General views on the chemistry of muscle contraction.
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[Biochemistry of muscle contraction].
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Adenine Nucleotides↗
Dynamic structural views of muscle contraction and its control.
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Animals↗
Some questions of general importance for the mechanics of muscle contraction.
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Animals↗
[Troponin components and regulation of muscle contraction].
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Animals↗
Selegiline, an MAO-B inhibitor, attenuates airway smooth muscle contraction in the rat trachea.
Selegiline is widely used for Parkinson's disease and sometimes for Alzheimer's disease. It is reported to affect intracellular Ca(2+) concentration. Since intracellular Ca(2+) is partly regulated by phosphatidylinositol (PI) response and is important for smooth muscle contraction, selegiline may affect airway smooth muscle tension. We examined the effects of selegiline on acetylcholine (ACh)- and KCl-induced contractile and PI responses in rat trachea. The trachea was cut into 3-mm-wide ring segments or 1-mm-wide slices. ACh (3 microM, 50% effective dose) or KCl (40 mM) was added, and ring relaxation was induced by the addition of selegiline. Tracheal slices were incubated with [(3)H]myo-inositol and 3 microM ACh in the presence of selegiline, and [(3)H]inositol monophosphate (IP(1)) was measured. Selegiline dose-dependently attenuated ACh- and KCl-induced tracheal ring contractions. Fifty-percent inhibitory doses (ID50) of selegiline against ACh- and KCl-induced contraction were 120 +/- 30 microM and 80 +/- 20 microM, respectively. Basal and ACh-induced IP(1) accumulation were 2.20 +/- 0.20 Bq and 7.88 +/- 0.23 Bq, respectively, and selegiline at a dose of 1000 microM attenuated ACh-induced IP(1) accumulation (5.44 +/- 0.30 Bq). These results suggest that selegiline inhibits contractile responses through the inhibition of voltage-operated Ca(2+) channels and the PI response.
Acetylcholine↗
[Ca2+]-dependent myosin phosphorylation in phorbol diester stimulated smooth muscle contraction.
Phorbol diesters, potent activators of protein kinase C, can produce a slow contraction in arterial smooth muscle. Such observations have prompted proposals that protein kinase C may have direct regulatory functions in contraction. In this paper, we present evidence that [Ca2+]-dependent myosin light chain phosphorylation is responsible for the contraction induced by low-dose phorbol diester and during force development in response to high-dose phorbol diester stimulation. The relationships between myoplasmic [Ca2+], myosin phosphorylation, and steady-state stress induced by low-dose phorbol dibutyrate were similar to those observed with contractile agonists. However, prolonged exposure to high-dose phorbol dibutyrate induced high stress with elevated phosphorylation that was not associated with elevations in aequorin-estimated [Ca2+]. Our results suggest that phorbol diesters can increase myoplasmic [Ca2+], and the resulting increase in myosin phosphorylation quantitatively explains the contraction.
Animals↗
Niels Stensen's geometrical theory of muscle contraction (1667): a reappraisal.
From reading the Elementorum Myologiae Specimen of 1667 by Niels Stensen (Steno), I assert that the text and illustrations contain an observation-based theory on the mechanics of muscle contraction: (1) Based on the study of the structure and motion of several muscles in different animals and in man, Stensen described the contraction of parallel equally long motor fibers formated as uni- or multipennate structures, each forming a parallelepipedon between parallel tendon plates. The parallelepipedon was used as a model allowing Stensen to apply mathematical methods in the argumentation. When the motor fibers contract, the tendons move in parallel planes, the muscle shortens, but the distance between the tendon planes does not change. There will appear a swelling, even if the volume of the model remains the same. Therefore, the swelling observed during contraction, according to Stensen, is no argument for an increase in muscle bulk and no argument against contraction without any change of muscle volume. (2) In the first century after its proposal, different arguments were published against Stensen's theory: in 1680 by Borelli (De Motu Animalium), 1694 by Bernoulli (De Motu Musculorum), 1743 by Boerhaave (Praelectiones), and 1762 by Haller (Elementa Physiologiae). When read today, these arguments are irrelevant, erroneous, or without scientific documentation. However, by the end of the 18th century, Stensen's theory all but disappeared from the science literature. (3) Anatomical and biomechanical studies published after 1980 show that the foundation and applicability of Stensen's theory are still valid. (4) While earlier considered to be perhaps Stensen's weakest work, arguments are presented to reappraise Elementorum as one of Stensen's significant publications and as a significant work in the biomechanical sciences.
Biomechanical Phenomena↗
Enhanced Ca2+ sensitization of the bronchial smooth muscle contraction in antigen-induced airway hyperresponsive rats.
To investigate the alteration in acetylcholine (ACh)-induced increase in Ca2+ sensitization of bronchial smooth muscle contraction concurrent with the airway hyperresponsiveness (AHR), the ACh-induced increases in cytosolic Ca2+ ([Ca2+]) level and contractile response were simultaneously determined by using Fura-2 loaded bronchial smooth muscle. The left main bronchi were isolated from AHR rats which were sensitized and repeatedly challenged with DNP-Ascaris antigen. The tissue ring preparations were incubated in loading solution containing 10 microM Fura-2AM for 3 hr at room temperature. Then the isometrical contraction and [Ca2+]i (F340/F380) were monitored. Although the ACh (10(-3) M)-induced contractile response in AHR group (322 +/- 60 % of 60 mM K+ induced contraction) was significantly greater than that in control animals (173 +/- 15 %, p<0.05), the ACh (10(-3) M)-induced increase in [Ca2+]i was without significant difference between the two groups (128 +/- 15 and 171 +/- 29% of 60 mM K+ -induced increase in [Ca2+]i, respectively). These findings suggest that an augmentation of ACh-induced Ca2+ sensitization may occur in bronchial smooth muscle of the rats with antigen-induced AHR.
Acetylcholine↗
Effects of training with eccentric muscle contractions on exercise performance, energy expenditure, and body temperature.
To study the effects of exercise training with eccentric muscle contractions on body temperatures, energy cost, and performance capacity, six human subjects were tested before and after a 5-week training program of eccentric exercise. Exercise was performed as leg cycling on a motor-driven ergometer at power levels ranging 252-316 W. Training consisted of three sessions/week for 1 h/session. As a result of the training, VO2, fH, and mean skin temperature were lowered for each subject at the same absolute exercise intensities. Ability to continue exercise as indicated by endurance time improved with training. Before training, four subjects terminated exercise after 30 min because of localized leg exhaustion and one subject could not continue longer than 45 min. After training, all six subjects completed 45 min of the exercise test without difficulty. Esophageal and muscle temperatures evidenced no changes as a result of training. It was concluded that the inability of subjects to perform eccentric exercise in the untrained state was not related to muscle temperature.
Adult↗
Healing over and muscle contraction in toad hearts.
The influence of temperature, contractures, and CA²⁺ on the processes of healing over and muscle contraction was investigated in toad myocardium by simultaneously measuring the size of the injury potential and the twitch tension. Stimulation with single pulses and electrically induced contractures of short duration (2-3 seconds) markedly increased the rate of healing, and epinephrine (10⁻⁶ g/ml) increased the effectiveness of stimulation. Other results supported the view that the healing process was largely dependent on temperature, since at 15°C or 10°C the rate of healing over was greatly reduced. The effect of temperature was probably related to a reduction in Ca²⁺ uptake. A possible change in junctional conductance produced by low temperature probably was not the reason for the decrease in rate of healing. Strontium, which replaces Ca²⁺ in the mechanical process, was also a good substitute for Ca²⁺ in healing over. The results stress the parallelism between the healing process and the contractile process in heart muscle.
Action Potentials↗
Reflex stimulation of cardiac sympathetic nerve activity during static muscle contraction in cats.
Reflex response of cardiac sympathetic nerve activity (CSNA) during static contraction of the triceps surae muscle was studied using anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. CSNA increased 48 +/- 13% immediately after the onset of contraction, which was abolished by cutting the L4-S1 dorsal roots. This rapid increase in CSNA preceded rises in heart rate (13 +/- 1 beats/min) and arterial blood pressure (33 +/- 6 mmHg). When tension development was altered by changing the frequency of ventral root stimulation or the initial muscle length, the CSNA increase depended on the tension developed. Passive stretch of the muscle, which primarily activates mechanoreceptors, increased CSNA by 41 +/- 22%. When the contraction was sustained for 5 min, CSNA remained elevated throughout the contraction despite a fall in tension, suggesting that the later increase in CSNA is caused by factors other than a mechanical event of contraction (e.g., metabolic products). Thus it is suggested that cardiac sympathetic outflow is stimulated due to a reflex arising from the contracting muscle. The increase in CSNA at the initiation of contraction is likely to be caused by a reflex from muscle mechanoreceptors, which is followed by a subsequent increase due to a reflex from muscle metaboreceptors.
Animals↗
Involvement of p42/44 MAPK and RhoA protein in augmentation of ACh-induced bronchial smooth muscle contraction by TNF-alpha in rats.
Bronchial asthma is characterized by chronic inflammation of airway tissues and nonspecific airway hyperresponsiveness (AHR), but the underlying mechanisms of AHR have yet to be elucidated. Recently, tumor necrosis factor-alpha (TNF-alpha) has been identified as a proinflammatory cytokine that might be important in the hyperresponsiveness of airway tissue. We have investigated the effects of SB-203580 (a p38 MAPK inhibitor), U-0126 (an inhibitor of p42/44 MAPK activation), and cycloheximide (an inhibitor of protein synthesis) on TNF-alpha-augmented ACh-induced bronchial smooth muscle contraction. We have also investigated the phosphorylation of p42/44 MAPK and upregulation of RhoA protein by TNF-alpha. Treatment of rat bronchial smooth muscles with TNF-alpha (300 and 1,000 ng/ml for 24 h) resulted in a significant upward shift in the concentration-response curve to ACh, but not to high K(+), compared with control tissues. The effect of TNF-alpha was completely blocked by pretreatment with U-0126 or cycloheximide, but not with SB-203580. Immunoblotting demonstrated that p42/44 MAPK was phosphorylated and RhoA protein was increased in bronchial tissue by TNF-alpha. Furthermore, the TNF-alpha-induced upregulation of RhoA protein was abolished by U-0126 pretreatment. In conclusion, we suggest that TNF-alpha might be one of the important mediators involved in the pathogenesis of augmented bronchial smooth muscle contractility in AHR. For the first time, we have demonstrated that augmentation of ACh-induced contractile response evoked by TNF-alpha was mediated by synthesis of protein, such as RhoA, through activation of p42/44, but not p38 MAPK, in rat bronchial smooth muscle.
Acetylcholine↗
Ca2+ activation of smooth muscle contraction: evidence for the involvement of calmodulin that is bound to the triton insoluble fraction even in the absence of Ca2+.
Smooth muscle contraction is activated by phosphorylation of the 20-kDa light chains of myosin catalyzed by Ca(2+)/calmodulin (CaM)-dependent myosin light chain kinase (MLCK). According to popular current theory, the CaM involved in MLCK regulation is Ca(2+)-free and dissociated from the kinase at resting cytosolic free Ca(2+) concentration ([Ca(2+)](i)). An increase in [Ca(2+)](i) saturates the four Ca(2+)-binding sites of CaM, which then binds to and activates actin-bound MLCK. The results of this study indicate that this theory requires revision. Sufficient CaM was retained after skinning (demembranation) of rat tail arterial smooth muscle in the presence of EGTA to support Ca(2+)-evoked contraction, as observed previously with other smooth muscle tissues. This tightly bound CaM was released by the CaM antagonist trifluoperazine (TFP) in the presence of Ca(2+). Following removal of the (Ca(2+))(4)-CaM-TFP(2) complex, Ca(2+) no longer induced contraction. The addition of exogenous CaM to TFP-treated tissue at a [Ca(2+)] subthreshold for contraction or even in the absence of Ca(2+) (presence of 5 mm EGTA), followed by washout of unbound CaM, restored Ca(2+)-induced contraction; this required MLCK activation, since it was blocked by the MLCK inhibitor ML-9. The data suggest, therefore, that a specific pool of cellular CaM, tightly bound to myofilaments at resting [Ca(2+)](i), or even in the absence of Ca(2+), is responsible for activation of contraction following a local increase in [Ca(2+)]. This mechanism would allow for localized changes in [Ca(2+)] in regions of the cell distant from the myofilaments to regulate distinct Ca(2+)-dependent processes without triggering a contractile response. Immobilized CaM, therefore, resembles troponin C, the Ca(2+)-binding regulatory protein of striated muscle, which is also bound to the thin filament in a Ca(2+)-independent manner.
Animals↗
Quantitative evaluation of the silent period, evoked by transcranial magnetic stimulation during sustained muscle contraction, in normal man and in patients with stroke.
It is well known that transcranial stimulation, delivered during sustained muscle contraction, evokes a temporary suppression of motor activity (silent period). The aim of the present study was to further analyze this inhibition in 20 healthy subjects and in 10 patients with previous stroke. Transcranial magnetic stimulation was performed at the vertex, recording responses from first dorsal interosseus (FDI) muscle. Normative data were provided from the control group. The results indicate a narrow range of onset latency, a wide interindividual variation of duration but small interside differences and a sufficient intraindividual stability. As the duration showed an approximately linear increase with increasing stimulus intensities, a standardized paradigm was employed, applying individually adjusted stimulus strengths of 50% above the threshold able to evoke a silent period. There was no relationship between silent period parameters and 1) age, 2) body length, and 3) innervation force. In the patient group, silent period duration was significantly prolonged when recordings were obtained from the affected side. This finding might prove to be an interesting new parameter in the investigation of motor disturbance due to previous stroke. With regard to the physiological basis of the phenomenon, spinal and cortical influences are discussed.
Adolescent↗
A new method for evaluation of intestinal muscle contraction properties: studies in normal subjects and in patients with systemic sclerosis.
Systemic sclerosis is a connective tissue disease that involves the gastrointestinal (GI) tract. Seventy-five per cent of systemic sclerosis patients experience symptoms arising from oesophagus. The intestine has less frequently been subject for studies than the oesophagus. When the small intestine becomes involved, nausea, vomiting, bloating, diarrhoea and malabsorption may occur. Previous studies have shown decreased and abnormal intestinal motility, dilatation and a stiffer wall. The aim was to study muscle mechanics in systemic sclerosis patients using novel analysis of intestinal muscle contraction force-velocity and power. A volume-controlled duodenal ramp-distension protocol was used in nine patients and eight healthy controls. The wall stretch ratio, tension, shortening velocity and muscle power were computed from pressure and cross-sectional area data recorded by an impedance planimetry system. The tension-stretch ratio relation obtained in patients was shifted to the left, indicating a stiffer wall. The in vivo tension-shortening velocity relationship was quantified using Hill's equation. The maximum preload tension (tension at zero velocity) was lower in the patients than in the healthy controls (P < 0.001). The muscle power was lowest in the patients. An association was found between the duration of the disease and the maximum stretch ratio (P < 0.05). The study represents the first data with application of in vivo muscle force-velocity relations in patients with gastrointestinal diseases. Systemic sclerosis patients had increased stiffness and impaired muscle dynamics of the duodenum. Decreased muscle function and increased wall stiffness may explain the GI symptoms reported in this patient group.
Algorithms↗
Stretch of contracting muscle fibres: evidence for regularly spaced active sites along the filaments and enhanced mechanical performance.
Single frog skeletal muscle fibres were stretched during fused tetanic contractions. The force increase during stretch exhibited a breakpoint at a mean critical length change of 16.6 nm per half sarcomere that was independent of stretch velocity and sarcomere length. The early decaying extra force after stretch (component 2) was removed by a small quick release, leaving a longer lasting component (component 3). The amplitude of release required increased with time up to the angle in the force record during stretch, was constant for the remainder of the stretch and decreased with time after the end of stretch; it was consistently less than the critical amplitude of stretch (above). Component 3 occurred at sarcomere lengths above 2.3 microns and was amplitude dependent. The final force after stretch was usually higher than the isometric force at the starting length of the stretch. Non-uniformity as a cause of this component was examined by (a) laser diffraction studies which showed sarcomere stretch at all locations and (b) 0.6-0.7 mm long segments along the entire fibre which all elongated during stretch. After stretch the sarcomeres and segments were significantly more stable than during control isometric tetani. Segments which were clamped by a servo system demonstrated component 3. Shortening during contraction followed by stretch back to the starting length led to nearly as much force enhancement as stretch alone, suggesting that component 3 is not due to a passive elastic element recruited during activation. An increase in temperature decreased components 1 (velocity dependent force during stretch) and 2 but increased component 3. The critical length features of component 2 suggest a cross-bridge mechanism. However, the sarcomere length dependence of all components differs from that of isometric force and from predictions based on filament overlap.
Animals↗
Chronic muscle contraction headache: the importance of depression and anxiety.
Seventy consecutive patients presenting with a clinical diagnosis of chronic muscle contraction headache over a two-year period were evaluated for depression and anxiety scores, along with other possible aetiological factors in this form of headache. Fifty-five of these patients (33 from a hospital neurology clinic and 22 from a local general practice) completed a double-blind study to evaluate flupenthixol 0.5 mg twice daily, diazepam 5 mg twice daily and placebo as prophylactic agents. Patients evaluated in the hospital neurology clinic had more frequent headaches of longer duration, higher analgesic consumption and higher depression, but no higher anxiety scores than those in general practice. Flupenthixol and diazepam were both significantly superior to placebo in reducing headaches and analgesic consumption. The trend was for flupenthixol to be superior to diazepam without reaching statistical significance. Flupenthixol was significantly better than diazepam and placebo in the reduction of Hamilton depression scores. This effect was independent of the effect on headache and analgesic reduction.
Adolescent↗