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At least 19 recordsLinked to original sources
PubMed2001

The use of optical flow to characterize muscle contraction.

Muscle contraction is usually measured and characterized with force and displacement transducers. The contraction of muscle fibers, however, evokes in the tissue a two and even three-dimensional displacement field, which is not properly quantified by these transducers because they provide just a single scalar quantity. This problem can be circumvented by using optical measurements and standard tools of computer vision, developed for the analysis of time varying image sequences. By computing the so called optical flow, i.e. the apparent motion of points in a time varying image sequence, it is possible to recover a two-dimensional motion field, describing rather precisely the displacement caused by muscle contraction in a flattened piece of skin. The obtained two-dimensional optical flow can be further analyzed by computing its elementary deformation components, providing a novel and accurate characterization of the contraction induced by different motoneurons. This technique is demonstrated analyzing the displacement caused by muscle contraction in the skin of the leech, Hirudo medicinalis. The proposed technique can be applied to monitor and characterize all contractions in almost flat tissues with enough visual texture.

Action Potentials↗
PubMed1987

The insulin-like effect of muscle contraction.

Muscle contraction results in an increase in membrane permeability to glucose. The actual mechanism by which contractile activity increases membrane permeability is unknown. However, kinetic studies suggest that this increase is due to an increase in the number of glucose transporters associated with the plasma membrane. This is also suggested by the recent finding that cytochalsin B, which competitively inhibits the binding of glucose to the glucose transporter in the plasma membrane, prevents activation of the glucose transport process by muscle contraction. Unlike insulin-stimulated glucose transport, in which permeability is reversed rapidly upon removal of the insulin, the increase in membrane permeability following contractile activity can persist for many hours. It has also been reported that the stimulatory effects of insulin and contraction are additive, and that prostaglandin E2 augments the effect of insulin on glucose transport but has no effect on contraction-facilitated glucose transport. Collectively, these findings suggest that insulin and contractile activity increase membrane permeability to glucose by independent mechanisms. An increase in membrane permeability is only partially responsible for the increase in glucose uptake during exercise in vivo. With an increase in muscle activity, there is an increase in delivery of glucose and insulin to the muscle as a result of an increase in muscle blood flow. Glucose uptake may also be facilitated by an increase in the insulin sensitivity of the muscle. The increases in muscle blood flow and insulin sensitivity may be associated with activation of the kinin-prostaglandin system of the muscle. The increase in muscle insulin sensitivity may also involve an increase in insulin binding to its receptors on the sarcolemma. It should be noted that the increase in insulin binding associated with contractile activity requires the presence of epinephrine. Muscle glycogen may also affect the rate of glucose uptake during exercise. During prolonged, moderately intense exercise, glucose uptake increases as the muscle glycogen level declines. This increase in glucose uptake is inversely related to the glucose-6-phosphate concentration of the cell. During high-intensity exercise, the rate of glycogenolysis is rapid, resulting in the accumulation of glucose-6-phosphate and free glucose. Thus, it appears that the rate-limiting step in glucose uptake during exercise is shifted from transport to glucose phosphorylation, and that this shift is mediated by the intracellular glucose-6-phosphate concentration, which is influenced by the rate of muscle glycogen catabolism.

Adenosine Triphosphate↗
PubMed1983

The molecular basis of muscle contraction.

Muscle contraction takes place by the cyclic interaction of two-stranded helical actin filaments with protuberances from the myosin filaments known as cross-bridges. The nature of the contractile process demands that the myosin cross-bridge be highly polymorphic. Biochemical evidence points to the cross-bridge having a domain structure such that contraction may be a manifestation of the rearrangement of these subunits. An essential step in contraction may be the initial binding of a small hinged domain of the cross-bridge (the 'nose-cone') to actin, followed by a series of changes ending in the formation of a second union (the rigor bond) with an actin monomer in the neighbouring strand of the actin helix.

Actins↗
PubMed1998

Elastic bending and active tilting of myosin heads during muscle contraction.

Muscle contraction is driven by a change in shape of the myosin head region that links the actin and myosin filaments. Tilting of the light-chain domain of the head with respect to its actin-bound catalytic domain is thought to be coupled to the ATPase cycle. Here, using X-ray diffraction and mechanical data from isolated muscle fibres, we characterize an elastic bending of the heads that is independent of the presence of ATP. Together, the tilting and bending motions can explain force generation in isometric muscle, when filament sliding is prevented. The elastic strain in the head is 2.0-2.7 nm under these conditions, contributing 40-50% of the compliance of the muscle sarcomere. We present an atomic model for changes in head conformation that accurately reproduces the changes in the X-ray diffraction pattern seen when rapid length changes are applied to muscle fibres both in active contraction and in the absence of ATP. The model predictions are relatively independent of which parts of the head are assumed to bend or tilt, but depend critically on the measured values of filament sliding and elastic strain.

Actins↗
PubMed1993

Structure of the actin-myosin complex and its implications for muscle contraction.

Muscle contraction consists of a cyclical interaction between myosin and actin driven by the concomitant hydrolysis of adenosine triphosphate (ATP). A model for the rigor complex of F actin and the myosin head was obtained by combining the molecular structures of the individual proteins with the low-resolution electron density maps of the complex derived by cryo-electron microscopy and image analysis. The spatial relation between the ATP binding pocket on myosin and the major contact area on actin suggests a working hypothesis for the crossbridge cycle that is consistent with previous independent structural and biochemical studies.

Actins↗
PubMed2006

Mechanics of actomyosin bonds in different nucleotide states are tuned to muscle contraction.

Muscle contraction and many other cell movements are driven by cyclic interactions between actin filaments and the motor enzyme myosin. Conformational changes in the actin-myosin binding interface occur in concert with the binding of ATP, binding to actin, and loss of hydrolytic by-products, but the effects of these conformational changes on the strength of the actomyosin bond are unknown. The force-dependent kinetics of the actomyosin bond may be particularly important at high loads, where myosin may detach from actin before achieving its full power stroke. Here we show that over a physiological range of rapidly applied loads, actomyosin behaves as a "catch" bond, characterized by increasing lifetimes with increasing loads up to a maximum at approximately 6 pN. Surprisingly, we found that the myosin-ADP bond is possessed of longer lifetimes under load than rigor bonds, although the load at which bond lifetime is maximal remains unchanged. We also found that actomyosin bond lifetime is ultimately dependent not only on load, but loading history as well. These data suggest a complex relationship between the rate of actomyosin dissociation and muscle force and shortening velocity. The 6-pN load for maximum bond lifetime is near the force generated by a single myosin molecule during isometric contraction. This raises the possibility that all catch bonds between load-bearing molecules are "mechanokinetically" tuned to their physiological environment.

Actomyosin↗
PubMed1992

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↗
PubMed1991

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↗
PubMed1991

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↗
PubMed2005

Mechanical effects of muscle contraction do not blunt sympathetic vasoconstriction in humans.

Sympathetic vasoconstrictor responses are blunted in the vascular beds of contracting muscle (functional sympatholysis), but the mechanism(s) have been difficult to elucidate. We tested the hypothesis that the mechanical effects of muscle contraction blunt sympathetic vasoconstriction in human muscle. We measured forearm blood flow (Doppler ultrasound) and calculated the reductions in forearm vascular conductance (FVC) in response to reflex increases in sympathetic activity evoked via lower body negative pressure (LBNP). In protocol 1, eight young adults were studied under control resting conditions and during simulated muscle contractions using rhythmic forearm cuff inflations (20 inflations/min) with cuff pressures of 50 and 100 mmHg with the arm below heart level (BH), as well as 100 mmHg with the arm at heart level (HL). Forearm vasoconstrictor responses (%DeltaFVC) during LBNP were -26 +/- 2% during control conditions and were not blunted by simulated contractions (range = -31 +/- 3% to -43 +/- 6%). In protocol 2, eight subjects were studied under control conditions and during rhythmic handgrip exercise (20 contractions/min) using workloads of 15% maximum voluntary contraction (MVC) at HL and BH (similar metabolic demand, greater mechanical muscle pump effect for the latter) and 5% MVC BH alone and in combination with superimposed forearm compressions of 100 mmHg (similar metabolic demand, greater mechanical component of contractions for the latter). The forearm vasoconstrictor responses during LBNP were blunted during 15% MVC exercise with the arm at HL (-1 +/- 3%) and BH (-2 +/- 3%) compared with control (-25 +/- 3%; both P < 0.005) but were intact during both 5% MVC alone (-24 +/- 4%) and with superimposed compressions (-23 +/- 4%). We conclude that mechanical effects of contraction per se do not cause functional sympatholysis in the human forearm and that this phenomenon appears to be coupled with the metabolic demand of contracting skeletal muscle.

Adult↗
PubMed1984

Protein synthesis versus energy state in contracting muscles of perfused rat hindlimb.

The goal of these studies was to evaluate acute changes in protein metabolism in skeletal muscle in response to contractile activity. Rates of protein synthesis were measured by following L-[U-14C]phenylalanine incorporation into protein in muscles of the perfused rat hindlimb at rest, during 10 min of maximal isometric muscle contractions, and during 10 min of recovery. Synthesis measurements were carried out under conditions that ensured that the specific radioactivity of the tRNA-bound precursor amino acid was equal to that of extracellular phenylalanine. Protein degradation was estimated by measuring the release of Nt-methylhistidine. Rates of synthesis were markedly inhibited in response to muscle contractions in tibialis anterior, gastrocnemius, and plantaris but were unaffected in soleus. Rates of synthesis returned toward those observed in the resting condition during the recovery period. Rates of degradation were also markedly inhibited in response to muscle contractions. Decreased rates of synthesis correlated with reduced tissue contents of ATP and creatine phosphate, a reduced ATP/ADP, and an elevated tissue content of lactate. The results demonstrate that isometric contractions in muscles consisting of a high proportion of fast glycolytic fibers result in a marked depression in rates of protein synthesis that may be due to an altered energy state.

Amino Acids↗