Changes In Passive Tension Research Articles

Quantification of muscle co-contraction using supersonic shear wave imaging

Muscle stiffness estimated using shear wave elastography can provide an index of individual muscle force during isometric contraction and may therefore be a promising method for quantifying co-contraction. We estimated the shear modulus of the lateral gastrocnemius (LG) muscle using supersonic shear wave imaging and measured its myoelectrical activity using surface electromyography (sEMG) during graded isometric contractions of plantar flexion and dorsiflexion (n=7). During dorsiflexion, the average shear modulus was 26±6kPa at peak sEMG amplitude, which was significantly less (P=0.02) than that measured at the same sEMG level during plantar flexion (42±10kPa). The passive tension during contraction was estimated using the passive LG muscle shear modulus during a passive ankle rotation measured at an equivalent ankle angle to that measured during contraction. The passive shear modulus increased significantly (P<0.01) from the plantar flexed position (16±5kPa) to the dorsiflexed position (26±9kPa). Once this change in passive tension from joint rotation was accounted for, the average LG muscle shear modulus due to active contraction was significantly greater (P<0.01) during plantar flexion (26±8kPa) than at sEMG-matched levels of dorsiflexion (0±4kPa). The negligible shear modulus estimated during isometric dorsiflexion indicates negligible active force contribution by the LG muscle, despite measured sEMG activity of 19% of maximal voluntary plantar flexion contraction. This strongly suggests that the sEMG activity recorded from the LG muscle during isometric dorsiflexion was primarily due to cross-talk. However, it is clear that passive muscle tension changes can contribute to joint torque during isometric dorsiflexion.

Changes in Passive Tension of the Hamstring Muscles During a Simulated Soccer Match.

Passive muscle tension is increased after damaging eccentric exercise. Hamstring-strain injury is associated with damaging eccentric muscle actions, but no research has examined changes in hamstring passive muscle tension throughout a simulated sport activity. The authors measured hamstring passive tension throughout a 90-min simulated soccer match (SAFT90), including the warm-up period and every 15 min throughout the 90-min simulation. Passive hamstring tension of 15 amateur male soccer players was measured using the instrumented straight-leg-raise test. Absolute torque (Nm) and slope (Nm/°) of the recorded torque-angular position curve were used for data analysis, in addition to total leg range of motion (ROM). Players performed a 15-min prematch warm-up, then performed the SAFT90 including a 15-min halftime rest period. Reductions in passive stiffness of 20-50° of passive hip flexion of 22.1-29.2% (P < .05) were observed after the warm-up period. During the SAFT90, passive tension increased in the latter 20% of the range of motion of 10.1-10.9% (P < .05) concomitant to a 4.5% increase in total hamstring ROM (P = .0009). The findings of this study imply that hamstring passive tension is reduced after an active warm-up that includes dynamic stretching but does not increase in a pattern suggestive of eccentric induced muscle damage during soccer-specific intermittent exercise. Hamstring ROM and passive tension increases are best explained by improved stretch tolerance.

Abstract 253: Modeling of Pathologic Hypertophy with Cardiac Microtissues

Introduction: Pathological myocyte hypertrophy and fibroblast activation are key features of myocardial remodeling in hypertension and heart failure. Crosstalk between myocytes and fibroblasts contributes to the structural, mechanical, and electrical remodeling involved in various forms of heart failure. Replicating these responses in traditional 2D cell culture conditions has proven difficult. In this study, we utilized a novel platform to examine the cellular crosstalk and biological processes that underlie functional and structural changes in the 3D engineered tissues when exposed to pathological factors. We hypothesized that engineered cardiac tissues can report structural and functional responses to pathologic biochemical stimuli. Methods: These studies employ microfabricated polydimethylsiloxane (PDMS) templates to engineer arrays of 3D cardiac microtissues (CMT). Cantilevers within templates provide physiologically-relevant biomechanical loading to the CMTs, promote the appropriate organization of neonatal rat cardiac myocytes and fibroblasts, and report active and passive force generation in real time. Data was collected using fluorescent and confocal microscopy. Results: CMTs in a controlled mechanical environment demonstrate mechanical and structural changes within 24 hours of exposure to a cocktail of factors involved in maladaptive remodeling, including Transforming Growth Factor-β, Endothelin-1, and Angiotensin II. Analysis of 40 microtissues revealed that the percent change in passive tension was 45% higher (16.4 ± 10.3% vs. 61.1 ± 11.8%, p&lt;0.01) and in active tension 170% higher (24.9 ± 9.5% vs.196.1 ± 76.0%, p&lt;0.001) in treated CMTs compared to untreated CMTs. The percentage change in cross-sectional area of CMTs treated with pathological factors was 35% higher (-24.5 ± 15.6% vs.11.6 ± 7.9%, p&lt;0.001) than untreated samples. Conclusions: These findings demonstrate that the CMT model can be used to study and dissect the dynamics of pathological hypertrophy. Ongoing experiments are examining the distinct contributions of the pathologic growth factors, the relative contributions of fibroblasts and cardiomyocytes to the pathologic growth response, and the interactions between biomechanical and humoral inputs.

Influence of Passive Muscle Tension on Electromechanical Delay in Humans

BackgroundElectromechanical delay is the time lag between onsets of muscle activation and muscle force production and reflects both electro-chemical processes and mechanical processes. The aims of the present study were two-fold: to experimentally determine the slack length of each head of the biceps brachii using elastography and to determine the influence of the length of biceps brachii on electromechanical delay and its electro-chemical/mechanical processes using very high frame rate ultrasound.Methods/ResultsFirst, 12 participants performed two passive stretches to evaluate the change in passive tension for each head of the biceps brachii. Then, they underwent two electrically evoked contractions from 120 to 20° of elbow flexion (0°: full extension), with the echographic probe maintained over the muscle belly and the myotendinous junction of biceps brachii. The slack length was found to occur at 95.5 ± 6.3° and 95.3 ± 8.2° of the elbow joint angle for the long and short heads of the biceps brachii, respectively. The electromechanical delay was significantly longer at 120° (16.9 ± 3.1 ms; p<0.001), 110° (15.0 ± 3.1 ms; p<0.001) and 100° (12.7 ± 2.5 ms; p = 0.01) of elbow joint angle compared to 90° (11.1 ± 1.7 ms). However, the delay between the onset of electrical stimulation and the onset of both muscle fascicles (3.9 ± 0.2 ms) and myotendinous junction (3.7 ± 0.3 ms) motion was not significantly affected by the joint angle (p>0.95).ConclusionIn contrast to previous observations on gastrocnemius medialis, the onset of muscle motion and the onset of myotendinous junction motion occurred simultaneously regardless of the length of the biceps brachii. That suggests that the between-muscles differences reported in the literature cannot be explained by different muscle passive tension but instead may be attributable to muscle architectural differences.

Cardiac Titin

Titin constitutes the third myofilament of cardiac muscle, with a single giant polypeptide spanning from Z-disk to the M-band region of the sarcomere1 (Fig. 1). The ∼1.0 MDa region in the I-band is extensible and consists of tandemly arranged immunoglobulin (Ig)-like domains that make up proximal (near Z-disk) and distal (near A-I junction) segments, interspersed by the PEVK sequence (rich in proline, glutamate, valine, and lysine residues) and the N2B element2. Each functions as a distinct spring element3. The C-terminal ∼2 MDa of titin is located in the A-band and is inextensible. It is composed of regular arrays of Ig and fibronectin type 3 (Fn3) modules forming so-called super-repeats2. A-band titin may function as a molecular ruler, regulating assembly of the thick filament2,4,5. Titin's ∼250-kDa COOH-terminal region is an integral part of the M-band and contains a kinase domain6,7. As in the Z-disk, where titin filaments from opposite sarcomeres overlap, titin filaments from opposite half-sarcomeres overlap within the M-band, where they are interconnected by M-band proteins8. Thus, titin filaments with opposite polarity overlap in both Z-disk and M-band, forming a contiguous filament along the myofibril. In this review, we discuss titin's functions in the heart, with an emphasis on its role in diastolic function and the various mechanisms whereby passive stiffness can be tuned. Due to space constraints, it has not been possible to provide inclusive references to all original articles in the field. Figure 1 Schematic of titin in sarcomere. Differential splicing Titin is encoded by a single gene containing 368 exons. Multiple splice pathways in the I-band encoding region (∼230 exons) give rise to isoforms with different spring composition9. The three cardiac isoform classes are shown in Fig. 1. The relatively small ∼3.0 MDa isoform is known as N2B titin (it contains the N2B element)9. A second class also contains the N2A element, and is termed N2BA titin. N2BA titins have a longer PEVK segment and a variable number of additional Ig domains resulting in a ∼3.3-3.5 MDa size9. The third class includes isoforms that predominate in fetal-neonatal life which contain additional spring elements in both tandem Ig and PEVK regions, resulting in a ∼3.6-3.8 MDa size protein10-12. These isoforms gradually disappear during postnatal development. Regulation of the spring composition of titin in fetal-neonatal myocardium allows adjustment of diastolic filling properties during development.

Changes in passive tension after stretch of unexercised and eccentrically exercised human plantarflexor muscles

The study measured the effect of stretch on passive mechanical properties in unexercised and eccentrically exercised plantarflexor muscles, to obtain insight into how stretch might serve athletes as a warm-up strategy. Passive torque, voluntary contraction strength and muscle soreness were measured before and after a large amplitude stretch given before and after a period of eccentric exercise and at 0, 1, 2 and 24 h later. Stretch of the unexercised muscle led to a 20% fall in passive torque which recovered within an hour. About 40% of the fall could be recovered immediately with a voluntary contraction. After eccentric exercise there was a rise in passive torque by 20% at 2 h post-exercise. This rise was postulated to result from an injury contracture in muscle fibres damaged by the exercise. It was accompanied by a fall in maximum voluntary torque and the development of muscle soreness at 24 h. Stretch of the exercised muscle led to a fall in passive torque and rise in pain threshold. It is proposed that in response to a stretch there is a fall in passive tension in the muscle due to stable cross-bridges in sarcomeres which could be recovered with a voluntary contraction and an additional component attributable to the elastic filament, titin. The size of the fall was not significantly different between exercised and unexercised muscle. These observations provide a physiological basis for the effects of passive stretches on skeletal muscle and help to explain why they are used as a popular warm-up strategy.

Abstract 924: Aging Induces Titin Oxidation And Increases Passive Cardiomyocyte Stiffness

One of the hallmarks of aging is an increase in ventricular passive stiffness leading to diastolic heart failure, however, the molecular basis for this is unclear. The giant elastic protein titin, working as an entropic spring, is the major determinant of passive cardiomyocyte stiffness. We hypothesized that accumulation of oxidized titin in the aging heart results in increased cardiomyocyte passive stiffness and thereby contributes to diastolic dysfunction. We further hypothesized that an age-assocated disturbance in the ubiquitin/proteasome pathway plays a role in the accumulation of oxidized titin. Methods: Cardiomyocytes from adult (4 month) and aging (34 month) mouse hearts were isolated and chemically skinned and the passive force-sarcomere length relationship in single cells were obtained. Post-translational modification of titin was assessed in whole heart homogenates by determining the content of 1) titin carbonyls, a marker of irreversible protein oxidation, and 2) titin ubiquitinylation, a marker for proteasomal degradation. Results: Cardiomyocyte passive tension was significantly higher in the aging group (at SL=2.45 μm, 1008.4 ± 45.5 vs. 871.6 ± 48.3 μg; p&lt;0.05). While the total amount of titin was unchanged between both groups, the carbonyl content of titin was increased 3-fold with aging (p&lt;0.05). High molecular weight ubiquitin-conjugated proteins were increased with aging, which is consistent with a decrease in proteasomal activity with age. Surprisingly, titin ubiquitinylation was decreased with aging suggesting an impairment upstream of the proteasome, in titin-specific ubiquitin ligase activity. Furthermore, the muscle specific ubiquitin ligase MURF-2, which has been shown to interact with titin and play a role in muscle protein turnover, showed a significant shift from a high to low molecular weight isoform with aging. Conclusion: Our data suggests that an age-associated impairment in titin turnover contributes to accumulation of oxidatively modified titins with consequent impairment of cardiomyocyte stiffness. We speculate that the oxidation of titin will change the elastic properties of titin, directly accounting for the change in passive tension and contributing to diastolic dysfunction associated with aging.

Passive mechanical properties of the medial gastrocnemius muscle of the cat.

1. This is a report on the history dependence of the passive mechanical properties of the medial gastrocnemius muscle of the anaesthetised cat. 2. The muscle was conditioned with an isometric contraction at the test length, or at 3 mm longer than the test length and then returned to the test length, where the level of resting tension was measured, as well as tension changes during a slow stretch. 3. The level of resting tension depended on the form of conditioning and, at the optimum length for active tension, the history-dependent component was 9 % of the total passive tension. 4. During a slow stretch, tension initially rose steeply up to a yield point, beyond which it rose more gradually. The shape of the tension rise depended on the form of conditioning. The level of tension at the yield point consisted of a stretch-dependent component, the 'short-range tension' plus the resting tension for that length. 5. The short-range tension increased with muscle length to peak close to the optimum for active tension. The slope of the tension rise during a stretch, the short-range stiffness, peaked at 2 mm beyond the optimum. 6. The short-range tension was small immediately after a conditioning contraction but grew in size as the interval was increased up to 60 s, with a time constant of 9.9 +/- 0.6 s. After a series of conditioning movements, it recovered more rapidly, with a time constant of 6.6 +/- 0.5 s. 7. The history-dependent changes in passive tension and the response to stretch are interpreted in terms of the presence, in sarcomeres of resting muscle fibres, of crossbridges between actin and myosin which have very slow formation rates, both at rest and during movements.

Changes in passive tension of muscle in humans and animals after eccentric exercise.

1. This is a report of experiments on ankle extensor muscles of human subjects and a parallel series on the medial gastrocnemius of the anaesthetised cat, investigating the origin of the rise in passive tension after a period of eccentric exercise. 2. Subjects exercised their triceps surae of one leg eccentrically by walking backwards on an inclined, forward-moving treadmill. Concentric exercise required walking forwards on a backwards-moving treadmill. For all subjects the other leg acted as a control. 3. Immediately after both eccentric and concentric exercise there was a significant drop in peak active torque, but only after eccentric exercise was this accompanied by a shift in optimum angle for torque generation and a rise in passive torque. In the eccentrically exercised group some swelling and soreness developed but not until 24 h post-exercise. 4. In the animal experiments the contracting muscle was stretched by 6 mm at 50 mm s(-1) over a length range symmetrical about the optimum length for tension generation. Measurements of passive tension were made before and after the eccentric contractions, using small stretches to a range of muscle lengths, or with large stretches covering the full physiological range. 5. After 150 eccentric contractions, passive tension was significantly elevated over most of the range of lengths. Measurements of work absorption during stretch-release cycles showed significant increases after the contractions. 6. It is suggested that the rise in passive tension in both human and animal muscles after eccentric contractions is the result of development of injury contractures in damaged muscle fibres.

Differential changes in ACh-, motilin-, substance P-, and K(+)-induced contractility in rabbit colitis.

To test the hypothesis that the changes in intestinal contractility, which accompany inflammation of the gut, are agonist specific, we compared the response of inflamed strips to substance P (SP), motilin, ACh, and K(+) as a function of time. In parallel experiments, changes in the general mechanical properties (passive tension, optimal stretch) of the colitic tissue were evaluated. Colitis was induced by trinitrobenzenesulfonic acid, and rabbits were killed after 1, 2, 3, 5, or 8 days. Passive tension was increased starting from day 2 until day 8, and maximal active tension (T(max)) was generated at less stretch from day 5. A 50% decrease in T(max) was observed for ACh and K(+) between days 2 and 3 and for motilin and SP between days 3 and 5. For all compounds, T(max) returned to normal after 8 days. The pEC(50) value (negative logarithm of the concentration that induces 50% of the maximal contractile activity) for ACh was increased from day 3 until day 8 and for SP at day 3, whereas for motilin it was decreased at day 1. The changes in passive tension and optimal stretch indicate generalized structural alterations of smooth muscle tissue. However, the different time profiles of the changes in active tension and contractile potency for different contractile agents suggest that inflammation specifically affects receptor-mediated mechanisms.

Passive tension in rat hindlimb during suspension unloading and recovery: muscle/joint contributions.

Muscle/joint stiffness associated with disuse conditions or weightlessness may seriously impair movement and work capacity. The purposes of this study were 1) to develop a noninvasive model to measure rat hindlimb passive tension, 2) to describe changes in passive tension (i.e., flexibility) during whole body suspension and weight-bearing recovery, and 3) to determine relative contributions of the posterior hindlimb to passive tension. Male Sprague-Dawley rats were suspended (14 days) and reloaded (14 days). On days 0, 7, 14, 17, 21, and 28, animals were anesthetized and hindlimb passive tension was measured during ankle dorsiflexion. Seven days of suspension significantly increased passive tension. Recovery of passive tension occurred by 14 days of weight bearing. In suspended animals, increased passive tension was due to musculotendinous units (75%) rather than to the joint (25%). Increased passive tension did not appear to be due to a shorter muscle, but changes in muscle architecture, cytoskeletal proteins, or viscoelastic properties of the muscle and its connective tissue elements cannot be excluded.

A LOW PASS FILTER WITH AMPLIFIER FOR MEASUREMENT OF ACTIVE AND PASSIVE TENSIONS OF SKELETAL MUSCLE IN VITRO

When displaying and measuring passive and active twitch tensions developed by skeletal muscle in vitro, the problems of amplification may be resolved by recording two traces. One, recorded at relatively low gain, is used for measurements of twitch tension amplitude. The other, recorded simultaneously, is a modified version of the first trace, in which the voltage signals are passed through a suitably constructed low pass filter, amplified and displayed. This second trace, recorded at relatively high gain, is used for measurements of changes in passive tension and contracture responses of relatively small amplitude.