失血性休克状态下的心肌超微结构

应用家免失血性休克模型观察心肌的超微结构改变。结果发现(1)间盘两侧的心肌纤维呈区带性病变,肌膜呈扇形膨出;Z带互相靠近,肌节缩短;Z带断裂,肌原纤维走向紊乱;线粒体移位至距间盘较远的地区;(2)间盘区以外广大地区心肌纤维显示细胞内水肿;线粒体肿胀,脊破坏减少;肌原纤维灶性溶解;肌浆网小管稀少、断离、扩张及囊泡化等改变。这些改变使心肌的供能装置、收缩结构以及兴奋收缩偶联过程遭到破坏,妨碍心肌收缩功能,从而构成并发急性心功能不全的超微结构基础。     

Nebulin是Duchenne型肌营养不良症缺失基因的产物吗?

导致Duchenne型肌营养不良症(DMD)基因编码的mRNA约16千碱基对,如果该信息翻译成一个蛋白质,其大小约为500千道尔顿。肌肉中已知的最大的蛋白质是nebulin(550千道尔顿)和titin(大于1000千道尔顿),两种蛋白质均存在于暗带(由肌球蛋白粗丝组成的肌节)和明带(含连到Z线的肌动蛋白细丝的肌节)的连接处。作者检查了5例DMD病人无变性的肌纤维,在某些肌节的暗带和明带连接处可见细丝紊乱,同时将之与对照组的肌肉作比较。作者还将肌活检标本制备的肌原纤维沉淀物用于电泳,应用此技术,研究了30例DMD病人(2.5个月到7岁)和25名对照     

1—5 蟾蜍和蛙缝匠肌的肌节长度测定

肌节是肌肉收缩的最小机能单位,肌肉作功能力的大小与其长度有密切关系,了解肌节长度及其变化对了解肌肉的力学性质具有重要意义。然而,在活体标本特别是直接测量在体骨骼肌肌节长度非常困难。迄今为止,尚未见到有关直接测量在体肌肉肌节长度的方法。我们应用激光衍射法直接测量了蟾蜍和蛙缝匠肌的在体肌节长度,现将结果报导如下。结果:离体实验牵拉肌肉从松弛状态直至肌肉断裂,观察肌肉和肌节长度关系,结果发现这两种动物骨髂肌的肌肉和肌节长度关系并未出现预期的线性关系,所获曲线略呈S型。蟾蜍缝匠机完全松弛时的肌节长度为2.10±0.03μm(n=11):SLf(固定     

用ODO冷冻断裂法观察人膈肌细胞的超微结构

扫描电镜观察人横纹肌细胞的超微结构,尚未见有报道。作者应用ODO(锇酸-二甲基亚砜-锇酸)冷冻断裂扫描电镜制样技术,对人膈肌细胞进行观察。人膈肌属横纹肌,其肌细胞呈长圆柱形,横径为12～18μm。由35～40个肌细胞组成肌束。肌细胞表面被有肌质膜,肌质膜外有一层由蛋白粘多糖构成的细丝状基板。据作者的观察,1个肌细胞含有170～380条肌原纤维,其横径为1.5μm。一条肌原纤维有许多A带(暗带)和1带(明带),前者宽1.25μm,后者宽0.6μm,A带中央的H带清     

葡萄糖-6-磷酸酶在大白鼠心肌细胞超微结构的定位

葡萄糖-6-磷酸酶(G6Pase)是内质网的标志酶,本研究观察了大白鼠左心室心肌细胞的G6Pase的定位。实验结果表明,G6Pase活性遍布于心肌细胞的肌浆网(内质网)腔内,包括肌原纤维之间的肌浆网小管、肌膜下池和核膜。尤其是酶的反应产物在肌原纤维处显示了肌浆网小管的特征性分布:即在A带处肌浆网小管排列紧密形成致密网格,而在I带处排列稀疏,形成多角形大网格。这种排列特点可能和肌肉的舒缩功能有关,在收缩时I带的细丝向A带粗丝处滑动,肌节缩短。在I带处肌浆网小管排列成大网格、稀疏,便于伸长或缩短,是适应性的分布。     

乙醇对豚鼠单个心房肌细胞L-型钙通道的影响

目的： 采用膜片钳全细胞记录方法，观察乙醇对分离的豚鼠单个心房肌细胞L-型钙电流（ICa.L）的影响。方法： 使用酶解方法获得豚鼠单个心房肌细胞，采用全细胞膜片钳记录技术观察不同浓度乙醇急性干预对ICa.L电流-电压曲线、激活曲线、失活曲线的影响。结果： 急性乙醇干预下，ICa.L的I-V曲线发生了变化，而失活曲线未发生变化，激活曲线仅在80mmol/L的时候发生了变化。在乙醇浓度≤45 mmol/L时可抑制ICa.L，而在≥50 mmol/L时可明显增大ICa.L，在45 mmol/L-50 mmol/L之间这两种作用发生了突然的转换。结论： 乙醇对于ICa.L的影响作用基本为非电压依赖性，但具有浓度依赖性，不同浓度的乙醇可对ICa.L产生不同甚至相反的作用，这有助于解释房颤和房扑之间的关系。     

模拟失重对大鼠比目鱼肌肌重和形态结构的影响

目的 研究模拟失重对大鼠抗重力肌—比目鱼肌的湿重、干重及形态结构的影响.方法 采用健康雌性Sprague-Dawlwy大鼠117只,按照体重配对原则随机分悬吊各组及其各自的对照组.采用组织学方法和透射电镜观察尾部悬吊法模拟失重状态下,比目鱼肌干、湿重体重比的变化,以及肌纤维的光镜结构与超微结构的变化.结果 与对照组相比,比目鱼肌干重体重比、湿重体重比在悬吊7d组即明显下降,悬吊14d组达峰值,此后有所回升.悬吊14d后的比目鱼肌,光镜下肌束结构紊乱,肌纤维面积和面积构成减少,肌纤维间间隙加大,结缔组织增生.电镜下可见肌原纤维分解,局部溶解,Z线排列紊乱、中断,肥厚层破坏,部分的纹带中出现坏死区.以上变化在解除悬吊7d时不能完全恢复.结论 尾部悬吊可致大鼠比目鱼肌萎缩,光镜结构和超微结构出现异常改变.     

用于测量单心肌细胞肌节运动的微机图象处理系统

分离的单心肌细胞在研究心脏力学及其电生理特性具有重要的作用。然而,过去很少有人同时研究心肌细胞的力学特性与电生理特性,其主要原因是缺乏同时记录细胞动作电位与测量肌节收缩的仪器系统。本文描述了一个解决此问题的仪器系统。该系统由显微镜、电极、摄象机、监视器、图象输入机、计算机和某些辅助电路组成。系统在记录动作电位的同时记录下细胞的图象,图象经图象输入数化后,输入计算机,运用数字图象处理技术,可测量收缩过程中肌节的长度。文中给出了运用此系统对豚鼠心室细胞进行研究的结果。实验结果表明,该系统是研究肌节兴奋——收缩的重要工具,它克     

老年亚临床甲减患者骨代谢生化指标的变化

目的:测定老年亚临床甲减患者骨代谢生化指标及探讨其临床意义。方法:采用放射免疫分析与电 化学发光免疫分析法观察了30例老年亚临床甲减患者,30例老年健康人S-BGP、TSH和FT4水平,同时观察 了两组血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、 载脂蛋白A1(ApoA1)、载脂蛋白B100(ApoB100)以及钙离子(Ca2 )的浓度变化。结果:①30例老年亚临床甲减 患者S-BGP浓度为(2.78±0.96)μg/L,30例老年健康人S-BGP浓度为(3.9±1.48)μg/L。两组比较差异 非常显著(P<0.01)。②30例老年亚临床甲减患者血清Ca2 浓度为(2.16±0.17)mmol/L,30例老年健康人 血清Ca2 浓度为(2.31±0.21)mmol/L,两组比较差异非常显著(P<0.01)。③30例老年亚临床甲减患者TC 和LDL-C水平分别为(5.58±0.41)mmol/L和(3.67±0.36)mmol/L,与老年健康组比较差异非常显著(P< 0.01)。结论:由于Ca2 浓度的降低,导致骨丢失,S-BGP浓度降低可能是老年亚临床甲减患者骨质疏松的主 要原因。     

应用MARS人工肝治疗急慢性重型肝炎临床研究

探讨分子吸附再循环系统(MARS)人工肝支持系统治疗重型肝炎的疗效和安全性。方法7例重型肝炎患者在内科综合治疗同时,加用MARS人工肝治疗。MARS人工肝治疗每次持续6～8h。结果7例重型肝炎患者在MARS治疗后,血总胆红素和总胆酸分别由(410.90±256.99)μmol/L和(107.37±69.78)μmol/L降至(310.60±88.97)μmol/L和(60.96±36.27)μmol/L(P<0.001);肌苷和尿素分别由(234.43±90.83)mmol/L和(12.64±5.29)mmol/L降至(93.29±45.27)mmol/L和(6.59±3.73mmol/L(P<0.05);凝血酶原时间(PT)和活化部分凝血酶时间(APTT)分别由(26.81±)13.01s)和(57.54±18.44)s缩短至(17.98±4.52)s和(40.57±11.14)s(P<0.05MARS治疗前后患者血K 、Na 、白细胞和);血小板无显著改变(P>0.05);在MARS治疗期间患者血压、脉搏稳定。4例合并肝肾综合征(HRS)患者中,2例经MARS治疗病情好转,肾功能改善。结论MARS人工肝支持系统是治疗重型肝炎及合并HRS有效和安全的方法。     

尼古丁对大鼠气道平滑肌细胞内钙离子浓度及膜瞬时受体电位通道mRNA表达的影响

目的 观察尼古丁刺激大鼠气道平滑肌细胞(ASMC)后细胞内基础钙离子浓度的改变及平滑肌细胞膜瞬时受体电位通道(TRPC1,TPRC6)mRNA表达水平变化.方法 不同浓度尼古丁[O(对照组)、10、20、50、100μg/L]刺激大鼠气道平滑肌细胞,作用24及48 h后,采用Incyte细胞内钙浓度检测系统观察细胞内钙离子浓度的变化.提取细胞总RNA,反转录成cDNA,实时定量PCR方法检测细胞TRPC1和TRPC6 mRNA表达量变化.结果 20、50、100μg/L的尼古丁刺激大鼠气道平滑肌细24和48 h后,细胞内基础钙离子浓度均较对照组明显升高[(117.99±19.39)、(122.89±17.91)、(124.70±17.93)nmol/L比(85.85±12.60)nmol/L;(142.07±18.99)、(162.27±19.91)、(207.30±26.56)nmol/L比(98.04±2.39)nmol/L,均P＜0.05].而细胞中TRPC1和TPRC6 mRNA相对浓度也均较对照组显著升高(P＜0.05),其中,100μg/L尼古丁刺激气道平滑肌细胞48 h后,细胞内基础钙离子浓度和TRPC6 mRNA相对表达量均较刺激24 h后的明显升高(P＜0.05).结论 尼古丁可能通过上调大鼠气道平滑肌细胞膜瞬时受体电位通道TRPC1和TPRC6的表达而导致大鼠气道平滑肌细胞内基础钙离子浓度增加.     

MCU在高糖诱导心肌H9c2细胞凋亡中的作用机制

目的:探讨线粒体钙离子单向转运体(mitochondrial calcium uniporter,MCU)在高糖(high glucose,HG)诱导心肌H9c2细胞凋亡中的作用机制。方法:将心肌H9c2细胞随机分为3组:对照(control)组,5.5 mmol/L葡萄糖处理细胞;HG组,25 mmol/L葡萄糖处理细胞;精胺(spermine,Sp)干预(HG+Sp)组,25 mmol/L葡萄糖和5μmol/L Sp共同处理细胞。Western blot检测H9c2细胞MCU、caspase-9和caspase-3蛋白的表达;RT-qPCR检测H9c2细胞MCU的mRNA水平;Rhod-2 AM探针检测线粒体内Ca2+的荧光强度;吸光度法检测丙酮酸脱氢酶(pyruvate dehydrogenase,PDH)的活性;萤火虫萤光素酶检测细胞裂解液ATP的浓度;JC-1染色法检测线粒体膜电位(mitochondrial membrane potential,Δψm);MitoSOXTM染色法检测线粒体活性氧簇(reactive oxygen species,ROS)水平。结果:与control组相比,HG组MCU mRNA和蛋白水平、线粒体内Ca2+浓度、PDH活性、细胞ATP浓度及Δψm降低(P<0.05),而ROS水平及caspase-9和caspase-3凋亡蛋白表达增加(P<0.05);与HG组相比,HG+Sp组线粒体内Ca2+浓度、PDH活性、细胞ATP浓度和Δψm增加(P<0.05),而ROS水平及caspase-9和caspase-3凋亡蛋白表达降低(P<0.05)。结论:高糖通过降低MCU表达导致其活性下降,从而促进心肌H9c2细胞凋亡,其机制可能与线粒体的钙离子稳态失衡、三羧酸循环障碍和线粒体功能损伤有关。     

High frequency characteristics of elasticity of skeletal muscle fibres kept in relaxed and rigor state

Summary The viscoelastic properties of crossbridges in rigor state are studied by means of application of small length changes, completed within 30 s, to isometric skinned fibre segments of the iliofibularis muscle of the frog in relaxed and rigor state and measurement of the tension response. Results are expressed as a complex Young's modulus, the real part of which denotes normalized stiffness, while the imaginary part denotes normalized viscous mechanical impedance. Young's modulus was examined over a wide frequency range varying from 5 Hz up to 50 kHz. Young's modulus can be interpreted in terms of stiffness and viscous friction of the half-sarcomere or in terms of elastic changes in tension and recovery upon a step length change.The viscoelastic properties of half-sarcomeres of muscle fibre segments in rigor state showed strong resemblance to those of activated fibres in that shortening a muscle fibre in rigor state resulted in an immediate drop in tension, after which half of the drop in tension was recovered. The following slower phases of tension recovery—a subsequent drop in tension and slow completion of tension recovery—as seen in the activated state, do not occur in rigor state. The magnitude of Young's moduli of fibres in rigor state generally decreased from a value of 3.12×10⁷ N m^-2 at 40 kHz to 1.61×10⁷ N m^-2 at about 100 Hz.Effects of increased viscosity of the incubation medium, decreased interfilament distance in the relaxed state and variation of rigor tension upon frequency dependence of complex Young's modulus have been investigated. Variation of tension of crossbridges in rigor state influenced to some extent the frequency dependence of the Young's modulus. Recovery in relaxed state is not dependent on the viscosity of the medium. Recovery in rigor is slowed down at raised viscosity of the incubation medium, but less than half the amount expected if viscosity of the medium would be the cause of internal friction of the half-sarcomere. Internal friction of the half-sarcomere in the relaxed fibre at the same interfilament distance as in rigor is different from internal friction in rigor. It will be concluded that time necessary for recovery in rigor cannot be explained by friction due to the incubation medium. Instead, recovery in rigor expressed by the frequency dependence of the Young's modulus has to be due to intrinsic properties of crossbridges. These intrinsic properties can be explained by the occurrence of state transitions of crossbridges in rigor. Similarity of Young's modulus of fibre segments in the activated state and in rigor in the frequency range above 5 kHz strongly suggests that the same state transitions occur in force generating crossbridges in the activated fibre.     

The function of elastic proteins in the oscillatory contraction of insect flight muscle

Oscillatory contraction of asynchronous insect flight muscle is activated by periodic stretches at constant low concentrations of Ca²⁺. The fibres must be relatively stiff to respond to small length changes occurring at high frequency. Several proteins in the flight muscle may determine the overall stiffness of the fibres. The Drosophila sallimus (sls) gene codes for multiple isoforms with a modular structure made up of immunoglobulin (Ig) and elastic PEVK domains, unique sequence, and a few fibronectin (Fn) domains at the end of the molecule. Kettin, derived from the sls gene, has Ig domains separated by linker sequences and is bound to actin near the Z-disc; the C-terminus is associated with the end of the A-band. Flight muscle also has longer isoforms of Sls, with extensible PEVK sequence, and C-terminal Fn domains; all extend from the Z-disc to the end of the A-band. Projectin, from a different gene, has repeating modules of Fn and Ig domains, and is associated with the end of thick filaments; tandem Ig and PEVK domains at the N-terminus are in the I-band. Projectin, kettin and other Sls isoforms form a mechanical link between thick and thin filaments; all are probably part of the connecting filaments, which branch from the thick filaments and are linked to actin near the Z-disc. The elasticity of fibres may depend on the relative amounts of those isoforms with extensible PEVK sequence. Flightin is bound on the outside of thick filaments and maintains the stiffness necessary for the transmission of stress along the filaments. Insect flight muscle has multiple elastic proteins to give the sarcomere the optimum compliance necessary for high frequency oscillatory contraction.     

Co-ordinated electron microscopy and X-ray studies of glycerinated insect flight muscle. II. Electron microscopy and image reconstruction of muscle fibres fixed in rigor,in ATP and in AMPPNP

Summary This paper presents electron microscopy, supported by optical diffraction and filtering of images from 100 nm and 25 nm sections, to complement the companion report of X-ray diffraction monitoring (immediately preceding this article) performed on the same insect flight muscle specimens during fixation, dehydration and embedding. GlycerinatedLethocerus fibre bundles initially fixed in rigor, in ATP relaxing buffer, or in 1mM AMPPNP at 2° C, gave thin-section images from each state whose optical transforms match the distinctive X-ray diffraction patterns from the embedded samples. For rigor and relaxed states, this extends and confirms a long-known correlation between X-ray patterns and EM image regularities. For the AMPPNP state, such correlation is here fully developed for the first time, and involves a new and distinctive EM image pattern of the crossbridge array, clearly different from a previously reported structure in AMPPNP-treated muscles that appears identical to fixed relaxed muscle. We found this latter artifact of AMPPNP-relaxed structure in many fibres from our best AMPPNP specimen, but could identify other fibres which retained the distinctive AMPPNP structure, known to be dominant in this specimen from the X-ray pattern. The true AMPPNP structure shows features of both the ATP-relaxed and rigor crossbridge patterns, not as separate patches, but hybridized uniformly along each filament and throughout each affected sarcomere and fibre. It presents a 14.5 nm repeat of striping and lateral projections along thick filaments, together with variously angled crossbridge attachments to actin that form a 38.7 nm repeat of diffuse chevrons or deltoids replacing the more clearly delinated rigor double chevrons. The associated optical transform has the typical AMPPNP features, that is, it has in common with rigor a strong 19.3 nm layer line and strong second to fourth row line sampling on the 38.7 nm layer line, it has in common with relaxed patterns a strong 14.5 nm meridional and layer line, but it uniquely shows no intensity at the first row line on the 38.7 nm layer line (the 10.3 X-ray reflection), where rigor and relaxed transforms always show high intensity. The processing artifacts which intensify the 10.3 reflection, and produce the weak 19.3 nm layer line (a gain of intensity for ATP but a loss for the AMPPNP state), throughout ATP specimens and in those analogue-treated fibres showing AMPPNP-relaxed structure, might indicate trapping and accumulation of minority populations within the native equilibrium distribution of crossbridge conformations in each nucleotide state.     

虎杖甙对心肌细胞钙的调节作用

目的:观察虎杖甙(polydatin,PD)对大鼠心肌细胞内游离钙浓度([Ca²⁺]i)的影响,以探讨PD增强心肌细胞收缩性的作用机制。方法:用荧光染料Fluo-3-AM标记细胞,在粘附式细胞仪上测定细胞[Ca²⁺]i的变化。结果:给予PD后心肌[Ca²⁺]i升高。但不同细胞群的[Ca²⁺]i升幅不一致。10min后有些细胞[Ca²⁺]i仅升至起始浓度的111.80%±2.22%,有些细胞内钙则急升到最初的224.00%±24.33%。当先用EGTA或维拉帕米分别预孵育10min后再加PD,细胞[Ca²⁺]i则呈持续下降趋势,10min后[Ca²⁺]i下降至起始浓度的53.00%±9.20%和52.00%±7.07%。给予TTX预处理后再加PD,[Ca²⁺]i也下降为起始值的72.67%±12.70%。与单纯PD作用相比都有显著差异。结论:PD可通过增加心肌[Ca²⁺]i而增强心肌收缩性,其作用可能与钙、钠通道开放有关。     

Perspective on the role of P2X-purinoceptor activation in human vas deferens contractility

The contractile actions of α,β-methylene ATP (α,β-meATP) and ATP and the effects of K(+) channel blockers in longitudinal and circular muscles of human vas deferens were investigated with a view to clarifying the functional importance of P2X(1)-purinoceptor activation and K(+) channels in modulating contractility of the tissues. The results provide an experiment-based perspective for resolving differing reports on purinergic activation of the tissues and uncertain roles of large-conductance Ca(2+)-activated K(+) (BK(Ca)) and voltage-gated delayed rectifier K(+) (K(V)) channels. α,β-Methylene ATP (3-100 μm) evoked suramin-sensitive contractions of longitudinal muscle but rarely of circular muscle. ATP (0.1-3 mm) less reliably activated only longitudinal muscle contractions. These were enhanced by ARL 67156 (100 μm), but a different ectonucleotidase inhibitor, POM 1, was ineffective. Both muscle types were unresponsive to ADP-βS (100 μm), a P2Y-purinoceptor agonist. Longitudinal muscle contractions in response to α,β-meATP were enhanced by FPL 64176 (1 μm), an L-type Ca(2+) agonist, TEA (1 mm), a non-specific K(+) channel blocker, 4-aminopyridine (0.3 mm), a selective blocker of K(V) channels, and iberiotoxin (0.1 μm), a selective blocker of BK(Ca) channels. Quiescent circular muscles responded to α,β-meATP reliably in the presence of FPL 64176 or iberiotoxin. Apamin (0.1 μm), a selective blocker of small conductance Ca(2+)-activated K(+) (SK(Ca)) channels had no effect in both muscle types. Y-27632 (1-10 μm) reduced longitudinal muscle contractions in response to α,β-meATP, suggesting involvement of Rho-kinase-dependent contractile mechanisms. The results indicate that P2X(1)-purinoceptor stimulation elicits excitatory effects that: (a) lead to longitudinal muscle contraction and secondary activation of 4-aminopyridine-sensitive (K(V)) and iberiotoxin-sensitive (BK(Ca)) K(+) channels; and (b) are subcontractile in circular muscle due to ancillary activation of BK(Ca) channels. The novel finding of differential action by P2X(1)-purinoceptor agonists in the muscle types has functional implication in terms of the purinergic contribution to overall contractile function of human vas deferens. The modulatory effects of K(V) and BK(Ca) channels following P2X(1)-purinoceptor activation may be pivotal in providing the crucial physiological mechanism that ensures temporal co-ordination of longitudinal and circular muscle contractility.     

Ultrastructural changes in myocardial cells of rats fed a low protein diet

 Ultrastructural changes in the ventricular myocardial cells in rats fed a low protein diet were examined by electron microscopy. The most striking changes were observed in the I-band region of the sarcomeres, which occurred very occasionally in myofibrils. In the sarcomere affected the I-band region was often fractured and/or disintegrated on one side, leaving an extended space, while the opposing I-band region disappeared along with dislocation of the intact A-band toward the adjacent Z-line. This dislocation was presumably attributed to the elasticity of titins connecting between the end of thick filaments and the Z-line. Fractured I-band regions were often accompanied by the dilated sarcoplasmic reticulum in the close vicinity of them. In some myofibrils the streaming and/or disruption of the Z-line were occasionally observed where disarrangement of thick and thin myofilaments were usually present. The study suggests that the fracture of the I-band region, consisting of actin and titin filaments, and the streaming of the Z-line of myofibrils are due to a proteolytic action of calpain and/or cathepsin L, which are activated by leaked Ca²⁺ ion and/or by modification of internal circumstances of the cytoplasm induced by a low protein diet, thus resulting in a low cardiac output. Received: 22 April 1998 / Accepted: 7 September 1998     

The complex Young's modulus of skeletal muscle fibre segments in the high frequency range determined from tension transients

Summary Stiffness measurements of muscle fibres are often based on application of a length change at one end of the muscle fibre and recording of the following tension change at the other end. In this study a method is developed to determine in the high frequency range (up to 40 kHz) the complex Young's modulus of skeletal muscle fibre as a function of frequency from the tension transient, following a rapid stepwise length change completed within 40 s. For this purpose both a new mechanical moving part of the displacement generating system and a force transducer with a high natural frequency (70 kHz) had to be developed. In addition to stiffness measurements of a silk fibre to test the displacement generating system and the method of analysis, stiffness of skeletal muscle fibres in relaxed and rigor state have been measured. The complex Young's moduli of relaxed muscle fibres as well as muscle fibres in rigor state are frequency dependent. In both cases the complex Young's modulus increases smoothly with increasing frequency over a range of 250 Hz up to 40 kHz. The phase angles of the responses remained almost constant at a value of 0.3 radians for a fibre in rigor and 0.6 radians for a relaxed fibre. This leads to the conclusion that for muscle fibres in rigor state the recovery in the tension response to a step length change shows a continuous distribution of relaxation times rather than a few discrete ones. Results of our stiffness measurements are compared with results obtained from current viscoelastic models used to describe stiffness of muscle fibre in this frequency range. The frequency dependence of stiffness of muscle fibres in rigor state suggests that the frequency used has to be taken into account while determining the elastic range of a crossbridge.