甲状腺功能亢进大鼠比目鱼肌肌浆网Ca2+-ATP酶活性增高可加速强直收缩疲劳

甲状腺功能亢进(甲亢)时甲状腺素分泌增加,不仅使具有神经支配的慢缩型肌纤维向快缩型转化,而且改变骨骼肌的强直收缩功能.因此,甲亢性肌病的肌肉乏力可能与骨骼肌强直收缩易发生疲劳有关.本实验在离体条件下,观测甲亢4周引起的大鼠慢缩肌--比目鱼肌(soleus, SOL)单收缩与间断强直收缩功能的变化.结果显示,甲亢4周大鼠体重明显低于同步对照组[(292±13)g vs (354±10)g],但SOL湿重没有明显改变[(107.3±8.6)mg vs (115.1±6.9)mg].甲亢大鼠SOL单收缩张力达到峰值的时间(time to peak tension, TPT)、从峰值降至75%舒张时间(time from peak tension to 75% relaxation, TR75)均明显缩短;强直收缩的TR75也明显缩短[(102.8±4.1)ms vs (178.8±15.8)ms];强直收缩的最适频率从对照组的100Hz增加到140Hz;间断强直收缩期间容易发生疲劳.甲亢大鼠SOL肌浆网Ca2 -ATP酶(sarcoplasmic-reticulum Ca2 -ATPase, SERCA)活性增高.采用SERCA特异性抑制剂CPA (1.0μmol/L)处理后,对照组与甲亢大鼠SOL间断强直收缩的TR75均延长,同时不易出现疲劳.5.0μmol/L CPA灌流虽可进一步抵抗甲亢大鼠SOL间断强直收缩引起的疲劳,但强直收缩期间的静息张力却明显升高.将CPA浓度增至10.0μmol/L,甲亢大鼠SOL间断强直收缩又趋向易发生疲劳.这些结果提示,与心肌相同,骨骼肌肌纤维SERCA活性亦可影响单收缩与强直收缩的舒张时间,SERCA活性升高可加速间断强直收缩发生疲劳.     

萎缩比目鱼肌间断强直收缩疲劳后恢复速率的影响因素

为研究模拟失重大鼠萎缩比目鱼肌强直收缩疲劳后恢复速率的影响因素,采用尾部悬吊模拟失重大鼠模型及离体骨骼肌条灌流技术,观测其在不同收缩模式下疲劳后的恢复过程。正常大鼠离体比目鱼肌条实验显示,10s短时程（S10P）与300s长时程（L10P）强直收缩轻度疲劳[强直收缩最大张力（P0）下降10％]后,在20min恢复期末,均可恢复至疲劳前P0,且恢复程度不受疲劳持续时间的影响;轻度疲劳后,在灌流液中加入10μmol／L钌红抑制肌浆网Ca^2＋释放功能,恢复速率减慢,恢复程度最大仅至94％P0,然后呈下降趋势,提示轻度疲劳可能仅抑制肌原纤维功能。60s短时程（S50P）与300s长时程（L50P）强直收缩中度疲劳（P0下降50％）后,在20min恢复期末,收缩张力分别恢复至95％P0和90％P0,表明中度疲劳持续时间影响恢复的速率;相同条件中度疲劳后,在灌流液中加入5mmol／L咖啡因促进肌浆网Ca62＋释放功能,恢复速率明显加快,无论疲劳持续时间长短,5min便可完全恢复,提示中度疲劳不仅抑制肌原纤维功能,还抑制肌浆网Ca^2＋释放功能。尾部悬吊1周的大鼠比目鱼肌明显萎缩,其重量／体重之比仅为对照大鼠的60％。采用短与长持续时间的轻与中度疲劳作用后,在20min恢复期末,收缩张力分别恢复至94％P0（S10P）、95％P0（L10P）、92％P0（S50P）、84％P0（L50P）,均与同步对照组有显著差异。以上结果提示：模拟失重1周大鼠萎缩的比目鱼肌,轻度与中度疲劳均可抑制肌原纤维功能与肌浆网Ca^2＋释放功能,使恢复速率减慢。     

兔膈肌力学模式对慢性电刺激的适应性改变和细胞外Ca2+变化的影响研究

目的 :研究兔膈肌肌条力学对不同频率慢性电刺激 (CES)的适应性变化特征和细胞外Ca2 变化对其力学特征的影响。方法 :测定正常对照组和CES组的颤搐收缩张力 (Pt)、峰值张力时间 (TPT)、1/ 2松驰时间 (1/ 2RT)、强直颤搐收缩张力 (Po)、疲劳指数 (FI)和疲劳恢复指数 (FRI) ;观察在无Ca2 Hank’s液和标准Hank’s液时肌条收缩张力消失和恢复的时间差异。结果 :①同对照组作比较 ,10Hz和 2 0Hz组的Pt、Po、Pt/Po明显降低 (P <0 .0 1) ,TPT和 1/ 2Rt明显延长 (P <0 .0 1) ,FI和FRI明显下降 (P <0 .0 1)。 5 0Hz和 10 0Hz组出现完全相反的效应 (P<0 .0 1)。②细胞外Ca2 变化对CES各组肌条收缩张力的降低和恢复均有明显的影响 ,但以 10Hz和 2 0Hz组尤为显著 ,其收缩张力在较短的时间内明显降低 (P <0 .0 5 )。结论 :①膈肌肌条力学模式在不同频率CES后呈现出明显的频率依赖性 ;②细胞外Ca2 变化对慢性低频电刺激后的膈肌肌条力学的影响明显增加     

兔膈肌力学模式对慢性电刺激的适应性改变和细胞外Ca …

目的：研究兔膈肌肌条力学对不同频率慢性电刺激（ＣＥＳ）的适应性变化特征和细胞外Ｃａ＾２＋变化夺其力学特征的影响。方法：测定正常对照组和ＣＥＳ组的颤搐收缩张力（Ｐｔ）、峰值张力时间（ＴＰＴ）、１／２松弛时间（１／２ＲＴ）、强直颤搐收缩张力（Ｐｏ）、疲劳指数（ＦＩ）和疲劳恢复指数（ＦＲＩ）;观察在无Ｃａ＾２＋Ｈａｎｋ’ｓ液和标准Ｈａｎｋ’ｓ液时肌条收缩张力消失和恢复的时间差异。结果：①同对照组作比较,     

兼受快肌和慢肌神经支配的大鼠慢肌或快肌纤维的肌-腱接头都没有乙酰胆碱敏感性

在大鼠慢肌比目鱼肌(SOL)肌纤维的肌-腱接头(MTJ)上有较高的乙酰胆碱(ACh)敏感牲,而快肌伸趾长肌(EDL)的 MTJ却没有。SOL 肌纤维受 EDL神经交叉支配后,其 MTJ的 ACh敏感性消失,此点 Miledi等已有报道。本文首先验证了与此相对称的结果,即EDL 肌纤维受 SOL神经交叉支配后,其 MTJ获得与正常 SOL肌纤维 MTJ相似的 ACh敏感性,从而进一步肯定了MTJ 的ACh 敏感性的出现是由特殊神经支配决定的。本文的主要结果是:兼受 SOL神经和 EDL神经支配的EDL和SOL的纤维,其MTJ都没有AGh 敏感性。这一结果的兴趣,不但在于它显示当两种神经支配同时存在时,快肌神经的影响压倒慢肌神经,而且还在于此结果与以往用其他指标进行的双神经支配肌纤维实验的结果形成鲜明的对照:用 M-ATPase 组织化学染色和Z带宽度等变化为指标,在双神经支配肌纤维中,慢肌神经的影响总压倒快肌神经。我们也观察了长期电刺激对MTJ ACh敏感性的影响。SOL经“慢”型刺激2—3周后,其 MTJ的 ACh敏感性虽有降低,但不及“快”型刺激显著。综合各种有关的观察,本文对双神经支配肌纤维的 MTJ没有 ACh敏感性这一主要结果的解释进行了讨论。     

模拟失重降低大鼠心肌细胞对异丙肾上腺素的反应性

本文旨在研究模拟失重对大鼠单个心肌细胞无负荷收缩功能的影响以及对异丙肾上腺素(isoproterenol,ISO)反应性的变化.采用人鼠尾部悬吊法在地面模拟失重状态,4周后以胶原酶I消化分离心肌细胞,分别对左、右两心室心肌细胞进行收缩功能测量.结果显示,悬吊4周大鼠(悬吊组)左,右心室心肌细胞的长度和宽度与正常大鼠(对照组)相比均无显著差异.随刺激频率增加,对照组与悬吊组大鼠心肌细胞缩短幅值均逐步增加.在1.0、2.0与4.0 Hz刺激下,对照组大鼠左心室心肌细胞缩短幅值分别为(8.50±1.26)%、(9.00±1.38)%与(9.23±1.83)%,右心室心肌细胞缩短幅值分别为(9.80±2.48)%、(10.03±2.48)%与(10.28±2.27)%;与对照组大鼠相比,在1.0与2.0Hz刺激下,悬吊组大鼠左心室心肌细胞无负荷缩短幅值分别降低12.2%、10.9%(P《0.05),右心室则分别降低16.5%、16.3%(P《0.05);但是在4.0 Hz刺激下却无显著性改变.与同一频率刺激下的对照组大鼠相比,悬吊组大鼠左、右心室心肌细胞达到缩短峰值的时程(time to peak shortening,TPS)明显缩短(P《0.05);而从缩短峰值至75%舒张的时程(TR75)则明显延长(P《0.05).在各刺激频率下,悬吊组大鼠左、右心室心肌细胞缩短(+dL/dtmax)与舒张(-dL/dtmax)速度均未发生明显改变.用1、5、10 nmol/L ISO灌流达稳态水平后,对照组大鼠心肌细胞缩短幅值分别增加了(10.63±0.83)%、(35.06±5.22)%和(71.64±6.83)%;而悬吊组大鼠心肌细胞缩短幅值仅增加(5.75±0.76)%、(23.97±4.50)%和(26.38±8.13)%,均有显著性差异(P《0.05,P《0.01).用10、50、100 nmol/L forskolin 灌流达稳定水平后,对照组大鼠心肌细胞缩短幅值分别增加了(3.04±0.27)%、(9.81±2.66)%、(20.20±3.47)%;而悬吊组大鼠心肌细胞缩短幅值仅增加了(1.42±0.53)%、(3.83±1.71)%、(5.49±4.08)%,均有显著性差异(P《0.05).以上结果表明,模拟失重4周降低人鼠心肌细胞无负荷缩短幅值以及对ISO的反应性.     

2 Hz与100 Hz刺激在诱导大鼠视皮层长持续长时程增强中的不同作用

在哺乳动物的视皮层,多种不同参数的刺激可诱导出长时程增强(long-term potentiation,LTP)现象。但关于刺激参数与持续时间长于3h的长持续LTP(long lasting LTP,L-LTP)之间关系的研究较少。本研究用3周龄的大鼠视皮层脑片标本,在Ⅳ层刺激而在Ⅱ／Ⅲ层记录场电位,待场电位稳定后施加强直刺激诱导LTP,探讨2Hz与100Hz的强直刺激在诱发持续时间长于3h的L-LTP中的作用。结果表明,多于300个脉冲不同频率的刺激可稳定地诱导出L-LTP;2Hz与100Hz的刺激诱发的L-LTP有明显不同的表达形式,100Hz刺激可诱导出较大的L-LTP;频率相同而脉冲数不同的强直刺激诱发的L-LTP有相同的表达形式。以上结果提示,不同频率的强直刺激诱发的L-LTP机制可能不同;相同频率的刺激(脉冲数不同)诱发的L-LTP可能有相同的机制。     

在改变大鼠比目鱼肌纤维类型特征中不活动不同于去神经

在本工作中,用河豚毒素长期阻断坐骨神经,使大鼠快肌伸趾长肌(EDL)和慢肌比目鱼肌(SOL)完全不活动,观察了这些不活动肌肉在收缩特性,三磷酸腺苷酶(M-ATPase)组织化学染色和 Z-带宽度等方面的变化,并把它们与去神经产生的变化作了比较。在 EDL,不活动与去神经引起的变化相同,即收缩变慢,各类纤维比例和Z-宽度无明显变化,但是对于SOL,则有一些差别。去神经的SOL的收缩变慢,而不活动的SOL却变快。与此同时,去神经基本上不改变SOL中各类纤维比例,而不活动的SOL中,Ⅱ型纤维增加一倍。本文讨论了在改变大鼠比目鱼肌纤维类型特征中,不活动不同于去神经的可能原因。     

肌球蛋白抑制剂BDM对骨骼肌收缩功能的非特异性作用

目的:探讨萎缩骨骼肌单位面积上等长收缩最大张力(Pt)降低的机理.方法:采用肌球蛋白ATP酶抑制剂BDM(Butanedione monoxime)灌流,观测其对离体骨骼肌肌条等长收缩功能的影响.结果:研究表明,BDM可使比目鱼肌(SOL)与趾长伸肌(EDL)等长收缩Pt明显降低,BDM对骨骼肌收缩功能的抑制呈剂量依赖性关系,且完全可逆.低浓度BDM(1 mmol/L)仅降低骨骼肌等长收缩的Pt而不影响其收缩时程,高浓度(10 mmol/L)下使收缩时程明显缩短.与SOL相比,在10mmol/LBDM作用下,使EDL等长收缩Pt降低一半的时间明显加快.无论在低浓度还是高浓度下,BDM对EDL肌球蛋白ATP酶活性的抑制作用均大于SOL.在相同浓度下,BDM对Pt的抑制程度远远大于对肌球蛋白ATP酶活性的抑制.结论:这些结果提示骨骼肌横桥功能降低可能是其等长收缩pt下降的原因之一;BDM并非特异型肌球蛋白ATP酶抑制剂,可对兴奋-收缩偶联的多个环节产生影响.     

核磁共振检测大鼠早期癫痫源性脑损伤的动态发展特征

为探讨癫痫源性脑损伤形成早期不同脑区病理改变和行为发作的动态发展特征 ,本研究对大鼠右背侧海马 (hippocampus,HPC)施加慢性强直电刺激 (6 0Hz,2s,0 .4～ 0 .6mA)诱发癫痫发作 ,1次 /d。每天记录大鼠原发性湿狗样抖动 (wetdogshakes,WEDS)频率 ,分别对大鼠施加电刺激 2、4、6、8和 10d后进行核磁共振成像 (T2 weightedmagneticresonanceimage ,T2 WI)检测 ,并对鼠脑进行了组织学切片鉴定。结果表明 :与空白对照组相比较 ,(1)施加 2d强直电刺激时 ,大鼠双侧背部侧脑室 (lateralventricle,LV)区域呈现对称性T2 WI信号绝对值增加 (n =4,左侧P =0 .0 0 18;右侧P =0 .0 0 10 ) ;施加 6d强直电刺激时 ,大鼠呈现植入电极对侧中、腹部LV区域T2 WI信号值增加 (n =5 ,P =0 .0 0 73;P =0 .0 2 49) ;施加 8d强直电刺激后 ,大鼠仅出现植入电极对侧腹部LV区域T2 WI信号值增加 (n =3,P =0 .0 34 0 ) ;施加 10d强直电刺激后 ,大鼠植入电极同侧腹部LV区域T2 WI信号值增加 (n =4,P =0 .0 10 7) ;(2 )随着强直电刺激天数增加 ,大鼠原发性WEDS频率高峰期出现在第 4个刺激日 ,然后WEDS频率下降 ,与T2 WI信号强度增加之间呈高度负相关关系 (相关系数r =- 0 .987,P <0 .0 2 ) ;(3)组织学切片鉴定 :T2 WI检测LV信号异     

Skeletal muscle fatigue in vitro is temperature dependent

Our purpose was to determine the effect of temperature on the fatigability of isolated soleus and extensor digitorum longus (EDL) muscles from rats during repeated isometric contractions. Muscles (70-90 mg) were studied at 20-40 degrees C in vitro. Fatigability was defined with respect to both the time and number of stimuli required to reach 50% of the force (P) developed at the onset of the fatigue test. Fatigue was studied during stimulation protocols of variable [force approximately 70% of maximum force (Po)] and constant frequency (28 Hz). Results for soleus and EDL muscles were qualitatively similar, but fatigue times were longer for soleus than for EDL muscles. During the variable-frequency protocol, development of approximately 70% of Po required an increase in stimulation frequency as temperature increased. During stimulation at these frequencies, fatigue time shortened as temperature increased. For both fatigue protocols, the relationship between temperature and the number of stimuli required to reach fatigue followed a bell-shaped curve, with maximum values at 25-30 degrees C. The temperature optimum for maximizing the number of isometric contractions to reach fatigue reflects direct effects of temperature on muscle function.     

Effects of modulators of sarcoplasmic Ca2+ release on the development of skeletal muscle fatigue.

The reduced release of Ca2+ from sarcoplasmic reticulum (SR) is considered a major determinant of muscle fatigue. In the present study, we investigated whether the presence of dantrolene, an established inhibitor of SR Ca2+ release, or caffeine, a drug facilitating SR Ca2+ release, modifies muscle fatigue development. Accordingly, the effects of Ca2+ release modulators were analyzed in vitro in mouse fast-twitch [extensor digitorum longus (EDL)] and slow-twitch (soleus) muscles, fatigued by repeated short tetani (40 Hz for 300 ms, 0.5 s(-1) in soleus and 60 Hz for 300 ms, 0.3 s(-1) in EDL, for 6 min). Caffeine produced a substantial increase of tetanic tension of both EDL and soleus muscles, whereas dantrolene decreased tetanic tension only in EDL muscle. In both EDL and soleus muscles, 5 microM dantrolene did not affect fatigue development, whereas 20 microM dantrolene produced a positive staircase during the first 3 min of stimulation in EDL muscle and a slowing of fatigue development in soleus muscle. The development of the positive staircase was abolished by the addition of 15 microM ML-7, a selective inhibitor of myosin light chain kinase. On the other hand, caffeine caused a larger and faster loss of tension in both EDL and soleus muscles. The results seem to indicate that the changes in fatigue profile induced by caffeine or dantrolene are mainly due to the changes in the initial tetanic tension caused by the drugs, with the resulting changes in the level of contraction-dependent factors of fatigue, rather than to changes in the SR Ca2+ release during fatigue development.     

The effects of neuropeptide Y on skeletal muscle contractile properties in streptozotocin diabetic rats

Diabetes induces changes in the structural, biochemical, electrical, and contractile properties of skeletal muscles. Neuropeptide Y (NPY) administered locally can induce angiogenesis in a rat ischemic limb model and restore the contractile function of the ischemic muscle. The effects of NPY on the contractile characteristics of limb skeletal muscles were examined in streptozotocin-induced diabetic rats. Rats were treated with sham pellets (control groups) or NPY-containing pellets (1 mg of NPY/pellet, 14 days releasing time) administered locally to the rat hind limb 2 months after induction of diabetes. Contractile properties and fatigability of the slow-twitch soleus and fast-twitch gastrocnemius medials muscle were compared in control (sham), control NPY, diabetic (sham), and diabetic NPY groups. In order to induce fatigue trains of repetitive tetanic stimulation were used (600 ms/1 s simulation-rest cycle per train, 112 trains at an 85-Hz fusion frequency). Two months of untreated diabetes significantly prolonged soleus contraction and slowed its relaxation, but had minimal effects on soleus tension. NPY ameliorated the diabetic effects on soleus speed-related contractile properties, restoring its contraction and relaxation times. Diabetes significantly reduced gastrocnemius medials tetanic tension, leaving its contractile characteristics mostly unaffected. NPY partially restored gastrocnemius tetanic tension production capacity. Diabetes significantly increased fatigability of both muscles, which was partially restored by NPY, as evidenced by restored endurance of soleus muscle. The results suggest that NPY administered locally tends to normalize muscle performance and improve fatigue resistance of skeletal muscles in streptozotocin diabetes. Further examination is needed to establish the mechanisms of local NPY action on muscle contractile properties in streptozotocin-induced diabetes.     

Fatigue and contraction of slow and fast muscles in hypokinetic/hypodynamic rats

This investigation examined the effects of hypokinesia/hypodynamia (H/H) on fatigability and contractile properties of rat soleus (S) and gastrocnemius (G) muscles. Whole-body suspension for 1 wk was used to eliminate hindlimb load-bearing functions and simultaneously permit voluntary isotonic contractions. Train stimulations (45/min, 16 min) resulted in significantly (P less than 0.05) faster rates of fatigue to lower asymptotes in G from H/H rats. Fatigue in the S was minimal at this stimulation frequency and differences between H/H and control animals were not significant. Contractile properties (twitch and tetanic) were measured before and after train stimulations. H/H suspension resulted in an increased twitch tension in G. However, H/H did not change train or tetanic tensions per gram or other G contractile properties. Peak twitch, train, and tetanic tensions, time to peak tension, one-half relaxation time, and twitch and tetanic peak rates of tension development and decline were unchanged by H/H in S muscles. These results indicate that 1 wk of H/H-induced muscle atrophy significantly increases fatigability in G but does not effect contractile properties of fast-twitch (G) or slow-twitch (S) muscles.     

Functional deficits in skeletal muscle grafts

Individual skeletal muscle fibers degenerate and regenerate with minimal functional deficits. When whole skeletal muscles are grafted in rats or cats by standard grafting techniques, revascularization and reinnervation must occur spontaneously. Under these circumstances, contraction times and maximum velocities of shortening eventually return to control values, but a significant deficit is observed in maximum tetanic tension. Grafts made with anastomosis of nerves or with nerves left intact have smaller deficits in tension development than do standard grafts made without nerve repair. The measurement of contractile properties of single motor units in extensor digitorum longus (EDL) muscles and in EDL grafts in rats indicates that the decreased maximum tetanic tension of whole grafts is due to a 10-20% decrease in the maximum tetanic tension of individual motor units, whereas standard grafts also show a 40-45% decrease in the number of motor units. Compared with control values, the fatigability of 100-mg grafts in rats is decreased, whereas larger 3-g grafts in cats show an increased fatigability. The deficits observed in large grafts can be reduced, but not eliminated, by grafting with neurovascular anastomoses.     

Effect of pulmonary TNF-α overexpression on mouse isolated skeletal muscle function

TNF-α is a proinflammatory cytokine that is involved in numerous pathological processes including chronic obstructive pulmonary disease (COPD). In the present study, we used a transgenic mouse model that overexpresses TNF-α in the lung (Tg(+)) to test the hypothesis that chronic exposure to TNF-α (as seen in COPD) reduces skeletal muscle force production and fatigue resistance, particularly under low Po(2) conditions. At 7-12 mo, body and muscle weight of both extensor digitorum longus (EDL) and soleus were significantly smaller in Tg(+) compared with littermate wild-type (WT) mice; however, the body-to-muscle weight ratio was not different between groups. EDL and soleus muscles were subjected to in vitro fatiguing contractile periods under high (～550 Torr) and low Po(2) (～40 Torr). Although all muscles were less fatigue-resistant during low Po(2) compared with high Po(2), only the soleus fatigued more rapidly in Tg(+) mice (～12%) compared with WT at high Po(2). The maximal tension of EDL was equally reduced in Tg(+) mice (28-34% decrease from WT under both Po(2) conditions); but for soleus this parameter was smaller only under low Po(2) in Tg(+) mice (～31% decrease from WT). The peak rate of relaxation and the peak rate of contraction were both significantly reduced in Tg(+) EDL muscles compared with WT EDL under low Po(2) conditions, but not in soleus. These results demonstrate that TNF-α upregulation in the lung impairs peripheral skeletal muscle function but affects fast- and slow-twitch muscles differentially at high and low Po(2).     

Recovery in skeletal muscle contractile function after prolonged hindlimb immobilization

Contractile properties of slow-twitch soleus (SOL), fast-twitch extensor digitorum longus (EDL), and fast-twitch superficial region of the vastus lateralis were determined in vitro (22 degrees C) in rats remobilized after prolonged (3 mo) hindlimb immobilization (IM). For all muscles the muscle-to-body weight ratio was significantly depressed by IM, and the ratios failed to completely recover even after 90 days. The contractile properties of the fast-twitch muscles were less affected by IM than the slow-twitch SOL. The IM shortened the SOL isometric twitch duration due to a reduced contraction and half-relaxation time. These parameters returned to control levels by the 14th day of recovery. Peak tetanic tension (Po, g/cm2) declined with IM by 46% in the SOL but showed no significant change in the fast-twitch muscles. After IM the SOL Po (g/cm2) recovered to control values by 28 days. The recovery of Po in absolute units (g) was considerably slower and did not return to control levels until 60 (SOL) to 90 (EDL) days. The maximum shortening velocity was not altered by IM in any of the muscles studied. These results demonstrate that both fast- and slow-twitch skeletal muscles possess the ability to completely recover normal contractile function following prolonged periods of hindlimb IM.     

Contractile properties of cat skeletal muscle after repetitive stimulation

The isometric and force-velocity properties of the fast-twitch flexor digitorum longus (FDL) and slow-twitch soleus muscles were investigated immediately after and during recovery from a fatiguing stimulus regime (40 Hz for 330 ms every second for 180 s) in the anesthetized cat. The amplitude of the isometric twitch of FDL was unaffected but in soleus it remained depressed for much of the recovery period. Immediately after stimulation the twitch time to peak of FDL increased to 140% of the control (prefatigue) value and then reverted to control values. The maximum isometric tetanic tension (Po) developed by FDL was reduced to 67% of control values immediately after the stimulus regime, whereas soleus declined to 93% of control. Recovery of maximum force development was achieved after 45 min in FDL and after 15 min in soleus. The maximum speed of shortening of FDL was reduced to 63% of control values immediately after fatigue; despite some recovery within the first 30 min, it remained depressed during the remainder of the recovery period (up to 300 min). Maximum speed of shortening was unaltered in soleus. The a/Po value transiently increased to 176% of control values in FDL immediately after the fatigue regime but promptly returned to control values. Force-velocity properties of soleus were not affected by the stimulus regime. It is concluded that in FDL changes in the maximum speed of shortening and maximum isometric tension as a result of the stimulus regime are attributable to changes in the intrinsic behavior of cross-bridges and the metabolic status of the fibers, particularly in the fast-twitch fatigue-resistant fibers.