Smith Lori W, Smith John D, Criswell David S
Department of Kinesiology, Texas Woman's University, Denton 76201, USA.
J Appl Physiol (1985). 2002 May;92(5):2005-11. doi: 10.1152/japplphysiol.00950.2001.
The purpose of this study was to determine the necessity of nitric oxide (NO) for hypertrophy and fiber-type transition in overloaded (OL) skeletal muscle. Endogenous NO production was blocked by administering N(G)-nitro-L-arginine methyl ester (L-NAME; 0.75 mg/ml; approximately 100 mg x kg-1 x day-1) in drinking water. Thirty-eight female Sprague-Dawley rats (approximately 250 g) were randomly divided into four groups: control-nonoverloaded (Non-OL), control-OL, L-NAME-Non-OL, and L-NAME-OL. Chronic overload of the plantaris was induced bilaterally by surgical removal of the gastrocnemius and soleus. Rats in the Non-OL groups received sham surgeries. L-NAME treatment began 24 h before surgery and continued until the rats were killed 14 days postsurgery. Although OL induced hypertrophy in both control (+76%) and L-NAME (+39%) conditions (P < 0.05), mean plantaris-to-body mass ratio in the L-NAME-OL group was significantly lower (P < 0.05) than that in the control-OL group. Microphotometric analysis of histochemically determined fiber types revealed increases in cross-sectional area (P < 0.05) for all fiber types (types I, IIA, and IIB/X) in the OL plantaris from control rats, whereas L-NAME-OL rats exhibited increases only in type I and IIB/X fibers. SDS-PAGE analysis of myosin heavy chain (MHC) composition in the plantaris indicated a significant (P < 0.05) OL effect in the control rats. Specifically, the mean proportion of type I MHC increased 6% (P < 0.05), whereas the proportion of type IIb MHC decreased approximately 9% (P < 0.05). No significant OL effects on MHC profile were observed in the L-NAME rats. These data support a role of NO in overload-induced skeletal muscle hypertrophy and fiber-type transition.
本研究的目的是确定一氧化氮（NO）在超负荷（OL）骨骼肌肥大和纤维类型转变中的必要性。通过在饮用水中给予N（G）-硝基-L-精氨酸甲酯（L-NAME；0.75毫克/毫升；约100毫克×千克-1×天-1）来阻断内源性NO的产生。38只雌性Sprague-Dawley大鼠（约250克）随机分为四组：对照-非超负荷（Non-OL）组、对照-OL组、L-NAME-Non-OL组和L-NAME-OL组。通过双侧手术切除腓肠肌和比目鱼肌诱导比目鱼肌慢性超负荷。Non-OL组的大鼠接受假手术。L-NAME处理在手术前24小时开始，并持续到大鼠在手术后14天处死。尽管在对照（+76%）和L-NAME（+39%）条件下OL均诱导了肥大（P<0.05），但L-NAME-OL组的比目鱼肌与体重的平均比值显著低于对照-OL组（P<0.05）。对组织化学测定的纤维类型进行显微光度分析显示，对照大鼠的OL比目鱼肌中所有纤维类型（I型、IIA型和IIB/X型）的横截面积均增加（P<0.05），而L-NAME-OL大鼠仅I型和IIB/X型纤维增加。比目鱼肌肌球蛋白重链（MHC）组成的SDS-PAGE分析表明，对照大鼠中存在显著的（P<0.05）OL效应。具体而言，I型MHC的平均比例增加了6%（P<0.05），而IIb型MHC的比例下降了约9%（P<0.05）。在L-NAME大鼠中未观察到对MHC谱的显著OL效应。这些数据支持NO在超负荷诱导的骨骼肌肥大和纤维类型转变中起作用。
