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At least 703 records · Page 39Linked to original sources
PubMed2006

An anomalous muscle linking superior and inferior rectus muscles in the orbit.

Dissections of the bilateral orbits in a 45-year-old female cadaver, who had no ocular movement disorders in her lifetime, revealed anomalous muscles linking the superior and inferior rectus muscles. The muscles, situated between the optic nerve and the lateral rectus muscle, originated from the annulus of Zinn and branched off two heads; one inserted into the medial inferior side of the superior rectus muscle and the other inserted into the central superior side of the inferior rectus muscle. Each insertion was located on a distal site of the myoneural junction of each rectus muscle. Histological investigations showed that the muscles had a striated muscle structure. No definite nerve insertion was observed in the muscles. Although this type of anomalous muscle has been reported in a few Caucasian cases, the present study is the first report in an Asian person. Anomalous orbital structures, which are a rare cause of strabismus, are important in the differential diagnosis of intra-orbital space-occupying lesions, rather than the differential diagnosis of strabismus.

Asian People↗
PubMed1990

The use of an electrically activated valve to control preload and provide maximal muscle blood flow with a skeletal-muscle ventricle.

A new method for optimally loading a skeletal muscle-wrapped pouch to act as a blood pump is described. The method takes advantage of the fact that the high preload pressure required for a forceful contraction needs to be present for only a short time. By using an electrically controlled valve to delay pouch filling until just before muscle contraction, pouch diastolic pressure can be kept low, which in turn maintains a high muscle capillary blood flow. The intrapouch precontraction pressure can be controlled by selecting the appropriate valve-open time (VOT). The pumping capabilities of untrained rectus abdominis and latissimus dorsi muscles were evaluated using a hydraulic circulatory system in a ten dog study (weight range 20-32.7 kg). The afterload was constant at 100 mmHg, and the pouch precontraction pressure, selected by choice of the VOT, was the test variable. It was found that for maximum pouch output, a precontraction pressure of 60-100 mmHg was required, being attained in this hydraulic model with a VOT of 400-500 msec. Typical pouch outputs were 400-600 mL/min with a muscle contraction rate of 40/min. Muscle capillary blood flow, measured with a periarterial electromagnetic flowmeter, varied inversely with pouch diastolic pressure and was near zero during tetanic muscle contraction. In one animal, a pouch output of 200 mL/min or more was maintained for more than 20 hours of continuous pumping without fatigue. In a related experiment, the method was applied to pump blood in a 32.7 kg dog, in which the muscle-wrapped pouch was connected between the descending thoracic aorta and the abdominal aorta. A pouch output of about 400 mL/min was obtained when the muscle was contracted 30 times/min and the VOT was 400 msec. This flow represented about 20% of the animal's cardiac output. This study demonstrates that by delaying pouch filling until just before the muscle is to be contracted, a low pouch diastolic pressure can be maintained, thereby maximizing muscle capillary blood flow and, in turn, providing the best opportunity for prolonged pumping.

Animals↗
PubMed2006

Effect of swimming on myostatin expression in white and red gastrocnemius muscle and in cardiac muscle of rats.

The aim of this study was to test the hypothesis that swimming training might impact differentially myostatin expression in skeletal muscles, depending on fibre type composition, and in cardiac muscle of rats. Myostatin expression was analysed by real time reverse transcriptase-polymerase chain reaction, Western blot and immunohistochemistry of the red deep portion (mainly composed of slow and type II A fibres) and in the superficial, white portion (composed of fast type II X and II B fibres) of the gastrocnemius muscle in adult male Wistar rats: (i) subjected to two consecutive swimming bouts for 3 h; (ii) subjected to intensive swimming training for 4 weeks; and (iii) sedentary control rats. Myostatin mRNA content was in all cases higher in white than in red muscles. Two bouts of swimming did not alter myostatin expression, whereas swimming training for 4 weeks resulted in a significant reduction of myostatin mRNA contents, significant both in white and red muscles but more pronounced in white muscles. Western blot did not detect any change in the amount of myostatin protein. Immunohistochemistry showed that, in control rats, myostatin was localized in presumptive satellite cells of a few muscle fibres. After training, the number of myostatin-positive spots decreased significantly. Myostatin mRNA content in cardiac muscle was lower than in skeletal muscle and was significantly increased by swimming training. In conclusion, the results obtained showed that intense training caused a decreased expression of myostatin mRNA in white and red skeletal muscles but an increase in cardiac muscle.

Animals↗
PubMedDate not supplied

Hypothyroidism prolongs and increases mdx muscle precursor proliferation and delays myotube formation in normal and dystrophic limb muscle.

Hypothyroidism (induced by 8 weeks of oral 0.05% propylthiouracil) heightened the phenotype of mdx mouse dystrophin-deficient myopathy to more closely resemble human Duchenne muscular dystrophy. Muscle repair after crush injury to the tibialis anterior muscle (TA) in hypothyroid mdx mice showed decreased myotube formation and delayed debris removal. To investigate whether reduced muscle precursor cell proliferation can account for the effects of hypothyroidism on repair from injury, immunocytochemistry for neural cell adhesion molecule (NCAM) on muscle precursor cells and autoradiography to detect DNA synthesis were performed in control and mdx TA. The proportions of labelled polymorphonuclear leukocyte nuclei (PMN), myotube nuclei (MN), and total mononuclear cell nuclei (TLN, the majority being muscle precursors) were counted in defined areas of regenerating TA after 2 and 4 days recovery. MN and the numbers of activated satellite cell nuclei on intact fibers were counted in surviving areas. In the same muscle, earlier phases of regeneration were observed in areas distal than proximal to the injury. At 2 days of regeneration, labelled PMN were increased in treated compared with untreated mdx TA. In distal areas at 4 days, fewer muscle precursors had recently fused to myotubes in treated than in untreated mdx. In proximal areas 4 days (relatively late in repair), TLN data suggested that muscle precursor proliferation was greater in hypothyroid compared with untreated mdx TA. NCAM immunostaining was consistent with proliferation data and confirmed that there were more muscle precursors in mdx than in control regenerating muscle. These results suggest that hypothyroidism prolongs and increases the phase of replication by mdx muscle precursors and delays precursor fusion into myotubes in regeneration.

Animals↗
PubMed1994

Experimental approaches in muscle metabolism: hindlimb perfusion and isolated muscle incubations.

The perfusion of rat hindlimb muscles and the isolated in vitro muscle preparation are usually the preferred methods for investigating muscle metabolism. In light of recent concerns about the incubated muscle preparation, we have examined the problems, the advantages, and the viability of these two experimental techniques, with focus on glucose metabolism. A major advantage of the hindlimb perfusion system is that it maintains its metabolic viability very well, and perfusions in resting muscles can be achieved successfully with cell-free media. However, variations in the perfused rat hindlimb procedures result in considerable differences in perfusate flow among muscles, making quantitative comparisons among perfusion procedures difficult. Metabolic viability has been identified as a problem in some isolated in vitro muscle preparations. We have provided criteria to avoid muscle hypoxia. Minimum levels of insulin seem to be a key requirement to maintaining the muscle's viability, and essential amino acids are required to retard an increase in the basal rate of glucose and amino acid uptake. Under such conditions metabolic viability can be maintained during prolonged incubations (9-30 h). Both the isolated in vitro muscle preparation and the hindlimb perfusion preparation are viable models for the study of muscle metabolism.

Animals↗
PubMed1991

Effect of muscle length on isometric stress and myosin light chain phosphorylation in gallbladder smooth muscle.

These experiments were designed to characterize the effect of muscle length on isometric stress, sensitivity to stimulation, and phosphorylation of the 20,000-Da myosin light chains in guinea pig gallbladder smooth muscle. Basal, active, and total isometric stress were determined in acetylcholine- or K(+)-treated (10(-4) M ACh, 80 mM KCl) muscle strips at 0.6-1.3 times the optimal muscle length (Lo) for isometric stress development. The effect of muscle length on the sensitivity to ACh and K+ was determined in cumulative dose-response experiments (10(-8) to 10(-4) M ACh, 10-80 mM KCl) at 0.7, 1.0, and 1.3 Lo. The effect of muscle length on myosin light chain phosphorylation was determined in ACh- or K(+)-treated (10(-4) M ACh, 80 mM KCl) muscle strips at 0.7, 1.0, and 1.3 Lo. In gallbladder smooth muscle, 1) active isometric stresses at 0.7 and 1.3 Lo were less than active isometric stress at 1.0 Lo; 2) the sensitivity of developed stress was similar at 1.0 and 1.3 Lo but decreased at 0.7 Lo; 3) the decline in isometric stress and sensitivity at 0.7 Lo was associated with reduced levels of phosphorylated myosin light chain; and 4) the decline in isometric stress at 1.3 Lo was not associated with reduced amounts of phosphorylated myosin light chain. These results suggest that the decline in active stress and sensitivity at short muscle lengths (L less than Lo) in gallbladder smooth muscle is due, at least in part, to decreases in the activation of the myofilaments. The decline in active isometric stress at long muscle lengths (L greater than Lo) is not due to changes in myofilament activation.

Acetylcholine↗
PubMed2002

Effect of rhythmic tetanic skeletal muscle contractions on peak muscle perfusion.

The purpose of this investigation was to examine the effect of rhythmic tetanic skeletal muscle contractions on peak muscle perfusion by using spontaneously perfused canine gastrocnemii in situ. Simultaneous pulsatile blood pressures were measured by means of transducers placed in the popliteal artery and vein, and pulsatile flow was measured with a flow-through-type transit-time ultrasound probe placed in the venous return line. Two series of experiments were performed. In series 1, maximal vasodilation of the muscles' vascular beds was elicited by infusing a normal saline solution containing adenosine (29.3 mg/min) and sodium nitroprusside (180 microg/min) for 15 s and then simultaneously occluding both the popliteal artery and vein for 5 min. The release of occlusion initiated a maximal hyperemic response, during which time four tetanic contractions were induced with supramaximal voltage (6-8 V, 0.2-ms stimuli for 200-ms duration at 50 Hz, 1/s). In series 2, the muscles were stimulated for 3 min before the muscle contractions were stopped for a period of 3 s; stimulation was then resumed. The results of series 1 indicate that, although contractions lowered venous pressure, muscle blood flow was significantly reduced from 2,056 +/- 246 to 1,738 +/- 225 ml x kg(-1) x min(-1) when contractions were initiated and then increased significantly to 1,925 +/- 225 ml x kg(-1) x min(-1) during the first 5 s after contractions were stopped. In series 2, blood flow after 3 min of contractions averaged 1,454 +/- 149 ml x kg(-1) x min(-1). Stopping the contractions for 3 s caused blood flow to increase significantly to 1,874 +/- 172 ml x kg(-1) x min(-1); blood flow declined significantly to 1,458 +/- 139 ml x kg(-1) x min(-1) when contractions were resumed. We conclude that the mechanical action of rhythmic, synchronous, maximal isometric tetanic skeletal muscle contractions inhibits peak muscle perfusion during maximal and near-maximal vasodilation of the muscle's vascular bed. This argues against a primary role for the muscle pump in achieving peak skeletal muscle blood flow.

Adenosine↗
PubMed2004

Training-induced changes in muscle CSA, muscle strength, EMG, and rate of force development in elderly subjects after long-term unilateral disuse.

The ability to develop muscle force rapidly may be a very important factor to prevent a fall and to perform other tasks of daily life. However, information is still lacking on the range of training-induced neuromuscular adaptations in elderly humans recovering from a period of disuse. Therefore, the present study examined the effect of three types of training regimes after unilateral prolonged disuse and subsequent hip-replacement surgery on maximal muscle strength, rapid muscle force [rate of force development (RFD)], muscle activation, and muscle size. Thirty-six subjects (60-86 yr) were randomized to a 12-wk rehabilitation program consisting of either 1) strength training (3 times/wk for 12 wk), 2) electrical muscle stimulation (1 h/day for 12 wk), or 3) standard rehabilitation (1 h/day for 12 wk). The nonoperated side did not receive any intervention and thereby served as a within-subject control. Thirty subjects completed the trial. In the strength-training group, significant increases were observed in maximal isometric muscle strength (24%, P < 0.01), contractile RFD (26-45%, P < 0.05), and contractile impulse (27-32%, P < 0.05). No significant changes were seen in the two other training groups or in the nontrained legs of all three groups. Mean electromyogram signal amplitude of vastus lateralis was larger in the strength-training than in the standard-rehabilitation group at 5 and 12 wk (P < 0.05). In contrast to traditional physiotherapy and electrical stimulation, strength training increased muscle mass, maximal isometric strength, RFD, and muscle activation in elderly men and women recovering from long-term muscle disuse and subsequent hip surgery. The improvement in both muscle mass and neural function is likely to have important functional implications for elderly individuals.

Aged↗
PubMed1992

Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure.

BACKGROUND: The purpose of this study was to investigate the prevalence of skeletal muscle atrophy and its relation to exercise intolerance and abnormal muscle metabolism in patients with heart failure (HF). METHODS AND RESULTS: Peak VO2, percent ideal body weight (% IBW), 24-hour urine creatinine (Cr), and anthropometrics were measured in 62 ambulatory patients with HF. 31P magnetic resonance spectroscopy (MRS) and imaging (MRI) of the calf were performed in 15 patients with HF and 10 control subjects. Inorganic phosphorus (Pi), phosphocreatine (PCr), and intracellular pH were measured at rest and during exercise. Calf muscle volume was determined from the sum of the integrated area of muscle in 1-cm-thick contiguous axial images from the patella to the calcaneus. A reduced skeletal muscle mass was noted in 68% of patients, as evidenced by a decrease in Cr-to-height ratio of less than 7.4 mg/cm and/or upper arm circumference of less than 5% of normal. Calf muscle volume (MRI) was also reduced in the patients with HF (controls, 675 +/- 84 cm3/m2; HF, 567 +/- 112 cm3/m2; p less than 0.05). Fat stores were largely preserved with triceps skinfold of less than 5% of normal and/or IBW of less than 80% in only 8% of patients. Modest linear correlations were observed between peak VO2 and both calf muscle volume per meter squared (r = 0.48) and midarm muscle area (r = 0.36) (both p less than 0.05). 31P metabolic abnormalities during exercise were observed in the patients with HF, which is consistent with intrinsic oxidative abnormalities. The metabolic changes were weakly correlated with muscle volume (r = -0.42, p less than 0.05). CONCLUSIONS: These findings indicate that patients with chronic HF frequently develop significant skeletal muscle atrophy and metabolic abnormalities. Atrophy contributes modestly to both the reduced exercise capacity and altered muscle metabolism.

Exercise↗
PubMed1984

Rabbit papillary muscle myosin isozymes and the velocity of muscle shortening.

Rabbits, ages 4-24 weeks, were injected with saline or thyroxine (150 micrograms/kg) for 7 days, and force-velocity curves were generated using papillary muscles from these hearts by a method described previously. In addition, the structure and relative amounts of myosin isozymes from papillary muscles and from 3- to 5-mg segments of the left and right ventricular free wall were analyzed by polyacrylamide gel electrophoresis under native and denatured conditions. We found that rabbit papillary muscles may contain up to three isozymic forms of myosin (V1, V2, and V3) and that their relative amounts change with age of the rabbit and with thyroxine treatment. There were no differences between papillary muscles and ventricular free wall in the molecular weight of light chain1 (27,000) and light chain2 (21,500) of heavy chain alpha or in the peptide map of heavy chain alpha nor were there any differences between papillary muscles and the ventricular free wall in the molecular weight of light chain1 (27,000) and light chain2 (21,500) of heavy chain beta or in the peptide map of heavy chain beta. However, the relative amounts of myosin isozymes in the ventricular free walls and papillary muscles may not be identical within the same heart. Analysis of the force-velocity curves indicated that the speed of papillary muscle shortening is correlated with the relative amount of V1 myosin present in each papillary muscle. Papillary muscles that contain 100% V1 myosin shorten, under zero load, approximately six times faster than papillary muscles that contain 100% V3 myosin. Our results indicate that changes in the relative amounts of myosin isozymes are responsible, at least in part, for sustained alterations in the speed of papillary muscle shortening.

Animals↗
PubMed2006

Muscle wasting and impaired muscle regeneration in a murine model of chronic pulmonary inflammation.

Muscle wasting and increased circulating levels of inflammatory cytokines, including TNF-alpha, are common features of chronic obstructive pulmonary disease. To investigate whether inflammation of the lung is responsible for systemic inflammation and muscle wasting, we adopted a mouse model of pulmonary inflammation resulting from directed overexpression of a TNF-alpha transgene controlled by the surfactant protein C (SP-C) promoter. Compared with wild-type mice, SP-C/TNF-alpha mice exhibited increased levels of TNF-alpha in the circulation and increased endogenous TNF-alpha expression in skeletal muscle, potentially reflecting an amplificatory response to circulating TNF-alpha. Decreased muscle and body weights observed in SP-C/TNF-alpha mice were indicative of muscle wasting. Further evaluation of the SP-C/TNF-alpha mouse musculature revealed a decreased muscle regenerative capacity, shown by attenuated myoblast proliferation and differentiation in response to reloading of disuse-atrophied muscle, which may contribute to skeletal muscle wasting. Importantly, incubation of cultured myoblasts with TNF-alpha also resulted in elevated TNF-alpha mRNA levels and inhibition of myoblast differentiation. Collectively, our results demonstrate that chronic pulmonary inflammation results in muscle wasting and impaired muscle regeneration in SP-C/TNF-alpha mice, possibly as a consequence of an amplificatory TNF-alpha expression circuit extending from the lung to skeletal muscle.

Animals↗
PubMed2005

Phenotypic flexibility of skeletal muscles during long-distance migration of garden warblers: muscle changes are differentially related to body mass.

Mass changes of skeletal muscles occur in a variety of species during the migratory period. Phenotypic flexibility of flight muscle mass is considered to represent adaptations of the flight muscle to changing power requirements associated with changes in body mass. We analyzed the relationship between muscle masses and body mass for garden warblers (Sylvia borin) sampled during spring migration in Tanzania, Ethiopia, and Egypt, and during autumn migration in Turkey. Flight muscle mass was positively related to body mass of warblers at only one of the four sites, in Egypt where warblers had just arrived after a long migratory flight. Analysis of covariance (ANCOVA) revealed a significant interaction term between sampling site and body mass (P < .001), indicating that flight muscle and body mass differed from site to site. We therefore question the idea that changing power requirements associated with changes in body mass cause mass changes of the flight muscle. We further suggest that different migration strategies across different landscapes shape the relationship between flight muscle and body mass. Flights across major ecological barriers may cause substantial catabolism of flight muscle protein until the limit necessary for flight, while migration across "common landscape," which enables a bird to land and to feed and/or drink, may occur without the need to catabolize flight muscle protein. However, a differential relationship between flight muscle mass and body mass described here for a long-distance migrant seems as well to occur in a short-distance migrant and is therefore unlikely to be part of an adaptive syndrome typical for long-distance migration.

Adipose Tissue↗
PubMed1996

Skeletal muscle content of membrane glycoprotein PC-1 in obesity. Relationship to muscle glucose transport.

Membrane glycoprotein PC-1, an inhibitor of insulin signaling, produces insulin resistance when overexpressed in cells transfected with PC-1 cDNA. In the present study, we determined whether PC-1 plays a role in the insulin resistance of skeletal muscle in obesity. Rectus abdominus muscle biopsies were taken from patients undergoing elective surgery. Subjects included both NIDDM patients (n = 14) and nondiabetic patients (n = 34) across a wide range of BMI values (19.5-90.1). Insulin-stimulated glucose transport was measured in incubated muscle strips, and PC-1 content, enzymatic activity, and insulin receptor content were measured in solubilized muscle extracts. Increasing BMI correlated with both an increase in the content of PC-1 in muscle (r = 0.55, P < 0.001) and a decrease in insulin stimulation of muscle glucose transport (r = -0.58, P = 0.008). NIDDM had no effect on either PC-1 content or glucose transport for any given level of obesity. Insulin stimulation of muscle glucose transport was negatively related to muscle PC-1 content (r = -0.68, P = 0.001) and positively related to insulin receptor content (r = 0.60, P = 0.005). Multivariate analysis indicated that both skeletal muscle PC-1 content and insulin receptor content, but not BMI, were independent predictors of insulin-stimulated glucose transport. Muscle PC-1 content accounted for 42% and insulin receptor content for 17% of the variance in glucose transport values. These studies raise the possibility that increased expression of PC-1 and a decreased insulin receptor content in skeletal muscle may be involved in the insulin resistance of obesity.

Adult↗
PubMed1997

Phenotypic characterization of rambouillet sheep expression the callipyge gene: III. Muscle weights and muscle weight distribution.

Paternal half-sibling Rambouillet ram lambs (n = 18) representing two muscle phenotypes were slaughtered at 54.5 kg to evaluate the effect of the callipyge gene on muscle mass. Lambs were produced from a sire that was heterozygous for the callipyge gene. Nineteen muscles were dissected from the right side of each carcass to evaluate muscle weights relative to carcass weight. Excised muscle mass as significantly higher (42%) for lambs exhibiting a callipyge muscle phenotype than for half-siblings. In the pelvic limb, all excised muscles except the peronius tertius were larger in lambs expressing the callipyge gene (P < .001). In the torso, the longissimus (P < .001), psoas major (P < .001), and psoas minor (P < .01) were larger in lambs with the callipyge phenotype. In the thoracic limb, the biceps brachii (P < .001) triceps brachii (P < .002), and extensor carpi radialis (P < .01) were larger in lambs with the callipyge phenotype. Total pelvic limb (P < .001) torso (P < .001), and thoracic muscle weights were higher (P < .01) in lambs with the callipyge phenotype. Callipyge lambs had a higher (P < .01) percentage of excised muscle weight in the pelvic limb and torso and a lower (P < .01) percentage in the thoracic limb when compared to controls. These data indicate that the magnitude of expression of the callipyge gene is dependent upon the location of the muscle on the body and that the increased muscle mass was concentrated in the leg and loin.

Animals↗
PubMed1995

Anatomical studies on the extensor pollicis et indicis accessorius muscle and the extensor indicis radialis muscle in Japanese.

Anatomical studies on the extensor pollicis et indicis accessorius and extensor indicis radialis muscles were conducted on 952 upper limbs from 476 Japanese adult cadavers. Each anomalous muscle occurred between the extensor pollicis longus proprius and extensor indicis proprius muscles in the dorsum of the forearm and hand. The extensor pollicis et indicis accessorius muscle was present in 13 of the limbs (1.4%). It was not coexistent with another anomalous muscle of the extensor digitorum profundus mass in 9 cases, and it was coexistent with that muscle in 4. The extensor indicis radialis muscle was present in 34 limbs (3.6%). It was accompanied by another anomaly of the extensor digitorum profundus mass in 5 cases, and not accompanied by that muscle in 29. The extensor pollicis et indicis accessorius and extensor indicis radialis muscles were innervated by the posterior interosseus nerve of the radial nerve. It seems that the former anomalous muscle supplies the extensor control of the thumb and index finger, and the latter one of the index finger only. Each anomalous muscle was considered to be differentiating on the radial side of the extensor digitorum profundus mass in humans.

Arm↗
PubMed2001

[Insulin effect on metabolism in skeletal muscles and the role of muscles in regulation of glucose homeostasis].

Insulin enhances glucose disposal, storage and oxidation in muscles. It control the metabolites required in the muscle and is involved in maintaining glucose homeostasis. Insulin is considered to be an anabolic hormone in that it promotes the synthesis of protein and glycogen and it inhibits the degradation of these compounds in muscle tissue. Glucose normally provides energy sources for tissues of the body, its uptake by muscle requires a secretion of insulin. The initial step of glucose utilization requires the transport of glucose into the cells. The transport across certain cell membranes such as muscle is regulated by insulin. The insulin-receptor complex stimulates the cellular uptake of glucose. Insulin stimulates the uptake of amino acids into cells and simulates protein synthesis in muscle tissue. With insulin deficiency, amino acids are mobilized from muscle and transported to the liver. Physiological increase in insulin suppresses lypolysis in skeletal muscle but in supra-physiological increases this suppression of intramuscular lypolysis is inadequate, resulting in increased availability of nonestrified fatty acids which can represent a potential mechanism involved in insulin resistance in muscle. Patients with diabetes mellitus are characterized by insulin deficiency (type 1) or peripheral insulin resistance (type 2) demonstrated by decreased insulin action on glucose utilization in muscle. Muscle tissue has been considered to be a major regulator of systemic glucose homeostasis.

Amino Acids↗
PubMed1990

Muscle elasticity: effect of muscle length and temperature.

The present study describes a new method which allows the determination of muscle elasticity by applying quick releases at one end of a muscle and measuring the resulting tension drops at both ends, and simultaneously the propagation time of the mechanical impulse. The elasticity determined by both methods was examined on resting as well as on tetanized frog muscles (Rana esculenta, M. flexor hallucis brevis) in relation to muscle length and at two different temperatures 1 degree C and 20 degrees C. The average propagation velocity of the mechanical impulse of resting muscle was 55.7 +/- 4.7 m/s and of the contracting muscle 104.8 +/- 24.7 m/s at 1 degree C (L0, n = 6), which corresponds to elasticities of 3.3 +/- 0.5 N/mm2 and 14.4 +/- 6.2 N/mm2, respectively. The elasticity modulus calculated from the tension drop was for the resting muscle 2.3 +/- 0.5 N/mm2 and for the contracting muscle 11.1 +/- 2.1 N/mm2 (L0, 1 degree C, n = 6). When the muscle length is varied, the elasticity modulus corresponds to the length-tension relation of the resting and the isometrically contracting muscle. There is a strong correlation between the elasticity moduli which was determined by both methods for measurement of resting (r = 0.99, n = 19, p less than 0.05) and contracting muscle (r = 0.97, n = 19, p less than 0.05). This relation between elasticity and tetanic tension, i.e. filament overlap at constant temperature, can be interpreted in accordance with the sliding filament theory. But if the temperature is increased from 1 degree C to 20 degrees C, an increase of the tetanic tension (Q10 = 1.56) and a decrease of the elasticity measured by both methods (Q10 of 0.86 and 0.84) were obtained. This suggests that the increased tetanic force is generated by a smaller number of attached cross-bridges, but with a higher amount of force generated by each cross-bridge.

Animals↗
PubMed1989

Ca2+ transport in muscle. A study of the Ca2+-transport ATPases in smooth muscle.

The Ca2+-transport ATPases of smooth muscle were studied. It was concluded that smooth muscle expresses at least two different Ca2+-transport ATPases. One is present in the plasma membrane with an Mr of 140-130 kDa it is stimulated by calmodulin and it could be purified by affinity chromatography on immobilized calmodulin. This ATPase could be reconstituted in artificial membrane vesicles that were then able to catalyze an ATP-dependent Ca2+-uptake. This Ca2+-transport ATPase could also be stimulated by partial proteolysis and by negatively charged phospholipids. Polyclonal and monoclonal antibodies were found to inhibit this ATPase and concomitantly the Ca2+-transport specifically in plasma membranes and not in the endoplasmic reticulum. This plasma-membrane Ca2+ pump from smooth muscle is controlled by cGMP via phosphorylation of a phosphatidylinositol kinase which phosphorylates phosphatidylinositol to phosphatidylinositol-monophosphate for which a specific binding site exists on the Ca2+-transport ATPase. The catalytic phosphoprotein intermediate of this ATPase can be easily demonstrated and this forms a highly sensitive method to detect the presence of the ATPase in different smooth muscles and even in non-muscle sources as the kidney. A second type of Ca2+ pump with an Mr of 100 kDa is found in smooth-muscle endoplasmic reticulum. By means of its catalytic phosphointermediate this pump could be characterized as similar to the cardiac/slow muscle isoform of the sarcoplasmic reticulum Ca2+ pumps, but different from the fast skeletal-muscle isoform. Immunological studies confirmed this conclusion. This endoplasmic reticulum Ca2+ pump in smooth muscle is regulated by cAMP and cGMP via phosphorylation of phospholamban. Once Ca2+ is accumulated in the lumen of the endoplasmic reticulum, it can be bound to calsequestrin. The calsequestrin of smooth muscle appears to be a similar isoform as that found in cardiac muscle. The Ca2+-transport ATPases were found to be inhibited by fluoroaluminate complexes without the involvement of GTP-binding proteins.

Biological Transport, Active↗