Widrick J J, Trappe S W, Costill D L, Fitts R H
Department of Biology, Marquette University, Milwaukee, Wisconsin 53201, USA.
Am J Physiol. 1996 Aug;271(2 Pt 1):C676-83. doi: 10.1152/ajpcell.1996.271.2.C676.
Gastrocnemius muscle fiber bundles were obtained by needle biopsy from five middle-aged sedentary men (SED group) and six age-matched endurance-trained master runners (RUN group). A single chemically permeabilized fiber segment was mounted between a force transducer and a position motor, subjected to a series of isotonic contractions at maximal Ca2+ activation (15 degrees C), and subsequently run on a 5% polyacrylamide gel to determine myosin heavy chain composition. The Hill equation was fit to the data obtained for each individual fiber (r2 > or = 0.98). For the SED group, fiber force-velocity parameters varied (P < 0.05) with fiber myosin heavy chain expression as follows: peak force, no differences: peak tension (force/fiber cross-sectional area), type IIx > type IIa > type I; maximal shortening velocity (Vmax, defined as y-intercept of force-velocity relationship), type IIx = type IIa > type I; a/Pzero (where a is a constant with dimensions of force and Pzero is peak isometric force), type IIx > type IIa > type I. Consequently, type IIx fibers produced twice as much peak power as type IIa fibers, whereas type IIa fibers produced about five times more peak power than type I fibers. RUN type I and IIa fibers were smaller in diameter and produced less peak force than SED type I and IIa fibers. The absolute peak power output of RUN type I and IIa fibers was 13 and 27% less, respectively, than peak power of similarly typed SED fibers. However, type I and IIa Vmax and a/Pzero were not different between the SED and RUN groups, and RUN type I and IIa power deficits disappeared after power was normalized for differences in fiber diameter. Thus the reduced absolute peak power output of the type I and IIa fibers from the master runners was a result of the smaller diameter of these fibers and a corresponding reduction in their peak isometric force production. This impairment in absolute peak power production at the single fiber level may be in part responsible for the reduced in vivo power output previously observed for endurance-trained athletes.
通过针吸活检从五名中年久坐男性(SED组)和六名年龄匹配的耐力训练大师级跑步者(RUN组)获取腓肠肌纤维束。将单个化学通透的纤维段安装在力传感器和位置电机之间,在最大Ca2+激活(15℃)下进行一系列等张收缩,随后在5%聚丙烯酰胺凝胶上运行以确定肌球蛋白重链组成。将希尔方程拟合到每个单独纤维获得的数据(r2≥0.98)。对于SED组,纤维力-速度参数随纤维肌球蛋白重链表达而变化(P<0.05),如下所示:峰值力,无差异;峰值张力(力/纤维横截面积),IIx型>IIa型>I型;最大缩短速度(Vmax,定义为力-速度关系的y轴截距),IIx型=IIa型>I型;a/Pzero(其中a是具有力的维度的常数,Pzero是峰值等长力),IIx型>IIa型>I型。因此,IIx型纤维产生的峰值功率是IIa型纤维的两倍,而IIa型纤维产生的峰值功率比I型纤维大约多五倍。RUN组的I型和IIa型纤维直径较小,产生的峰值力比SED组的I型和IIa型纤维少。RUN组I型和IIa型纤维的绝对峰值功率输出分别比类似类型的SED纤维的峰值功率低13%和27%。然而,SED组和RUN组之间I型和IIa型的Vmax和a/Pzero没有差异,并且在对纤维直径差异进行功率归一化后,RUN组I型和IIa型的功率缺陷消失。因此,大师级跑步者的I型和IIa型纤维绝对峰值功率输出降低是这些纤维直径较小以及相应的峰值等长力产生减少的结果。单纤维水平上绝对峰值功率产生的这种损害可能部分导致了先前观察到的耐力训练运动员体内功率输出降低。