Increased fatigue of isovelocity vs. isometric contractions of canine diaphragm

A comparison of fatigue as a loss of force with repeated contractions over time was performed in canine respiratory muscle by isometric (nonshortening) and isovelocity (shortening) contractions. In situ diaphragm muscle strips were attached to a linear ergometer and electrically stimulated (30 or 40 Hz) via the left phrenic nerve to produce either isometric (n = 12) or isovelocity (n = 12) contractions (1.5 s) from optimal muscle length (Lo = 8.8 cm). Similar velocities of shortening between isovelocity experiments [0.19 +/- 0.02 (SD) Lo/S] were produced by maximizing the mean power output (Wmax = 210 +/- 27 mW/cm2) that could be developed over 1.5 s when displacement was approximately 0.30 Lo. Initial peak isometric tension was 1.98 kg/cm2, whereas initial peak isovelocity tension was 1.84 kg/mc2 (P less than 0.01) or 93% of initial isometric tension. Fatigue trials of 5 min were conducted on muscles contracting at a constant duty cycle (0.43). At the end of the trials, peak isovelocity tension had fallen to 50% of initial isometric tension (P less than 0.01), whereas peak isometric tension had only fallen by 27%. These results indicate that muscle shortening during force production has a significant influence on diaphragm muscle fatigue. We conclude that the effects of shortening on fatigue must be considered in models of respiratory muscle function, because these muscles typically shorten during breathing.     

The measurement of force/velocity relationships of fresh and fatigued human adductor pollicis muscle

The purpose of the study was to obtain force/velocity relationships for electrically stimulated (80 Hz) human adductor pollicis muscle (n = 6) and to quantify the effects of fatigue. There are two major problems of studying human muscle in situ; the first is the contribution of the series elastic component, and the second is a loss of force consequent upon the extent of loaded shortening. These problems were tackled in two ways. Records obtained from isokinetic releases from maximal isometric tetani showed a late linear phase of force decline, and this was extrapolated back to the time of release to obtain measures of instantaneous force. This method gave usable data up to velocities of shortening equivalent to approximately one-third of maximal velocity. An alternative procedure (short activation, SA) allowed the muscle to begin shortening when isometric force reached a value that could be sustained during shortening (essentially an isotonic protocol). At low velocities both protocols gave very similar data (r2 = 0.96), but for high velocities only the SA procedure could be used. Results obtained using the SA protocol in fresh muscle were compared to those for muscle that had been fatigued by 25 s of ischaemic isometric contractions, induced by electrical stimulation at the ulnar nerve. Fatigue resulted in a decrease of isometric force [to 69 (3)%], an increase in half-relaxation time [to 431 (10)%], and decreases in maximal shortening velocity [to 77 (8)%] and power [to 42 (5)%]. These are the first data for human skeletal muscle to show convincingly that during acute fatigue, power is reduced as a consequence of both the loss of force and slowing of the contractile speed.     

The effect of shortening history on isometric and dynamic muscle function

Despite numerous reports on isometric force depression, few reports have quantified force depression during active muscle shortening (dynamic force depression). The purpose of this investigation was to determine the influence of shortening history on isometric force following active shortening, force during isokinetic shortening, and velocity during isotonic shortening. The soleus muscles of four cats were subjected to a series of isokinetic contractions at three shortening velocities and isotonic contractions under three loads. Muscle excursions initiated from three different muscle lengths but terminated at a constant length. Isometric force produced subsequent to active shortening, and force or shortening velocity produced at a specific muscle length during shortening, were compared across all three conditions. Results indicated that shortening history altered isometric force by up to 5%, force during isokinetic shortening up to 30% and shortening velocity during isotonic contractions by up to 63%. Furthermore, there was a load by excursion interaction during isotonic contractions such that excursion had the most influence on shortening velocity when the loads were the greatest. There was not a velocity by excursion interaction during isokinetic contractions. Isokinetic and isotonic power–velocity relationships displayed a downward shift in power as excursions increased. Thus, to discuss force depression based on differences in isometric force subsequent to active shortening may underestimate its importance during dynamic contractions. The presence of dynamic force depression should be realized in sport performance, motor control modeling and when controlling paralyzed limbs through artificial stimulation.     

A three-dimensional muscle model: a quantified relation between form and function of skeletal muscles

A three-dimensional muscle model with complex geometry is described and tested against experimental data. Using this model, several muscles were constructed. These muscles have equal optimum length but differ in architecture. The force exerted by the constructed muscles, in relation to their actual length and velocity of shortening, is discussed. Generally speaking, the constructed muscles with considerable pennation have great fiber angles, a great physiological cross section, a narrow active and steep passive length-force relation, and a low maximal velocity of shortening. The maximal power (force times velocity) delivered by the constructed muscles is shown to be almost independent of the architecture of the muscles. The steepness of the passive length-force relation is determined mainly by the shortest fibers within the group of constructed muscles, whereas maximal velocity of shortening and the width of the active length-force relation are determined mainly by the longest fibers. The validity of the three-dimensional muscle model with respect to some morphological and functional characteristics is tested. Length-force relations of constructed muscles are compared with the actual length-force relations of mm. gastrocnemii mediales and mm. semimembranosi of male Wistar rats. Moreover, actual fiber angle, fiber length, and muscle thickness of three mm. gastrocnemii mediales are compared with values found for constructed muscles. It is concluded that the three-dimensional muscle model closely approximates the actual muscle form and function.     

Theoretical and experimental behaviour of the muscle viscosity coefficient during maximal concentric actions

The aim of this study was to calculate the theoretical variation of the nonlinear damping factor (B) as a function of the muscle shortening velocity, and then to compare the theoretical values with the experimental data obtained on both the elbow flexor and the ankle extensor muscles. The theoretical variation of the B factor was determined from a muscle model consisting of a contractile component in parallel with a viscous damper both in series with an elastic component, and by using, the charateristic equation of the force velocity curve. In this muscle model, the viscous element modelled the inability of the muscle to generate as big a contracting force (while shortening) as possible under isometric conditions. Eight volunteer subjects performed maximal concentric elbow flexions and ankle extensions on an isokinetic ergometer at angular velocities of 60, 120, 180, 240, 300 and 360°·s^–1, and held two maximal isometric actions at an elbow angle of 90° (0° corresponds to the full extension) and at an ankle angle of 0° (0° corresponds to the foot flexion of 90° relative to the leg axis). From these measurements, the force and the shortening velocity values of each muscle were determined by using a musculo-skeletal model of the joint. The results showed that the theoretical behaviour of the B factor would seem to be dependent on the shortening velocity and on the parameter which varies according to the muscle fibre type composition and affects the curvature of the force-velocity curve (a_f). For each muscle group, the experimental data of B fitted with the theoretical equation, and the best fit was obtained for an of of 0.28 for the ankle extensor and of 0.32 for the elbow flexor muscles. These results indicated that from the muscle model used in the present study it is possible to describe the mechanical behaviour of the muscle during maximal concentric action.     

Muscular force production after concentric contraction

The steady-state force following active shortening does not reach the maximum isometric force associated with the final length. Isolated extensor digitorum longus and soleus muscles from mice (NMRI strain) were used to investigate the force produced by a muscle, and some parameters hypothetically influencing this shortening-induced force depression. The muscles were pre-stimulated at fixed length, shortened and then held isometrically to give maximum post-shortening forces, before de-stimulation. The shortening magnitude was 0.18, 0.36 or 0.72mm (about 2-7% of optimal length), time of shortening was chosen as 0.03, 0.06 and 0.12s, and final length as +0.72, 0 and -0.72mm, related to optimal length. The mechanical work during active shortening was evaluated by integrating the product of force and shortening velocity over the shortening period. The results show a positive correlation between the force depression and the mechanical work, whereas the force depression was not correlated to the velocity of shortening. Depression of the passive force component was also observed following all stimulations. Experiments show that the fully stimulated redevelopment of isometric force following concentric contraction follows a time function similar to the creation of force when isometric muscle is initially stimulated. The conclusion is that the isometric force development after active shortening can be well described by an asymptotic force which is decided by the produced work, and the initial isometric time constant.     

Effect of theophylline on the velocity of diaphragmatic muscle shortening

The present study examined the effect of theophylline on the shortening velocity of submaximally activated diaphragmatic muscle (i.e., muscles were activated by the use of a level of stimulation, 50 Hz, within the range of phrenic neural firing frequencies achieved during breathing, whereas maximum activation is achieved at 300 Hz). Experiments were performed in vitro on strips of diaphragmatic muscle obtained from 21 Syrian hamsters. Muscle shortening velocity was assessed during isotonic contractions against a range of afterloads, and Hill's characteristic equation was used to calculate velocity at zero load. In addition, unloaded shortening velocity was also measured by the slack test, i.e., from the time required for muscles to take up slack after a sudden reduction in muscle length. Theophylline (160 mg/l) increased the velocity of muscle shortening against a wide range of external loads (0-14 N/cm2) and increased the extrapolated unloaded velocity of shortening from 6.4 +/- 0.9 to 7.9 +/- 1.1 (SE) lengths/s (P less than 0.01). Theophylline reduced the time required to take up slack for any given step change in muscle length, increasing the unloaded velocity of shortening assessed by the slack test from 7.6 +/- 0.9 to 9.3 +/- 1.1 lengths/s (P less than 0.002). The effect of theophylline on diaphragmatic shortening velocity was evident at concentrations as low as 40 mg/l and increased progressively as theophylline concentrations were increased to 320 mg/l. Theophylline increased the shortening velocity of fatigued as well as fresh muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasticity in canine airway smooth muscle

The large volume changes of some hollow viscera require a greater length range for the smooth muscle of their walls than can be accommodated by a fixed array of sliding filaments. A possible explanation is that smooth muscles adapt to length changes by forming variable numbers of contractile units in series. To test for such plasticity we examined the muscle length dependence of shortening velocity and compliance, both of which will vary directly with the number of thick filaments in series. Dog tracheal smooth muscle was studied because its cells are arrayed in long, straight, parallel bundles that span the length of the preparation. In experiments where muscle length was changed, both compliance and velocity showed a strong dependence on muscle length, varying by 1.7-fold and 2.2-fold, respectively, over a threefold range of length. The variation in isometric force was substantially less, ranging from a 1.2- to 1.3-fold in two series of experiments where length was varied by twofold to an insignificant 4% variation in a third series where a threefold length range was studied. Tetanic force was below its steady level after both stretches and releases, and increased to a steady level with 5-6 tetani at 5 min intervals. These results suggest strongly that the number of contractile units in series varies directly with the adapted muscle length. Temporary force depression after a length change would occur if the change transiently moved the filaments from their optimum overlap. The relative length independence of the adapted force is explained by the reforming of the filament lattice to produce optimum force development, with commensurate changes of velocity and compliance.     

In vivo estimation of contraction velocity of human vastus lateralis muscle during "isokinetic" action.

To determine the shortening velocities of fascicles of the vastus lateralis muscle (VL) during isokinetic knee extension, six male subjects were requested to extend the knee with maximal effort at angular velocities of 30 and 150 degrees /s. By using an ultrasonic apparatus, longitudinal images of the VL were produced every 30 ms during knee extension, and the fascicle length and angle of pennation were obtained from these images. The shortening fascicle length with extension of the knee (from 98 to 13 degrees of knee angle; full extension = 0 degrees ) was greater (43 mm) at 30 degrees /s than at 150 degrees /s (35 mm). Even when the angular velocity remained constant during the isokinetic range of motion, the fascicle velocity was found to change from 39 to 77 mm/s at 150 degrees /s and from 6 to 19 mm/s at 30 degrees /s. The force exerted by a fascicle changed with the length of the fascicle at changing angular velocities. The peak values of fascicle force and velocity were observed at approximately 90 mm of fascicle length. In conclusion, even if the angular velocity of knee extension is kept constant, the shortening velocity of a fascicle is dependent on the force applied to the muscle-tendon complex, and the phenomenon is considered to be caused mainly by the elongation of the elastic element (tendinous tissue).     

High ionic strength and low pH detain activated skinned rabbit skeletal muscle crossbridges in a low force state

The effects of varying pH and ionic strength on the force-velocity relations and tension transients of skinned rabbit skeletal muscle were studied at 1-2 degrees C. Both decreasing pH from 7.35 to 6.35 and raising ionic strength from 125 to 360 mM reduced isometric force by about half and decreased sarcomere stiffness by about one-fourth, so that the stiffness/force ratio was increased by half. Lowering pH also decreased maximum shortening velocity by approximately 29%, while increasing ionic strength had little effect on velocity. These effects on velocity were correlated with asymmetrical effects on stiffness. The increase in the stiffness/force ratio with both interventions was manifest as a greater relative force change associated with a sarcomere length step. This force difference persisted for a variable time after the step. At the high ionic strength the force difference was long- lasting after stretches but relaxed quickly after releases, suggesting that the structures responsible would not impose much resistance to steady-state shortening. The opposite was found in the low pH experiments. The force difference relaxed quickly after stretches but persisted for a long time after releases. Furthermore, this force difference reached a constant value of approximately 8% of isometric force with intermediate sizes of release, and was not increased with larger releases. This value was almost identical to the value of an internal load that would be sufficient to account for the reduction in maximum velocity seen at the low pH. The results are interpreted as showing that both low pH and high ionic strength inhibit the movement of crossbridges into the force-generating parts of their cycle after they have attached to the actin filaments, with very few other effects on the cycle. The two interventions are different, however, in that detained bridges can be detached readily by shortening when the detention is caused by high ionic strength but not when it is caused by low pH.     

Effect of osmotic compression on the force-velocity properties of glycerinated rabbit skeletal muscle cells

The force-velocity relations of single glycerinated rabbit psoas muscle fibers at 5 degrees C were studied at maximum and half-maximum activation in the presence of 0 (control) and 39-145 g/liter dextran T-70. Resting fiber diameter decreased progressively to approximately 70% of the nondextran control as the dextran concentration was increased. Isometric force at full activation increased to a maximum of 136% of control at 111 g/liter dextran and then fell to 80% of control in 145 g/liter dextran. Maximum velocity, which fell to 49% of the control value in the highest concentration of dextran, was nearly constant at approximately 65% control over the range of 58-111 g/liter dextran. Relative maximum power, which gives an estimate of changes in intermediate velocity, was not significantly reduced by dextran concentrations up to 76 g/liter, but then fell progressively to 62% of control in the highest concentration of dextran. At half-maximum activation, maximum velocity and relative maximum power were not significantly different from the values at full activation. The results obtained at partial activation indicate that the decline of velocity seen in the presence of dextran is not due to a passive internal load and that the dextran does not cause a viscous resistance to shortening. The increased velocity in the absence of dextran can be explained by the reduced ability of cross-bridges to resist shortening, as proposed by Goldman (1987. Biophys. J. 51:57).     

Influence of an active pre-stretch on fatigue of skeletal muscle

In activities such as running, many muscles of the lower extremities appear to be actively stretched before they are allowed to shorten. In this study we investigated the effect of an active pre-stretch on the fatigability of muscles. Thus muscle contractions were compared in which shortening was preceded by an active isometric phase or by an active stretch. Rat medial gastrocnemius muscle-tendon complexes (with arrested blood flow) performed a series of ten repeated contractions (1.s-1) with either an active stretch or an isometric phase preceding the shortening. Contraction duration (0.45 s), and shortening duration (0.3 s), distance (6 mm) and velocity (20 mm.s-1) were the same in both types of contraction. Work output during the ten shortening phases was approximately 40% higher in the contractions with an active pre-stretch; in contrast, high-energy phosphate utilization was similar. Over the ten repeated contractions reduction of work output during the shortening phases of both types of contraction was similar in absolute terms (approx. 9.5 mJ). It is suggested that all the extra work performed during the shortening phases after a pre-stretch originated from sources other than cross-bridge cycling, which are hardly affected by fatigue. However, reduction of work output in relative terms, which is how the reduction is often expressed in voluntary exercise, was less after a pre-stretch (26% vs 32%), giving the impression of protection against fatigue by an active pre-stretch.     

Isoproterenol attenuates myosin phosphorylation and contraction of tracheal muscle

The effects of isoproterenol on isometric force, unloaded shortening velocity, and myosin phosphorylation were examined in thin muscle bundles (0.1-0.2 mm diam) dissected from lamb tracheal smooth muscle. Methacholine (10(-6) M) induced rapid increases in isometric force and in phosphorylation of the 20,000-Da myosin light chain. Myosin phosphorylation remained elevated during steady-state maintenance of isometric force. The shortening velocity peaked at 15 s after stimulation with methacholine and then declined to approximately 45% of the maximal value by 3 min. Isoproterenol pretreatment inhibited methacholine-stimulated myosin light chain phosphorylation, shortening velocity, and force during the early stages of force generation. However, the inhibitory effect of isoproterenol on force and myosin phosphorylation is proportionally greater than that on shortening velocity. Isoproterenol pretreatment also caused a rightward non-parallel shift in the methacholine dose-response curves for both isometric tension and myosin light chain phosphorylation. These data demonstrate that isoproterenol attenuates the contractile properties of airway smooth muscles by affecting the rate and extent of myosin light chain phosphorylation, perhaps through a mechanism that involves the synergistic interaction of myosin light chain kinase phosphorylation and Ca2+ metabolism.     

Does the speed of shortening affect steady-state force depression in cat soleus muscle?

It has been stated repeatedly for the past 50 years that the steady-state force depression following shortening of an activated muscle depends on the speed of shortening. However, these statements were based on results from experiments in which muscles were shortened at different speeds but identical activation levels. Therefore, the force during shortening was changed in accordance with the force-velocity relationship of muscles: that is, increasing speeds of shortening were associated with decreasing forces, and vice versa. Consequently, it is not possible at present to distinguish whether force depression is caused by the changes in speed, as frequently stated, or the associated changes in force, or both. The purpose of this study was to test if force depression depends on the speed of shortening. We hypothesized that force depression was dependent on the force but not the speed of contraction. Our prediction is that the amount of force depression after shortening contractions at different speeds could be similar if the force during contraction was controlled at a similar level. Cat soleus muscles (n=7) were shortened by 9 or 12 mm at speeds of 3, 9, and 27 mm/s, first with a constant activation during shortening (30Hz), then with activation levels that were reduced (<30Hz) for the slow speeds (3 and 9 mm/s) to approximate the shortening forces of the fast speed contractions (27 mm/s). If done properly, force depression could be precisely matched at the three different speeds, indicating that force depression was related to the force during the shortening contraction but not to the speed. However, in order to match force depression, the forces during shortening had to be systematically greater for the slow compared to the fast speeds of shortening, suggesting that force depression also depends on the level of activation, as force depression at constant activation levels can only be matched if the force during shortening, evaluated by the mechanical work, is identical. Therefore, we conclude that force depression depends on the force and activation level during shortening, but does not depend on the speed of shortening as has been assumed for half a century. These results support, but do not prove, the current hypothesis that force depression is caused by a stress-related cross-bridge inhibition in the actin-myosin overlap zone that is newly formed during muscle shortening.     

Evidence for increased low force cross-bridge population in shortening skinned skeletal muscle fibers: implications for actomyosin kinetics.

The dynamic characteristics of the low force myosin cross-bridges were determined in fully calcium-activated skinned rabbit psoas muscle fibers shortening under constant loads (0.04-0.7 x full isometric tension Po). The shortening was interrupted at various times by a ramp stretch (duration, 10 ms; amplitude, up to 1.8% fiber length) and the resulting tension response was recorded. Except for the earlier period of velocity transients, the tension response showed nonlinear dependence on stretch amplitude; i.e., the magnitude of the tension response started to rise disproportionately as the stretch exceeded a critical amplitude, as in the presence of inorganic phosphate (Pi). This result, as well as the result of stiffness measurement, suggests that the low force cross-bridges similar to those observed in the presence of Pi (presumably A.M.ADP.Pi) are significantly populated during shortening. The critical amplitude of the shortening fibers was greater than that of isometrically contracting fibers, suggesting that the low force cross-bridges are more negatively strained during shortening. As the load was reduced from 0.3 to 0.04 P0, the shortening velocity increased more than twofold, but the amount of the negative strain stayed remarkably constant (approximately 3 nm). This This insensitiveness of the negative strain to velocity is best explained if the dissociation of the low force cross-bridges is accelerated approximately in proportion to velocity. Along with previous reports, the results suggest that the actomyosin ATPase cycle in muscle fibers has at least two key reaction steps in which rate constants are sensitively regulated by shortening velocity and that one of them is the dissociation of the low force A.M.ADP.Pi cross-bridges. This step may virtually limit the rate of actomyosin ATPase turnover and help increase efficiency in fibers shortening at high velocities.     

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.     

Atrophy, but not necrosis, in rabbit skeletal muscle denervated for periods up to one year

Our understanding of the effects of long-term denervation on skeletal muscle is heavily influenced by an extensive literature based on the rat. We have studied physiological and morphological changes in an alternative model, the rabbit. In adult rabbits, tibialis anterior muscles were denervated unilaterally by selective section of motor branches of the common peroneal nerve and examined after 10, 36, or 51 wk. Denervation reduced muscle mass and cross-sectional area by 50–60% and tetanic force by 75%, with no apparent reduction in specific force (force per cross-sectional area of muscle fibers). The loss of mass was associated with atrophy of fast fibers and an increase in fibrous and adipose connective tissue; the diameter of slow fibers was preserved. Within fibers, electron microscopy revealed signs of ultrastructural disorganization of sarcomeres and tubular systems. This, rather than the observed transformation of fiber type from IIx to IIa, was probably responsible for the slow contractile speed of the muscles. The muscle groups denervated for 10, 36, or 51 wk showed no significant differences. At no stage was there any evidence of necrosis or regeneration, and the total number of fibers remained constant. These changes are in marked contrast to the necrotic degeneration and progressive decline in mass and force that have previously been found in long-term denervated rat muscles. The rabbit may be a better choice for a model of the effects of denervation in humans, at least up to 1 yr after lesion. force; shortening velocity; electron microscopy; histochemistry     

Frequency-dependent power output and skeletal muscle design

Cyclically contracting muscles provide power for a variety of processes including locomotion, pumping blood, respiration, and sound production. In the current study, we apply a computational model derived from force–velocity relationships to explore how sustained power output is systematically affected by shortening velocity, operational frequency, and strain amplitude. Our results demonstrate that patterns of frequency dependent power output are based on a precise balance between a muscle's intrinsic shortening velocity and strain amplitude. We discuss the implications of this constraint for skeletal muscle design, and then explore implications for physiological processes based on cyclical muscle contraction. One such process is animal locomotion, where musculoskeletal systems make use of resonant properties to reduce the amount of metabolic energy used for running, swimming, or flying. We propose that skeletal muscle phenotype is tuned to this operational frequency, since each muscle has a limited range of frequencies at which power can be produced efficiently. This principle also has important implications for our understanding muscle plasticity, because skeletal muscles are capable of altering their active contractile properties in response to a number of different stimuli. We discuss the possibility that muscles are dynamically tuned to match the resonant properties of the entire musculoskeletal system.     

Relative shortening velocity in locomotor muscles: turkey ankle extensors operate at low V/V(max)

The force-velocity properties of skeletal muscle have an important influence on locomotor performance. All skeletal muscles produce less force the faster they shorten and typically develop maximal power at velocities of approximately 30% of maximum shortening velocity (V(max)). We used direct measurements of muscle mechanical function in two ankle extensor muscles of wild turkeys to test the hypothesis that during level running muscles operate at velocities that favor force rather than power. Sonomicrometer measurements of muscle length, tendon strain-gauge measurements of muscle force, and bipolar electromyographs were taken as animals ran over a range of speeds and inclines. These measurements were integrated with previously measured values of muscle V(max) for these muscles to calculate relative shortening velocity (V/V(max)). At all speeds for level running the V/V(max) values of the lateral gastrocnemius and the peroneus longus were low (<0.05), corresponding to the region of the force-velocity relationship where the muscles were capable of producing 90% of peak isometric force but only 35% of peak isotonic power. V/V(max) increased in response to the demand for mechanical power with increases in running incline and decreased to negative values to absorb energy during downhill running. Measurements of integrated electromyograph activity indicated that the volume of muscle required to produce a given force increased from level to uphill running. This observation is consistent with the idea that V/V(max) is an important determinant of locomotor cost because it affects the volume of muscle that must be recruited to support body weight.     

Muscle-induced accelerations at maximum activation to assess individual muscle capacity during movement

Analyses of muscle-induced accelerations provide insight into how individual muscles contribute to motion. In previous studies, investigators have calculated muscle-induced accelerations on a per unit force basis to assess the potential of individual muscles to contribute to motion. However, because muscle force is a function of muscle activation, length, and shortening velocity, examining induced accelerations per unit force does not take into account how the capacity of individual muscles to produce force changes during movement. Alternatively, calculating a muscle's induced accelerations at maximum activation considers the extent to which the muscle can produce force during movement, as well as the potential of the muscle to accelerate the joints at each instant due to its moment arm(s) and the dynamics of the system. We computed both quantities for the major lower extremity muscles active during the stance phase of normal gait. We found that analyzing the induced accelerations at maximum activation in some cases led to a different interpretation of the muscles’ potential actions than analyzing the induced accelerations per unit force. For example, per unit force, gluteus maximus has a very large potential to accelerate the knee during single limb stance, but only a small potential to accelerate the knee at maximum activation due to this muscle operating in suboptimal regions of its force–length–velocity curve during the majority of stance. This new analysis technique will be useful in studying abnormal movement, when altered kinematics may influence the capacity of muscles to accelerate joints due to altered lengths and shortening velocities.