Number Of Sarcomeres Research Articles

Myofascial force transmission and tendon transfer for patients suffering from spastic paresis: A review and some new observations

The current rationale of clinical practice in spastic tendon transfer surgery is based on four assumptions: (1) changes in muscle fiber length (serial number of sarcomeres) determine the available length range and joint excursion, (2) muscle cross-sectional area determines the maximal force output, (3) fiber length and muscle force are invariable functions of muscle length, (4) there is an invariable relation between the elastic force and the active force exerted by the sarcomeres. The validity of these assumptions is discussed. Additionally, some new perspectives in muscle research are discussed and myofascial force transmission is introduced as a co-determinant for the outcome of tendon transfer by presenting some exploratory observations.

The effects of cilazapril and valsartan on the mRNA and protein expressions of atrial calpains and atrial structural remodeling in atrial fibrillation dogs

Owing to relative inefficacy and side effects of currently available antiarrhythmic drugs, current interest has shifted to treatments that target atrial fibrillation (AF) substrate. It has been suggested that calpain-induced atrial structural remodelling is under the control of renin-angiotensin system during AF. The purpose of this study is to investigate the effects of cilazapril and valsartan on the mRNA and protein expression of atrial calpains and atrial structural remodelling in AF dogs induced by chronic rapid atrial pacing. Twenty-seven dogs were randomly divided into sham-operated group (n = 6), control group (n = 7), cilazapril group (n = 7) and valsartan group (n = 7). One thin silicon plaque containing 4 pairs of electrodes was sutured to each atrium. A pacemaker was implanted in a subcutaneous pocket and attached to a screw-in epicardial lead in the right atrial appendage. The dogs in control group, cilazapril group and valsartan group were paced at 400 beats per minutes for 6 weeks. The dogs in cilazapril and valsartan groups received cilazapril (1mg x kg(-1)x d(-1)) or valsartan (30mg x kg(-1) x d(-1)) 1 week before rapid atrial pacing until pacing stop respectively. Transthoracic and transoesophageal echocardiographic examinations were performed in order to detect the changes of left atrium volume and contractile function. The inducibility and duration of AF were measured in all the groups. The expressions of atrial calpain I and calpain II mRNA were semi-quantified by reverse transcription-polymerase chain reaction. The protein levels of calpain I and calpain II in atrial myocardium were measured by Western-blot method. Pathohistological and ultrastructural changes in atrial tissue were tested by light and electron microscopy. Compared with the sham-operated control group, dramatic smaller left atrium and left atrial appendage volumes and significant higher atrial contractile function were observed in the cilazapril and valsartan groups. After 6-week atrial tachy-pacing, the mRNA and protein expressions of calpain I increased dramatically in the control group than that in the sham group, tissue calpain protein expression in all groups significantly correlated with the myolysis (r = 0.89, P < 0.01). Cilazapril and valsartan could significantly inhibit the gene and protein expressions of calpain I. No differences were found in the expression of calpain II mRNA and protein between the groups. Compared with atrial myocytes obtained from sham dogs, atrial myocytes from the control group dogs showed a reduced number of sarcomeres, a significant higher myolytic area of atria (24.3% vs. 3.1%, P < 0.01), increased vacuolization and dissolution. Cilazapril and valsartan could effectively prevent the pathohistological and ultrastructural changes induced by chronic rapid atrial pacing, dramatically decrease the area of myolysis (P < 0.05) and significantly reduce the inducibility and duration of AF. The expression of calpain I mRNA and protein increased remarkably in AF dogs. Cilazapril and valsartan can inhibit calpain I up-regulation, suppress atrial structural remodeling, and prevent the induction and promotion of AF in chronic rapid atrial pacing dogs.

To breathe or not to breathe: the respiratory muscles and COPD

The respiratory muscles are unique among skeletal muscles in that they are required to work without sustained rest throughout life. It is not surprising, therefore, that the ventilatory pump has been the subject of intense investigation over the past 30 years, with particular interest in the ability

The Magnitude of Muscle Strain Does Not Influence Serial Sarcomere Number Adaptations Following Eccentric Exercise

Eccentric exercise, when performed by a muscle that is unaccustomed to that type of contraction, results in a delayed onset of muscle soreness (DOMS). A prolonged exposure to eccentric exercise leads to the disappearance of the signs and symptoms associated with DOMS, which has been referred to as the repeated bout effect (RBE). Although the mechanisms underlying the RBE remain unclear, several mechanisms have been proposed, including the idea of an increase in serial sarcomere number following exercise induced muscle damage. However, in the traditional DOMS and RBE protocols, muscle injury has been treated as a global parameter, with muscle force and strain assumed to be uniform throughout the muscle. PURPOSE: To assess the effects of muscle-tendon unit strain, fiber strain, joint torque and injury on serial sarcomere number adaptations in four regions of the tibialis anterior muscle (TA) following long-term eccentric exercise training. METHODS: Three groups of New Zealand White (NZW) rabbits were subjected to chronic repetitive eccentric exercise bouts (3x/week) of the ankle dorsiflexors for 6 weeks. These eccentric exercise protocols (P1, P2, P3) consisted of identical muscle tendon unit (MTU) strain, but muscle length and activation timing were systematically altered resulting in changes of joint torque and fiber strain. RESULTS: Following chronic eccentric exercise, serial sarcomere number adaptations in the central superficial region of the TA differed significantly between the three eccentric exercise protocols (+2.7±1.4%[P1],+7.6±0.9%[P2],+6.4±1.1%[P3], p<.05), even though MTU strains were not significantly different (+5.0±.0.2%[P1], +5.0±.0.5%[P2], +5.2±.0.7%[P3], p=.973). Peak torque (0.6±0.02Nm[P1], 0.7±0.03Nm[P2], 0.7±0.03Nm[P3]), and relaxation fiber strain (+2.5±0.2%[P1], +7.7±0.2%[P2], +7.8±0.2%[P3]), during eccentric exercise were the best predictors of serial sarcomere number (r2=.99 and r2=.94, respectively) across all three protocols. In addition, serial sarcomere number adaptations were not uniform across the four regions of the muscle following all three exercise protocols. CONCLUSION: MTU strain does not appear to be the primary cause for sarcomerogenesis (the RBE), as fiber strain and torque were the best predictors for cellular adaptations following chronic eccentric exercise. Ultimately, the differential adaptations within the muscle may be explained by the non-uniform architecture between regions of the muscle, resulting in differential local fiber strains, injury and adaptation. This work was supported by the CIHR Bone and Joint Training Program, the CIHR Research Chair Program, and NSERC of Canada

The magnitude of muscle strain does not influence serial sarcomere number adaptations following eccentric exercise

It is generally accepted that eccentric exercise, when performed by a muscle that is unaccustomed to that type of contraction, results in a delayed onset of muscle soreness (DOMS). A prolonged exposure to eccentric exercise leads to the disappearance of the signs and symptoms associated with DOMS, which has been referred to as the repeated bout effect (RBE). Although the mechanisms underlying the RBE remain unclear, several mechanisms have been proposed, including the serial sarcomere number addition following exercise induced muscle damage. In the traditional DOMS and RBE protocols, muscle injury has been treated as a global parameter, with muscle force and strain assumed to be uniform throughout the muscle. To assess the effects of muscle‐tendon unit strain, fiber strain, torque and injury on serial sarcomere number adaptations, three groups of New Zealand White (NZW) rabbits were subjected to chronic repetitive eccentric exercise bouts of the ankle dorsiflexors for 6 weeks. These eccentric exercise protocols consisted of identical muscle tendon unit (MTU) strain, but other mechanical factors were systematically altered. Following chronic eccentric exercise, serial sarcomere number adaptations were not identical between the three eccentric exercise protocols, and serial sarcomere number adaptations were not uniform across all regions of the muscle. Peak torque and relaxation fiber strain were the best predictors of serial sarcomere number across all three protocols. Therefore, MTU strain does not appear to be the primary cause for sarcomerogenesis, and differential adaptations within the muscle may be explained by the nonuniform architecture of the muscle, resulting in differential local fiber strains.

Side‐to‐side linking of myocardial cells in hypertrophic cardiomyopathy: Whole heart microscopic observation with tangential sections

By cross-section or longitudinal section, it is difficult to investigate longitudinal features of myocardial cells in the whole heart. Here, introducing the use of tangential sections to obtain longitudinal aspect of myocardial cells in any part of myocardium, the authors evaluated myocardium in the left ventricle in 10 normal hearts and four hearts with hypertrophic cardiomyopathy (HCM). Tangential sections were obtained by peeling the superficial layer of myocardium. After peeling the whole surface, secondary deep layer was peeled. These procedures were repeated more than five times through the wall. Intercalated discs (ICD) were observed immunohistochemically with anti-N-cadherin and antidesmoplakin. In normal hearts, myocardial cells were cut longitudinally and ran parallel in tangential sections. They linked end-to-end with simple and regular ICD with average lengths of 120-130 microm and average sarcomere numbers of 56-65. In HCM hearts, many myocardial cells were cut almost longitudinally running approximately parallel in tangential sections. Myocardial cells frequently showed side-to-side linking characterized by skewed ICD, indistinct ICD counterparts, and longitudinally arranged ICD. Two young HCM hearts had circle-shaped ICD and vacuole-like structures highlighted by immunostaining for N-cadherin, which were actually extracellular structures comparable with irregular side-to-side linking. It is considered that side-to-side linking of myocardial cells is a characteristic microscopic feature in HCM rather than myocardial disarray.

The magnitude of muscle strain does not influence serial sarcomere number adaptations following eccentric exercise

It is generally accepted that eccentric exercise, when performed by a muscle that is unaccustomed to that type of contraction, results in a delayed onset of muscle soreness (DOMS). A prolonged exposure to eccentric exercise leads to the disappearance of the signs and symptoms associated with DOMS, which has been referred to as the repeated bout effect (RBE). Although the mechanisms underlying the RBE remain unclear, several mechanisms have been proposed, including the serial sarcomere number addition following exercise induced muscle damage. In the traditional DOMS and RBE protocols, muscle injury has been treated as a global parameter, with muscle force and strain assumed to be uniform throughout the muscle. To assess the effects of muscle-tendon unit strain, fiber strain, torque and injury on serial sarcomere number adaptations, three groups of New Zealand White (NZW) rabbits were subjected to chronic repetitive eccentric exercise bouts of the ankle dorsiflexors for 6 weeks. These eccentric exercise protocols consisted of identical muscle tendon unit (MTU) strain, but other mechanical factors were systematically altered. Following chronic eccentric exercise, serial sarcomere number adaptations were not identical between the three eccentric exercise protocols, and serial sarcomere number adaptations were not uniform across all regions of the muscle. Peak torque and relaxation fiber strain were the best predictors of serial sarcomere number across all three protocols. Therefore, MTU strain does not appear to be the primary cause for sarcomerogenesis, and differential adaptations within the muscle may be explained by the nonuniform architecture of the muscle, resulting in differential local fiber strains.

Differential serial sarcomere number adaptations in knee extensor muscles of rats is contraction type dependent

Sarcomerogenesis, or the addition of sarcomeres in series within a fiber, has a profound impact on the performance of a muscle by increasing its contractile velocity and power. Sarcomerogenesis may provide a beneficial adaptation to prevent injury when a muscle consistently works at long lengths, accounting for the repeated-bout effect. The association between eccentric exercise, sarcomerogenesis and the repeated-bout effect has been proposed to depend on damage, where regeneration allows sarcomeres to work at shorter lengths for a given muscle-tendon unit length. To gain additional insight into this phenomenon, we measured fiber dynamics directly in the vastus lateralis (VL) muscle of rats during uphill and downhill walking, and we measured serial sarcomere number in the VL and vastus intermedius (VI) after chronic training on either a decline or incline grade. We found that the knee extensor muscles of uphill walking rats undergo repeated active concentric contractions, and therefore they suffer no contraction-induced injury. Conversely, the knee extensor muscles during downhill walking undergo repeated active eccentric contractions. Serial sarcomere numbers change differently for the uphill and downhill exercise groups, and for the VL and VI muscles. Short muscle lengths for uphill concentric-biased contractions result in a loss of serial sarcomeres, and long muscle lengths for downhill eccentric-biased contractions result in a gain of serial sarcomeres.

Adaptation of muscle size and myofascial force transmission: a review and some new experimental results

This paper considers the literature and some new experimental results important for adaptation of muscle fiber cross-sectional area and serial sarcomere number. Two major points emerge: (1) general rules for the regulation of adaptation (for in vivo immobilization, low gravity conditions, synergist ablation, tenotomy and retinaculum trans-section experiments) cannot be derived. As a consequence, paradoxes are reported in the literature. Some paradoxes are resolved by considering the interaction between different levels of organization (e.g. muscle geometrical effects), but others cannot. (2) An inventory of signal transduction pathways affecting rates of muscle protein synthesis and/or degradation reveals controversy concerning the pathways and their relative contributions. A major explanation for the above is not only the inherently limited control of the experimental conditions in vivo, but also of in situ experiments. Culturing of mature single Xenopus muscle fibers at high and low lengths (allowing longitudinal study of adaptation for periods up to 3 months) did not yield major changes in the fiber cross-sectional area or the serial sarcomere number. This is very different from substantial effects (within days) of immobilization in vivo. It is concluded that overall strain does not uniquely regulate muscle fiber size. Force transmission, via pathways other than the myotendinous junctions, may contribute to the discrepancies reported: because of substantial serial heterogeneity of sarcomere lengths within muscle fibers creating local variations in the mechanical stimuli for adaptation. For the single muscle fiber, mechanical signalling is quite different from the in vivo or in vitro condition. Removal of tensile and shear effects of neighboring tissues (even of antagonistic muscle) modifies or removes mechanical stimuli for adaptation. It is concluded that the study of adaptation of muscle size requires an integrative approach taking into account fundamental mechanisms of adaptation, as well as effects of higher levels of organization. More attention should be paid to adaptation of connective tissues within and surrounding the muscle and their effects on muscular properties.

The Effect of Rate of Distraction Osteogenesis on Structure and Function of Anterior Digastric Muscle Fibers

The authors hypothesized that distraction at a rate of 3 mm/day, compared with mandibular distraction at a rate of 1 mm/day, would produce a maladaptive response in adjacent muscles of mastication. The authors further hypothesized that the maladaptive response would manifest at the single fiber level by means of increased sarcomeric heterogeneity, decreased maximum force output, and increased susceptibility to stretch-induced injury. In an ovine model, distraction osteogenesis of the right hemimandible was performed at either 1 mm/day for 21 days (n = 2) or 3 mm/day for 7 days (n = 2) to achieve a total distraction distance of 21 mm. The left hemimandibles served as controls. After a consolidation period of 2 days, the anterior digastric muscles were harvested; in six randomly selected single fibers from each muscle, maximum calcium-activated force (Po) was measured at optimal sarcomere length. The amount of damage to the sarcomeres in each fiber was assessed microscopically. To test susceptibility to contraction-induced injury, each fiber was given an activated stretch of 20 percent. Compared with control fibers and fibers distracted at 1 mm/day, maximum tetanic force (Po) was significantly lower in fibers distracted at 3 mm/day. Compared with control fibers, specific Po (Po/cross-sectional area) was lower in fibers distracted at 3 mm/day. The number of sarcomeres appearing damaged in fibers distracted at 3 mm/day was significantly higher than in control fibers or in fibers distracted at 1 mm/day. A greater deficit in Po was observed after a single activated stretch in fibers distracted at 3 mm/day than in control fibers or in fibers distracted at 1 mm/day. The authors conclude that distraction of the anterior digastric muscle in sheep at 3 mm/day produces a maladaptive response in the muscle fibers but a rate of 1 mm/day is tolerated by the muscle fibers. These data are consistent with the hypothesis that distraction of skeletal muscle at high rates results in increased heterogeneity of sarcomere lengths and that this increase in heterogeneity is the most likely potential mechanism resulting in whole muscle force deficits and in increased susceptibility to stretch-induced injury in distracted muscles.

Effect of passive stretching on the immobilized soleus muscle fiber morphology

The aim of the present study was to determine the effect of stretching applied every 3 days to the soleus muscle immobilized in the shortened position on muscle fiber morphology. Eighteen 16-week-old Wistar rats were used and divided into three groups of 6 animals each: a) the left soleus muscle was immobilized in the shortened position for 3 weeks; b) during immobilization, the soleus was stretched for 40 min every 3 days; c) the non-immobilized soleus was only stretched. Left and right soleus muscles were examined. One portion of the soleus was frozen for histology and muscle fiber area evaluation, while the other portion was used to identify the number and length of serial sarcomeres. Immobilized muscles (group A) showed a significant decrease in weight (44 +/- 6%), length (19 +/- 7%), serial sarcomere number (23 +/- 15%), and fiber area (37 +/- 31%) compared to the contralateral muscles (P < 0.05, paired Student t-test). The immobilized and stretched soleus (group B) showed a similar reduction but milder muscle fiber atrophy compared to the only immobilized group (22 +/- 40 vs 37 +/- 31%, respectively; P < 0.001, ANOVA test). Muscles submitted only to stretching (group C) significantly increased the length (5 +/- 2%), serial sarcomere number (4 +/- 4%), and fiber area (16 +/- 44%) compared to the contralateral muscles (P < 0.05, paired Student t-test). In conclusion, stretching applied every 3 days to immobilized muscles did not prevent the muscle shortening, but reduced muscle atrophy. Stretching sessions induced hypertrophic effects in the control muscles. These results support the use of muscle stretching in sports and rehabilitation.

Effect of one stretch a week applied to the immobilized soleus muscle on rat muscle fiber morphology.

We determined the effect of stretching applied once a week to the soleus muscle immobilized in the shortened position on muscle fiber morphology. Twenty-six male Wistar rats weighing 269 +/- 26 g were divided into three groups. Group I, the left soleus was immobilized in the shortened position for 3 weeks; group II, the soleus was immobilized in the shortened position and stretched once a week for 3 weeks; group III, the soleus was submitted only to stretching once a week for 3 weeks. The medial part of the soleus muscle was frozen for histology and muscle fiber area evaluation and the lateral part was used for the determination of number and length of serial sarcomeres. Soleus muscle submitted only to immobilization showed a reduction in weight (44 +/- 6%, P = 0.002), in serial sarcomere number (23 +/- 15%) and in cross-sectional area of the fibers (37 +/- 31%, P < 0.001) compared to the contralateral muscles. The muscle that was immobilized and stretched showed less muscle fiber atrophy than the muscles only immobilized (P < 0.05). Surprisingly, in the muscles submitted only to stretching, fiber area was decreased compared to the contralateral muscle (2548 +/- 659 vs 2961 +/- 806 microm(2), respectively, P < 0.05). In conclusion, stretching applied once a week for 40 min to the soleus muscle immobilized in the shortened position was not sufficient to prevent the reduction of muscle weight and of serial sarcomere number, but provided significant protection against muscle fiber atrophy. In contrast, stretching normal muscles once a week caused a reduction in muscle fiber area.

Popping sarcomere hypothesis explains stretch-induced muscle damage.

1. Exercise that involves stretching a muscle while active cause microscopic areas of damage, delayed onset muscle soreness and adaptation to withstand subsequent similar exercise. 2. Longer muscle lengths are associated with greater damage and recent animal experiments show that it is the length relative to optimum that determines the damage. 3. In humans, walking down stairs, taking two at a time, increases the length of the muscle during the lengthening and increases the delayed onset muscle soreness. 4. The observed pattern of damage is consistent with explanations based on sarcomere length instabilities. 5. The pattern of adaptation is consistent with the number of sarcomeres in series in a muscle being modulated by exercise, especially the range of muscle lengths over which eccentric exercise regularly occurs.

Effects of strain on contractile force and number of sarcomeres in series of Xenopus laevis single muscle fibres during long-term culture

The aim of the present study is to test whether mechanical strain uniquely regulates muscle fibre atrophy/hypertrophy and adaptation of the number of sarcomeres in series within mature muscle fibres in vitro . Mature single muscle fibres from Xenopus laevis illiofibularis muscle were cultured (4-97 days) while kept at negative strain ( approximately 20% below passive slack length, 'short fibres') or at positive strain ( approximately 5% over passive slack length, 'long fibres'). Before and after culture the number of sarcomeres in series was determined using laser diffraction. During culture, twitch and tetanic force characteristics were measured every day. Survival time of long fibres was substantially less than that of short fibres. Of the long fibres 40% died or became inexcitable within 1 week, whereas this did not occur for short fibres. During culture, twitch and tetanic force of all short fibres increased substantially. Regression analysis showed that the post-culture number of sarcomeres in series was not significantly changed compared to the number before culture. It is concluded that culture at negative strain does not result in atrophy or a reduction of the number of sarcomeres in series, even after 97 days. For the long fibres we did not detect any hypertrophy as tetanic force remained stable or decreased slowly, while twitch force varied. Regression analysis of the change of the number of sarcomeres in series as a function of the culture time showed a positive slope ( P=0.054). Two out of four long fibres that were cultured for at least 2 weeks showed an increase in the number of sarcomeres of 4-5%. Compared with in vivo adaptation to mechanical stimuli this is much less than would be expected. The data suggest that strain may not be the only factor that regulates hypertrophy and the number of sarcomeres in series.

Tension- and afferent input-associated responses of neuromuscular system of rats to hindlimb unloading and/or tenotomy.

Responses of electromyogram (EMG) in soleus muscle and both afferent and efferent neurograms at the fifth lumbar (L(5)) segmental level of spinal cord were investigated during acute and chronic unloading induced by hindlimb suspension and/or tenotomy in adult rats. The soleus EMG and afferent neurogram decreased 88 and 37%, respectively, relative to those at quadrupedal posture on the floor after acute hindlimb suspension that causes passive shortening of soleus due to ankle plantarflexion. However, the afferent neurogram (P < 0.05) and soleus EMG (P > 0.05) recorded on the floor increased after tenotomy of synergists. Furthermore, the afferent input was inhibited when the soleus EMG disappeared after tenotomy of soleus. The afferent neurogram and EMG of the soleus showed correlated responses to a variety of treatments, suggesting that the afferent neurogram recorded at the L(5) segmental level reflects the neural input associated with the activity level of the soleus predominantly. The level of efferent neurogram decreased after acute hindlimb suspension but was not influenced significantly by tenotomy of synergists and/or soleus itself. The EMG and afferent neurograms remained low up to the 4th day but recovered to the preexperimental levels within 14 days, due to reorganization of sarcomere number and length, as well as the shortening of muscle fiber length and recovery of tension development. It is suggested that the levels of EMG and afferent neurogram associated with antigravity muscle are closely related to the tension development of the muscle.

The mode of myofibril remodelling in human skeletal muscle affected by DOMS induced by eccentric contractions.

Myofibrillar Z-disc streaming and loss of the desmin cytoskeleton are considered the morphological hallmarks of eccentric contraction-induced injury. The latter is contradicted by recent studies where a focal increase of desmin was observed in biopsies taken from human muscles with DOMS. In order to determine the effects of eccentric contraction-induced alterations of the myofibrillar Z-disc, we examined the distribution of alpha-actinin, the Z-disc portion of titin and the nebulin NB2 region in relation to actin and desmin in DOMS biopsies. In biopsies taken 2-3 days and 7-8 days after exercise, we observed a significantly higher number of fibres showing focal areas lacking staining for alpha-actinin, titin and nebulin than in biopsies taken from control or 1 h after exercise. None of these proteins were part of Z-disc streamings but instead they were found in distinct patterns in areas characterised by altered staining for desmin and actin. These were preferentially seen in regions with increased numbers of sarcomeres in parallel myofibrils. We propose that these staining patterns represent different stages of sarcomere formation. These findings therefore support our previous suggestion that muscle fibres subjected to eccentric contractions adapt to unaccustomed activity by the addition of new sarcomeres.

Gene expression in response to muscle stretch.

In studying the way the musculoskeletal system adapts, it is important to consider how the different tissues interact with each other. During growth, and in response to changes in posture, the functional length of muscle is adjusted by altering the number of sarcomeres in series to the optimum for force generation and power output. In some cases, insufficient adaptation gives rise to problems such as muscle contracture. Stretch has marked effects on muscle mass with eccentric contraction being the most effective form of exercise for building muscles. As far as the mechanism is concerned, the current authors have cloned the deoxyribonucleic acid (cDNA) of a splice variant of the insulinlike growth factor gene that is produced by active muscle that seems to be the factor that controls local tissue repair, maintenance, and remodeling. This new growth factor has been called mechanogrowth factor to distinguish it from the liver insulin growth factors, which have a systemic mode of action. The discovery of the locally produced insulinlike growth factor seems to provide the link between the mechanical stimulus and the activation of gene expression.

The effect of the amount of limb lengthening on skeletal muscle.

The adaptation of tibialis anterior muscles after 20% and 30% gradual limb lengthening was evaluated. Eight skeletally mature neutered male goats had 20% (n = 4) or 30% (n = 4) tibial distraction at a rate of 0.25 mm three times per day. Muscles from lengthened and contralateral control limbs were harvested on completion of distraction. Fiber length and sarcomere length were measured followed by calculation of sarcomere number and muscle fiber-to-bone lengthening ratio. Fiber length and sarcomere number after 20% and 30% limb lengthening were significantly greater in the distracted muscles, whereas no difference in sarcomere length was detected. The difference in muscle fiber length and sarcomere number between distracted and control limbs was greater in the 30% than in the 20% group. The disproportion between the amounts of muscle fiber and bone length increase was similar after 20% and 30% lengthening. The results show that muscular adaptation continues during 20% to 30% limb lengthening by increasing fiber length. It seems that this increase occurs through serial sarcomere addition rather than sarcomere length alteration. The higher rate of musclerelated clinical complications after limb lengthening beyond 20% does not seem to be related to a failure of muscle fiber contractile elements to adapt to increasing limb length.

THE ADDITION OF SARCOMERES IN SERIES IS THE MAIN PROTECTIVE MECHANISM FOLLOWING ECCENTRIC EXERCISE

Sore muscles following unaccustomed eccentric exercise is a common experience. One remarkable aspect of this is the rapid training. A single bout of exercise can provide significant protection against muscle damage and soreness from subsequent bouts. Several studies have shown that such training also increases the optimum muscle length and/or the number of sarcomeres. The present study aimed to test whether this accounts for all the protection. Rats were trained for up to 30 minutes per day on a treadmill, either inclined to 16° (concentrically biased exercise) or declined to 16° (eccentrically biased exercise) for one week. The decline rats were found to have smaller optimum knee angles, or longer muscle lengths, for torque generation by vastus intermedius muscles than the incline rats. When test eccentric contractions were given over the same range of knee angles for each training group, the decline rats showed less damage. When the differences in the optimum length were accounted for and the eccentric contractions were given over the same portion of the torque angle curve, there was no difference between the two groups in the amount of damage that they suffered, suggesting that the shift in optimum was responsible for all of the protection.

LENGTHENING CONTRACTIONS DO NOT INCREASE SERIAL SARCOMERE NUMBER IN EXTENSOR DIGITORUM LONGUS MUSCLES OF MICE

PURPOSE: To test the hypothesis that a protocol of lengthening contractions that induces protection from contraction-induced injury increases serial sarcomere number. METHODS: Extensor digitorum longus (EDL) muslces from male C57B1/6 mice (3 mo old; n = 8) were subjected to a protocol of controlled lengthening contractions shown previously to induce protection from subsequent lengthening contraction-induced injury. The protocol consisted of 75 stretches of 20% strain relative to optimal fiber length (Lf) at 1 Lf/s, with stretches initiated 100 ms after beginning of 150 Hz stimulation and occurring once each 4 s. Two weeks after the protocol, EDL muscles were harvested, fixed in 8% paraformaldehyde, small fiber bundles were teasted from each of the 4 bellies of the muscle, and serial sarcomere numbers were estimated by dividing bundle length (measured under a dissecting microscope) by sarcomere length (measure using laser diffiraction). RESULTS: Sarcomere numbers were significantly smaller (p < 0.05) for bellies supplying digits 2and 3 (mean + SE: 2359 + 41, 2405 + 60, respectively) than for bellies supplying digits 4 and 5 (2684 + 61, 2721 + 74, respectively). However, sarcomere number was not significantly different for muscle exposed to lengthening contractions (2521 + 45) compared with control muscle (2564 + 56) either when compared by 2-way analysis of variance or when comparing across bellies using t tests. CONCLUSION: A protocol of lengthening contractions that induces protection from subsequent contraction-induced injury did not increase serial sarcomere number in the mouse extensor digitorum longus. Supported by NIA AG-06157, AG-00114.