Duration Of Stretch Research Articles

Duration of neuronal stretch correlates with functional loss.

Postoperative cranial nerve weakness or paralysis is not uncommon in many otolaryngologic surgical procedures. Our study used a rat model to test the hypothesis that the length of time that a nerve is under tension may be an important variable in the amount of postoperative paresis. Forty Sprague-Dawley rats were divided into 4 groups that underwent either a sham operation or a traction injury for 1, 2, or 5 minutes. The traction injury was performed with a vessel loop placed around the sciatic nerve with 50 g of tension. Traction injury for 1 or 2 minutes did not result in any statistical differences in the motor capabilities of the lower limb. However, those animals with a stretch injury for 5 minutes had a significant loss of function (P < 0.01) when compared with all other groups. Histologic examination of nerves harvested on postoperative day 7 showed no evidence of mechanical injury. This study demonstrates that even minimal tension, if maintained for a significant amount of time, may result in postoperative weakness.

Duration of neuronal stretch correlates with functional loss

Postoperative cranial nerve weakness or paralysis is not uncommon in many otolaryngologic surgical procedures. Our study used a rat model to test the hypothesis that the length of time that a nerve is under tension may be an important variable in the amount of postoperative paresis. Forty Sprague-Dawley rats were divided into 4 groups that underwent either a sham operation or a traction injury for 1, 2, or 5 minutes. The traction injury was performed with a vessel loop placed around the sciatic nerve with 50 g of tension. Traction injury for 1 or 2 minutes did not result in any statistical differences in the motor capabilities of the lower limb. However, those animals with a stretch injury for 5 minutes had a significant loss of function ( P < 0.01) when compared with all other groups. Histologic examination of nerves harvested on postoperative day 7 showed no evidence of mechanical injury. This study demonstrates that even minimal tension, if maintained for a significant amount of time, may result in postoperative weakness. (Otolaryngol Head Neck Surg 2001;124:641-4.)

THE EFFECTS OF ACTIVE ISOLATED VS STATIC STRETCHING ON FLEXIBILITY

To evaluate the effect of Active Isolated Stretching (Al) versus Static Stretching (SS) on hamstring and low back flexibility, 30 subjects (24 female, 6 male, age 22.6 ± 1.3 yr, body mass 65.5 ± 3.1 kg and height 166 ± 18 cm) were randomly assigned to one of three groups (AI, SS, Control). Supervised intervention was conducted three times per week with an equal duration of stretch (60 sec) for the AI and SS groups. The control group (C) was evaluated at three intervals without intervention. Sit and Reach (SR) and hip flexion by goniometer (G) were obtained at weeks 0, 7, and 13. The following results were obtained:Table: No Caption Available.Statistical analysis by ANOVA revealed significant difference (p < .05) only with the G measurements of the AI trial. Although the technique of measurement and procedures were identical for each assessment, all groups revealed variability in their baseline. Flexibility variation in a group of young subjects with baseline flexibility in the 60th percentile may not be unusual. Significant change in a precise measure of flexibility (G) without changes in a general measure of flexibility (SR) may in part be attributed to the accuracy of the instrument. A low dose (3 sessions per week at 60 sec/session) of flexibility intervention may be insufficient to elicit measurable changes in range of motion.

Orientation and length of mammalian skeletal myocytes in response to a unidirectional stretch.

Effects of mechanical forces exerted on mammalian skeletal muscle cells during development were studied using an in vitro model to unidirectionally stretch cultured C2C12 cells grown on silastic membrane. Previous models to date have not studied these responses of the mammalian system specifically. The silastic membrane upon which these cells were grown exhibited linear strain behavior over the range of 3.6-14.6% strain, with a Poisson's ratio of approximately 0.5. To mimic murine in utero long bone growth, cell substrates were stretched at an average strain rate of 2.36%/day for 4 days or 1.77%/day for 6 days with an overall membrane strain of 9.5% and 10.6%, respectively. Both control and stretched fibers stained positively for the contractile protein, alpha-actinin, demonstrating muscle fiber development. An effect of stretch on orientation and length of myofibers was observed. At both strain rates, stretched fibers aligned at a smaller angle relative to the direction of stretch and were significantly longer compared to randomly oriented control fibers. There was no effect of duration of stretch on orientation or length, suggesting the cellular responses are independent of strain rate for the range tested. These results demonstrate that, under conditions simulating mammalian long bone growth, cultured myocytes respond to mechanical forces by lengthening and orienting along the direction of stretch.

CAMP- and cGMP-independent stretch-induced changes in the contraction of rat atrium.

The stretch-induced changes in contraction force, cAMP and cGMP in isolated rat left atrium were studied. Increasing the diastolic intra-atrial pressure from 1 cmH2O to 8 cmH2O caused an immediate (<500 ms) increase in contraction force, the magnitude of which was 2.24+/-0.29 (n=6) times the force elicited by 1 cmH2O. This was followed by a slower, gradual increase of the force, which was maximal 8 min after the stretch (4.33+/-0.31, n=6). These phenomena were not accompanied by changes in the cAMP (n=24) or cGMP (n=24) concentrations within the tissue at any duration of stretch tested (2, 8, 20 and 36 min, n=6 at each time point). Furthermore, it was estimated that if the beta-adrenergic receptor agonist isoprenaline (100 nM) was used to produce an increase of the contraction force of the same magnitude as that induced by stretch, the cAMP concentration was greater (4.20+/-0.29 pmol/mg, n=5, P<0.001) when compared to that produced after 20 min of stretch (2.69+/-0.12 pmol/mg, n=6). Even without significantly changing the cGMP concentration, isoprenaline significantly increased the [cAMP]/[cGMP] ratio (3.4+/-0.36, n=5, P<0.01) compared to stretch (1.95+/-0.14, n=6). This result shows that in the rat atrium stretch does not regulate the production or breakdown of cyclic nucleotides (cAMP or cGMP). Thus it seems very unlikely that the effects of stretch on rat atrium function are caused by cAMP or cGMP.

Effects of baseline anxiety on response to kindling of the right medial amygdala

The effects of kindling of the right anterior medial amygdala of Wistar rats was studied. Kindling lastingly increased anxiety (decreased open-arm exploration) in the elevated plus-maze 1 week after the last kindled seizure, replicating previous findings. Changes in anxiety were independent of changes in exploration or activity in either the plus-maze or hole board. A new finding is the dependence on baseline behavior of kindling induced behavioral changes. Using a novel-retest paradigm, it was possible to retest rats in the plus-maze without changes in their open arm explorations. This permitted pretesting rats to determine their baseline levels of plus-maze anxiety. Controls proved to be stable in their plus-maze behavior over a retest interval of 3 weeks. Rats below the median level of Test 1 open-arm exploration were unaffected by kindling. Those above the Test 1 median level of open-arm exploration showed reduced exploration following kindling. Kindling did not affect closed-arm entries in the plus-maze in this analysis. However, it was discovered that rats with arm entries below a critical level on Test 1 showed an increase in closed-arm entries following kindling. These findings point out how baseline behaviors can interact with kindling to influence behavioral outcome. Risk assessment was unchanged by kindling in this study, unlike previous reports. Subtle changes in focus location within the medial amygdala may have altered the effects of kindling on risk assessment. The electrodes in this study were in a slightly but significantly different location in the medial amygdala than in previous studies. As in previous studies, risk assessment was measured as frequency and duration of stretch attend postures toward the open arm of the plus maze when the hind quarters were in the closed arms. Risk assessment was taken as a ratio of time spent in the closed arms of the maze. This study, along with others reviewed elsewhere, suggest that a complex set of factors contributes to the effects of kindling on behavior. The fact that previous studies have not taken them into account perhaps explains inconsistencies in the reported behavioral effects of kindling on behavior in rodents.

Up-Regulation of AT 1 and AT 2 Receptors in Postinfarcted Hypertrophied Myocytes and Stretch-Mediated Apoptotic Cell Death

To determine whether up-regulation of AT(1) and AT(2) receptors occurred in hypertrophied myocytes after infarction and whether AT(2) played a role in stretch-mediated apoptosis, left ventricular myocytes were dissociated from the surviving portion of the wall 8 days after coronary occlusion and cardiac failure in rats. Control cells were obtained from sham-operated animals. Myocytes were stretched in an equibiaxial stretch apparatus and angiotensin II (Ang II) formation and cell death were measured 3 and 12 hours later. AT(1) and AT(2) proteins were evaluated in freshly isolated myocytes and after stretch. The effects of AT(1) and AT(2) antagonists on stretch-induced Ang II synthesis and apoptosis were also established. Myocardial infarction increased AT(1) and AT(2) in myocytes and stretch further up-regulated these receptors. Ang II levels were higher in postinfarcted myocytes and this peptide increased with the duration of stretch in both groups of cells. Similarly, apoptosis increased with time in control and postinfarcted myocytes. Absolute values of Ang II and apoptosis were greater in myocytes from infarcted hearts at 3 and 12 hours after stretch. Addition of AT(1) blocker to cultures inhibited stretch-activated apoptosis in both myocyte populations as well as the generation of Ang II in postinfarcted myocytes. In contrast, AT(2) antagonists had no impact on these cellular events. In conclusion, Ang II stimulated cell death through AT(1) receptor activation, whereas ligand binding to AT(2) receptor did not alter Ang II concentration and apoptosis in normal and postinfarcted hypertrophied myocytes.

Stretch-mediated release of angiotensin II induces myocyte apoptosis by activating p53 that enhances the local renin-angiotensin system and decreases the Bcl-2-to-Bax protein ratio in the cell.

Physical forces activate apoptosis and gene expression, but the mechanism is unknown. For this purpose, adult myocytes were stretched in an equibiaxial stretch apparatus and the magnitude of cell death was examined 4 and 24 h later. The possibility of stretch-mediated activation of p53 and p53-dependent genes was evaluated at 30 min, 2, 4, 8, and 24 h. Myocyte apoptosis increased by 4.4- and 7.6-fold at 4 and 24 h after stretch. p53 binding to the promoter of angiotensinogen, AT1 receptor, and Bax also increased. Expression of angiotensinogen, AT1 receptor, p53, and Bax increased and Bcl-2 decreased in stretched myocytes. The changes in AT1 receptor, p53, Bax, and Bcl-2 became more apparent with the duration of stretch. Angiotensin II concentration in the medium increased at 10 min, reaching maximal levels at 1 and 20 h. The AT1 blocker, losartan, abolished apoptosis in stretched myocytes. Myocyte volume was not influenced by stretch. In conclusion, stretch-mediated release of angiotensin II is coupled with apoptosis and the activation of p53 which may be responsible for the prolonged upregulation of the local renin-angiotensin system and the increased susceptibility of myocytes to undergo apoptosis.

EMG-activity and muscular performance of lower leg during stretch-shortening cycle after cooling.

To test the effect of cooling on EMG-activity of muscles working as an agonist and antagonist in the lower leg, 12 men dressed in shorts and jogging shoes performed a drop-jump exercise after 60 min exposures to 27 degrees C and 10 degrees C. Cooling decreased mean skin temperature 5.6 +/- 0.4 degrees C (mean +/- SD, P < 0.001), whereas rectal temperature was unaffected. The muscle temperature measured from m. gastrocnemius medialis decreased 4.1 +/- 0.3 degrees C (P < 0.01) at the depth of 30 mm below skin surface. To find the optimal stretching velocity for potentiation of elastic energy, the drop-jump exercise was performed from six different bench heights (10, 20, 30, 40, 50, and 60 cm). The optimal velocity was not altered on account of cooling. In cooled subjects during the stretch phase of the drop jumps the EMG-activity of m. triceps surae complex (agonist) increased (P < 0.05-0.001) while the activity of m. tibialis anterior (antagonist) remained unchanged. After cooling during the shortening phase of the jumps the EMG-activity of m. triceps surae complex decreased (P < 0.05-0.001), whereas the activity of m. tibialis anterior increased (P < 0.05-0.001). In addition, after cooling the peak EMG-activity appeared on the average 28 ms earlier, which shifted the peak activity from the shortening phase (at 27 degrees C) to the stretch phase (at 10 degrees C). Cooling increased the mean duration of stretch and shortening phases by 28 +/- 3 ms (P < 0.001) and 23 +/- 2 ms (P < 0.001), respectively. The average force production during the shortening phase was 26% less (P < 0.05) after cooling, which resulted in a decreased rise of body centre of gravity (P < 0.05-0.01). It is concluded that during a stretch-shortening cycle cooling alters the EMG-activity of agonist and antagonist muscles on a contradictory manner and results in an earlier peak EMG-activity. Therefore, alterations in motor unit recruitment could be responsible for the prolonged muscle contraction and decreased force production on account of cooling.

Effect of a brief stretch on time course of shortening after a quick release in guinea pig tenea coli.

To examine the origin of velocity deceleration in the shortening of smooth muscle, guinea pig tenea coli which contracts isometrically in a high-potassium solution was released quickly (1st release), restretched to the original length, kept at this length for 0.06-0.2s and quickly released again (2nd release). The muscle shortened isotonically under the same very-light load after the 1st and 2nd releases. The length change of the muscle during shortening was examined using a video camera. The rapid shortening phase, seen after the 1st release, which followed the instantaneous, elastic recoil and lasted for about 0.3s, disappeared after the 2nd release. This effect was prominent when the stretch duration was short. The time course of the slow phase of shortening subsequent to the rapid one was not affected by stretching. These results suggest that the rapid shortening phase is due largely to adjust of the cross-bridges between the thick and thin filaments to the change from an isometric to an isotonic contraction, while the slow phase reflects a steady turnover in the cross-bridges. The velocity of the slow shortening phase reached a maximum before the isometric force peaked and decreased as the activation level was lowered by reducing the external Ca2+ concentration from 2.5 to 0.5 mM. This suggests that the steady turnover rate of the cross-bridges depends on the phase of contraction and level of activation. The cause of the gradual velocity decrease in the slow phase of shortening was discussed.

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.

Stretch-induced enhancement of contractions in uterine smooth muscle of rats.

1. We studied the effect of servo-controlled stretch of smooth muscle strips from rat uterus on tension and intracellular Ca2+ concentration ([Ca2+]i, using fura-2 as an indicator) at 30 degrees C. 2. When quiescent uterine muscle strips were stretched at a ramp time of 0.5 s by multiples of 5% of the resting muscle length (L0) up to 40%, forty-two out of sixty muscle strips responded with a transient active contraction and a [Ca2+]i increase. The minimum excursion of stretch required for contraction was 26.3 +/- 7.5% of L0 (mean +/- S.D.). The peak response had an all-or-none property and was almost independent of the duration of stretch. 3. Stretches of 30 or 35% of L0 induced contraction in most cases when rapidly applied in 0.2-0.5 s, but slowly applied stretch (ramp duration of 5-10 s) rarely induced contraction. 4. The stretch-induced response was inhibited by the removal of extracellular Ca2+ or by the addition of 10 nM nicardipine. However, it was unaffected by 1 microM tetrodotoxin, 1 microM atropine or by 10 microM cyclopiazonic acid, an inhibitor of Ca2+-ATPase in intracellular Ca2+ stores. 5. When a stretch of 15-35% of L0 was applied during the relaxation phase of 10 nM oxytocin-induced rhythmic contractions, the first contraction after the stretch occurred earlier than that expected from the control rhythm. However, the frequency of the subsequent rhythm returned to almost the control level even during continued application of stretch, although the half-width of rhythmic contractions was increased during stretch. 6. The present study demonstrates that stretch of uterine muscle induces a transient contraction due to Ca2+ influx, which is myogenic and dependent on the excursion and velocity of stretch. The all-or-none property of the stretch-induced contractions suggests initiation of Ca2+ spikes. Furthermore, stretch modulates the oxytocin-induced rhythmic contractions.

Prolonged static muscle stretch reduces spasticity - But for how long should it be held?

The rehabilitation of patients with upper motor neurone lesions often necessitates the reduction of spasticity before normal movement patterns can be taught. One proven technique is that of prolonged stretch to the affected muscle. However, the duration of the stretch has not been defined. This study aimed to investigate which of the following durations of prolonged muscle stretch - two, ten or thirty minutes - was optimal in reducing spasticity in spastic quadriceps femoris muscles of adult patients following cerebral vascular accidents or head trauma. The degree of spasticity was measured by the use of four methods, prior to, and after stretching. Twenty-nine spastic muscles were stretched for the three durations on different occasions, and the data analysed using the student's T-test.Results indicated that the most beneficial duration of prolonged muscle stretch in decreasing spasticity was ten minutes.

The Effect of Time on Static Stretch on the Flexibility of the Hamstring Muscles

To date, there are no reports comparing duration of static stretch in humans on joint range of motion (ROM) and hamstring muscle flexibility. The purpose of this study was to examine the length of time the hamstring muscles should be placed in a sustained stretched position to maximally increase ROM. Fifty-seven subjects (40 men, 17 women), ranging in age from 21 to 37 years and with limited hamstring muscle flexibility (ie, 30 degrees loss of knee extension measured with femur held at 90 degrees of hip flexion), were randomly assigned to one of four groups. Three groups stretched 5 days per week for 15, 30, and 60 seconds, respectively. The fourth group, which served as a control group, did not stretch. Before and after 6 weeks of stretching, flexibility of the hamstring muscles was determined by measuring knee extension ROM with the femur maintained in 90 degrees of hip flexion. Data were analyzed with a 4 x 2 analysis of variance (group x test) for repeated measures on one variable. The data analysis revealed a significant group x test interaction, indicating that the change in flexibility was dependent on the duration of stretching. Further post hoc analysis revealed that 30 and 60 seconds of stretching were more effective at increasing flexibility of the hamstring muscles (as determined by increased ROM of knee extension) than stretching for 15 seconds or no stretching. In addition, no significant difference existed between stretching for 30 seconds and for 1 minute, indicating that 30 seconds of stretching the hamstring muscles was as effective as the longer duration of 1 minute. The results of this study suggest that a duration of 30 seconds is an effective time of stretching for enhancing the flexibility of the hamstring muscles. Given the information that no increase in flexibility of the hamstring muscles occurred by increasing the duration of stretching from 30 to 60 seconds, the use of the longer duration of stretching for an acute effect must be questioned.

The relationship between duration of stimulus per day and the extent of hypertrophy of slow-tonic skeletal muscle in the fowl, Gallus gallus

1. 1. Passive stretch stimulus ranging from 30 min to 8 hr per day were studied on the slow twitch latissimus dorsi muscle (ALD) of the fowl for a 5-week period. 2. 2. A significant increase in the mass of the ALD was observed in all daily durations of stretch stimulus applied. Nearly 50% of the mass increase that occurred with stretch of 8 hr per day was obtained from durations of stretch as short as 30 min per day. 3. 3. Given that stretch is the equal of dynamic loading with respect to increasing muscle mass, it is concluded that stretch stimulation periods as short as 30 min per day may be just as effective as longer durations when hypertrophy is the desired result, such as following fracture, or muscle building in order to enhance athletic performance. 4. 4. In fact it may be that longer durations of daily stimulus may be detrimental to the muscle as the functional capacity may be compromised.

Progressive stretch overload of skeletal muscle results in hypertrophy before hyperplasia

Intermittent stretch of the anterior latissimus dorsi (ALD) muscle produces fiber hypertrophy without fiber hyperplasia (J. Appl. Physiol. 74: 1893-1898, 1993). This study was undertaken to determine if a progressive increase in load and duration of stretch would induce extremely large muscle fiber areas or if the fibers would reach a critical size before the onset of fiber hyperplasia. Weights ranging from 10 to 35% of the bird's mass were attached to the right wing of 26 adult quail while the left wing served as the intra-animal control. The stretch protocol was as follows: day 1 (10% wt), days 2 and 3 (rest), day 4 (15% wt), days 5-7 (rest), day 8 (20% wt), days 9 and 10 (rest), days 11-14 (25% wt), days 15 and 16 (rest), and days 17-38 (35% wt). Birds were killed after 12, 16, 20, 24, and 28 days of stretch not including rest days. Muscle mass increased 174% (12 days), 196% (16 days), 225% (20 days), 264% (24 days), and 318% (28 days). Muscle length increased 60% (12 days), 34% (16 days), 59% (20 days), 50% (24 days), and 51% (28 days). Mean fiber area increased 111% (12 days), 142% (16 days), 75% (20 days), 90% (24 days), and 39% (28 days). Fiber number, which was measured histologically, increased significantly by 82% only in the 28 days of stretch group. The percentage of slow tonic fibers did not change for any of the time points examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of muscle fiber hypertrophy and hyperplasia in intermittently stretched avian muscle.

In the chronic stretch model, muscle fiber hyperplasia precedes fiber hypertrophy [Alway et al. Am. J. Physiol. 259 (Cell Physiol. 28): C92-C102, 1990]. This study was undertaken to determine if an intermittent stretch protocol would induce fiber hypertrophy without fiber hyperplasia. A weight equalt to 10% of the bird's mass was attached to the right wing of seven adult quail while the left wing served as the intra-animal control. The weight was attached to the wing for 24-h periods interspersed with a 48- to 72-hr rest interval. The actual stretch time was 5 days while the length of the treatment period was 15 days. Muscle mass and length increased significantly 53.1 +/- 9.0 and 26.1 +/- 7.3% in the stretched anterior latissimus dorsi. Fiber number, which was determined from a histological section in the midregion of the muscle, did not change (control 1,651.6 +/- 94.8; stretch 1,626.0 +/- 70.9). The slow tonic fiber areas increased significantly an average of 28.6 +/- 5.7%, whereas the fast fibers increased 18.5 +/- 8.4% when compared with control values. Mean fiber area (average of slow and fast fibers) increased significantly by 27.8 +/- 6.0% in the stretched anterior latissimus dorsi. There were no differences in the percentage of slow fibers or volume density of noncontractile tissue. These data indicate that muscle adapts differently to intermittent stretch than it does to chronic stretch despite an equivalent load and stretch duration. In contrast to chronic stretch, 5 days of intermittent stretch produces muscle fiber hypertrophy without fiber hyperplasia.

Stretch-induced electromyographic activity and torque in spastic elbow muscles. Differential modulation of reflex activity in passive and active motor tasks.

Stretch-evoked electromyographic (EMG) activity and torque signals have been studied in elbow joint muscles of both sides of patients with spastic hemiparesis and healthy subjects. In order to reveal differences in the generation of muscle tone between clinical assessment and functional movement, stretches of different velocities and amplitudes were applied during passive and quasi-functional active motor tasks. In spastic patients the strength and duration of the EMG responses following stretching of flexor and extensor muscles during both passive and active tasks were dependent on the stretch velocity and duration, respectively. This effect was seen on both the spastic and unaffected side. Under passive conditions EMG activity after stretching was negligible in the limb muscles of healthy subjects, of small amplitude in unaffected limbs of the patients, but was strong in affected muscles. Under active conditions, the amplitude of the early (M1) component of the EMG signal was larger, while the later components (M2 and M3) were smaller. These differences were due more to a change in reflex gain than to a change in reflex threshold when the stretch velocity signal was the basis for calculation. It is suggested that in spastic paresis, modulation of stretch-induced EMG activity in the spastic limb becomes restricted to a smaller range with a poor ability to switch off under passive conditions. Furthermore, the reflex EMG activity suffers a reduced facilitation under active conditions. In comparison with unaffected limbs the stretch-evoked torque on the affected side was increased under passive conditions (due to the extra EMG activity) and decreased under active conditions (due to a reduced EMG activity). An increased torque to EMG ratio was found in spastic flexor and extensor muscles during active tasks. This is thought to be due to changes in mechanical muscle fibre properties suffered as a consequence of defective muscle activation following cerebral lesions. The consequences for clinical assessment of muscle tone and therapy of spastic movement disorder are discussed.

Effects of prestretch at the onset of stimulation on mechanical work output of rat medial gastrocnemius muscle-tendon complex

Work output of rat gastrocnemius medialis (GM) muscle (N = 5) was measured for stretch-shortening contractions, in which initiation of stretch occurred prior to the onset of activation, and for contractions with an isometric prephase. Duration of the active prephase (prestretch and pre-isometric) varied from 20 to 200 ms. Subsequent shortening (from optimum length + 4 mm to optimum length -2mm) lasted 150 ms. Stretch velocities of 5, 10 and 20 mm s-1 were used, and the shortening velocity was 40 mm s-1. The effects of several combinations of active stretch duration and active stretch amplitude were compared. Using force-compliance characteristics, the work of the contractile element (CE), elastic energy storage and release of the undamped series elastic component (SEC) were distinguished. During shortening, an extra amount of work output was produced, induced by active stretch, of which the largest contribution (70-80%) was due to higher elastic energy release. Enhancement of the storage and utilization of elastic energy during the stretch-shortening cycle, caused by higher transition-point forces (i.e. force at onset of shortening), increased with active stretch amplitude and was associated with a net loss of work, probably due to cross-bridge detachment during active stretch. Net work over the stretch-shortening cycle remained positive for all prestretch contractions, indicating that when a muscle performs this type of contraction, it is able to contribute to work performance on body segments. It is concluded that, in stretch-shortening movements of rat GM muscle, maximal positive work output is incompatible with maximal net work output. Consequences for complex movements in vivo are discussed.

Optimal duration of static stretching exercises for improvement of coxo-femoral flexibility.

The purpose of this study was to determine the effect of different durations of static stretching exercises on coxo-femoral (hip) flexibility. The experimental group, consisting of 20 sedentary women (20-30 years of age), participated in an exercise programme of static stretching exercises with emphasis on the hamstring muscles. The programme lasted for 10 weeks and consisted of two 50-min sessions per week. A control group of 15 sedentary women did not participate in the programme. Hip flexibility was determined before, during and at the end of the programme by means of a goniometric measuring technique developed by us and described elsewhere. Three sub-groups were formed, each following the same programme except that the duration of the static stretch differed (group 1, 10 s; group 2, 20 s; group 3, 30 s). The ANOVA tests showed that for all groups - the control group excepted - the hip flexibility had improved significantly after 10 weeks (P less than 0.05). No significant differences in hip flexibility were noted between the three subgroups at the end of the programme. This finding suggests that a duration of 10 s static stretching is sufficient for improving coxo-femoral flexibility.