Active Length-tension Relationships Research Articles

The effect of varying musculotendinous length on the construction of triceps surae length-tension curves

Introduction: Exercise-induced muscle damage (EIMD) occurs after a bout of unaccustomed exercise, which has effects that peak approximately two days post exercise. Uncertainty exists about the mechanisms and the reliability of some measures of EIMD. A change in the active length-tension relationship of a muscle is often used as a determinant of EIMD, but can be difficult to measure in-vivo. The aim of this experiment was to determine if active length–tension curves could be accurately constructed from the triceps surae muscle group, in vivo, using a commercially available isokinetic dynamometer.

Whole muscle length-tension relationships are accurately modeled as scaled sarcomeres in rabbit hindlimb muscles

An a priori model of the whole active muscle length-tension relationship was constructed utilizing only myofilament length and serial sarcomere number for rabbit tibialis anterior (TA), extensor digitorum longus (EDL), and extensor digitorum II (EDII) muscles. Passive tension was modeled with a two-element Hill-type model. Experimental length-tension relations were then measured for each of these muscles and compared to predictions. The model was able to accurately capture the active-tension characteristics of experimentally-measured data for all muscles (ICC=0.88±0.03). Despite their varied architecture, no differences in predicted versus experimental correlations were observed among muscles. In addition, the model demonstrated that excursion, quantified by full-width-at-half-maximum (FWHM) of the active length-tension relationship, scaled linearly (slope=0.68) with normalized muscle fiber length. Experimental and theoretical FWHM values agreed well with an intraclass correlation coefficient of 0.99 ( p<0.001). In contrast to active tension, the passive tension model deviated from experimentally-measured values and thus, was not an accurate predictor of passive tension (ICC=0.70±0.07). These data demonstrate that modeling muscle as a scaled sarcomere provides accurate active functional but not passive functional predictions for rabbit TA, EDL, and EDII muscles and call into question the need for more complex modeling assumptions often proposed.

Length-Tension Relationships Are Similar Between Cardiac Myocytes And Skeletal Muscle Fibers

According to the Frank-Starling relationship increased ventricular volume increases ventricular output, which helps match peripheral energy supply with demand. The cellular basis for this relationship is, in large part, the myofilament length-tension relationship. The length-tension relationship in maximally activated skinned preparations is relatively shallow and similar between cardiac myocytes and skeletal muscle fibers. During twitch activations the length tension relationship becomes steeper in both cardiac and skeletal muscle; however, it remains unclear whether length dependence of tension differs between striated muscle cell types during submaximal activations. The purpose of this study was to compare myofilament length-tension relationships between cardiac myocytes, fast-twitch and slow twitch skeletal muscle fibers during half-maximal calcium activations. For these experiments, passive and active sarcomere length-tension relationships were characterized in skinned rat left ventricular cardiac myocytes, fast-twitch and slow-twitch skeletal muscle fibers. For active length-tension relationships, cells were mounted between a force transducer and motor and activated to yield 50-65% maximal force after which isometric force was measured over a range of ascending limb sarcomere lengths monitored by IonOptix SarLen system. Passive tension was considerably greater in cardiac myocytes (3.5 ± 2.5 kN/m2 at 2.30 ± 0.04μm) compared to both fast-twitch (1.1 ± 0.8 kN/m2 at 2.70 ± 0.07μm) and slow-twitch (1.4 ± 0.5 kN/m2 at 2.70 ± 0.07μm) muscle fibers. Active myofilament length-tension relationships were considerably shallower in slow-twitch fibers compared to fast-twitch fibers. Interestingly, cardiac myocytes exhibited two distinct populations of length-tension relationships, one nearly identical to fast-twitch fibers and the other similar to slow-twitch fibers. These results indicate that cardiac myocytes exhibit length-tension relationships very similar to skeletal muscle fibers. The finding of two populations of cardiac myocyte length-tension relationships suggests a mode for adjusting Frank-Starling relationships following acute and/or chronic ventricular adaptations.

Length-tension relationships of small arteries, veins, and lymphatics from the rat mesenteric microcirculation

The passive and active length-tension relationships of isolated rat mesenteric lymphatics ( approximately 150 microm ID), and adjacent small arteries ( approximately 240 microm) and veins ( approximately 275 microm) were compared under isometric conditions using a wire myograph. About 60% of the lymphatic vessels developed spontaneous contractions in physiological saline solution at nominal preload. To maximally activate smooth muscle, 145 mM K(+) + 5 x 10(-5) M norepinephrine was used for arteries, and 145 mM K(+) + 1 x 10(-6) M substance P was used for lymphatics and veins. In response, arteries exhibited monotonic force development to a plateau level, whereas lymphatics and veins showed biphasic force development, consisting of a transient force peak followed by partial relaxation to a plateau over approximately 5 min. The passive and the active length-tension curves were similar in shape among all three vessels. However, the maximal active tension of arteries (3.4 +/- 0.42 mN/mm) was significantly greater than peak active tension (0.59 +/- 0.04 mN/mm) or plateau tension (0.20 +/- 0.04 mN/mm) in small veins and greater than peak active tension (0.34 +/- 0.02 mN/mm) or plateau tension (0.21 +/- 0.02 mN/mm) in lymphatics. Maximal active medial wall stress was similar between lymphatics and veins but was approximately fivefold higher in small arteries. For lymphatics, the pressure calculated from the optimal preload was significantly higher than that found previously in isobaric studies of isolated lymphatics, suggesting the capacity to operate at higher than normal pressures for increased responsiveness. Our results represent the first mechanical comparisons of arterial, venous, and lymphatic vessels in the same vasculature.

The Impact of Mechanical Ventilation on Immature Airway Smooth Muscle: Functional, Structural, Histological, and Molecular Correlates

Preterm infants exposed to mechanical ventilation often develop airway dysfunction and bronchopulmonary dysplasia. The mechanisms of mechanical ventilation-induced airway injury are currently unknown. This study correlates the age-related effects of mechanical ventilation on airway function with structural alterations at the tissue, cellular, ultrastructural, and molecular levels. Mechanically ventilated and nonventilated tracheal rings were obtained from premature and newborn lambs. In tissue baths, the passive and active length-tension relationships and dose-response characteristics of the tracheal rings were determined. Fixed tracheal rings were digested and the resulting isolated smooth muscle cells measured. Rings were analyzed by light and electron microscopy. Additionally, protein was extracted from the tracheal smooth muscle and myosin heavy chain isoforms were separated by SDS-polyacrylamide gel electrophoresis and analyzed by densitometry. Mechanical ventilation resulted in a significant decrease of both the slope of the passive length-stress relationship and of maximal force generation, with both effects being most pronounced in the newborn age group. These age-related functional alterations correlated with a decrease in smooth muscle cell length and a disruption of ultrastructural architecture, which were also most pronounced in the older groups. Furthermore, mechanical ventilation resulted in epithelial denudation at all ages. There were no acute statistically significant effects of mechanical ventilation on myosin heavy chain isoform expression. This study demonstrates age-related effects of mechanical ventilation on the passive and active characteristics of tracheal function and provides a structural analysis of potential mechanisms. The mechanisms behind these functional differences involve ultrastructural changes in cell length, tissue matrix, and disruption of epithelial integrity. These findings help elucidate the pathogenesis of ventilator-induced airway injury.

Rises in whole muscle passive tension of mammalian muscle after eccentric contractions at different lengths.

This is a report of experiments carried out on the medial gastrocnemius muscle of the anesthetized cat, investigating the effects of eccentric contractions carried out at different muscle lengths on the passive and active length-tension relationships. In one series of experiments, the motor supply to the muscle was divided into three approximately equal parts; in the other, whole muscles were used. Fifty eccentric contractions were carried out over different regions of the active length-tension curve for each partial or whole muscle. Active and passive length-tension curves were measured before and after the eccentric contractions. When eccentric contractions were carried out at longer lengths, there was a larger shift of the optimum length for active tension in the direction of longer muscle lengths and a larger fall in peak isometric tension. Passive tension was higher immediately after the eccentric contractions, and if the muscle was left undisturbed for 40 min, it increased further to higher values, particularly after contractions at longer lengths. A series of 20 passive stretches of the same speed and amplitude and covering the same length range as the active stretches, reduced the passive tension which redeveloped over a subsequent 40-min period. It is hypothesized that there are two factors influencing the level of passive tension in a muscle after a series of eccentric contractions. One is injury contractures in damaged muscle fibers tending to raise passive tension; the other is the presence of disrupted sarcomeres in series with still-functioning sarcomeres tending to reduce it.

New animal model for the study of postmenopausal coronary and cerebral artery function: the Watanabe heritable hyperlipidemic rabbit fed on a diet avoiding phytoestrogens

Objective: To evaluate the effect of estrogen replacement therapy (ERT) on the functional characteristics of coronary and cerebral arteries in a new rabbit model for postmenopausal vascular function.Methods: Female ovariectomized Watanabe heritable hyperlipidemic (WHHL) rabbits were randomized to treatment for 16 weeks with either 17β-estradiol or placebo. The chow used was semi-synthetic,thereby avoiding the influence of phytoestrogens. Ring segments of cerebral and coronary arteries were mounted for isometric tension recordings in myographs. The passive and active length-tension relationshipsfor electromechanical (high potassium), pharmacomechanical (histamine) and combined electro- and pharmacomechanical (high potassium plus histamine) contraction were evaluated.Results: Treatmentwith 17β-estradiol significantly changed the active length-tension relationship for the electromechanical response in the proximal coronary arteries. No changes were observed for the passive length-tensionrelationships.Conclusions: Long-term treatment with 17β-estradiol lowered the electromechanical tonus of atherosclerotic coronary arteries proximally, where the atherosclerosis is mostdeveloped. This could be one of the mechanisms behind the putative protective effect of hormone replacement therapy against ischemic heart disease. The study presents a promising new animal model for theinvestigation of postmenopausal coronary and cerebral artery function. The data correspond well with epidemiological observations in postmenopausal women.

Effect of ischemia and partial outflow obstruction on rat bladder function.

We investigated the effects of ischemia induced by ligation of the bilateral internal iliac arteries following partial outlet obstruction on changes in detrusor function in rat. Rats were divided into three groups: sham-operated control rats, rats with partial outlet obstruction, and rats with obstruction+ischemia. Bladder function was studied by the in vitro organ bath technique 7 days after surgery. The weight of the bladder was significantly increased in both the obstruction and obstruction+ischemia groups. The obstruction+ischemia group exhibited a greater increase in weight. The passive length-tension relationship of detrusor muscle strips showed that tissue elasticity was decreased and the active length-tension relationship demonstrated that the peak response was observed at a shorter tissue length in the obstruction+ischemia group compared with the other two groups. There was no difference in the passive and active length-tension relationships between the control group and the obstruction group. The contractile response to various kinds of stimulation (field stimulation, bethanechol, ATP, and KCl) increased in the obstruction group and decreased in the obstruction+ischemia group. These findings suggest that partial outflow obstruction alone increased bladder contractility in response to stimuli. However, ischemia reduced the contractility and elasticity of the bladder wall.

Incorporation of muscle architecture into the muscle length-tension relationship

A mathematical model of the muscle active length-tension relationship has been developed. It integrates the functional basis of different muscle arrangements into a mathematical description of the contractile element. The model is complex enough to represent many of the mechanical and architectural properties of active muscle. Yet, it is simple enough that only two parameters (muscle fiber optimal length, muscle belly optimal length) are needed to scale the model to a specific actuator.

The active length-tension relationship in human uterine muscle

The active length-tension relationship in standard strips of human myometrium was studied using constant velocities of elongation to stretch the muscle and electrical stimulation to induce contraction. The position of the active tension maximum was not directly related to the length of the muscle but upon the tension developed in the passively stretched muscle. The position of the passive length-tension curve could be varied by changing the velocity of elongation, by sequential pulls, and by stress relaxation at a constant length. The peak of active tension occurred at a point on the passive tension curve of 15.0 Gm. ± 6.2 for the pregnant and 14.1 Gm. ± 7.6 for the nonpregnant uterus.