shortening velocity
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Introduction. One of the risk factors for cardiovascular diseases is the toxic metal pollution of the industrial area and the environment. Lead is the most critical of toxic metals. In industrial conditions, the body’s exposure to harmful substances is often combined with muscular work of varying severity. It has not been studied enough how these combinations influence the development of pathological processes associated with harmful exposure. Materials and methods. The subchronic experiment was carried out on white outbred male rats for six weeks. Intoxication was simulated by repeated intraperitoneal injections of lead acetate three times a week. Running was chosen to model the muscle exercise at a 25 m/min speed for 10 minutes 5 days a week. We performed biochemical and electrocardiographic studies. Blood pressure parameters were recorded. Muscle contractility was studied on isolated multicellular preparations of the right ventricular myocardium in isometric and physiological contraction modes. The ratio of myosin heavy chains was determined by the polyacrylamide gel electrophoresis. The sliding velocity of reconstituted thin filaments on myosin using an in vitro motility assay. Results. Physical exercise under lead intoxication normalized the level of calcium and the angiotensin-converting enzyme activity in the blood serum, the voltage of the isoelectric line and the amplitude of the T wave on the electrocardiogram. The combined action of lead and physical exercise showed an increase in the creatinine kinase-MB level. We found that the effect of exercise under lead intoxication on myocardial contractility was ambiguous. The maximum isotonic shortening velocity in trabeculae was normalized, but the maximum rate of strength development in the isometric mode in the papillary muscles decreased to a greater extent than under lead intoxication. The maximum sliding velocity of reconstituted thin filaments and myosin and the heavy chain ratio was partly normalized. Conclusion. In general, muscle exercise attenuated the lead cardiotoxic effects.

AbstractPennate muscle is characterized by muscle fibers that are oriented at a certain angle (pennation angle) relative to the muscle’s line of action and rotation during contraction. This fiber rotation amplifies the shortening velocity of muscle, to match loading conditions without any control system. This unique variable gearing mechanism, which characterized by Architecture Gear Ratio (AGR), is involves complex interaction among three key elements: muscle fibers, connective tissue, and the pennation angle. However, how three elements determine the AGR of muscle-like actuator is still unknown. This study introduces a Himisk actuator that arranges five contractile units at a certain pennation angle in a flexible matrix, the experiment and simulation results demonstrated that the proposed actuator could vary AGR automatically in response to variable loading conditions. Based on this actuator, we present a series of actuators by simulations with the varying pennation angle (P), elastic modulus of the flexible matrix (E), and number of contractile units (N) to analyze their effects on AGR, and their interaction by three-factor analysis of variance. The results demonstrated that P and N effect on the AGR significantly, while E effects on AGR slightly, which supported the idea that the P is the essential factor for the AGR, and N is also an important factor due to the capability of force generation. This provides a better understanding of mechanical behavior and an effective optimizing strategy to muscle-like soft actuator.

During jumping by kangaroo rats, the musculotendon work contributions across all joints are not well understood. Namely, measures of external joint work do not provide information on the contributions from individual muscles or in-series elastic structures. In this study, we examined the functional roles of a major ankle extensor muscle, lateral gastrocnemius (LG), and of a major knee extensor muscle, vastus lateralis (VL), through in vivo sonomicrometry and electromyography techniques, during vertical jumping by kangaroo rats. Our data showed that both muscles increased shortening and activity with higher jumps. We found that knee angular velocity and VL muscle shortening velocity were coupled in time. In contrast, the ankle angular velocity and LG muscle shortening velocity were decoupled, and rapid joint extension near the end of the jump produced high power outputs at the ankle joint. Further, the decoupling of muscle and joint kinematics allowed the LG muscle to prolong the period of shortening velocity near optimal velocity (Vopt), which likely enabled the muscle to sustain maximal power generation. These observations were consistent with a LG tendon that is much more compliant than that of the VL.

Abstract Introduction Ventricular arrhythmias (VA) and heart failure (HF) are the major complications following myocardial infarction (MI). In both conditions, there is a key role for perturbed calcium homeostasis of which the underlying mechanisms remain unclear. A preclinical model that faithfully presents most of the features of MI-induced HF has been lacking. The complexity of this syndrome means that animal modelling is difficult. As the hearts of large animals share many electrophysiological similarities to humans, ovine modelling of cardiac diseases could better reflect human pathologies than in small mammals. Question Is it possible to develop a clinically relevant ovine model with moderate cardiac dysfunction following myocardial infarction? Methods MI was induced in sheep by inflating an angioplasty balloon distal to the second diagonal branch of the left anterior descending artery for 90 min. Cardiac function was monitored for 20 weeks using electrocardiography (ECG), echocardiography, blood biochemical analysis, and subjective signs of cardiac deterioration (lethargy, dyspnoea, and cough). 20 weeks post-MI, the animals were humanely killed and single left ventricular myocytes were isolated from the infarct border zone. Changes in cellular electrophysiology and intracellular calcium concentration were monitored using whole-cell patch technique in voltage-clamp mode and the calcium sensitive fluorescent indicator Fura-2 (K5 salt). Results By using minimally invasive procedures, we obtained a survival rate of 80% (n=15). During surgery, our data show clinical features of ischaemia, including changes in the ECG features (elevation of the ST and T segment, left bundle branch block and/or pathological Q waves) and elevation of the cardiac biomarker such as troponin I. Following MI, we observed a decline in ejection fraction (−25±3%, p<0.0001) and an increase in whole animal arrhythmias (incidence of VA 72 hours post-MI, ∼70%). On cardiac removal apico-septal transmural necrosis / scarring was evident. Importantly, the L-type calcium current (ICaL) was decreased in MI cells compared to healthy cells (−1.87±0.73 pA/pF, p<0.05), but isoprenaline had no effet on ICaL (0.48±1.2 pA/pF, p=0.70) in MI cells. Moreover, the amplitude of the systolic calcium transient (−0.33±0.1 F/F0, p<0.05) and the sarcoplasmic reticulum calcium content (−23±7 μmol/L, p<0.01) were also decreased. The shortening velocity of the sarcomere was also decreased in MI cells (−0.55±0.18 μm/s, p<0.01). Conclusion We successfully established an ovine MI model using minimally invasive procedure which displays a moderately impaired cardiac function, reduced contractility, and pro-arrhythmic electrophysiological remodelling. Future analysis will examine the role of the L-type calcium channel with respect to the excitation-contraction coupling process and myocyte contractility and how we can improve therapeutic strategies towards VA and HF. FUNDunding Acknowledgement Type of funding sources: Foundation. Main funding source(s): British Heart Foundation

Changes in muscle shape could play an important role during contraction allowing to circumvent some limits imposed by the fascicle force–velocity (F–V) and power–velocity (P–V) relationships. Indeed, during low-force high-velocity contractions, muscle belly shortening velocity could exceed muscle fascicles shortening velocity, allowing the muscles to operate at higher F–V and P–V potentials (i.e., at a higher fraction of maximal force/power in accordance to the F–V and P–V relationships). By using an ultrafast ultrasound, we investigated the role of muscle shape changes (vastus lateralis) in determining belly gearing (muscle belly velocity/fascicle velocity) and the explosive torque during explosive dynamic contractions (EDC) at angular accelerations ranging from 1000 to 4000°.s–2. By means of ultrasound and dynamometric data, the F–V and P–V relationships both for fascicles and for the muscle belly were assessed. During EDC, fascicle velocity, belly velocity, belly gearing, and knee extensors torque data were analysed from 0 to 150 ms after torque onset; the fascicles and belly F–V and P–V potentials were thus calculated for each EDC. Absolute torque decreased as a function of angular acceleration (from 80 to 71 Nm, for EDC at 1000 and 4000°.s–1, respectively), whereas fascicle velocity and belly velocity increased with angular acceleration (P < 0.001). Belly gearing increased from 1.11 to 1.23 (or EDC at 1000 and 4000°.s–1, respectively) and was positively corelated with the changes in muscle thickness and pennation angle (the changes in latter two equally contributing to belly gearing changes). For the same amount of muscle’s mechanical output (force or power), the fascicles operated at higher F–V and P–V potential than the muscle belly (e.g., P–V potential from 0.70 to 0.56 for fascicles and from 0.65 to 0.41 for the muscle belly, respectively). The present results experimentally demonstrate that belly gearing could play an important role during explosive contractions, accommodating the largest part of changes in contraction velocity and allowing the fascicle to operate at higher F–V and P–V potentials.

AbstractMaximal muscular power production is of fundamental importance to human functional capacity and feats of performance. Here, we present a synthesis of literature pertaining to physiological systems that limit maximal muscular power during cyclic actions characteristic of locomotor behaviours, and how they adapt to training. Maximal, cyclic muscular power is known to be the main determinant of sprint cycling performance, and therefore we present this synthesis in the context of sprint cycling. Cyclical power is interactively constrained by force-velocity properties (i.e. maximum force and maximum shortening velocity), activation-relaxation kinetics and muscle coordination across the continuum of cycle frequencies, with the relative influence of each factor being frequency dependent. Muscle cross-sectional area and fibre composition appear to be the most prominent properties influencing maximal muscular power and the power-frequency relationship. Due to the role of muscle fibre composition in determining maximum shortening velocity and activation-relaxation kinetics, it remains unclear how improvable these properties are with training. Increases in maximal muscular power may therefore arise primarily from improvements in maximum force production and neuromuscular coordination via appropriate training. Because maximal efforts may need to be sustained for ~15-60 s within sprint cycling competition, the ability to attenuate fatigue-related power loss is also critical to performance. Within this context, the fatigued state is characterised by impairments in force-velocity properties and activation-relaxation kinetics. A suppression and leftward shift of the power-frequency relationship is subsequently observed. It is not clear if rates of power loss can be improved with training, even in the presence adaptations associated with fatigue-resistance. Increasing maximum power may be most efficacious for improving sustained power during brief maximal efforts, although the inclusion of sprint interval training likely remains beneficial. Therefore, evidence from sprint cycling indicates that brief maximal muscular power production under cyclical conditions can be readily improved via appropriate training, with direct implications for sprint cycling as well as other athletic and health-related pursuits.

[Purpose] The purpose of this study was to investigate the effects of a high-fat high-sucrose (HFHS) diet on previously reported adaptations of cardiac morphological and contractile properties to resistance training.[Methods] Twelve-week-old rats participated in 12-weeks of resistance exercise training and consumed an HFHS diet. Echocardiography and skinned cardiac muscle fiber bundle testing were performed to determine the structural and mechanical adaptations.[Results] Compared to chow-fed sedentary animals, both HFHS- and chow-fed resistance-trained animals had thicker left ventricular walls. Isolated trabecular fiber bundles from chow-fed resistance-trained animals had greater force output, shortening velocities, and calcium sensitivities than those of chow-fed sedentary controls. However, trabeculae from the HFHS resistance-trained animals had greater force output but no change in unloaded shortening velocity or calcium sensitivity than those of the chow-fed sedentary group animals.[Conclusion] Resistance exercise training led to positive structural and mechanical adaptations of the heart, which were partly offset by the HFHS diet.

Abstract Introduction: Fatigue is defined as a loss in the capacity for developing force and/or velocity of a muscle which is reversible by rest. The aim was to evaluate non-invasively the fatigue and recovery of the inspiratory ribcage muscles during two endurance tests in healthy subjects. Methods: 22 subjects were evaluated before, during and after performing a respiratory endurance test with normocapnic hyperpnea (NH) and inspiratory pressure threshold load (IPTL). Simultaneous measurements of muscle activity (electromyography), tissue oxygenation (NIRS), pressure (nasal inspiratory pressure), and volume (optoelectronic plethysmography) were performed. Results: There was a decrease in the maximum relaxation rate (MRR) and increase in the time constant (τ) after the IPTL test (p <0.05) and a decrease in the peak pressure generated in SNIP after both protocols (p <0.05). Additionally, there was a decrease in shortening velocity and mechanical power only after the IPTL test (p <0.05). The inspiratory ribcage muscles showed a linear drop in the median frequency in the IPTL test and an exponential drop in the NH test, which was not significant for the development of fatigue and there was a linear increase in the NIRS variables in both protocols. Conclusion: It was concluded that the inspiratory ribcage muscles undergo changes after performing an endurance test with NH and IPTL. Additionally, the development of fatigue in these muscles and their consequent changes are more evident in the protocol with IPTL.

AbstractMuscle fatigue is a complex phenomenon enclosing various mechanisms. Despite technological advances, these mechanisms are still not fully understood in vivo. Here, simultaneous measurements of pressure, volume, and ribcage inspiratory muscle activity were performed non-invasively during fatigue (inspiratory threshold valve set at 70% of maximal inspiratory pressure) and recovery to verify if inspiratory ribcage muscle fatigue (1) leads to slowing of contraction and relaxation properties of ribcage muscles and (2) alters median frequency and high-to-low frequency ratio (H/L). During the fatigue protocol, sternocleidomastoid showed the fastest decrease in median frequency and slowest decrease in H/L. Fatigue was also characterized by a reduction in the relative power of the high-frequency and increase of the low-frequency. During recovery, changes in mechanical power were due to changes in shortening velocity with long-lasting reduction in pressure generation, and slowing of relaxation [i.e., tau (τ), half-relaxation time (½RT), and maximum relaxation rate (MRR)] was observed with no significant changes in contractile properties. Recovery of median frequency was faster than H/L, and relaxation rates correlated with shortening velocity and mechanical power of inspiratory ribcage muscles; however, with different time courses. Time constant of the inspiratory ribcage muscles during fatigue and recovery is not uniform (i.e., different inspiratory muscles may have different underlying mechanisms of fatigue), and MRR, ½RT, and τ are not only useful predictors of inspiratory ribcage muscle recovery but may also share common underlying mechanisms with shortening velocity.