌肉相比,在术后30天内,肌肉质量和横截面积从28%平行增加到52%。与年龄匹配的对照组相比,肥大肌肉的比力在协同肌肉消融后第1天和第3天下降了38%,在第5~30d下降了28%。仅在第1天,间质间隙比对照组的20.4+/-1微升/100 mg增加了38%。术后7d内蛋白浓度下降15%,结缔组织蛋白浓度无明显变化。平均纤维横截面积增加的相对幅度小于肌块的相对幅度,直到消融后第7天。单个核细胞在第3~30天出现束间间隙的浸润,光镜下未见肌纤维损伤的迹象。最初的功能缺陷部分是由于间质间隙的扩大和蛋白质浓度的降低;后来的功能缺陷可能是细胞内的变化。
The purpose was to study selected structural changes associated with the deficit in maximum specific force (N/cm2) during the early development of skeletal muscle hypertrophy. Ablation of gastrocnemius and plantaris muscles was performed bilaterally in 35-day-old rats (n = 41), and the soleus muscle was studied from days 1 to 30 thereafter. Compared with control muscles from age-matched unoperated rats (n = 48), muscle mass and cross-sectional area increased in parallel from 28 to 52% over the 30-day postoperative period. Specific force of hypertrophied muscle was depressed 38% at days 1 and 3, and by 28% from days 5 to 30 after synergistic muscle ablation compared with age-matched control values. Interstitial space was 38% greater than the control value of 20.4 +/- 1 microliters/100 mg at day 1 only. Protein concentration was depressed 15% for 7 days after the ablation operation, and connective tissue protein concentration was unchanged. The relative magnitude of increased mean fiber cross-sectional area was less than that of muscle mass until day 7 after ablation. Mononuclear cell infiltration in interfascicular spaces occurred from days 3 to 30 without light microscopic evidence of muscle fiber injury. Initial functional deficits are explained in part by an enlarged interstitial space and decreased protein concentration; later deficits are likely accounted for by intracellular changes.