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PubMed1992

Role of Ia muscle spindle afferents in post-contraction and post-vibration motor effect genesis.

Experiments carried out on 14 human subjects showed that long-lasting involuntary tonic motor responses occurred after the offset of muscle vibration (70 Hz, 0.5 mm, duration 30 s). These post-vibratory biceps and triceps brachii motor responses were compared with the motor responses observed in the same subjects after performing an isometric contraction of the same duration, i.e., post-contraction responses, or the so-called 'Kohnstamm phenomenon'. The results show the existence of close similarities between these two types of motor after-effect, particularly as regards the muscle sites where they develop, their amplitudes and their temporal patterns (latencies and offset times). Neither type of excitatory post-effect can be elicited by co-contracting or co-stimulating two antagonist muscles at the same frequency. Lastly, visual stimulation can cause both types of motor response to switch from one muscle to its antagonist. Comparative analysis of the spindle proprioceptive activities recorded in response to either vibration or isometric contractions suggests that these motor after-effects may both result from the fact that the spindle afferents from agonist and antagonist muscles are asymmetrically activated in these two particular situations.

Electromyography↗

PubMed1988

Differential effects of (-)-norepinephrine and of (+/-)-isoproterenol on cardiac contraction, an uptake phenomenon.

Concentration-dependent inotropic effects of (-)-norepinephrine and of (+/-)-isoproterenol were compared in isometrically contracting guinea pig papillary muscles stimulated at a frequency of 0.2 Hz. (-)-Norepinephrine (0.1-100 mumol/l) elicited a positive inotropic effect that was not antagonized by carbachol, failed to produce a positive inotropic staircase after resumption of stimulation and shortened relaxation time in a concentration-dependent fashion.(+/-)-Isoproterenol had a dual action: at low and moderately effective concentrations (1-30 nmol/l), the positive inotropic effect was antagonized by carbachol, a positive inotropic staircase was elicited and time to peak force was shortened. At (+/-)-isoproterenol concentrations exceeding an EC80 for the positive inotropic effect (greater than 30 nmol/l), relaxation time became shorter, staircase and carbachol-induced antagonism became less pronounced until at 300 nmol/l inotropic effects of (+/-)-isoproterenol resembled closely those of (-)-norepinephrine. Cyclic AMP derivatives and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine mimicked (+/-)-isoproterenol in their inotropic actions. Impairment of neuronal uptake caused (-)-norepinephrine 1) to produce (+/-)-isoproterenol-like effects on the isometric contraction, 2) to induce a positive inotropic staircase and 3) to become sensitive to carbachol-induced antagonism. The results are compatible with the concept that neuronal uptake produces a distribution of (-)-norepinephrine within the papillary muscle which allows predominantly high concentrations of (-)-norepinephrine to become effective in the receptor compartment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Electromyogram changes during sustained contraction after resistance training in women in their 3rd and 8th decades.

The present study aimed at investigating the neuromuscular adaptations to 6 weeks of resistance training in women in their third (6 experimental, 8 controls) and eighth decades (8 experimental, 8 controls). The surface electromyogram (sEMG) was measured from the biceps brachii muscle during constant-force isometric contractions lasting 12 s at 80% of maximal voluntary contraction (MVC). All the signals were analysed adopting in the time domain the root mean square (RMS) as a measure of amplitude and in the frequency domain the median frequency (MDF) of the power spectrum. Quantitative analysis was performed from the 3rd to the 6th second, to describe the early phase of the contraction ("Early"), starting from point at which 80% of the MVC was reached, and from the 9th to the 12th second, to describe the last part of the constant-force sustained contraction ("Late"). After training, the MVC increased by 22.4% in the young (P < 0.0001) and by 13.4% in the older (P < 0.05) women. The "Early" RMS increased by 60.4% with respect to the pre-training condition in the young (P < 0.01) but not in the older women. In contrast, the "Late" RMS increased by 46.7% in the older (P < 0.05) but not in the young women. The MDF remained unchanged in both groups. These results indicate that young and older women showed different training-induced adaptation of the motor unit (MU) activation pattern, in order to keep a constant level of force during a sustained isometric contraction at 80% of MVC.

Adolescent↗

PubMed2004

Peripheral muscle endurance and the oxidative profile of the quadriceps in patients with COPD.

BACKGROUND: Based on previously reported changes in muscle metabolism that could increase susceptibility to fatigue, we speculated that patients with chronic obstructive pulmonary disease (COPD) have reduced quadriceps endurance and that this will be correlated with the proportion of type I muscle fibres and with the activity of oxidative enzymes. METHODS: The endurance of the quadriceps was evaluated during an isometric contraction in 29 patients with COPD (mean (SE) age 65 (1) years; forced expiratory volume in 1 second 37 (3)% predicted) and 18 healthy subjects of similar age. The electrical activity of the quadriceps was recorded during muscle contraction as an objective index of fatigue. The time at which the isometric contraction at 60% of maximal voluntary capacity could no longer be sustained was used to define time to fatigue (Tf). Needle biopsies of the quadriceps were performed in 16 subjects in both groups to evaluate possible relationships between Tf and markers of muscle oxidative metabolism (type I fibre proportion and citrate synthase activity). RESULTS: Tf was lower in patients with COPD than in controls (42 (3) v 80 (7) seconds; mean difference 38 seconds (95% CI 25 to 50), p<0.001). Subjects in both groups had evidence of electrical muscle fatigue at the end of the endurance test. In both groups significant correlations were found between Tf and the proportion of type I fibres and citrate synthase activity. CONCLUSION: Isometric endurance of the quadriceps muscle is reduced in patients with COPD and the muscle oxidative profile is significantly correlated with muscle endurance.

Aged↗

PubMed2002

Genistein attenuates postischemic depressed myocardial function by increasing myofilament Ca2+ sensitivity in rat myocardium.

The present study investigated whether genistein, a broad-spectrum tyrosine kinase inhibitor, could increase the myofilament Ca(2+) sensitivity and partially reverse postischemic depressed myocardial function. Left ventricular papillary muscles were isolated from adult Wistar rats and loaded with the Ca2+ indicator, aequorin. The use of fluorocarbon immersion with hypoxia simulated a model of ischemia. Myofilament responsiveness to Ca2+ was evaluated from force-[Ca2+]i relationship recorded during tetani in papillary muscles. Protein levels of troponin I (TnI) were measured in postischemic papillary muscles with the Western blot technique. Isometric contraction was depressed during the period of ischemia and remained low after 60 min of reoxygenation without a corresponding significant change of peak [Ca2+]i in the control group (n = 7). In contrast, the depression of isometric contraction was ameliorated during ischemia in muscle preparations in the presence of genistein (2 micro M; n = 8), and postischemic depressed myocardial contractility partially recovered after a 60-min reperfusion. The myofilament Ca2+ responsiveness was significantly increased in papillary muscles in the presence of genistein. Protein levels of TnI were reduced in postischemic papillary muscles, whereas genistein partially restored decreased protein levels of TnI. Our results reveal that genistein produces an effective attenuation of postischemic depressed myocardial function and improves myofibrillar Ca2+ responsiveness in rat myocardium.

Actin Cytoskeleton↗

PubMed1993

Increased susceptibility of EDL muscles from mdx mice to damage induced by contractions with stretch.

Absence of dystrophin in mdx muscles may render the muscle more susceptible to damage when submitted to high stress levels. To test this, typically slow (soleus) and fast (EDL) limb muscles of dystrophic (mdx) and normal (C57BL/10) mice were submitted (in vitro) to a series of isometric contractions, followed by a series of contractions with stretches. Muscle injury was assessed by monitoring the force signal. Membrane damage was evaluated by bathing the muscle in Procion Red, a dye that does not penetrate intact fibres, and subsequent analysis by light microscopy. After isometric contractions, only a very small force drop (< 3% of maximal isometric force) was observed which indicated that no injury had occurred in soleus and EDL muscles in either mdx or C57 strains. After contractions with a stretch, a force drop of 10% was observed in soleus muscles from both strains and in EDL muscles from C57 mice. However, in mdx mice EDL muscles displayed an irreversible force drop of 40-60%. Histological analysis of the muscles indicates that force drop is associated with membrane damage. These results show that EDL muscles from mdx mice are more vulnerable than their controls, supporting the structural role hypothesis for dystrophin. Furthermore, they suggest that contractions with stretches may contribute to the muscle damage and degeneration observed in DMD-patients.

Animals↗

PubMed1997

Short- and long-latency reflex responses during different motor tasks in elbow flexor muscles.

Stretch reflex responses in three elbow flexor muscles - the brachioradialis and the short and long heads of the biceps brachii - were studied during different motor tasks. The motor tasks were iso-velocity (8 deg/s) elbow flexion movements in which the muscles performed shortening or lengthening contractions, or were isometric contractions. Care was taken to maintain constant background electromyographic (EMG) activity in the brachoradialis muscle at a 50-deg elbow angle across the tasks by changing the magnitude of the initial load. During each task, mechanical perturbations (duration 170 ms) were applied at pseudorandom intervals when the elbow angle was 50 deg. The magnitude of the perturbation was varied across tasks in order to induce an elbow extension velocity of 80 deg/s over the first 50 ms after the onset of perturbation. The stretch reflex EMG responses in all muscles varied across the three tasks, despite a constant EMG level and similar perturbation-induced angular velocity in the direction of elbow extension. In particular, both the short- and long-latency reflex EMG components were reduced during the lengthening contractions. Further, the task-dependent variations in the early (M2) and the late (M3) components of the long-latency reflex were different, i.e., the magnitude of M3 was considerably enhanced during the shortening task as compared with that of M2. These findings suggest that central modification was responsible for the task-dependent modulation of late EMG responses.

Adult↗

PubMed1991

Dynamic X-ray diffraction of skeletal muscle contraction: structural change of actin filaments.

The X-ray diffraction pattern recorded during contraction shows that the force generation of a muscle proceeds upon interaction of the actin and myosin heads in the incommensurate structural framework of the thin and thick filaments. In this molecular framework the binding of myosin heads to actin filaments is thought to occur on a random basis. Such an actomyosin structure would not produce constructive interference between scattered X-rays from the bound heads and the thin filaments. The characteristic intensity changes of the thin filament layer lines that occur during contraction suggest strongly that the actin structure is varied by interaction with the myosin heads, in a manner that is quite different from that in the rigor state. Variability of the time courses of the intensity changes of the various layer lines indicates that structural change within the thin filament does not take place uniformly and that some different structural processes are involved during contraction At the plateau of isometric contraction, the thin filament structure as a whole assumes a more four-stranded nature due to the changes in the actin structure and tropomyosin position. Our present results imply that the changes of actin structure induced by interaction with myosin heads would be responsible for the regulation as well as force generation in muscle contraction.

Actins↗

PubMed1998

Cocaine augments contractility of the pregnant human uterus by both adrenergic and nonadrenergic mechanisms.

OBJECTIVE: Our purpose was to evaluate the mechanisms of cocaine's effect on both spontaneous and agonist-induced contractility of pregnant human myometrium. STUDY DESIGN: Myometrium was obtained from 42 women at term who were undergoing cesarean section. Myometrial strips were suspended in contraction baths and isometric contractions were measured. Tissue was exposed to various combinations of cocaine, prazosin, desipramine, benzoylecgonine, and procaine. Spontaneous contractility and the contractile responses to increasing concentrations of methoxamine and oxytocin were measured and compared. RESULTS: Cocaine increased spontaneous myometrial contractility by more than threefold. Prazosin, an alpha-adrenergic antagonist, blocked this effect only for the first 35 minutes of exposure. The cumulative concentration-response to the alpha-adrenergic agonist methoxamine was increased by cocaine in terms of both sensitivity and maximal response. The maximal response to oxytocin, but not the sensitivity, was increased by cocaine by an effect that could not be blocked by prazosin. CONCLUSION: Cocaine augments spontaneous and agonist-induced contractility of pregnant human myometrium by mechanisms that appear to be both alpha-adrenergic and nonadrenergic in nature.

Adrenergic alpha-Agonists↗

PubMed2002

Intracellular beta-blockade: overexpression of Galpha(i2) depresses the beta-adrenergic response in intact myocardium.

OBJECTIVE: Increased levels of inhibitory G proteins have been observed in heart failure, but their physiological relevance in mediating the reduced beta-adrenergic response is largely unknown. METHODS: To evaluate the functional consequences of Galpha(i2) overexpression, we studied myocardial contraction in intact isometric contracting cardiac rabbit trabeculae and isolated myocytes after adenovirus-mediated gene transfer of Galpha(i2). RESULTS: Neither Galpha(i2) nor lacZ (control) overexpression altered baseline contractile force. After 72 h of continuous contractions, developed force (F(dev)) increased after addition of 1 microM isoproterenol by 28.5+/-9.7 mN/mm(2) in the control group, which was unchanged from the initial response at t=0 h (23.7+/-3.8 mN/mm(2)). In sharp contrast, in preparations transfected with AdGalpha(i2), the response to isoproterenol was significantly attenuated (5.9+/-2.0 vs. 27.6+/-4.2 mN/mm(2), t=72 vs. 0 h, respectively, P<0.01). In a primary culture of transfected isolated myocytes from a nearly identical baseline, isoproterenol increased cell shortening by 3.1+/-0.6% in the lacZ transfected myocytes, but only by 1.3+/-0.5% in Galpha(i2) transfected myocytes (t=72 h, P<0.01). In Galpha(i2) transfected myocytes, pertussis toxin restored beta-adrenergic responsiveness, indicating specificity of attenuation by the transgene. CONCLUSIONS: Overexpression of Galpha(i2) attenuates the positive inotropic effects of beta-adrenergic stimulation in myocardium. In addition, the method we developed allows investigation of a causal link between altered protein expression and subsequent alterations in contractile function in a physiological relevant in vitro manner.

Adenoviridae↗

PubMed2000

Scalp distribution of the earliest cortical somatosensory evoked potential to tibial nerve stimulation: proposal of a new recording montage.

OBJECTIVE: To investigate the most reliable method to record the earliest cortical somatosensory evoked potential (SEP) after tibial nerve stimulation. The 'gating' phenomenon was used to dissociate the overlapping cortical SEP components. METHODS: In 11 subjects we recorded the scalp SEPs at rest, during the voluntary (active gating) and passive (passive gating) foot movement and during the isometric calf muscle contraction (isometric gating). RESULTS: At the vertex the P40 amplitude was reduced in all the gating conditions. Instead, both the P40 response recorded in the parietal region ipsilateral to the stimulation (indicated as P40par) and the fronto-temporal N37 potential were reduced in amplitude only during the passive foot movement. CONCLUSIONS: The same behaviour of the N37 and P40par potentials suggests that they can represent the opposite counterparts of the same dipolar generator. Instead, the real P40 amplitude, which is affected in all the gating conditions, is recorded at the vertex and might be generated by a different source. We conclude that the montage obtained by referring a temporal electrode contralateral to the stimulation to an ipsilateral parietal lead can reliably record the earliest cortical component (N37/P40par) after tibial nerve stimulation.

Adult↗

PubMed2003

The ACh-induced contraction in rat aortas is mediated by the Cys Lt1 receptor via intracellular calcium mobilization in smooth muscle cells.

1. Our previously published data indicate that an endogenously produced 5-lipoxygenase metabolite can strongly contract isolated endothelium-preserved rat aortic strips when cyclo-oxygenase isoenzymes are inhibited. Therefore, we decided to investigate if cysteinyl-containing leukotrienes (Cys Lts) are involved in this endothelium-dependent contraction. 2. The isometric contraction of endothelium-preserved rat aortic strips was recorded in preparations preincubated with 5 microM indomethacin and precontracted with phenylephrine, adjusting resting tension at 0.7 g. Acetylcholine (ACh) contracted control strips. Montelukast and MK-571, selective type 1 Cys Lts receptor (Cys Lt(1)) antagonists and the Cys Lt(1)/Cys Lt(2) (type 2 Cys Lts receptor) antagonist BAYu9773 dose-dependently prevented ACh-induced contraction, their IC(50)s being 2.2, 3.1 and 7.9 nM respectively. The leukotriene B4 receptor antagonist U75302 was far less potent (IC(50) 1.5 microM). 3. In rat aorta smooth muscle cells (RASMs), Western blot analysis showed the presence of Cys Lt(1) and Cys Lt(2) receptors, the Cys Lt(1) receptor being predominantly expressed. 4. In fura-2 loaded RASMs, LTD4 (0.01-100 nM) and LTC4 (200-800 nM) dose-dependently increased intracellular calcium concentration ([Ca(2+)](i)). Montelukast (1-100 nM) reduced LTD4-induced [Ca(2+)](i) increase, its IC(50) being approximately 10 nM. BAY u9773 exhibited significantly low effectiveness. 5. LTD4 (10 nM) induced a redistribution of smooth muscle actin fibres throughout the cytoplasm as visualized by confocal microscopy. 6. In conclusion, Cys Lt(1) activation by endogenously produced Cys Lts, can contract rat aortas, while Cys Lt(2) only marginally influences aortic tone. Intracellularly, this effect is mediated by an increase in [Ca(2+)](i). Therefore, Cys Lts, by inducing vascular contraction, can contribute to systemic hypertension.

Acetylcholine↗

PubMed2002

The muscular wisdom hypothesis in human muscle fatigue.

The muscular wisdom hypothesis proposed that the slowing of the motor unit discharge rate during sustained maximal isometric contractions serves to minimize fatigue. The purpose of this review is to examine the applicability of the muscular wisdom hypothesis during other forms of contraction, i.e., prolonged submaximal isometric or dynamic contractions.

Humans↗

PubMed1992

Craniomandibular disorders and masticatory muscle function.

The heading craniomandibular disorders covers a wide range of abnormal and pathologic conditions accompanied by orofacial pain and impaired mandibular function, the masticatory muscles and the temporomandibular joints being the structures most frequently involved. Prevalences of severe craniomandibular disorders accompanied by headache and facial pain urgently in need of treatment are 1-2% in children, about 5% in adolescents, and 5-15% in adults, with higher values in women than in men. With respect to physiology and ergonomics, masticatory muscles are comparable to other human skeletal muscles, e.g. of shoulder, neck and lower back. Therefore these muscles share pathogenesis, symptoms and signs of muscular disorders caused by prolonged, low-level static contractions or intermittent isometric contractions at higher levels. Since the same elements of performance in the masticatory muscles are influenced by occlusal factors, they link the development of muscular fatigue, discomfort and pain to the dental occlusion. Furthermore, changes of the occlusal surfaces, e.g. due to dental treatment, may influence the performance of the masticatory muscles, and consequently interfere with local muscular function.

Adolescent↗

PubMed1990

Load and length regulation of cardiac energetics.

Crossbridge cycling and consequent energy utilization during contraction are subject to physiologic regulation by load and length; the length effect on the sensitivity of troponin C to a given [Ca2+]i is an important, newly defined mechanism for this length regulation in cardiac muscle. Further, energy utilization persists throughout the cardiac contraction, demonstrably for isometric contractions initiated at optimal length, and is continuously modulated by length changes during variably loaded twitch contractions. The extent, rate, and time of load-induced length changes during myocardial contraction appear to be the primary variables affecting crossbridge activity and energetics. Load and length regulation of the properties of the heart represents a remarkably simple and direct biological response to the physiologic input and role in this organ. This mechanism is utilized by the heart in response to its dynamic loading environment both for long-term adaptation of cardiac mass to chronic load alterations, as discussed here recently (23), and for short-term adaptation of cardiac mechanics and energetics to instantaneous load alterations, as discussed above. It is probably no coincidence, given their central physiologic importance, that both of these most basic adaptive responses of the heart are simultaneously coming to be understood at the molecular level.

Animals↗

PubMed1990

Enhanced calcium uptake of cardiac sarcoplasmic reticulum in exercise-trained old rats.

To determine whether endurance exercise training initiated during senescence improves the slower calcium transport of cardiac sarcoplasmic reticulum in senescent rats, three groups of male Fischer 344 rats were used: sedentary mature (SM), 11-12 mo of age; sedentary old (SO), 23-24 mo of age; and exercised old (EO), 23-24 mo of age. The EO rats ran on a motor-driven treadmill 5 days/wk for 8-10 wk while two other groups remained sedentary. The contraction duration of isometrically contracting papillary muscle was prolonged in the SO rats compared with the SM group, resulting from both a longer time-to-peak tension and a longer half-relaxation time. Chronic exercise improved the papillary muscle contractile function of the EO group to that observed in the younger SM rats. More importantly, the exercise regime ameliorated the slower oxalate-supported, ATP-dependent calcium transport observed in the SO group so that the EO and SM groups were the same. In contrast, the calcium-activated myosin adenosinetriphosphatase activity, which was slower in the SO group, was not altered after exercise training, so that both senescent groups were slower than the SM rats. Thus the increased calcium transport by the cardiac sarcoplasmic reticulum may be one of the potential mechanisms underlying the improvement of myocardial performance with chronic exercise initiated during senescence.

Aging↗

PubMed1990

Variable series elasticity accounts for Fenn effects of skeletal and cardiac muscles.

The Fenn effect differs between skeletal and cardiac muscles in the magnitude of energy consumption of shortening contraction relative to isometric contraction at the same preload. The former is typically greater than the latter in the skeletal muscle, whereas the former is smaller than the latter in the cardiac muscle. The present theoretical study examined whether the different Fenn effects could be accounted for by different compliances of the series elasticity (SE) in different muscles. A two-element model consisting of an idealized contractile element (CE) and an SE was used. The compliance of the SE was assumed to be variable. Results show that the skeletal Fenn effect can be simulated when SE is stiff and the cardiac Fenn effect can be simulated when SE is compliant. Moreover, when SE is compliant the total work of CE approximates for force-length area, which has been proposed as a measure of the total mechanical energy and shown to correlate linearly with myocardial oxygen consumption.

Biomechanical Phenomena↗

PubMed2003

Elastase-induced suppression of endothelin-mediated Ca2+ entry mechanisms of vascular contraction.

Abdominal aortic aneurysm (AAA) is associated with increased endothelin (ET-1), both systemically and locally in the aorta. Also, elastase activity is increased in human AAA, and elastase perfusion of the aorta induces aneurysm formation in animal models of AAA. However, whether elastase directly affects the ET-1-induced mechanisms of aortic smooth muscle contraction is unclear. Isometric contraction and 45Ca2+ influx were measured in aortic strips isolated from male Sprague-Dawley rats and treated with elastase (5 U/mL). To avoid degradation of the extracellular matrix proteins by elastase, experiments were performed in the presence of elastin (10 mg/mL). In normal Krebs solution (2.5 mmol/L Ca2+), ET-1 (10(-7) mol/L) caused contraction of aortic strips that was inhibited by elastase (5 U/mL). The elastase-induced inhibition of ET-1 contraction was slow in onset (4.6+/-0.4 minutes), time-dependent, complete in 34+/-3 minutes, and reversible. In Ca2+-free Krebs solution, caffeine (25 mmol/L) caused a small contraction that was not inhibited by elastase, suggesting that elastase does not inhibit Ca2+ release from the intracellular stores. Membrane depolarization by 96 mmol/L KCl, which stimulates Ca2+ entry from the extracellular space, caused a contraction that was inhibited by elastase in a concentration-dependent, time-dependent, and reversible fashion. The reversible inhibitory effects of elastase, particularly in the presence of elastin, suggest that they are not due to dissolution of the extracellular matrix or smooth muscle contractile proteins. Elastase also inhibited ET-1 and KCl-induced 45Ca2+ influx. Thus, elastase directly inhibits ET-1-induced Ca2+ entry mechanisms of vascular smooth muscle contraction, which may explain the role of elastase and ET-1 during the development of AAA.

Animals↗