In this section, our goal is to illustrate the analysis of the discrete system presented in the previous section for the Huxley’57 model and the Piazzesi–Lombardi’95 model, which we chose as a representative of the multi-site, multi-state models. These illustrations serve several purposes. We ﬁrst want to demonstrate that the thermodynamics identities established at the discrete level are satisﬁed in the numerical simulations. Then, we want to show that the ability to compute the thermodynamical balances numerically allows to gain additional insight into the physiology of musclecontraction. Additionally, for the Piazzesi–Lombardi’95 model, we compare our simulation results with that obtained in the original paper as a further validation of our approach.
The fatigue slope (Slope T50) and the fatigable area under the curve (F AUCT50) are useful parameters to describe muscle functionality in this test. The calcula- tion of functional indices of approximate force contribu- tions of fatigable and fatigue-resistant muscle fibers may enable us to distinguish functional drug effects on myo- fiber subtypes. However, using Fmin as a cutoff to approximate the contribution of fatigue-resistant muscle fibers to the total force before the curve center is likely to result in an underestimate, because those fibers do show some fatiguing during the latter part of the muscle fatiguing test. Therefore the fatigable index might also be higher than estimated. In the Dex study, this effect might skew the comparison of the functional index ratios between vehicle and Dex treated groups, since Fmin is very similar in both groups and therefore rela- tively larger in the weaker Dex treated rats. Nonetheless, comparing functional indices and their ratios within a study should provide relevant information about differ- ences in fiber type composition of the tested leg muscles.
Knee is the largest and most complicated joint in human body, which plays an important role in human motions. Currently, there are few musculoskeletal models for knee joint have been developed. Moreover, some researchers did not study the subject- specific musculoskeletal geometry, which is vital to calculate musclecontraction force and to understand each muscle’s contribution to total muscular torque. To match specific subjects, the geometry path can be scaled based on relative distances between pairs of markers obtained from a motion-capture system. However, the motion-capture system is quite expensive. Furthermore, the applications of these models were limited to clinical diagnosis and management of orthopaedic conditions. 12, 16 Hence, their potential
It is generally accepted that combat sports ath- letes strive to improve their muscle perfor- mance, however, they also habitually attempt to reduce their body-mass before the competi- tion voluntarily. The integration of such delete- rious, physically stressful factors may promote the exercise-induced muscle damage (EIMD). The EIMD is usually associated with muscle fatigue, increased plasma levels of muscle proteins, mus- cle fibre damage, inflammation and impairments in muscle functioning . Currently, invasive blood sampling is the most frequently reported diagnostic tool used to monitor the EIMD and denote muscle fatigue in athletes . In this con- text, Magal et al.  showed that muscle sore- ness after eccentrically induced EIMD response was positively related to fibre type distribution (r = 0.51, p=0.04), whereas there was no correla- tion between fibre type distribution and creatine kinase (CK) activity. This may be due to a greater recruitment of type II muscle fibres in the high- intensity eccentric exercise that is commonly used in controlled EIMD studies. Furthermore, type II fibres have been found to be more sus- ceptible to disruption compared to type I, indi- cating that athletes with a greater proportion of type II muscle fibres might also facilitate higher EIMD responses in other models for inducing the EIMD response [3-5].
Prior to the 1950s, it had been assumed that muscle activation and force production were associated with the shortening of the thick filaments in the centre of sarcomeres. It was thought that activation (calcium release) caused the myosin filaments that comprise the thick, A-band filaments to be transformed from a helix-like configuration into a coil-like configuration (Fig. 1), thereby causing muscle shortening and force production. Specifically, the long myosin filaments that were aligned in long strands were thought to undergo calcium-induced shortening at specific points, thereby producing muscle activation. However, Hugh Huxley hinted at the idea that thick filaments did not shorten upon activation (Huxley, 1953), and he and Andrew Huxley then published their seminal work on the sliding filament theory (Huxley and Niedergerke, 1954; Huxley and Hanson, 1954) where they argued independently that thick filaments did not shorten. Rather, they suggested that musclecontraction occurred through the relative sliding of the thick and thin filaments (Fig. 1). Three years later, Andrew Huxley then provided the first molecular and mathematical framework of how this relative sliding of the two sets of filaments was supposed to occur: the cross-bridge theory (Huxley, 1957). His theory was based on the idea that there are uniformly arranged side projections (cross-bridges) on the thick filaments that interact cyclically with specific attachment points on the thin filaments, thereby pulling the thin past the thick filaments. These interactions by the cross-bridges were driven partially by Brownian motion and partially by the hydrolysis of adenosine triphosphate (ATP), one ATP per cross-bridge cycle. The theory proposed in 1957 had two cross-bridge states, one attached and one detached. Hugh Huxley then proposed that cross- bridge action likely involved rotation (Huxley, 1969), a concept adapted by Andrew Huxley and extended to multiple attachment states (Huxley and Simmons, 1971). This multiple-state model had the advantage that it could explain force transients following quick stretches or releases. Although cross-bridge models with more than 20 states have been described in the literature, commonly cross- bridge action and musclecontraction are described by models that
The uterus is the pivotal organ responsible for reproduction, it is responsible for the implantation of the fertilised embryo, where it then sustains the growing foetus and at term the myometrium becomes active in order to expel the foetus. The human uterus is a pear shaped organ, around 6-8cm long in the non-pregnant state, and consists of three layers; the serosa, endometrium, and the smooth muscle layer the myometrium. Despite the big difference between the human and Wistar rat (Rattus norvegicus) in gross anatomy, at the myometrial level they are remarkably similar. The human uterus is a simplex, consisting of one single organ, while the uterus of the Wistar rat along with other rodents and primitive mammals is duplex. As such they possess two uterine horns, each leading from an ovary to the vagina, allowing for multiple offspring (Figure 1.1.a).
removed. Contractions caused by potassium depolarization also were depressed, indicating the effect of IL-1 is not specific to the alpha-adrenoceptor agonist. The inhibitory effect of IL- 1 was concentration-dependent (0.2 to 20 ng/ml), and eliminated by pretreatment with cycloheximide (20 micrograms/ml). Indomethacin (10(-5) M) did not prevent the inhibition caused by IL-1. These studies identify IL-1 as a potent inhibitor of vascular contraction, via an endothelium-independent mechanism. Studies with inhibitors suggest that the action of IL-1 is independent of prostanoid synthesis, and may involve synthesis of protein.
The complex biomechanical actions, such as urination or voluntary control of defecation, cannot be completed in a normal manner if muscular or connective tissues have altered mechanical properties (passive and/or active). As the pelvic floor muscle resting tone decreases and connective tissue (ligament) laxity ensues, a significant anatomic distortion can develop, which could lead to a decrease in contractive capa- bilities and physiologic malfunction. Even more damaging can be the avulsion of pelvic floor muscle and more severe connective tissue disruption, which are not readily reversible without a surgical intervention. The intent of this manuscript is to demonstrate how one can evaluate these changes in the mechanical properties of pelvic floor structures (muscular and connective tissues) using vaginal tactile imaging to gain a better understanding of an individual patient’s pelvic floor dysfunction, and thereby ultimately improve guidance toward optimal selection from the various surgical and nonsurgical therapeutic choices available.
When the hand is in the correct position, mounted cush- ion pads (see 4a, 4 in Fig. 2) are moved towards the extremity (arm and hand) using spindles powered by elec- tro-motors (see 4b in Fig. 2d) and set into position. The power of the electro-motors is limited so that even with full power no harm could be done to the test subjects. The precise position of these cushions is determined by elec- tronic measurement recorders (see 4c in Fig. 2d), which save the positional information from the first session and can, therefore, automatically be moved into the exact position at later sessions [16-18]. The extremity setting design can take in right or left, pronated or supinated hands. If the examination of another muscle, for instance an adductor of the leg, is required the extremity setting module can be removed at the axle and another module specific for the setting of larger muscles can be mounted in its position. [16,17,19]
body wall muscles in ala1 (top left) and UAS-ala (top middle) larvae without prior heat-shock treatment, and ala1 (bottom left) and UAS-ala (bottom middle) after they were subjected to a 1 h heat-shock treatment at 37°C. Driving expression of ala peptide inhibitor in muscle tissue, independently of heat shock, did not attenuate the effects of DPKQDFMRFamide (top right) or in the controls (bottom right). The peptide was applied at the downward pointing arrows by continuous perfusion. (B) Left: average muscle tonus change induced by DPKQDFMRFamide in ala1 larvae and the control, UAS-ala larvae. Larvae of the two genetic lines showed similar increases in tonus in response to peptide treatment. Heat-shock treatment, which increases the expression of calcium/calmodulin- dependent protein kinase (CaMKII) inhibitory protein in ala1 flies, but not in UAS-ala flies, potentiated DPKQDFMRFamide-induced contractions in both ala1 and UAS-ala larvae (t-test for independent samples, *P<0.05). No significant difference was observed between the responses in heat-shocked ala1 and UAS- ala larvae (t-test for independent samples, P>0.05). Middle: average muscle tonus change induced by DPKQDFMRFamide (1 μmol l −1 ) in Canton-S larvae in
First, we observed that coordinated GDL activity is necessary for locomotion. We activated GDLs in all segments simultaneously by driving ChR2(T159C) (Berndt et al., 2011) with GDL-GAL4. All individual larvae stopped moving upon presentation of blue light (10 out of 10; [Figure 7A and Video 6]). Larval abdominal segments were paralyzed but, interestingly, they could still move their thoracic segments, which do not participate in peristaltic wave propagation. To control for a poten- tial startle response to blue light (Xiang et al., 2010), we confirmed these findings using thermoge- netics and dTRPA1 (Pulver et al., 2009). Larvae showed very slow and uncoordinated locomotion at a restrictive temperature at which dTRAPA1 expression is driven (32 ˚ C; p<0.001; Figure 7B–D). To determine the nature of this locomotion blockage, we activated all GDLs by ChR2(T159C) in a semi- intact preparation where we could monitor muscle contractions using mhc::GFP (Hughes and Thomas, 2007). We found that muscles relaxed when all GDLs were active (Figure 7E), contrary to the whole-body contraction (hunch) normally observed as part of the startle response elicited by blue light (Ohyama et al., 2013; Vogelstein et al., 2014). To exclude that neurons in the GDL- GAL4 expression pattern other than GDLs played a role in this muscle relaxation, we used tsh- GAL80 to suppress expression in abdominal segments, and this rescued the immobilization pheno- type (Video 6). These results were confirmed using optogenetic CsChrimson-mediated activation of GDLs and a different driver line, R15C11-LexA; this resulted in similar phenotypes (Figure 7—figure supplement 1 and Video 6).
independent of tail-beat frequency over a range of swimming speeds (Webb et ad. 1984). In contrast, the optimal strain amplitude for isolated flight muscle of the tobacco hawkmoth (Manduca sexta )t increases with temperature (Stevenson and Josephson, 1990). However, this again parallels the in vivo situation since low amplitude wing movements are used to warm the thoracic temperature prior to flight (Stevenson and Josephson, 1990). Electromyography of mackeral swimming at 1-14 bodylengths s”^ show that the number of muscle action potentials per cycle decreases with increasing swimming speed (C.S. Wardle pers. comm). The functional
We were unable to obtain rigorous measurements of wingbeat amplitude using lateral and dorsal views because a bird’s wingtip goes through a different arc than its humerus during flapping flight (Scholey, 1983). Amplitude of wingbeat may have varied inversely with frequency, thus maintaining constant contractile velocity during flapping, in agreement with the fixed-gear hypothesis (Rayner, 1985). However, in kinematic terms, a glide is a modified long-duration flap with an amplitude of 0 ˚ and a velocity of contraction of 0 m s 21 . We inferred the presence of isometric contractions of the pectoralis during glides in budgerigars by comparing simultaneous EMGs with wingtip position in lateral perspective (Fig. 6) (see also Goldspink et al. 1978). Whereas the progressive wing flexion during intermittent non-flapping phases reflects a continuum (Fig. 5), neuromuscular activity patterns clearly distinguish flap-gliding and flap- bounding flight. During glides (Fig. 6), the pectoralis was active, undergoing an isometric contraction. During bounds, (Fig. 7) the pectoralis was inactive. We consider intermediate-posture non-flapping periods to be modified bounds because the pectoralis muscle was always inactive during these phases. For glides, similar EMG patterns have been reported in herring gulls (Larus argentatus) (Goldspink et al. 1978) and American kestrels (Falco sparverius) (Meyers, 1991); however, our data provide the first insight into neuromuscular control during a bound.
acetylcholine produced tension and occurred at 80 V. Upper esophageal and gastric muscle were not inhibited. The inhibitory response of the LES muscle was antagonized by tetrodotoxin and hexamethonium but not by other specific antagonists. Adrenergic nerve destruction following 6-hydroxydopamine also did not abolish the LES inhibition. These data indicate that the distal esophagus, at the zone of the manometrically determined LES, is characterized by a nonadrenergic neural inhibitory system. We suggest that these nerves may mediate LES relaxation.
Inguinal structures, as living entities that move and func- tion cannot really be appreciated either by dissection on cadavers or operations on patients under general or spinal anaesthesia. Live demonstration of movements of the posterior wall and the musculo-aponeurotic structures around the inguinal canal during the acts of internal ab- dominal 'blows' (raised intra abdominal pressure) is so far not possible. Imaging of the inguinal canal in patients, with or without hernia, on sonography machines is also not satisfactory because of the small size of the canal and the fact that all structures are seen in black and white. Many operations developed to date deal only with the anatom- ical aspects of the repair. Any failure in these operations is be- cause the physiological aspects have not been considered while developing a new operating technique. The author has devel- oped a new technique  of pure tissue repair of any type of inguinal hernia without a mesh, based on the concept of constructing a strong and physiologically dynamic pos- terior wall to the inguinal canal with the help of the exter- nal oblique muscle and its aponeurosis. A strip of the external oblique aponeurosis gives replacement to the ab- sent aponeurotic extensions in the posterior wall, making it strong, and the additional strength of the external ob- lique muscle to the weakened internal oblique and the transversus abdominis muscle keeps it physiologically dynamic. The first recorded observation of dynamic activ- ity in the internal ring of a living nonanaesthetized hu- man being was done in only one patient by Tobin et al. Many such studies of dynamic activity in the internal ring have been done in dogs. Peacock EE  states that little is known about the muscular activity in the internal ring because conventional repair of groin hernia does not ade- quately expose the normal muscle fibers. Preperitoneal ex- posure is, of course, performed in an anaesthetized patient; consequently little information has been ac-
No obvious differences were detected between the myosin heavy chains of the arm and cone regions using the low percentage 4.75 % polyacrylamide-SDS gel and CNBr peptide- mapping techniques (Fig. 1). Separate attempts to separate myosin heavy chains using glycerol-SDS-polyacrylamide gels also failed to resolve any differences in the myosin heavy chain (MHC) composition of cone versus arm regions. While electrophoresis of the bass myofibrils did not reveal any significant arm versus cone differences in any of the major contractile proteins (Fig. 2), a significant difference in thin filament proteins was discovered longitudinally. In both the arm and cone regions, a longitudinal shift occurs in the ratio of two thin filament proteins, identified through column chromatography as two troponin T (TnT) isoforms (Fig. 3). Rostral muscle samples, A1–A5, are composed primarily of the faster migrating protein, TnT-2 (M r 28,120), while caudal