Force during stretches of rat skeletal muscles after hypertonia at short and long lengths

Following injection of tetanus toxin into rat gastrocnemius muscle to produce hypertonia, plantar flexor muscles were allowed to shorten (S, n=5) without restraint or held lengthened (L, n=3) by splinting. Saline injected rats served as control (n=5). One week after injection, peak forces during 3 stretches with passive muscles and acute isometric force deficits produced by 15 stretches of electrically stimulated muscles were examined under pentobarbital anesthesia. Isometric force and mass of plantar flexors were similar in S rats but 16% lower in L rats compared to control. Peak passive forces were highest in S rats but not different between L rats and control. At the end of the stretch protocol, isometric force deficits were 26% larger in S rats compared to L rats and 17% smaller in L rats compared to control. Acute isometric force deficits produced by stretches of active skeletal muscles were dependent on the muscle length maintained during hypertonia. Our animal model could be used to test rehabilitation interventions during hypertonia of skeletal muscles.     

Fatigue during sustained maximal voluntary contraction of different muscles in humans: dependence on fibre type and body posture

Nine healthy men, aged between 25 and 35 years, performed sustained maximal voluntary contractions (MVC) of foot plantar, foot dorsal, and finger flexor muscles. Contractions lasted 10 min and were followed by short test contractions at 30% MVC during recovery. Two positions of the working extremity high or low were established by different body postures (supine or sitting). Under these conditions, studies of force, integrated electromyogram (iEMG), blood pressure, and heart rate showed firstly that force decreased throughout the first few minutes of maximal contraction but reached a near steady-state value after 5 to 6 min. Secondly, force decay and steady-state level depended on muscle group and body position. When sitting (low leg), muscles with a high incidence of slow twitch fibres (plantar flexors) showed a slower force decay and a higher relative steady-state force than fast dorsal flexor muscles. When supine (high leg), plantar and dorsal flexor muscles reached about the same low level of relative steady-state force. Changes in iEMG, blood pressure, and heart rate did not differ in the two positions. Thirdly, during recovery, plantar flexor muscles showed higher iEMG values as well as higher values of blood pressure and heart rate when supine than when sitting. Recovery of dorsal flexor muscles was little affected by body posture. Fourthly, force development and recovery of predominantly fast finger flexor muscles were almost independent of arm position. It was concluded that muscle fibre composition was the main factor in determining endurance capacity. However, endurance was influenced by changes in the hydrostatic blood pressure component.(ABSTRACT TRUNCATED AT 250 WORDS)     

Residual force enhancement after lengthening is present during submaximal plantar flexion and dorsiflexion actions in humans.

Stretch of an activated muscle causes a transient increase in force during the stretch and a sustained, residual force enhancement (RFE) after the stretch. The purpose of this study was to determine whether RFE is present in human muscles under physiologically relevant conditions (i.e., when stretches were applied within the working range of large postural leg muscles and under submaximal voluntary activation). Submaximal voluntary plantar flexion (PF(v)) and dorsiflexion (DF(v)) activation was maintained by providing direct visual feedback of the EMG from soleus or tibialis anterior, respectively. RFE was also examined during electrical stimulation of the plantar flexion muscles (PF(s)). Constant-velocity stretches (15 degrees /s) were applied through a range of motion of 15 degrees using a custom-built ankle torque motor. The muscles remained active throughout the stretch and for at least 10 s after the stretch. In all three activation conditions, the stable joint torque measured 9-10 s after the stretch was greater than the isometric joint torque at the final joint angle. When expressed as a percentage of the isometric torque, RFE values were 7, 13, and 12% for PF(v), PF(s), DF(v), respectively. These findings indicate that RFE is a characteristic of human skeletal muscle and can be observed during submaximal (25%) voluntary activation when stretches are applied on the ascending limb of the force-length curve. Although the underlying mechanisms are unclear, it appears that sarcomere popping and passive force enhancement are insufficient to explain the presence of RFE in these experiments.     

Effect of stretching training on the viscoelastic properties of human tendon structures in vivo.

The purpose of this study was to examine whether stretching training altered the viscoelastic properties of human tendon structures in vivo. Eight men performed the stretching training for 3 wk. Before and after the stretching training, the elongation of the tendon and aponeurosis of medial gastrocnemius muscle was directly measured by ultrasonography while the subjects performed ramp isometric plantar flexion up to the voluntary maximum, followed by a ramp relaxation. The relationship between the estimated muscle force (Fm) and tendon elongation (L) during the ascending phase was fitted to a linear regression, the slope of which was defined as stiffness of tendon structures. The percentage of the area within the Fm-L loop to the area beneath the curve during ascending phase was calculated as an index representing hysteresis. To assess the flexibility, the passive torque of the plantar flexor muscles was measured during the passive stretch from 0 degrees (anatomic position) to 25 degrees of dorsiflexion with a constant velocity of 5 degrees/s. The slope of the linear portion of the passive torque-angle curve during stretching was defined as flexibility index. Flexibility index decreased significantly after stretching training (-13.4 +/- 4.6%). On the other hand, the stretching training produced no significant change in stiffness but significantly decreased hysteresis from 19.9 +/- 11.7 to 12.5 +/- 9.5%. The present results suggested that stretching training affected the viscosity of tendon structures but not the elasticity.     

Severity of contraction-induced injury is affected by velocity only during stretches of large strain.

Our purpose was to investigate the effect of velocity of stretch on contraction-induced injury to whole skeletal muscles. Single stretches provide an effective method for studying factors that initiate contraction-induced injury. We tested the null hypothesis that the severity of injury is not dependent on the velocity of the stretch. From the plateau of maximum isometric contractions, extensor digitorum longus muscles of mice were administered single stretches in situ of 30--50% strain relative to muscle fiber length (L(f)) at rates of 1--16 L(f)/s. The magnitude of injury was represented by the isometric force deficit 1--10 min after the stretch. Although the null hypothesis was not supported because the force deficit was affected by velocity (r(2) = 0.09), the effect was relatively weak and was not significant except at the largest strain. Velocity had no effect on peak or average force or work input, factors established to have significant relationships with the force deficit. Velocity may play a minor role in contraction-induced injury, but its importance is negligible relative to that of strain.     

Active force inhibition and stretch-induced force enhancement in frog muscle treated with BDM.

There is evidence that the stretch-induced residual force enhancement observed in skeletal muscles is associated with 1) cross-bridge dynamics and 2) an increase in passive force. The purpose of this study was to characterize the total and passive force enhancement and to evaluate whether these phenomena may be associated with a slow detachment of cross bridges. Single fibers from frog lumbrical muscles were placed at a length 20% longer than the plateau of the force-length relationship, and active and passive stretches (amplitudes of 5 and 10% of fiber length and at a speed of 40% fiber length/s) were performed. Experiments were conducted in Ringer solution and with the addition of 2, 5, and 10 mM of 2,3-butanedione monoxime (BDM), a cross-bridge inhibitor. The steady-state active and passive isometric forces after stretch of an activated fiber were higher than the corresponding forces measured after isometric contractions or passive stretches. BDM decreased the absolute isometric force and increased the total force enhancement in all conditions investigated. These results suggest that total force enhancement is directly associated with cross-bridge kinetics. Addition of 2 mM BDM did not change the passive force enhancement after 5 and 10% stretches. Addition of 5 and 10 mM did not change (5% stretches) or increased (10% stretches) the passive force enhancement. Increasing stretch amplitudes and increasing concentrations of BDM caused relaxation after stretch to be slower, and because passive force enhancement is increased at the greatest stretch amplitudes and the highest BDM concentrations, it appears that passive force enhancement may be related to slow-detaching cross bridges.     

The neuromuscular demands of toe walking: a forward dynamics simulation analysis

Toe walking is a gait deviation with multiple etiologies and often associated with premature and prolonged ankle plantar flexor electromyographic activity. The goal of this study was to use a detailed musculoskeletal model and forward dynamical simulations that emulate able-bodied toe and heel-toe walking to understand why, despite an increase in muscle activity in the ankle plantar flexors during toe walking, the internal ankle joint moment decreases relative to heel-toe walking. The simulations were analyzed to assess the force generating capacity of the plantar flexors by examining each muscle's contractile state (i.e., the muscle fiber length, velocity and activation). Consistent with experimental measurements, the simulation data showed that despite a 122% increase in soleus muscle activity and a 76% increase in gastrocnemius activity, the peak internal ankle moment in late stance decreased. The decrease was attributed to non-optimal contractile conditions for the plantar flexors (primarily the force-length relationship) that reduced their ability to generate force. As a result, greater muscle activity is needed during toe walking to produce a given muscle force level. In addition, toe walking requires greater sustained plantar flexor force and moment generation during stance. Thus, even though toe walking requires lower peak plantar flexor forces that might suggest a compensatory advantage for those with plantar flexor weakness, greater neuromuscular demand is placed on those muscles. Therefore, medical decisions concerning whether to reduce equinus should consider not only the impact on the ankle moment, but also the expected change to the plantar flexor's force generating capacity.     

An ankle-foot orthosis powered by artificial pneumatic muscles

We developed a pneumatically powered orthosis for the human ankle joint. The orthosis consisted of a carbon fiber shell, hinge joint, and two artificial pneumatic muscles. One artificial pneumatic muscle provided plantar flexion torque and the second one provided dorsiflexion torque. Computer software adjusted air pressure in each artificial muscle independently so that artificial muscle force was proportional to rectified low-pass-filtered electromyography (EMG) amplitude (i.e., proportional myoelectric control). Tibialis anterior EMG activated the artificial dorsiflexor and soleus EMG activated the artificial plantar flexor. We collected joint kinematic and artificial muscle force data as one healthy participant walked on a treadmill with the orthosis. Peak plantar flexor torque provided by the orthosis was 70 Nm, and peak dorsiflexor torque provided by the orthosis was 38 Nm. The orthosis could be useful for basic science studies on human locomotion or possibly for gait rehabilitation after neurological injury.     

Effect of passive stretch on intracellular nitric oxide and superoxide activities in single skeletal muscle fibres: influence of ageing

Skeletal muscle is repeatedly exposed to passive stretches due to the activation of antagonist muscles and to external forces. Stretch has multiple effects on muscle mass and function, but the initiating mechanisms and intracellular signals that modulate those processes are not well understood. Mechanical stretch applied to some cell types induces production of reactive oxygen species (ROS) and nitric oxide that modulate various cellular signalling pathways. The aim of this study was to assess whether intracellular activities of ROS and nitric oxide were modulated by passive stretches applied to single mature muscle fibres isolated from young and old mice. We developed a novel approach to apply passive stretch to single mature fibres from the flexor digitorum brevis muscle in culture and to monitor the activities of ROS and nitric oxide in situ by fluorescence microscopy. Passive stretch applied to single skeletal muscle fibres from young mice induced an increase in dihydroethidium oxidation (reflecting intracellular superoxide) with no increase in intracellular DAF-FM oxidation (reflecting nitric oxide activity) or CM-DCFH oxidation. In contrast, in fibres isolated from muscles of old mice passive stretch was found to induce an increase in intracellular nitric oxide activities with no change in DHE oxidation.     

Analysis of stretch responses of a myocybernetic model muscle fibre

The characteristics of the response to stretch of a muscle fibre are investigated using a validated model of skeletal muscle. It is found that the model correctly predicts all the peculiar features of the stretch response: the initial rapid force rise; the subsequent slower rise; the slow decay of the force upon termination of the elongation; and the dependence of these phenomena upon stretching velocity and muscle length. The hypothesis explaining these phenomena is discussed in detail.     

Relation between the ankle joint angle and the maximum isometric force of the toe flexor muscles

The purpose of this study was to investigate the relationships between the ankle joint angle and maximum isometric force of the toe flexor muscles. Toe flexor strength and electromyography activity of the foot muscles were measured in 12 healthy men at 6 different ankle joint angles with the knee joint at 90 deg in the sitting position. To measure the maximum isometric force of the toe flexor muscles, subjects exerted maximum force on a toe grip dynamometer while the activity levels of the intrinsic and extrinsic plantar muscles were measured. The relation between ankle joint angle and maximum isometric force of the toe flexor muscles was determined, and the isometric force exhibited a peak when the ankle joint was at 70–90 deg on average. From this optimal neutral position, the isometric force gradually decreased and reached its nadir in the plantar flexion position (i.e., 120 deg). The EMG activity of the abductor hallucis (intrinsic plantar muscle) and peroneus longus (extrinsic plantar muscle) did not differ at any ankle joint angles. The results of this study suggest that the force generation of toe flexor muscles is regulated at the ankle joint and that changes in the length-tension relations of the extrinsic plantar muscle could be a reason for the force-generating capacity at the metatarsophalangeal joint when the ankle joint angle is changed.     

Adaptation of muscle coordination to altered task mechanics during steady-state cycling

The objective of this work was to increase our understanding of how motor patterns are produced during movement tasks by quantifying adaptations in muscle coordination in response to altered task mechanics. We used pedaling as our movement paradigm because it is a constrained cyclical movement that allows for a controlled investigation of test conditions such as movement speed and effort. Altered task mechanics were introduced using an elliptical chainring. The kinematics of the crank were changed from a relatively constant angular velocity using a circular chainring to a widely varying angular velocity using an elliptical chainring. Kinetic, kinematic and muscle activity data were collected from eight competitive cyclists using three different chainrings--one circular and two different orientations of an elliptical chainring. We tested the hypotheses that muscle coordination patterns (EMG timing and magnitude), specifically the regions of active muscle force production, would shift towards regions in the crank cycle in which the crank angular velocity, and hence muscle contraction speeds, were favorable to produce muscle power as defined by the skeletal muscle power-velocity relationship. The results showed that our hypothesis with regards to timing was not supported. Although there were statistically significant shifts in muscle timing, the shifts were minor in absolute terms and appeared to be the result of the muscles accounting for the activation dynamics associated with muscle force development (i.e. the delay in muscle force rise and decay). But, significant changes in the magnitude of muscle EMG during regions of slow crank angular velocity for the tibialis anterior and rectus femoris were observed. Thus, the nervous system used adaptations to the muscle EMG magnitude, rather than the timing, to adapt to the altered task mechanics. The results also suggested that cyclists might work on the descending limb of the power-velocity relationship when pedaling at 90 rpm and sub-maximal power output. This finding might have important implications for preferred pedaling rate selection.     

Residual force enhancement contributes to increased performance during stretch-shortening cycles of human plantar flexor muscles in vivo

It is well known that muscular force production is history-dependent, which results in enhanced (RFE) and depressed (RFD) steady-state forces after stretching and shortening, respectively. However, it remains unclear if force-enhancing mechanisms can contribute to increased performance during in vivo stretch-shortening cycles (SSCs) of human locomotor muscles. The purpose of this study was to investigate whether RFE-related mechanisms contribute to enhanced force and power output during SSCs of the human plantar flexor muscles. Net ankle torques of fourteen participants were measured during and after pure isometric, pure stretch, pure shortening, and SSC contractions when the triceps surae muscles were electrically stimulated at a submaximal level that resulted in 30% of their maximum isometric torque. Dynamic contractions were performed over an amplitude of 15°, from 5° plantar flexion to 10° dorsiflexion, at a speed of 120° s⁻¹. External ankle work during shortening was 11.6% greater during SSCs compared to pure shortening contractions (p = .003). Additionally, RFD after SSCs (8.6%) was reduced compared to RFD after pure shortening contractions (12.0%; p < .05). It is therefore concluded that RFE-related mechanisms contribute to increased performance following SSCs of human locomotor muscles. Since RFD after SSCs decreased although work during shortening was increased, we speculate that the relevant mechanism lies outside actin-myosin interaction. Finally, our data suggests that RFE might be relevant and beneficial for human locomotion whenever a muscle is stretched, but this needs to be confirmed.     

The mechanics of mouse skeletal muscle when shortening during relaxation

The dynamic properties of relaxing skeletal muscle have not been well characterised but are important for understanding muscle function during terrestrial locomotion, during which a considerable fraction of muscle work output can be produced during relaxation. The purpose of this study was to characterise the force-velocity properties of mouse skeletal muscle during relaxation. Experiments were performed in vitro (21 degrees C) using bundles of fibres from mouse soleus and EDL muscles. Isovelocity shortening was applied to muscles during relaxation following short tetanic contractions. Using data from different contractions with different shortening velocities, curves relating force output to shortening velocity were constructed at intervals during relaxation. The velocity component included contributions from shortening of both series elastic component (SEC) and contractile component (CC) because force output was not constant. Early in relaxation force-velocity relationships were linear but became progressively more curved as relaxation progressed. Force-velocity curves late in relaxation had the same curvature as those for the CC in fully activated muscles but V(max) was reduced to approximately 50% of the value in fully activated muscles. These results were the same for slow- and fast-twitch muscles and for relaxation following maximal tetani and brief, sub-maximal tetani. The measured series elastic compliance was used to partition shortening velocity between SEC and CC. The curvature of the CC force-velocity relationship was constant during relaxation. The SEC accounted for most of the shortening and work output during relaxation and its power output during relaxation exceeded the maximum CC power output. It is proposed that unloading the CC, without any change in its overall length, accelerated cross-bridge detachment when shortening was applied during relaxation.     

Relaxation kinetics following sudden Ca(2+) reduction in single myofibrils from skeletal muscle

To investigate the roles of cross-bridge dissociation and cross-bridge-induced thin filament activation in the time course of muscle relaxation, we initiated force relaxation in single myofibrils from skeletal muscles by rapidly (approximately 10 ms) switching from high to low [Ca(2+)] solutions. Full force decay from maximal activation occurs in two phases: a slow one followed by a rapid one. The latter is initiated by sarcomere "give" and dominated by inter-sarcomere dynamics (see the companion paper, Stehle, R., M. Krueger, and G. Pfitzer. 2002. Biophys. J. 83:2152-2161), while the former occurs under nearly isometric conditions and is sensitive to mechanical perturbations. Decreasing the Ca(2+)-activated force preceding the start of relaxation does not increase the rate of the slow isometric phase, suggesting that cycling force-generating cross-bridges do not significantly sustain activation during relaxation. This conclusion is strengthened by the finding that the rate of isometric relaxation from maximum force to any given Ca(2+)-activated force level is similar to that of Ca(2+)-activation from rest to that given force. It is likely, therefore, that the slow rate of force decay in full relaxation simply reflects the rate at which cross-bridges leave force-generating states. Because increasing [P(i)] accelerates relaxation while increasing [MgADP] slows relaxation, both forward and backward transitions of cross-bridges from force-generating to non-force-generating states contribute to muscle relaxation.     

Effects of stretch on work from fast and slow muscles of mice: damped and undamped energy release

Stretching active muscle increases the work performed during subsequent shortening. The effects of a preceding stretch on work done by the undamped or lightly damped series compliance (SC) and by the contractile component (CC), which includes cross bridges and damped elements, were assessed using mouse soleus (slow) and extensor digitorum longus (fast) muscles with limited tendon. Increasing stretch amplitude (0-10% fibre length) increased work done by the SC up to a limit, but did not effect work done by the CC. Increasing stretch velocity (10-100% Vmax) had almost no effect on work done by either component. Increasing the delay between the end of stretch and onset of shortening (0-60 ms) caused a decrease in SC work, with no effect on CC work. Recoil of the SC was responsible for 50-70% of the total work done during shortening after stretch. Usually only 10-40% of the energy imparted during the stretch was recovered as work during subsequent shortening; large stretches and long delays between stretch and shortening further reduced this recovery by one third to one fifth. Results are interpreted in the context of a loss of energy stored in the SC owing to forcible detachment of cross bridges with large stretches and cyclic detachment with long delays.     

Mechanical performance of artificial pneumatic muscles to power an ankle-foot orthosis

We developed a powered ankle-foot orthosis that uses artificial pneumatic muscles to produce active plantar flexor torque. The purpose of this study was to quantify the mechanical performance of the orthosis during human walking. Three subjects walked at a range of speeds wearing ankle-foot orthoses with either one or two artificial muscles working in parallel. The orthosis produced similar total peak plantar flexor torque and network across speeds independent of the number of muscles used. The orthosis generated approximately 57% of the peak ankle plantar flexor torque during stance and performed approximately 70% of the positive plantar flexor work done during normal walking. Artificial muscle bandwidth and force-length properties were the two primary factors limiting torque production. The lack of peak force and work differences between single and double muscle conditions can be explained by force-length properties. Subjects altered their ankle kinematics between conditions resulting in changes in artificial muscle length. In the double muscle condition greater plantar flexion yielded shorter artificial muscles lengths and decreased muscle forces. This finding emphasizes the importance of human testing in the design and development of robotic exoskeleton devices for assisting human movement. The results of this study outline the mechanical performance limitations of an ankle-foot orthosis powered by artificial pneumatic muscles. This orthosis could be valuable for gait rehabilitation and for studies investigating neuromechanical control of human walking.     

Acceleration of stretch activation in murine myocardium due to phosphorylation of myosin regulatory light chain

The regulatory light chains (RLCs) of vertebrate muscle myosins bind to the neck region of the heavy chain domain and are thought to play important structural roles in force transmission between the cross-bridge head and thick filament backbone. In vertebrate striated muscles, the RLCs are reversibly phosphorylated by a specific myosin light chain kinase (MLCK), and while phosphorylation has been shown to accelerate the kinetics of force development in skeletal muscle, the effects of RLC phosphorylation in cardiac muscle are not well understood. Here, we assessed the effects of RLC phosphorylation on force, and the kinetics of force development in myocardium was isolated in the presence of 2,3-butanedione monoxime (BDM) to dephosphorylate RLC, subsequently skinned, and then treated with MLCK to phosphorylate RLC. Since RLC phosphorylation may be an important determinant of stretch activation in myocardium, we recorded the force responses of skinned myocardium to sudden stretches of 1% of muscle length both before and after treatment with MLCK. MLCK increased RLC phosphorylation, increased the Ca(2+) sensitivity of isometric force, reduced the steepness of the force-pCa relationship, and increased both Ca(2+)-activated and Ca(2+)-independent force. Sudden stretch of myocardium during an otherwise isometric contraction resulted in a concomitant increase in force that quickly decayed to a minimum and was followed by a delayed redevelopment of force, i.e., stretch activation, to levels greater than pre-stretch force. MLCK had profound effects on the stretch activation responses during maximal and submaximal activations: the amplitude and rate of force decay after stretch were significantly reduced, and the rate of delayed force recovery was accelerated and its amplitude reduced. These data show that RLC phosphorylation increases force and the rate of cross-bridge recruitment in murine myocardium, which would increase power generation in vivo and thereby enhance systolic function.     

Molecular Basis of Force Development by Skeletal Muscles During and After Stretch

When activated skeletal muscles are stretched at slow velocities, force increases in two phases: (i) a fast increase, and (ii) a slow increase. The transition between these phases is commonly associated with the mechanical detachment of cross-bridges from actin. This phenomenon is referred to asforce enhancement during stretch. After the stretch, force decreases and reaches steady-state at levels that are higher than the force produced at the corresponding length during purely isometric contractions. This phenomenon is referred to asresidual force enhancement.The mechanisms behind the increase in force during and after stretch are still a matter of debate, and have physiological implications as human muscles perform stretch contractions continuously during daily activity. This paper briefly reviews the potential mechanisms to explain stretch forces, including an increased number of cross-bridges attached to actin, an increased strain in cross-bridges upon stretch, the influence of passive elements upon activation and sarcomere length non-uniformities.     

Tension relaxation after stretch in resting mammalian muscle fibers: stretch activation at physiological temperatures.

Tension responses to ramp stretches of 1-3% Lo (fiber length) in amplitude were examined in resting muscle fibers of the rat at temperatures ranging from 10 degrees C to 36 degrees C. Experiments were done using bundles of approximately 10 intact fibers isolated from the extensor digitorum longus (a fast muscle) and the soleus (a slow muscle). At low temperatures (below approximately 20 degrees C), the tension response consisted of an initial rise to a peak during the ramp followed by a complex tension decay to a plateau level; the tension decay occurred at approximately constant sarcomere length. The tension decay after a standard stretch at approximately 3-4.Lo/s contained a fast, an intermediate, and a (small amplitude) slow component, which at 10 degrees C (sarcomere length approximately 2.5 microns) were approximately 2000.s-1, approximately 150.s-1, and approximately 25.s-1 for fast fibers and approximately 2000.s-1, approximately 70.s-1 and approximately 8.s-1 for slow fibers, respectively. The fast component may represent the decay of interfilamentary viscous resistance, and the intermediate component may be due to viscoelasticity in the gap (titin, connectin) filament. The two- to threefold fast-slow muscle difference in the rate of passive tension relaxation (in the intermediate and the slow components) compares with previously reported differences in the speed of their active contractions; this suggests that "passive viscoelasticity" is appropriately matched to contraction speed in different muscle fiber types. At approximately 35 degrees C, the fast and intermediate components of tension relaxation were followed by a delayed tension rise at approximately 10.s-1 (fast fibers) and 2.5.s-1 (slow fibers); the delayed tension rise was accompanied by sarcomere shortening. BDM (5-10 mM) reduced the active twitch and tetanic tension responses and the delayed tension rise at 35 degrees C; the results indicate stretch sensitive activation in mammalian sarcomeres at physiological temperatures.