Muscle contraction: muscle fiber studies support solution data.
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Actins↗
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The effects of thyroxine treatment on slow- and fast-contracting skeletal muscle contractions of the cat and their cyclic AMP level.
1. The effects of thyroxine treatment on soleus and extensor digitorum longus (EDL) muscle contractions and their cyclic adenosine 3',5'-monophosphate (cyclic AMP) levels were examined in anaesthetized cats. 2. Thyroxine treatment decreased the tension of incomplete tetanic contractions of the soleus as well as the EDL muscles. The effect on tension of these muscles was not associated with an increase in the cyclic AMP level of the muscle as is the case with a beta 2-adrenoceptor agonist effect. 3. The results do not support the involvement of cyclic AMP in the tension depressant effect of thyroxine on contractions of skeletal muscle. 4. It is suggested that the muscle weakness and tremor observed in thyrotoxicosis and during administration of beta 2-adrenoceptor agonists are mediated by different mechanisms.
Animals↗
The effect of muscle vibration on human position sense during movements controlled by lengthening muscle contraction.
Muscle vibration studies suggest that during voluntary movement limb position is coded by muscle spindle information derived from the lengthening, antagonist muscle. However, these investigations have been limited to movements controlled by shortening contractions. This study further examined this property of kinesthesia during movements controlled by lengthening contraction. Subjects performed a horizontal flexion of the right forearm to a mechanical stop randomly positioned at 30, 50 and 70 degrees from the starting position. The movement was performed against a flexor load (1 kg) requiring contraction of the triceps muscle. Vision was occluded and movements were performed under three conditions: no vibration, vibration of the right biceps and vibration of the right triceps. The perceived position of the right forearm was assessed by instructing subjects to simultaneously match the right limb position with the left limb. Vibration of the shortening biceps muscle had no effect on limb matching accuracy. However, triceps vibration resulted in significant overestimation of the vibrated limb position (10-13 degrees). The variability in movement distance was uninfluenced by muscle vibration. During movements controlled by lengthening contraction, there is a concurrent gamma dynamic fusimotor input that would enhance primary afferent discharge. Despite this additional regulating input to the muscle spindle, it appears that muscle spindle information from the lengthening muscle is important for the accurate perception of limb movement and/or position.
Adult↗
Static muscle contraction reflexly increases adrenal sympathetic nerve activity in rats.
Little is known about the mechanisms responsible for activation of sympathoadrenal function during exercise. We hypothesized that sympathoadrenal discharge is activated at the onset of exercise by a reflex arising in the contracting muscle. Adrenal sympathetic nerve activity (SNA) was recorded during 1 min stimulation of the tibial nerve at two times motor threshold, before and during neuromuscular blockade, in 12 alpha-chloralose-anesthetized rats. Static muscle contractions, induced by stimulation before neuromuscular blockade, were repeated during ganglionic blockade (n = 6) to specifically test reflex activation of preganglionic activity to the adrenal gland. During static contraction, adrenal SNA rapidly increased (P less than 0.05) to a maximum of 89 +/- 12% above basal and then declined, reaching basal levels after 30 s of muscle contraction. Tibial nerve stimulation during neuromuscular blockade had no effect on adrenal SNA. In most rats, adrenal SNA decreased with ganglionic blockade, indicating postganglionic as well as preganglionic innervation of the adrenal gland. During ganglionic blockade, static muscle contractions elicited a 140 +/- 21% increase in adrenal preganglionic SNA. In conclusion, static muscle contraction reflexly increases SNA to the adrenal gland, providing a mechanism for sympathoadrenal activation at the onset of exercise.
Adrenal Glands↗
Pentobarbitone and skeletal muscle contractions: on the interaction with the effect elicited by the beta-adrenoceptor agonist, terbutaline.
The soleus, a slow-contracting muscle, and the extensor digitorum longus (EDL), a fast-contracting muscle from guinea-pig were prepared for isometric recording in vitro. Subtetanic contractions were evoked by transmural field-stimulation. Pentobarbitone increased the force of contraction in both muscles. In the soleus it shifted the stimulation frequency-response curve to the left. Terbutaline caused a decrease in the force of subtetanic contractions of the soleus, an effect which was dependent on the stimulation frequency. In the presence of pentobarbitone, the stimulation frequency had to be lowered by about 2 HZ in order to maintain the optimum response to terbutaline. The EDL responded to terbutaline with an increased force of contraction. In this case the stimulation frequency was less critical and the effects were the same in the presence and in the absence of pentobarbitone. Experiments with alpha-chloralose yielded results similar to those obtained with pentobarbitone.
Animals↗
[Control of isometric muscle contraction in muscle hypotonia of central origin: EMG mapping analysis].
Electromyographic and mechanographic investigations in patients with muscular hypotonia, which is, for instance, a side-effect after stereotactic treatment of tremor syndromes, permit the presumption that in this sensomotor open-loop situation the decreased muscular resistance to stretching during isometric contraction (initial stiffness) is caused by changes of muscular innervation pattern. Probably, the innervation pattern during tonic activity is changed by a shift of a more tonic motoneurone behaviour to motoneurone activities with predominantly phasic characteristics. In 17 controls and 4 patients with muscular hypotonia caused by stereotactic lesions of VIM area (treatment of tremor syndromes) the EMG of right and left side forearm flexors (especially the activity of the M. biceps brachii) was investigated by a sophisticated, topographically oriented 16-channel-surface-EMG-technique ("EMG-Mapping") during slight isometric contraction. EMG-Maps of forearm flexors (especially of M. biceps brachii) in patients with centrally evoked muscular hypotonia demonstrate that in these open-loop conditions the motor control is changed. For this the reason could be a shift of the activated motor units from a predominantly static to a more phasic functional behaviour. The latest results on muscular activation processes in cats support this presumption.
Adult↗
Rapid regeneration of the actin-myosin power stroke in contracting muscle.
At the molecular level, muscle contraction is the result of cyclic interaction between myosin crossbridges, which extend from the thick filament, and the thin filament, which consists mainly of actin. The energy for work done by a single crossbridge during a cycle of attachment, generation of force, shortening and detachment is believed to be coupled to the hydrolysis of one molecule of ATP. The distance the actin filament slides relative to the myosin filament in one crossbridge cycle has been estimated as 12 nm by step-length perturbation studies on single fibres from frog muscle. The 'mechanical' power stroke of the attached crossbridge can therefore be defined as 12-nm shortening with a force profile like that shown by the quick recovery of force following a length perturbation. According to this definition, power strokes cannot be repeated faster than the overall ATPase rate. Here, however, we show that the power stroke can be regenerated much faster than expected from the ATPase rate. This contradiction can be resolved if, in the shortening muscle, the free energy of ATP hydrolysis is used in several actin-myosin interactions consisting of elementary power strokes each of 5-10 nm.
Actins↗
Role of calcium and cyclic adenosine 3':5' monophosphate in regulating smooth muscle contraction. Mechanisms of excitation-contraction coupling in smooth muscle.
Caclium initiates smooth muscle contraction by activating an enzyme, myosin light chain kinase. This enzyme catalyzes the transfer of phosphate from adenosine triphosphate to the 20,000 dalton light chain of myosin. In its phosphorylated form myosin interacts with actin to produce muscle contraction. The mechanism by which calcium activates myosin kinase requires (1) the binding of calcium to a 16,500 dalton calcium-binding protein (calmodulin), and (2) the binding of calmodulin-calcium to a 125,000 dalton catalytic subunit. This two protein complex is the active form of myosin light chain kinase. Smooth muscle relaxation is mediated by cyclic adenosine 3':5' monophosphate (cyclic AMP). One nechanism by which the latter may exert a direct effect on actin-myosin interaction is through the activation of a cyclic AMP-dependent protein kinase that can phosphorylate the 125,000 dalton component of myosin light chain kinase. Phosphorylation of myosin light chain kinase decreases the activity of the enzyme, thus favoring the unphosphorylated form of myosin, which cannot interact with actin to produce smooth muscle contraction.
Actins↗
Caldesmon and thin-filament regulation of muscle contraction.
Smooth muscle contraction is regulated by phosphorylation of myosin and also possibly by the actin associated protein, caldesmon. The properties of caldesmon are discussed and compared with those of tropomyosin-troponin, the well characterized actin-based regulatory system of striated muscle. Caldesmon functions quite differently from tropomyosin-troponin. Under relaxing conditions tropomyosin-troponin does not affect the binding of myosin subfragment-1 to actin. In contrast, caldesmon strongly inhibits the binding of subfragment-1 to actin in the presence of ATP. This inhibition of binding parallels the decrease in ATPase activity that occurs as the caldesmon concentration is increased. Caldesmon has the opposite effect on the two headed myosin subfragment, heavy meromyosin. The apparent binding of skeletal heavy meromyosin increases slightly as the caldesmon concentration is increased, although the rate of ATP hydrolysis is inhibited. It is suggested that in the presence of caldesmon, myosin.ATP does not bind to the productive actin binding site but interacts with a distinct site on actin-caldesmon. This could lead to both an inhibition of ATP hydrolysis and an increase in resting stiffness of relaxed smooth muscle.
Actin Cytoskeleton↗
Changes in R-R interval at the start of muscle contraction in the decerebrate cat.
1. The effect on R-R interval of a brief hindlimb contraction, elicited by electrical stimulation of L7 ventral roots, was investigated in decerebrate cats. The first series of experiments was performed at both low and high carotid sinus pressure to vary the level of vagal tone. When carotid sinus pressure was elevated to increase vagal tone, contraction commenced 1 s later. 2. The change in R-R interval at low carotid sinus pressure was expressed as the difference between the mean of the five R-R intervals immediately preceding contraction and the mean of the last five R-R intervals at the end of a 5 s contraction. At high carotid sinus pressure, the change was expressed as the difference between the mean of the last five R-R intervals at the end of a 5 s contraction and the mean of five R-R intervals at an equivalent time after raising pressure alone. 3. Hindlimb contraction at low carotid sinus pressure produced a significant reduction in R-R interval from 359 +/- 25 (mean +/- S.E.M. n = 8) to 336 +/- 24 ms (P less than 0.005). At high carotid sinus pressure the response was enhanced with contraction producing a reduction in R-R interval from 474 +/- 45 to 419 +/- 47 ms (P less than 0.001). 4. The shortening of R-R interval produced by hindlimb contraction at high carotid sinus pressure, 55 +/- 8 ms, was significantly greater than that observed at low sinus pressure, 23 +/- 5 ms (P less than 0.001, n = 8, paired t test). This pattern of response was also seen at stimulation frequencies as low as 10 Hz. 5. In a second series of experiments, designed to determine the latency of the cardiac acceleration, the minimum latency between the onset of L7 ventral root stimulation and the end of the first shortened R-R interval was 687 +/- 29 ms (n = 5). 6. Atropine (0.4 mg kg-1, I.V.) prevented a 5 s contraction from producing any change in R-R interval. 7. These results indicate that afferent information originating from receptors in contracting muscles is responsible for producing an immediate shortening of R-R interval, which is mediated by vagal withdrawal. The possibility that the shortening of R-R interval at the start of contraction is linked to a reduction in arterial baroreceptor reflex sensitivity, possibly via inhibitory effects on neurones forming the central pathway of the baroreceptor reflex, is discussed.
Animals↗
Muscle contraction (tension) headache.
Muscle contraction headache is the most common headache afflicting mankind. Acute muscle contraction headache usually presents no problem in treatment and is a self-limited condition. Chronic muscle contraction headache presents a very difficult treatment problem. Patients are often dependent on drugs and treatment usually necessitates a multimodal approach. The pathophysiology of muscle contraction headache is unknown. There is much controversy as to whether muscle contraction is the primary cause of this condition or whether muscle contraction is merely another component of this syndrome. The extensive research now going on in the field of chronic pain should help clarify the issue.
Headache↗
Protein engineering and the study of muscle contraction in Drosophila flight muscles.
We describe an experimental approach to the use of genetics to study muscle contraction in Drosophila melanogaster. Mutations induced by in vitro mutagenesis are inserted into the genome of flies using P-element mediated transformation, permitting the effects of the mutant genes to be studied in vivo in the indirect flight muscles (IFMs). Details of how mechanical experiments can be performed on skinned IFMs, despite their small size, are provided. The effects of two in vitro actin mutations, G368E and E316K, are described. The problems of performing biochemical and biophysical experiments on the IFMs and their myofibrillar proteins are described, together with indications as to how these may be overcome.
Actins↗
[Muscle contraction headache and posture--with special reference to ischemic contraction of the posterior neck muscles].
Cause of muscle contraction headache (MCH) results from sustained contraction of scalp and posterior neck muscles. Recently, we published an effect of posture on the etiology of MCH. According to our data, head bending posture seems to be one of the main causes of sustained contraction of the posterior neck muscles. Wolff presented a hypothesis of ischemic contraction of these muscles as a cause of pain. However, about the blood flow of scalp or posterior neck muscles, only two reports were published so far. These two papers failed to demonstrate a reduction of blood flow in MCH patients, and neglected the effect of posture. The purpose of this report is to examine a change of blood flow of posterior neck muscles with the change of posture. A total of 40 patients with MCH were studied using laser doppler blood flow meter. Needle shaped probe with a diameter of 0.55 mm was inserted 15 mm into the posterior neck muscle. The angle between orbito-meatal line and horizontal plane were measured using a light helmet with goniometer. Surface EMG of the posterior neck muscles was recorded at the same time. In the case of controls who do not experience headache, the amplitude of EMG increases slightly with the bending posture (40 microV with OM line 20 degrees upward from the horizontal plane, 46 microV with OM line horizontal, and 52 microV when 30 degrees downward). In reverse to the increase of the EMG activity, blood flow of the neck muscles decreases (12 ml/100 g/min with OM line 20 degrees upward, 10.8 with OM line horizontal, 7.6 at 10 degrees down, 4.6 at 20 degrees down, and 4.1 at 30 degrees down).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[The influence of long-term isometric muscle contraction on the bioelectric muscle activity and on selected circulatory parameters].
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Adult↗
Regulation of a smooth muscle contraction: a hypothesis based on skinned fiber studies.
It seems clear that a simple Ca2+ dependent switch (MLC phosphorylation) cannot completely explain all of the disparate mechanical and energetic results obtained under numerous experimental conditions in numerous laboratories. Some of the problems of the simple switch model are that: 1. Force can be developed in the complete absence of increases in MLC phosphorylation; 2. Crossbridge cycling rate, as measured by either shortening velocity or directly by ATPase activity, can be regulated independent of changes in MLC phosphorylation; and 3. Ca2+ can directly influence both force and crossbridge cycling rate. Thus, we believe that there are two distinct Ca2+ dependent regulatory systems which normally act in parallel to contract smooth muscle. One of these is the Ca2+ dependent MLC phosphorylation-dephosphorylation. system which is likely to be responsible for the rapid development of force. The other is the hypothesized Ca2+ dependent system which is probably responsible for the slow development of force as well as the maintenance of previously developed force, represented in Figure 5 as K8. This second system involves a calmodulin-like protein with a higher Ca2+ sensitivity than that for the Ca(2+)-calmodulin-MLC kinase system. Under most conditions, the total force attained by smooth muscle in response to stimulation is the result of the concerted activation of both of these regulatory systems. The available information is consistent with this hypothesis of two regulatory systems functioning in parallel. In addition to the information presented in this chapter, work from a number of laboratories (Moreland and Ford, 1982; Fujiwara et al., 1989; Kitazawa et al., 1989; Somlyo et al., 1989; Kubota et al., 1990; Kitazawa and Somlyo, this volume) have suggested the possibility that a regulated MLC phosphatase may functionally alter the Ca2+ sensitivity of the contractile filaments. There is evidence suggesting that the sensitivity of MLC kinase to activation by Ca2+ and calmodulin may be regulated (Stull et al., this volume). Protein kinase C has been postulated to play an important role in the regulation of myofilament Ca2+ sensitivity (Nishimura et al., this volume). MgADP has been suggested to affect the kinetics of latchbridge attachment and detachment (Kerrick and Hoar, 1987; Nishimura and van Breemen, 1989). Cooperativity between crossbridges as described by Somlyo et al. (1988) and Siegman et al. (this volume) might also be an important component in the regulation of smooth muscle contraction.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Smooth operators. The molecular mechanics of smooth muscle contraction.
Smooth muscle cells squeeze the blood back to your heart, raise the hackles on your neck and change the F-stop of your eyes. The past year has provided penetrating new insights into their mechanism of contraction.
Animals↗
[Significance of flexed posture and neck instability as a cause of chronic muscle contraction headache].
Cause of a muscle contraction headache (MCH) is due to sustained contraction of the neck and head muscles. This is proved by the effect of local anesthesia and EMG findings. However, the pathophysiology of abnormal muscle contraction is still unclear. Also, there is no explanation about female's greater susceptibility to MCH. The purpose of our report is to study the mechanism of abnormal muscle contraction and to find out a way to prevent it. We have examined 826 (572 female & 254 male) patients with MCH using EMG and dynamic X-ray. Results are most of MCH patients have a tendency to bend their head downward at the onset of headache. EMG shows continuous discharge of the posterior neck muscles so long as they keep this posture. Once they look up, however, EMG discharge usually subsides. Therefore, these muscle contraction are not involuntary, but passive as the results of drooping head. In 12 patients, severe attack of MCH were temporarily alleviated by the local anesthesia to the suboccipital tender point. In patients complaining MCH of one side, they often have a tendency to bend their neck toward the opposite direction, thus contracting the painful side of the neck muscles. It is also found that looking up to make orbito-meatal line more than 10 degrees from horizontal plane is enough to minimize muscle contraction, and to prevent or alleviate headache. Not all people experience headache, though.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
[Ca2+], not diacylglycerol, is the primary regulator of sustained swine arterial smooth muscle contraction.
Sustained smooth muscle contraction has been proposed to be regulated by either 1) sustained increases in intracellular Ca2+ concentration [(Ca2+]i)-dependent myosin phosphorylation or 2) diacylglycerol-dependent protein kinase C activation. We measured diacylglycerol mass with the diacylglycerol kinase assay and myoplasmic [Ca2+] with aequorin in swine carotid medial smooth muscle. Sustained and significant increases in [Ca2+], myosin light chain phosphorylation, and isometric stress were observed with histamine or endothelin stimulation. Neither stimuli, however, induced significant increases in diacylglycerol mass. Relaxation of histamine-stimulated tissues was induced by removal of histamine or removal of extracellular CaCl2 in the continued presence of histamine. The rate of decline of both [Ca2+] and force was similar in both protocols, suggesting that removal of Ca2+ (without removing the stimulus) was equivalent to removal of the stimulus. These data suggest that [Ca2+]i is the primary regulator of sustained swine arterial smooth muscle contraction, whereas diacylglycerol has, at most, only a minor role.
Alkaloids↗